WO2025245127A1

WO2025245127A1 - Spirocyclic dihydropyranopyrimidine kras inhibitors

Info

Publication number: WO2025245127A1
Application number: PCT/US2025/030217
Authority: WO
Inventors: Shawn Cabral; Vincent Mascitti; Ludovic Jacky Gilbert DECULTOT; Jens-Martin HEROLD; Kevin D. HESP; James Paul LAJINESS; Andy Tsai
Original assignee: Treeline Biosciences, Inc
Current assignee: Treeline Biosciences, Inc
Priority date: 2024-05-21
Filing date: 2025-05-20
Publication date: 2025-11-27
Anticipated expiration: 2026-11-21

Abstract

This disclosure provides compounds of Formula ( AA ) Formula ( A ), Formula ( I ) (e.g., Formula ( I-a1 )), Formula ( II ) (e.g., Formula ( II-1 ), ( II-a ), ( II-a1 ), ( II-a2 ), or ( II-a3 )), Formula ( III ) (e.g., Formula ( III-1 )), Formula ( IV ) (e.g., Formula ( IV-a ), ( IV-a1 ), ( IV-b ), ( IV-b1 ), or ( IV-c )), or Formula ( B ) (e.g., Formula ( B-1 )), or pharmaceutically acceptable salts thereof, that inhibit a KRas protein. In some embodiments, the KRas protein has a dysregulation (e.g., the KRas protein is mutated or amplified). These compounds are useful, for example, for treating a disease, disorder, or condition in which increased and/or sustained (e.g., excessive) KRas activation, for example, KRas activation associated with a mutant KRas protein, contributes to the pathology and/or symptoms and/or progression of the disease, disorder, or condition (e.g., cancer) in a subject (e.g., a human). This disclosure also provides compositions containing compounds as disclosed herein, or pharmaceutically acceptable salts thereof, and methods of using and making the same.

Description

Spirocyclic Dihydropyranopyrimidine KRas Inhibitors CROSS-REFERENCE TO RELATED APPLICATIONS This application claims priority to U.S. Provisional Application Serial Nos.63/650,229, filed May 21, 2024; and 63/757,623, filed February 12, 2025, each of which is incorporated by reference in its entirety herein. SEQUENCE LISTING This application contains a Sequence Listing that has been submitted electronically as an XML file named “TRLN-008-021WO1_ST26_SL.XML.” The XML file, created on May 13, 2025, is 2,078 bytes in size. The material in the XML file is hereby incorporated by reference in its entirety. TECHNICAL FIELD This disclosure provides compounds of Formula (AA) Formula (A), Formula (I) (e.g., Formula (I-a1)), Formula (II) (e.g., Formula (II-1), (II-a), (II-a1), (II-a2), or (II-a3)), Formula (III) (e.g., Formula (III-1)), Formula (IV) (e.g., Formula (IV-a), (IV-a1), (IV-b), (IV-b1), or (IV-c)), or Formula (B) (e.g., Formula (B-1)), or pharmaceutically acceptable salts thereof, that inhibit a KRas GTPase (e.g., a KRas GTPase that has a dysregulation (referred to herein as a dysregulated KRas protein)). In some embodiments, the KRas protein is a dysregulated KRas protein that has a mutation (referred to herein as a mutant KRas protein). These compounds are useful, for example, for treating a disease, disorder, or condition in which increased and/or sustained (e.g., excessive) KRas activation, such as KRas activation associated with a mutant KRas protein, contributes to the pathology and/or symptoms and/or progression of the disease, disorder, or condition (e.g., cancer) in a subject (e.g., a human). This disclosure also provides compositions containing compounds of Formula (AA) Formula (A), Formula (I) (e.g., Formula (I-a1)), Formula (II) (e.g., Formula (II-1), (II-a), (II-a1), (II-a2), or (II-a3)), Formula (III) (e.g., Formula (III-1)), Formula (IV) (e.g., Formula (IV-a), (IV-a1), (IV-b), (IV-b1), or (IV- c)), or Formula (B) (e.g., Formula (B-1)), or pharmaceutically acceptable salts thereof, as well as methods of using and making the same. BACKGROUND The KRAS gene is frequently dysregulated (e.g., mutated or amplified) in various human cancers. Oncogenic mutations in KRas typically occur at hotspots in the protein such as at amino acids positions 12, 13, and 61. In some cases, a mutation can lead to maintenance of KRas activation (GTP-bound state), e.g., due to a deficiency of intrinsic GTPase activity and/or insensitivity for GTPase-activating proteins (GAPs) and consequent increased KRas signaling. Specifically, some of the most common protein mutations include those at position 12 (referred to herein as G12X) such as G12A, G12C, G12D, G12R, G12S, and G12V; position 13 (referred to herein as G13X) such as G13C, G13D, and G13V; and Q61 (referred to herein as Q61X), such as Q61E, Q61H, Q61K, Q61L, Q61P, and Q61R. KRas is widely recognized as a target for the design and development of therapies that can specifically bind and inhibit KRas signaling in cancer cells but had long been considered to be undruggable. Currently, there are few approved KRas-targeted therapies. SUMMARY This disclosure provides compounds of Formula (AA) Formula (A), Formula (I) (e.g., Formula (I-a1)), Formula (II) (e.g., Formula (II-1), (II-a), (II-a1), (II-a2), or (II-a3)), Formula (III) (e.g., Formula (III-1)), Formula (IV) (e.g., Formula (IV-a), (IV-a1), (IV-b), (IV-b1), or (IV-c)), or Formula (B) (e.g., Formula (B-1)), or pharmaceutically acceptable salts thereof, that inhibit a KRas protein (e.g., a dysregulated KRas protein, such as a mutant KRas protein). These compounds are useful, for example, for treating a disease, disorder, or condition in which increased KRas activation, such as KRas activation associated with a mutant KRas protein or KRas activation associated with KRas amplification, contributes to the pathology and/or symptoms and/or progression of the disease, disorder, or condition (e.g., cancer) in a subject (e.g., a human). This disclosure also provides compositions containing compounds of Formula (AA) Formula (A), Formula (I) (e.g., Formula (I-a1)), Formula (II) (e.g., Formula (II-1), (II- a), (II-a1), (II-a2), or (II-a3)), Formula (III) (e.g., Formula (III-1)), Formula (IV) (e.g., Formula (IV-a), (IV-a1), (IV-b), (IV-b1), or (IV-c)), or Formula (B) (e.g., Formula (B-1)), or pharmaceutically acceptable salts thereof, as well as methods of using and making the same. Provided herein are compounds of Formula (AA): or pharmaceutically acceptable salts thereof, wherein: Ring B, *, R^4a, R^4b, E¹, R¹, Y², and R³ are as defined herein. Also provided herein are compounds of Formula (A): Formula (A) or pharmaceutically acceptable salts thereof, wherein: Ring B, *, E¹, R¹, Y², and R³ are as defined herein. Also provided herein are compounds of Formula (I): Formula (I) or pharmaceutically acceptable salts thereof, wherein: Ring B, *, R¹, Y², and R³ are as defined herein. Also provided herein are pharmaceutical compositions comprising a compound of Formula (AA) Formula (A), Formula (I) (e.g., Formula (I-a1)), Formula (II) (e.g., Formula (II-1), (II-a), (II-a1), (II-a2), or (II-a3)), Formula (III) (e.g., Formula (III-1)), Formula (IV) (e.g., Formula (IV-a), (IV-a1), (IV-b), (IV-b1), or (IV-c)), or Formula (B) (e.g., Formula (B- 1)), or a pharmaceutically acceptable salt thereof, and a pharmaceutically acceptable carrier. Provided herein are methods for treating cancer in a subject in need thereof, the methods comprising administering to the subject a therapeutically effective amount of a compound of Formula (AA) Formula (A), Formula (I) (e.g., Formula (I-a1)), Formula (II) (e.g., Formula (II-1), (II-a), (II-a1), (II-a2), or (II-a3)), Formula (III) (e.g., Formula (III-1)), Formula (IV) (e.g., Formula (IV-a), (IV-a1), (IV-b), (IV-b1), or (IV-c)), or Formula (B) (e.g., Formula (B- 1)), or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as provided herein. Also provided herein are methods for treating cancer in a subject in need thereof, the methods comprising (a) determining that the cancer has a KRas dysregulation (e.g., a KRas mutation (e.g., a KRas G12A mutation, a KRas G12C mutation, a KRas G12D mutation, a KRas G12R mutation, a KRas G12S mutation, or a KRas G12V mutation)); and (b) administering to the subject a therapeutically effective amount of a compound of Formula (AA) Formula (A), Formula (I) (e.g., Formula (I-a1)), Formula (II) (e.g., Formula (II-1), (II-a), (II- a1), (II-a2), or (II-a3)), Formula (III) (e.g., Formula (III-1)), Formula (IV) (e.g., Formula (IV- a), (IV-a1), (IV-b), (IV-b1), or (IV-c)), or Formula (B) (e.g., Formula (B-1)), or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as provided herein. Provided herein are methods of treating a KRas-associated disease or disorder (e.g., a mutant KRas-associated disease or disorder (e.g., a G12A-associated cancer, a G12C- associated cancer, a KRas G12D-associated cancer, a KRas G12R-associated cancer, a G12S- associated cancer, or a KRas G12V-associated cancer)) in a subject, the methods comprising administering to a subject identified or diagnosed as having a KRas-associated disease or disorder a therapeutically effective amount of a compound of Formula (AA) Formula (A), Formula (I) (e.g., Formula (I-a1)), Formula (II) (e.g., Formula (II-1), (II-a), (II-a1), (II-a2), or (II-a3)), Formula (III) (e.g., Formula (III-1)), Formula (IV) (e.g., Formula (IV-a), (IV-a1), (IV-b), (IV-b1), or (IV-c)), or Formula (B) (e.g., Formula (B-1)), or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as provided herein. This disclosure also provides methods of treating a KRas-associated disease or disorder (e.g., a mutant KRas-associated disease or disorder (e.g., a KRas G12A-associated disease or disorder, a KRas G12C-associated disease or disorder, a KRas G12D-associated disease or disorder, a KRas G12R-associated disease or disorder, a KRas G12S-associated disease or disorder, or a KRas G12V-associated disease or disorder)) in a subject, the methods comprising: determining that the disease or disorder in the subject is a KRas-associated disease or disorder (e.g., a mutant KRas-associated disease or disorder (e.g., a KRas G12A-associated disease or disorder, a KRas G12C-associated disease or disorder, a KRas G12D-associated disease or disorder, a KRas G12R-associated disease or disorder, a KRas G12S-associated disease or disorder, or a KRas G12V-associated disease or disorder)); and administering to the subject a therapeutically effective amount of a compound of Formula (AA) Formula (A), Formula (I) (e.g., Formula (I-a1)), Formula (II) (e.g., Formula (II-1), (II-a), (II-a1), (II-a2), or (II-a3)), Formula (III) (e.g., Formula (III-1)), Formula (IV) (e.g., Formula (IV-a), (IV-a1), (IV-b), (IV-b1), or (IV-c)), or Formula (B) (e.g., Formula (B-1)), or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as provided herein. Further provided herein are methods of treating a KRas-associated cancer (e.g., a mutant KRas-associated cancer (e.g., a G12A-associated cancer, a G12C-associated cancer, a KRas G12D-associated cancer, a KRas G12R-associated cancer, a KRas G12S-associated cancer, or a KRas G12V-associated cancer)) in a subject, the methods comprising administering to a subject identified or diagnosed as having a KRas-associated cancer (e.g., a mutant KRas-associated cancer (e.g., a G12A-associated cancer, a G12C-associated cancer, a KRas G12D-associated cancer, a KRas G12R-associated cancer, a KRas G12S-associated cancer, or a KRas G12V-associated cancer)) a therapeutically effective amount of a compound of Formula (AA) Formula (A), Formula (I) (e.g., Formula (I-a1)), Formula (II) (e.g., Formula (II-1), (II-a), (II-a1), (II-a2), or (II-a3)), Formula (III) (e.g., Formula (III-1)), Formula (IV) (e.g., Formula (IV-a), (IV-a1), (IV-b), (IV-b1), or (IV-c)), or Formula (B) (e.g., Formula (B- 1)), or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as provided herein. This disclosure also provides methods of treating a KRas-associated cancer (e.g., a mutant KRas-associated cancer (e.g., a G12A-associated cancer, a G12C-associated cancer, a KRas G12D-associated cancer, a KRas G12R-associated cancer, a KRas G12S-associated cancer, or a KRas G12V-associated cancer)) in a subject, the methods comprising: determining that the cancer in the subject has a KRas dysregulation (e.g., a KRas G12A mutation, a KRas G12C mutation, a KRas G12D mutation, a KRas G12R mutation, a KRas G12S mutation, or a KRas G12V-mutation)); and administering to the subject a therapeutically effective amount of a compound of Formula (AA) Formula (A), Formula (I) (e.g., Formula (I-a1)), Formula (II) (e.g., Formula (II-1), (II-a), (II-a1), (II-a2), or (II-a3)), Formula (III) (e.g., Formula (III-1)), Formula (IV) (e.g., Formula (IV-a), (IV-a1), (IV-b), (IV-b1), or (IV-c)), or Formula (B) (e.g., Formula (B-1)), or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as provided herein. To facilitate understanding of the disclosure set forth herein, a number of terms are provided. Generally, the nomenclature used herein and the laboratory procedures in organic chemistry, medicinal chemistry, and pharmacology described herein are those well-known and commonly employed in the art. Unless defined otherwise, all technical and scientific terms used herein generally have the same meaning as commonly understood by one of ordinary skill in the art to which this disclosure belongs. Each of the patents, applications, published applications, and other publications that are mentioned throughout the specification and the attached appendices are incorporated herein by reference in their entireties. In the case of conflict between the present disclosure and any content incorporated by reference, the present disclosure controls. The details of one or more embodiments of the invention are set forth in the accompanying drawings and the description below. Other features and advantages of the invention will be apparent from the description and drawings, and from the claims. DETAILED DESCRIPTION This disclosure provides compounds of Formula (AA) Formula (A), Formula (I) (e.g., Formula (I-a1)), Formula (II) (e.g., Formula (II-1), (II-a), (II-a1), (II-a2), or (II-a3)), Formula (III) (e.g., Formula (III-1)), Formula (IV) (e.g., Formula (IV-a), (IV-a1), (IV-b), (IV-b1), or (IV-c)), or Formula (B) (e.g., Formula (B-1)), or pharmaceutically acceptable salts thereof, that inhibit a KRas protein (e.g., a dysregulated KRas protein, such as a mutant KRas protein). These compounds are useful, e.g., for treating a disease, disorder, or condition associated with a KRas dysregulation (e.g., a KRas mutation or amplification) in which increased and/or sustained (e.g., excessive) KRas activation contributes to the pathology and/or symptoms and/or progression of the disease, disorder, or condition (e.g., cancer) in a subject (e.g., a human). These compounds can also be useful, e.g., for treating a disease, disorder, or condition in which a mutant KRas protein (e.g., a resistance mutation) confers intrinsic resistance to one or more KRas inhibitors (e.g., a KRas inhibitor selective for a KRas G12C mutant protein), or to a non-KRas-targeted therapeutic agent. See, e.g., Misale, et al., Nature 486.7404 (2012): 532-536 and Awad, et al., New England Journal of Medicine 384.25 (2021): 2382-2393. This disclosure also provides compositions containing the compounds provided herein as well as methods of using and making the same. Ras family genes (e.g., KRAS, NRAS, and HRAS) were the first oncogenes identified and are some of the most commonly mutated of all discovered oncogenes. See, e.g., Hunter et al. Mol Cancer Res. 2015;13(9):1325-35. The Ras family are guanine nucleotide binding proteins generally found at the inner leaflet of the cell membrane. A wild type Ras protein becomes activated when bound to GTP, but it is inactive when bound to GDP. Normally, growth factors bind to extracellular receptors to induce nucleotide exchange with the help of guanine nucleotide exchange factors (GEF) (e.g., Son of sevenless homolog 1 (SOS1)). These GEFs allow GDP to dissociate from a Ras protein and GTP to bind. Ras proteins can interact with effector proteins such as cRAF when bound to GTP. Hydrolysis of GTP to form GDP can deactivate Ras proteins, and the hydrolysis can be achieved through the intrinsic GTPase activity, which may be enhanced by binding to a GTPase activating protein (GAP). There are 3 major RAS proteins in humans: KRas, HRas, and NRas. Some oncogenic KRas missense mutations can prevent or slow GTP hydrolysis and result in the accumulation of KRas in the active state. Signaling pathways associated with KRas are persistently activated in many cancers, where they participate in cellular growth and proliferation, differentiation, protein synthesis, glucose metabolism, cell survival, and inflammation. Mutant KRas proteins often have altered Raf affinity and/or altered intrinsic GTPase activity. See, for example, Table 1 reproduced from Hunter et al. Mol Cancer Res. 2015;13(9):1325-35. These changes and other factors can contribute to increased KRas signaling in mutant KRas proteins. Table 1 KRas inhibitors are described in, for example, International Publication Nos. WO 2024/112654; WO 2025/064848; WO 2025/038936; WO 2023/154766; WO 2023/143623; WO 2022/240971; WO 2020/236940; WO 2022/115439; WO 2023/086383; WO 2021/093758; WO 2022/135546; WO 2021/139748; WO 2022/251576; and WO 2023/025116. Additional examples of KRas inhibitors are described in, for example, International Publication Nos. WO 2022/132200; WO 2022/133038; WO 2023/150284; WO 2022/261154; WO 2023/183585; WO 2023/099592; WO 2023/099623; WO 2023/099624; WO 2023/099608; WO 2022/250170; WO 2022/173870; WO 2022/236578; WO 2022/237649; WO 2022/248885; WO 2022/256459; WO 2022/258974; WO 2022/266015; WO 2023/018809; WO 2023/018810; WO 2023/018812; WO 2023/020518; WO 2023/020519; WO 2023/020521; WO 2023/020523; WO 2023/046135; WO 2023/061294; WO 2023/097227; WO 2023/114733; WO 2023/137223; WO 2023/141300; WO 2023/138583; WO 2023/159086; WO 2023/159087; WO 2023/173016; WO 2023/173017; WO 2023/179703; WO 2023/125627; WO 2022/216762; WO 2024/030633; WO 2023/230190; and CN 116143806. Compound Embodiments Provided herein are compounds of Formula (AA): or pharmaceutically acceptable salts thereof, wherein: E¹ is N or CH; R¹ is selected from the group consisting of: (a) -H; (b) -N(R²)₂; (c) –N(R²)C(=O)R²; (d) -O-C_1-3 alkyl optionally substituted with 1-3 R^c; (e) C_1-6 alkyl optionally substituted with 1-3 R^c; and (f) -Z⁰–(Z¹)_m1-Z²; each R² is independently selected from the group consisting of: -H and C_1-6 alkyl optionally substituted with 1-3 R^c; Z⁰ is -N(R^f)- or -O-; m1 is 0 or 1; Z¹ is C_1-4 alkylene optionally substituted with 1-3 R^c; Z² is selected from the group consisting of: C3-10 cycloalkyl, 4-10 membered heterocyclyl, and 5-10 membered heteroaryl, each of which is optionally substituted with 1-3 R⁷, wherein: each R⁷ is independently selected from the group consisting of R^a and R^b; Ring B is wherein: the * marks the ring carbon atom common to both Ring B and ; X¹ is selected from the group consisting of a bond, S(O)_0-2, CH₂, CHR^L, C(R^L)₂, and O; X² and X³ are independently selected from the group consisting of: CH₂, CHR^L, C(R^L)2, O, and S(O)0-2, provided that no more than one of X¹, X², and X³ is selected from the group consisting of: O and S(O)_0-2; b1 is 0, 1, 2, or 3; R⁹ is selected from the group consisting of: -H, -OH, -NR^dR^e, and halo; each R¹⁰ is independently selected from the group consisting of R^a and R^b; each R^L is independently selected from the group consisting of C_1-3 alkoxy, -F, -CN, and C_1-3 alkyl optionally substituted with 1-3 R^c; or a pair of R^L on the same or different ring carbon atom(s) taken together with the ring atom(s) connecting them form a C_3-6 cycloalkyl ring; Y² is a bond or straight-chain C_1-6 alkylene optionally substituted with 1-6 R^Y; each R^Y is independently selected from the group consisting of: halo, cyano, -OH, oxo, C_1-6 alkoxy, C_1-6 haloalkoxy, C_1-6 alkyl, and C_1-6 haloalkyl, or a pair of R^Y on the same or different carbon atom(s) taken together with the atom(s) connecting them forms a C_3-6 cycloalkyl ring or 4-6 membered heterocyclyl ring, each of which is optionally substituted with 1-3 independently C_1-3 alkyl; R³ is selected from the group consisting of: (a) 4-15 membered heterocyclyl optionally substituted with 1-6 substituents independently selected from the group consisting of: R^a and R^b; and (b) -NR^dR^e; R^4a and R^4b are independently selected from the group consisting of: -H and C_1-3 alkyl optionally substituted with 1-3 R^c; each R^a is independently selected from the group consisting of: (a) halo; (b) cyano; (c) -OH; (d) oxo; (e) -C_1-6 alkoxy; (f) -C_1-6 haloalkoxy; (g) -NR^dR^e; (h) C(=O)C1-6 alkyl; (i) C(=O)C_1-6 haloalkyl; (j) C(=O)OH; (k) C(=O)OC_1-6 alkyl; (l) C(=O)OC_1-6 haloalkyl; (m) C(=O)N(R^f)₂; (n) S(O)_0-2(C_1-6 alkyl); (o) S(O)_0-2(C_1-6 haloalkyl); (p) S(O)_1-2N(R^f)₂; and (q) C_1-6 alkyl, C_2-6 alkenyl, or C_2-6 alkynyl, each optionally substituted with 1-6 R^c; each R^b is independently selected from the group consisting of: -(L^b)b-R^b1 and -R^b1, wherein: b is 1, 2, or 3; each -L^b is independently selected from the group consisting of: -O-, -N(H)-, -N(C_1-3 alkyl)-, -S(O)_0-2-, C(=O), and C_1-3 alkylene; and each R^b1 is independently selected from the group consisting of: C_3-10 cycloalkyl, 4-10 membered heterocyclyl, C_6-10 aryl, and 5-10 membered heteroaryl, each of which is optionally substituted with 1-3 R^g; each R^c is independently selected from the group consisting of: halo, cyano, -OH, -C_1- ₆ alkoxy, -C_1-6 haloalkoxy, -NR^dR^e, C(=O)C_1-6 alkyl, C(=O)C_1-6 haloalkyl, C(=O)OC_1-6 alkyl, C(=O)OC_1-6 haloalkyl, C(=O)OH, C(=O)N(R^f)₂, S(O)_0-2(C_1-6 alkyl), S(O)_0-2(C_1-6 haloalkyl), and S(O)_1-2N(R^f)₂; each R^d and R^e is independently selected from the group consisting of: H, C(=O)C_1-6 alkyl, C(=O)C_1-6 haloalkyl, C(=O)OC_1-6 alkyl, C(=O)OC_1-6 haloalkyl, C(=O)N(R^f)₂, S(O)_1- ₂(C_1-6 alkyl), S(O)_1-2(C_1-6 haloalkyl), S(O)_1-2N(R^f)₂, and C_1-6 alkyl optionally substituted with 1-3 R^h; each R^f is independently selected from the group consisting of: H and C_1-6 alkyl optionally substituted with 1-3 R^h; each R^g is independently selected from the group consisting of: R^h, C_1-3 alkyl, and C_1- ₃ haloalkyl; and each R^h is independently selected from the group consisting of: halo, cyano, -OH, -C_1- 6 alkoxy, -C1-6 haloalkoxy, -NH2, -N(H)(C1-3 alkyl), and -N(C1-3 alkyl)2-. In some embodiments of Formula (AA), R^4a is selected from the group consisting of: - H and C_1-3 alkyl optionally substituted with -OH or C_1-3 alkoxy. In some embodiments of Formula (AA), R^4b is -H. In some embodiments of Formula (AA), R^4a is selected from the group consisting of: - H and C_1-3 alkyl optionally substituted with -OH or C_1-3 alkoxy; and R^4b is -H. Also provided herein are compounds of Formula (A): Formula (A) or pharmaceutically acceptable salts thereof, wherein: E¹ is N or CH; R¹ is selected from the group consisting of: (a) -H; (b) -N(R²)₂; (c) –N(R²)C(=O)R²; (d) -O-C_1-3 alkyl optionally substituted with 1-3 R^c; (e) C_1-6 alkyl optionally substituted with 1-3 R^c; and (f) -Z⁰–(Z¹)m1-Z²; each R² is independently selected from the group consisting of: -H and C_1-6 alkyl optionally substituted with 1-3 R^c; Z⁰ is -N(R^f)- or -O-; m1 is 0 or 1; Z¹ is C_1-4 alkylene optionally substituted with 1-3 R^c; Z² is selected from the group consisting of: C_3-10 cycloalkyl, 4-10 membered heterocyclyl, and 5-10 membered heteroaryl, each of which is optionally substituted with 1-3 R⁷, wherein: each R⁷ is independently selected from the group consisting of R^a and R^b; Ring B is wherein: the * marks the ring carbon atom common to both Ring B and ; X¹ is selected from the group consisting of a bond, S(O)_0-2, CH₂, CHR^L, C(R^L)₂, and O; X² and X³ are independently selected from the group consisting of: CH₂, CHR^L, C(R^L)₂, O, and S(O)_0-2, provided that no more than one of X¹, X², and X³ is selected from the group consisting of: O and S(O)_0-2; b1 is 0, 1, 2, or 3; R⁹ is selected from the group consisting of: -H, -OH, -NR^dR^e, and halo; each R¹⁰ is independently selected from the group consisting of R^a and R^b; each R^L is independently selected from the group consisting of C_1-3 alkoxy, -F, -CN, and C_1-3 alkyl optionally substituted with 1-3 R^c; or a pair of R^L on the same or different ring carbon atom(s) taken together with the ring atom(s) connecting them form a C_3-6 cycloalkyl ring; Y² is a bond or straight-chain C_1-6 alkylene optionally substituted with 1-6 R^Y; each R^Y is independently selected from the group consisting of: halo, cyano, -OH, oxo, C_1-6 alkoxy, C_1-6 haloalkoxy, C_1-6 alkyl, and C_1-6 haloalkyl, or a pair of R^Y on the same or different carbon atom(s) taken together with the atom(s) connecting them forms a C_3-6 cycloalkyl ring or 4-6 membered heterocyclyl ring, each of which is optionally substituted with 1-3 independently C_1-3 alkyl; R³ is selected from the group consisting of: (a) 4-15 membered heterocyclyl optionally substituted with 1-6 substituents independently selected from the group consisting of: R^a and R^b; and (b) -NR^dR^e; each R^a is independently selected from the group consisting of: (a) halo; (b) cyano; (c) -OH; (d) oxo; (e) -C_1-6 alkoxy; (f) -C_1-6 haloalkoxy; (g) -NR^dR^e; (h) C(=O)C_1-6 alkyl; (i) C(=O)C_1-6 haloalkyl; (j) C(=O)OH; (k) C(=O)OC_1-6 alkyl; (l) C(=O)OC_1-6 haloalkyl; (m) C(=O)N(R^f)₂; (n) S(O)_0-2(C_1-6 alkyl); (o) S(O)_0-2(C_1-6 haloalkyl); (p) S(O)_1-2N(R^f)₂; and (q) C_1-6 alkyl, C_2-6 alkenyl, or C_2-6 alkynyl, each optionally substituted with 1-6 R^c; each R^b is independently selected from the group consisting of: -(L^b)_b-R^b1 and -R^b1, wherein: b is 1, 2, or 3; each -L^b is independently selected from the group consisting of: -O-, -N(H)-, -N(C_1-3 alkyl)-, -S(O)_0-2-, C(=O), and C_1-3 alkylene; and each R^b1 is independently selected from the group consisting of: C_3-10 cycloalkyl, 4-10 membered heterocyclyl, C_6-10 aryl, and 5-10 membered heteroaryl, each of which is optionally substituted with 1-3 R^g; each R^c is independently selected from the group consisting of: halo, cyano, -OH, -C_1- ₆ alkoxy, -C_1-6 haloalkoxy, -NR^dR^e, C(=O)C_1-6 alkyl, C(=O)C_1-6 haloalkyl, C(=O)OC_1-6 alkyl, C(=O)OC_1-6 haloalkyl, C(=O)OH, C(=O)N(R^f)₂, S(O)_0-2(C_1-6 alkyl), S(O)_0-2(C_1-6 haloalkyl), and S(O)_1-2N(R^f)₂; each R^d and R^e is independently selected from the group consisting of: H, C(=O)C1-6 alkyl, C(=O)C_1-6 haloalkyl, C(=O)OC_1-6 alkyl, C(=O)OC_1-6 haloalkyl, C(=O)N(R^f)₂, S(O)_1- 2(C1-6 alkyl), S(O)1-2(C1-6 haloalkyl), S(O)1-2N(R^f)2, and C1-6 alkyl optionally substituted with 1-3 R^h; each R^f is independently selected from the group consisting of: H and C_1-6 alkyl optionally substituted with 1-3 R^h; each R^g is independently selected from the group consisting of: R^h, C_1-3 alkyl, and C_1- ₃ haloalkyl; and each R^h is independently selected from the group consisting of: halo, cyano, -OH, -C_1- ₆ alkoxy, -C_1-6 haloalkoxy, -NH₂, -N(H)(C_1-3 alkyl), and -N(C_1-3 alkyl)₂-. In some embodiments, the compounds of Formula (A) are compounds of Formula (I): Formula (I) or pharmaceutically acceptable salts thereof, wherein: R¹ is selected from the group consisting of: a) -H; b) -N(R²)₂, wherein each R² is independently selected from the group consisting of: H and C_1-6 alkyl optionally substituted with 1-3 R^c; c) -O-C_1-3 alkyl optionally substituted with 1-3 R^c; d) C_1-6 alkyl optionally substituted with 1-3 R^c; and e) -Z⁰–(Z¹)_m1-Z², wherein: Z⁰ is -N(R^f)- or -O-; m1 is 0 or 1; Z¹ is C_1-4 alkylene optionally substituted with 1-3 R^c; Z² is selected from the group consisting of: C_3-10 cycloalkyl, 4-10 membered heterocyclyl, and 5-10 membered heteroaryl, each of which is optionally substituted with 1-3 R⁷, wherein: each R⁷ is independently selected from the group consisting of R^a and R^b; Ring B is wherein: the * marks the ring carbon atom common to both Ring B and ; X¹ is selected from the group consisting of a bond, S(O)_0-2, CH₂, CHR^L, C(R^L)₂, and O; X² and X³ are independently selected from the group consisting of: CH₂, CHR^L, C(R^L)₂, O, and S(O)_0-2, provided that no more than one of X¹, X², and X³ is selected from the group consisting of: O and S(O)_0-2; b1 is 0, 1, 2, or 3; R⁹ is selected from the group consisting of: H, OH, NR^dR^e, and halo; each R¹⁰ is independently selected from the group consisting of R^a and R^b; each R^L is independently selected from the group consisting of C_1-3 alkoxy, -F, CN, and C_1-3 alkyl optionally substituted with 1-3 R^c; a pair of R^L on the same or different ring carbon atom(s) taken together with the ring atom(s) connecting them form a C_3-6 cycloalkyl ring; Y² is a bond or straight-chain C_1-6 alkylene optionally substituted with 1-6 R^Y; each R^Y is independently selected from the group consisting of: halo, cyano, -OH, oxo, C_1-6 alkoxy, C_1-6 haloalkoxy, C_1-6 alkyl, and C_1-6 haloalkyl, or a pair of R^Y on the same or different carbon atom(s) taken together with the atom(s) connecting them forms a C_3-6 cycloalkyl ring or 4-6 membered heterocyclyl ring, each of which is optionally substituted with 1-3 independently selected C_1-3 alkyl; R³ is selected from the group consisting of: (a) 4-15 membered heterocyclyl optionally substituted with 1-6 substituents independently selected from the group consisting of: R^a and R^b; and (b) -NR^dR^e; each R^a is independently selected from the group consisting of: (a) halo; (b) cyano; (c) -OH; (d) oxo; (e) -C_1-6 alkoxy; (f) -C_1-6 haloalkoxy; (g) -NR^dR^e; (h) C(=O)C_1-6 alkyl; (i) C(=O)C_1-6 haloalkyl; (j) C(=O)OH; (k) C(=O)OC_1-6 alkyl; (l) C(=O)OC_1-6 haloalkyl; (m) C(=O)N(R^f)₂; (n) S(O)_0-2(C_1-6 alkyl); (o) S(O)_0-2(C_1-6 haloalkyl); (p) S(O)_1-2N(R^f)₂; and (q) C_1-6 alkyl, C_2-6 alkenyl, or C_2-6 alkynyl, each optionally substituted with 1-6 R^c; each R^b is independently selected from the group consisting of: -(L^b)_b-R^b1 and -R^b1, wherein: b is 1, 2, or 3; each -L^b is independently selected from the group consisting of: -O-, -N(H)-, -N(C_1-3 alkyl)-, -S(O)_0-2-, C(=O), and C_1-3 alkylene; and each R^b1 is independently selected from the group consisting of: C_3-10 cycloalkyl, 4-10 membered heterocyclyl, C_6-10 aryl, and 5-10 membered heteroaryl, each of which is optionally substituted with 1-3 R^g; each R^c is independently selected from the group consisting of: halo, cyano, -OH, -C_1- ₆ alkoxy, -C_1-6 haloalkoxy, -NR^dR^e, C(=O)C_1-6 alkyl, C(=O)C_1-6 haloalkyl, C(=O)OC_1-6 alkyl, C(=O)OC_1-6 haloalkyl, C(=O)OH, C(=O)N(R^f)₂, S(O)_0-2(C_1-6 alkyl), S(O)_0-2(C_1-6 haloalkyl), and S(O)_1-2N(R^f)₂; each R^d and R^e is independently selected from the group consisting of: H, C(=O)C_1-6 alkyl, C(=O)C_1-6 haloalkyl, C(=O)OC_1-6 alkyl, C(=O)OC_1-6 haloalkyl, C(=O)N(R^f)₂, S(O)_1- 2(C1-6 alkyl), S(O)1-2(C1-6 haloalkyl), S(O)1-2N(R^f)2, and C1-6 alkyl optionally substituted with 1-3 R^h; each R^f is independently selected from the group consisting of: H and C1-6 alkyl optionally substituted with 1-3 R^h; each R^g is independently selected from the group consisting of: R^h, C_1-3 alkyl, and C_1- ₃ haloalkyl; and each R^h is independently selected from the group consisting of: halo, cyano, -OH, -C_1- ₆ alkoxy, -C_1-6 haloalkoxy, -NH₂, -N(H)(C_1-3 alkyl), and -N(C_1-3 alkyl)₂-. In some embodiments of Formula (I), R¹ is -Z⁰–(Z¹)m1-Z², wherein: Z⁰ is -N(R^f)-; m1 is 0 or 1; Z¹ is C_1-4 alkylene optionally substituted with 1-3 R^c; Z² is selected from the group consisting of: C_3-10 cycloalkyl and 5-10 membered heteroaryl, each of which is optionally substituted with 1-3 R⁷, wherein: each R⁷ is independently selected from the group consisting of R^a and R^b; Ring B is wherein: X¹ is selected from the group consisting of a bond, S(O)_0-2, CH₂, CHR^L, C(R^L)₂, and O; X² and X³ are independently selected from the group consisting of: CH₂, CHR^L, C(R^L)₂, O, and S(O)_0-2, provided that no more than one of X¹, X², and X³ is selected from the group consisting of: O and S(O)_0-2; b1 is 0, 1, 2, or 3; R⁹ is selected from the group consisting of: H, OH, NR^dR^e, and halo; each R¹⁰ is independently selected from the group consisting of R^a and R^b; each R^L is independently selected from the group consisting of C_1-3 alkoxy, -F, CN, and C_1-3 alkyl optionally substituted with 1-3 R^c; a pair of R^L on the same or different ring carbon atom(s) taken together with the ring atom(s) connecting them form a C_3-6 cycloalkyl ring; Y² is a bond or straight-chain C_1-6 alkylene optionally substituted with 1-6 R^Y; each R^Y is independently selected from the group consisting of: halo, cyano, -OH, oxo, C_1-6 alkoxy, C_1-6 haloalkoxy, C_1-6 alkyl, and C_1-6 haloalkyl, or a pair of R^Y on the same or different carbon atom(s) taken together with the atom(s) connecting them forms a C_3-6 cycloalkyl ring or 4-6 membered heterocyclyl ring, each of which is optionally substituted with 1-3 independently selected C_1-3 alkyl; R³ is selected from the group consisting of: (a) 4-15 membered heterocyclyl optionally substituted with 1-6 substituents independently selected from the group consisting of: R^a and R^b; and (b) -NR^dR^e; each R^a is independently selected from the group consisting of: (a) halo; (b) cyano; (c) -OH; (d) oxo; (e) -C_1-6 alkoxy; (f) -C1-6 haloalkoxy; (g) -NR^dR^e; (h) C(=O)C_1-6 alkyl; (i) C(=O)C_1-6 haloalkyl; (j) C(=O)OH; (k) C(=O)OC_1-6 alkyl; (l) C(=O)OC_1-6 haloalkyl; (m) C(=O)N(R^f)₂; (n) S(O)_0-2(C_1-6 alkyl); (o) S(O)_0-2(C_1-6 haloalkyl); (p) S(O)_1-2N(R^f)₂; and (q) C_1-6 alkyl, C_2-6 alkenyl, or C_2-6 alkynyl, each optionally substituted with 1-6 R^c; each R^b is independently selected from the group consisting of: -(L^b)b-R^b1 and -R^b1, wherein: b is 1, 2, or 3; each -L^b is independently selected from the group consisting of: -O-, -N(H)-, -N(C1-3 alkyl)-, -S(O)_0-2-, C(=O), and C_1-3 alkylene; and each R^b1 is independently selected from the group consisting of: C_3-10 cycloalkyl, 4-10 membered heterocyclyl, C_6-10 aryl, and 5-10 membered heteroaryl, each of which is optionally substituted with 1-3 R^g; each R^c is independently selected from the group consisting of: halo, cyano, -OH, -C_1- ₆ alkoxy, -C_1-6 haloalkoxy, -NR^dR^e, C(=O)C_1-6 alkyl, C(=O)C_1-6 haloalkyl, C(=O)OC_1-6 alkyl, C(=O)OC_1-6 haloalkyl, C(=O)OH, C(=O)N(R^f)₂, S(O)_0-2(C_1-6 alkyl), S(O)_0-2(C_1-6 haloalkyl), and S(O)_1-2N(R^f)₂; each R^d and R^e is independently selected from the group consisting of: H, C(=O)C_1-6 alkyl, C(=O)C_1-6 haloalkyl, C(=O)OC_1-6 alkyl, C(=O)OC_1-6 haloalkyl, C(=O)N(R^f)₂, S(O)_1- ₂(C_1-6 alkyl), S(O)_1-2(C_1-6 haloalkyl), S(O)_1-2N(R^f)₂, and C_1-6 alkyl optionally substituted with 1-3 R^h; each R^f is independently selected from the group consisting of: H and C_1-6 alkyl optionally substituted with 1-3 R^h; each R^g is independently selected from the group consisting of: R^h, C_1-3 alkyl, and C_1- 3 haloalkyl; and each R^h is independently selected from the group consisting of: halo, cyano, -OH, -C_1- ₆ alkoxy, -C_1-6 haloalkoxy, -NH₂, -N(H)(C_1-3 alkyl), and -N(C_1-3 alkyl)₂-. In some embodiments of Formula (AA), Formula (A), or Formula (I), R¹ is selected from the group consisting of: a) -H; b) -N(R²)₂, wherein each R² is independently selected from the group consisting of: H and C_1-6 alkyl optionally substituted with 1-3 R^c; and c) -Z⁰–(Z¹)_m1-Z², wherein: Z⁰ is -N(R^f)-. In some embodiments of Formula (AA), Formula (A), or Formula (I), R¹ is -Z⁰–(Z¹)m1- Z². In some embodiments, Z¹ is -N(R^f)-. In some embodiments of Formula (AA), Formula (A), or Formula (I), Z⁰ is -N(C1-3 alkyl)-, wherein the C_1-3 alkyl portion of -N(C_1-3 alkyl)- is optionally substituted with 1-3 R^h. In some embodiments, Z⁰ is -N(C1-3 alkyl)- (e.g., -NMe-). In some embodiments of Formula (AA), Formula (A), or Formula (I), Z⁰ is -NH-. In some embodiments of Formula (AA), Formula (A), or Formula (I), m1 is 0; and Z² is C_3-10 cycloalkyl optionally substituted with 1-3 R⁷. In some embodiments, Z² is C_3-6 cycloalkyl optionally substituted with 1-3 R⁷, wherein each R⁷ is independently selected from the group consisting of: F, -OH, -CN, and C_1-3 alkyl optionally substituted with 1-3 F. In some embodiments, Z² is cyclopropyl optionally substituted with 1-3 R⁷, wherein each R⁷ is independently selected from the group consisting of: F, -OH, -CN, and C_1-3 alkyl optionally substituted with 1-3 F. In some embodiments, Z² is cyclobutyl optionally substituted with 1-3 R⁷, wherein each R⁷ is independently selected from the group consisting of: F, -OH, -CN, and C_1-3 alkyl optionally substituted with 1-3 F. In some embodiments of Formula (AA), Formula (A), or Formula (I), m1 is 0; and Z² is cyclopropyl or cyclobutyl, each optionally substituted with 1-3 R⁷, wherein each R⁷ is independently selected from the group consisting of: -F, -OH, -CN, and C_1-3 alkyl optionally substituted with 1-3 F. In some embodiments of Formula (AA), Formula (A), or Formula (I), Z² is (e.g., ). For example, Z² can be (e.g., ). In some embodiments of Formula (I), Z² is . In some embodiments of Formula (AA), Formula (A), or Formula (I), Z² is , , or . In some embodiments, each R⁷ is -F. In some embodiments, one R⁷ is -OH; and each remaining R⁷ if present is independently selected from the group consisting of: -F, -OH, -CN, and C_1-3 alkyl optionally substituted with 1-3 F. In some embodiments of Formula (AA), Formula (A), or Formula (I), Z⁰ is -N(C_1-3 alkyl)- (e.g., -NMe-) or -NH-; and Z² is C_3-6 cycloalkyl optionally substituted with 1-3 R⁷, wherein each R⁷ is independently selected from the group consisting of: -F, -OH, -CN, and C_1- ₃ alkyl optionally substituted with 1-3 F. In some embodiments, each R⁷ is -F. In some embodiments, one R⁷ is -OH; and each remaining R⁷ if present is independently selected from the group consisting of: -F, -OH, -CN, and C_1-3 alkyl optionally substituted with 1-3 F. In some embodiments of Formula (AA), Formula (A), or Formula (I), m1 is 0; and Z² is cyclopropyl or cyclobutyl, each optionally substituted with 1-3 R⁷, wherein each R⁷ is independently selected from the group consisting of: -F, -OH, -CN, and C_1-3 alkyl optionally substituted with 1-3 F. In some embodiments, each R⁷ is -F. In some embodiments, one R⁷ is -OH; and each remaining R⁷ if present is independently selected from the group consisting of: -F, -OH, -CN, and C1-3 alkyl optionally substituted with 1-3 F. In some embodiments of Formula (AA), Formula (A), or Formula (I), Z¹ is C1-3 alkylene optionally substituted with 1-2 R^c; and Z² is selected from the group consisting of: 4- 10 membered heterocyclyl and 5-10 membered heteroaryl, each of which is optionally substituted with 1-3 R⁷. In some embodiments of Formula (AA), Formula (A), or Formula (I), Z¹ is C_1-3 alkylene; and Z² is selected from the group consisting of: 4-6 membered heterocyclyl and 5- membered heteroaryl, each of which is optionally substituted with 1-2 R⁷. In some embodiments, Z² is selected from the group consisting of: tetrahydrofuranyl, piperidinyl, isoxazolyl, oxazolyl, and pyrazolyl, each of which is optionally substituted with 1-2 R⁷, wherein each R⁷ is independently selected from the group consisting of: -F, -OH, oxo, -CN, and C_1-3 alkyl optionally substituted with 1-3 F. For example, Z² can be selected from the group consisting of: tetrahydrofuranyl, isoxazolyl, and oxazolyl. In some embodiments of Formula (AA), Formula (A), or Formula (I), Z⁰ is -N(C_1-3 alkyl)-, wherein the C_1-3 alkyl portion of -N(C_1-3 alkyl)- is optionally substituted with 1-3 R^h; m1 is 0; and Z² is C_3-6 cycloalkyl optionally substituted with 1-3 R⁷, wherein each R⁷ is independently selected from the group consisting of: F, -OH, -CN, and C_1-3 alkyl optionally substituted with 1-3 F. In some embodiments of Formula (AA), Formula (A), or Formula (I), Z⁰ is -N(C_1-3 alkyl)-, wherein the C_1-3 alkyl portion of -N(C_1-3 alkyl)- is optionally substituted with 1-3 R^h; m1 is 0; and Z² is cyclopropyl optionally substituted with 1-3 R⁷, wherein each R⁷ is independently selected from the group consisting of: F, -OH, -CN, and C1-3 alkyl optionally substituted with 1-3 F. In some embodiments of Formula (AA), Formula (A), or Formula (I), Z⁰ is -N(C_1-3 alkyl)-, wherein the C_1-3 alkyl portion of -N(C_1-3 alkyl)- is optionally substituted with 1-3 R^h; m1 is 0; and Z² is (e.g., ). For example, Z² can be (e.g., ). In some embodiments of Formula (AA), Formula (A), or Formula (I), m1 is 1; Z¹ is C_1-3 alkylene optionally substituted with 1-2 R^c; and Z² is 5-10 membered heteroaryl, which is optionally substituted with 1-3 R⁷. In some embodiments of Formula (AA), Formula (A), or Formula (I) when m1 is 1, Z¹ is C_1-3 alkylene (e.g., C_2-3 alkylene); and Z² is 6-membered heteroaryl, which is substituted with one NH2 and further optionally substituted with 1-2 R⁷. In some embodiments of Formula (AA), Formula (A), or Formula (I) when m1 is 1, Z¹ is ; and Z² is pyridyl (e.g., 3-pyridyl), which is substituted with one NH₂ and further optionally substituted with 1-2 R⁷. For example, Z² can be . In some embodiments of Formula (AA), Formula (A), or Formula (I), Z⁰ is -N(C_1-3 alkyl)-, wherein the C_1-3 alkyl portion of -N(C_1-3 alkyl)- is optionally substituted with 1-3 R^h; m1 is 1; Z¹ is C_1-3 alkylene (e.g., C_2-3 alkylene); and Z² is 6-membered heteroaryl, which is substituted with one NH2 and further optionally substituted with 1-2 R⁷. In some embodiments of Formula (AA), Formula (A), or Formula (I), Z⁰ is -N(C_1-3 alkyl)-, wherein the C_1-3 alkyl portion of -N(C_1-3 alkyl)- is optionally substituted with 1-3 R^h; m1 is 1; Z¹ is ; and Z² is pyridyl (e.g., 3-pyridyl), which is substituted with one NH2 and further optionally substituted with 1-2 R⁷. For example, Z² can be . In some embodiments of Formula (AA), Formula (A), or Formula (I), R¹ is -N(H)-Z² or -N(C_1-3 alkyl)-Z², wherein Z² is a C_3-6 cycloalkyl optionally substituted with 1-3 R⁷, wherein: one R⁷ is -OH; and each remaining R⁷ if present is independently selected from the group consisting of: - F, -OH, -CN, and C_1-3 alkyl optionally substituted with 1-3 F. In some embodiments, Z² is C_3- ₆ cycloalkyl substituted with one -OH (e.g., Z² is or ). In some embodiments of Formula (AA), Formula (A), or Formula (I), R¹ is -N(R²)₂. In some embodiments of Formula (AA), Formula (A), or Formula (I), each R² is an independently selected C_1-3 alkyl optionally substituted with 1-3 R^c. In some embodiments of Formula (AA), Formula (A), or Formula (I), each R² is independently methyl or ethyl, each optionally substituted with 1-3 R^c, wherein each R^c present on R² is independently selected from the group consisting of: -F, cyano, -OH, -C_1-6 alkoxy, and -C_1-6 haloalkoxy. In some embodiments of Formula (AA), Formula (A), or Formula (I), R¹ is -N(Me)₂, - N(Et)₂, or -N(Me)Et. In some embodiments of Formula (AA), Formula (A), or Formula (I), R¹ is -N(R²)₂; and one R² is a C_2-6 alkyl substituted with -OH. In some embodiments, the other R² is -H or C_1-3 alkyl (e.g., -H or methyl). In some embodiments of Formula (AA), Formula (A), or Formula (I), R¹ is -H. In some embodiments of Formula (AA), Formula (A), or Formula (I), X¹ is selected from the group consisting of: CH2, CHR^L, and C(R^L)2. For example, X¹ can be CH2. In some embodiments of Formula (AA), Formula (A), or Formula (I), X¹ is a bond. In some embodiments of Formula (AA), Formula (A), or Formula (I), X² and X³ are independently selected from the group consisting of: CH₂, CHR^L, and C(R^L)₂. In some embodiments of Formula (AA), Formula (A), or Formula (I), X² and X³ are both CH₂. In some embodiments of Formula (AA), Formula (A), or Formula (I), X² is CH₂; and X³ is selected from the group consisting of: CHR^L and C(R^L)₂. In some embodiments of Formula (AA), Formula (A), or Formula (I), X² is CH₂; and X³ is CHR^L. For example, X² can be CH₂; and X³ can be CHMe. In some embodiments of Formula (AA), Formula (A), or Formula (I), one of X² and X³ is -O-; and the other of X² and X³ is selected from the group consisting of: CH₂, CHR^L, and C(R^L)₂. In some embodiments, X² is -O-; and X³ is CH₂ or CHMe. In some embodiments of Formula (AA), Formula (A), or Formula (I), R⁹ is para to - X³-. In some embodiments of Formula (AA), Formula (A), or Formula (I), R⁹ is -OH or - NH₂. For example, R⁹ can be -NH₂. In some embodiments, the compounds of Formula (I) are compounds of Formula (I- a1): Formula (I-a1) or pharmaceutically acceptable salts thereof, wherein: X¹ is a bond or CH₂; X² and X³ are independently selected from the group consisting of: CH₂, CHR^L, and C(R^L)₂; and b1 is 0, 1, or 2 (e.g., 0 or 1). In some embodiments of Formula (I-a1), X¹ is a bond. In some embodiments of Formula (I-a1), X¹ is CH₂. In some embodiments of Formula (I-a1), X² and X³ are independently selected from the group consisting of: CH₂, CHR^L, and C(R^L)₂. In some embodiments of Formula (I-a1), X² and X³ are both CH₂. In some embodiments of Formula (I-a1), X² is CH₂; and X³ is selected from the group consisting of: CHR^L and C(R^L)₂. For example, X² can be CH₂; and X³ can be CHMe. In some embodiments of Formula (I-a1), X¹ is CH₂; and X² and X³ are independently selected from the group consisting of: CH₂, CHR^L, and C(R^L)₂. In some embodiments, X² and X³ are both CH₂. In some embodiments, X² is CH₂; and X³ is selected from the group consisting of: CHR^L and C(R^L)₂. In some embodiments of Formula (I-a1), X¹ is CH₂; one of X² and X³ is -O-; and the other of X² and X³ is selected from the group consisting of: CH₂, CHR^L, and C(R^L)₂. In some embodiments, X² is -O-; and X³ is CH₂ or CHMe. In some embodiments of Formula (AA), Formula (A), or Formula (I) (e.g., Formula (I- a1)), b1 is 0, 1, or 2. In some embodiments of Formula (AA), Formula (A), or Formula (I) (e.g., Formula (I- a1)), b1 is 1 or 2. In some embodiments of Formula (AA), Formula (A), or Formula (I) (e.g., Formula (I- a1)), b1 is 1 or 2; and each R¹⁰ is independently selected from the group consisting of: -Cl, -F, -CN, and C_1-3 alkyl optionally substituted with 1-3 R^c. In some embodiments of Formula (AA), Formula (A), or Formula (I) (e.g., Formula (I- a1)), b1 is 1; R¹⁰ is ortho to R⁹; and R¹⁰ is -CN. In some embodiments of Formula (AA), Formula (A), or Formula (I) (e.g., Formula (I- a1)), b1 is 1; and R¹⁰ is -CN. In some embodiments of Formula (AA), Formula (A), or Formula (I) (e.g., Formula (I- a1)), b1 is 1 or 2; and each R¹⁰ is independently -Cl or -F. In some embodiments of Formula (AA), Formula (A), or Formula (I) (e.g., Formula (I- a1)), b1 is 1 or 2; 1-2 occurrence(s) of R¹⁰ is ortho to R⁹; and each R¹⁰ is independently -Cl or -F. In some embodiments of Formula (AA), Formula (A), or Formula (I) (e.g., Formula (I- a1)), Ring B is selected from the group consisting of: , , and , wherein: X² is -O- or -CH₂-; X³ is -CH₂- or -CHR^L-, wherein R^L is C_1-3 alkyl (e.g., methyl); and each R¹⁰ is independently selected from the group consisting of: -Cl, -F, -CN, and C_1-3 alkyl optionally substituted with 1-3 R^c. In some embodiments of Formula (AA), Formula (A), or Formula (I) (e.g., Formula (I- a1)), Ring B is selected from the group consisting of: and , wherein: X² is -O- or -CH₂-; X³ is -CH₂- or -CHR^L-, wherein R^L is C_1-3 alkyl (e.g., methyl); and each R¹⁰ is independently selected from the group consisting of: -Cl, -F, -CN, and C_1-3 alkyl optionally substituted with 1-3 R^c. In some embodiments of Formula (AA), Formula (A), or Formula (I) (e.g., Formula (I- a1)), Ring B is selected from the group consisting of: , , , , , , , and . In some embodiments of Formula (AA), Formula (A), or Formula (I) (e.g., Formula (I- a1)), Ring B is , wherein X³ is -CH₂- or -CHR^L-; and R^L is C_1-3 alkyl optionally substituted with 1-3 -F. In some embodiments, X³ is -CHR^L-. In some embodiments, R^L is methyl. In some embodiments of Formula (AA), Formula (A), or Formula (I) (e.g., Formula (I- a1)), Y² is -CH₂-. In some embodiments of Formula (AA), Formula (A), or Formula (I) (e.g., Formula (I- a1)), R³ is a 4-10 membered heterocyclyl optionally substituted with 1-6 substituents independently selected from the group consisting of: R^a and R^b. In some embodiments of Formula (AA), Formula (A), or Formula (I) (e.g., Formula (I- a1)), R³ is a 4-10 membered heterocyclyl having one ring nitrogen atom and 0-1 additional ring heteroatom selected from the group consisting of oxygen and nitrogen, wherein the heterocyclyl is optionally substituted with 1-6 R^a. In some embodiments of Formula (AA), Formula (A), or Formula (I) (e.g., Formula (I- a1)), R³ is a bicyclic 7-10 membered heterocyclyl optionally substituted with 1-6 R^a. In some embodiments of Formula (AA), Formula (A), or Formula (I) (e.g., Formula (I- a1)), R³ is optionally substituted with 1-3 R^a. In some embodiments of Formula (AA), Formula (A), or Formula (I) (e.g., Formula (I- a1)), R³ is optionally substituted with 1-3 substituents independently selected from the group consisting of: -F, -C_1-3 alkoxy, -C_1-3 haloalkoxy, and -OH. In some embodiments of Formula (AA), Formula (A), or Formula (I) (e.g., Formula (I- a1)), R³ is (e.g., ). In some embodiments of Formula (AA), Formula (A), or Formula (I) (e.g., Formula (I- a1)), the ring carbon atom labelled with * in Formula (I) has (S)-stereochemistry. In some embodiments, the compounds of Formula (I) are compounds of Formula (II): Formula (II) or pharmaceutically acceptable salts thereof, wherein: X¹ is selected from the group consisting of a bond, S(O)_0-2, CH₂, CHR^L, C(R^L)₂, and O; X² and X³ are independently selected from the group consisting of: CH₂, CHR^L, C(R^L)₂, O, and S(O)_0-2, provided that no more than one of X¹, X², and X³ is selected from the group consisting of: O and S(O)_0-2; b1 is 1 or 2; each R¹⁰ is independently selected from the group consisting of R^a and R^b; and each R^L is independently selected from the group consisting of C_1-3 alkoxy, -F, CN, and C_1-3 alkyl optionally substituted with 1-3 R^c; or one pair of R^L on the same or different ring carbon atom(s) taken together with the ring atom(s) connecting them form a C_3-6 cycloalkyl ring. In some embodiments, the compounds of Formula (I) (e.g., Formula (II)) are compounds of Formula of Formula (II-a): Formula (II-a) or pharmaceutically acceptable salts thereof, wherein: b4 is 0 or 1; and each R¹⁰ is independently selected from the group consisting of: -Cl, -F, -CN, and C_1-3 alkyl optionally substituted with 1-3 R^c. In some embodiments of Formula (II-a), b4 is 0. In some embodiments, the compounds of Formula (I) are compounds of Formula (III): Formula (III) or pharmaceutically acceptable salts thereof, wherein: X¹ is selected from the group consisting of a bond, S(O)_0-2, CH₂, CHR^L, C(R^L)₂, and O; X² and X³ are independently selected from the group consisting of: CH₂, CHR^L, C(R^L)₂, O, and S(O)_0-2, provided that no more than one of X¹, X², and X³ is selected from the group consisting of: O and S(O)_0-2; R⁹ is selected from the group consisting of: H, NR^dR^e, -OH, and halo; b4 is 0 or 1; each R¹⁰ is independently selected from the group consisting of R^a and R^b; and each R^L is independently selected from the group consisting of C_1-3 alkoxy, -F, CN, and C1-3 alkyl optionally substituted with 1-3 R^c; or one pair of R^L on the same or different ring carbon atom(s) taken together with the ring atom(s) connecting them form a C3-6 cycloalkyl ring. In some embodiments of Formula (III), R⁹ is -NH₂; and each R¹⁰ is independently selected from the group consisting of: -Cl, -F, -CN, and C_1-3 alkyl optionally substituted with 1-3 R^c. In some embodiments of Formula (II), (II-a), or (III), X¹ is CH₂ or CHR^L (e.g., CH₂). In some embodiments of Formula (II), (II-a), or (III), X² and X³ are independently selected from the group consisting of: CH₂, CHR^L, and C(R^L)₂. In some embodiments of Formula (II), (II-a), or (III), X¹ is CH₂; and X² and X³ are both CH₂. In some embodiments of Formula (II), (II-a), or (III), at least one (e.g., one) of X¹, X², and X³ is selected from the group consisting of: CHR^L and C(R^L)₂. In some embodiments, each R^L is independently selected from the group consisting of: CH₃, CF₃, CHF₂, and CH₂F. In some embodiments of Formula (II), (II-a), or (III), one of X¹, X², and X³ is CHR^L; and each remaining of X¹, X², and X³ is CH₂. In some embodiments, X¹ is CH₂; and X² and X³ are independently selected from the group consisting of: CH₂, CHR^L, and C(R^L)_2, provided that 1-2 of X² and X³ is independently CHR^L or C(R^L)₂. In some embodiments, each R^L is independently selected from the group consisting of: CH₃, CF₃, CHF₂, and CH₂F. In some embodiments of Formula (II), (II-a), or (III), X¹ is CH₂; X² is CH₂; and X³ is CHR^L. In some embodiments, each R^L is independently selected from the group consisting of: CH₃, CF₃, CHF₂, and CH₂F. For example, each R^L can be CH₃. In some embodiments of Formula (II), (II-a), or (III), X¹ is CH₂; X² is CH₂; and X³ is CHMe or CH₂ (e.g., CHMe). In some embodiments, the compounds of Formula (I) are compounds of Formula (IV): Formula (IV) or pharmaceutically acceptable salts thereof, wherein: X¹ is selected from the group consisting of a bond, S(O)_0-2, CH₂, CHR^L, C(R^L)₂, and O; X² and X³ are independently selected from the group consisting of: CH₂, CHR^L, C(R^L)₂, O, and S(O)_0-2, provided that at least one of X¹, X², and X³ is CHR^L or C(R^L)₂; further provided that no more than one of X¹, X², and X³ is selected from the group consisting of: O and S(O)_0-2; b1 is 0, 1 or 2; R⁹ is selected from the group consisting of: H, OH, NR^dR^e, and halo; each R¹⁰ is independently selected from the group consisting of R^a and R^b; and each R^L is independently selected from the group consisting of C_1-3 alkoxy, -F, CN, and C_1-3 alkyl optionally substituted with 1-3 R^c. In some embodiments, the compounds of Formula (I) (e.g., Formula (IV)) are compounds of Formula (IV-a): Formula (IV-a) or pharmaceutically acceptable salts thereof, wherein: each R¹⁰ is independently selected from the group consisting of: -Cl, -F, -CN, and C_1-3 alkyl optionally substituted with 1-3 R^c. In some embodiments of Formula (IV) or (IV-a), b1 is 1; and R¹⁰ is -CN. In some embodiments, the compounds of Formula (I) (e.g., Formula (IV)) are compounds of Formula (IV-b): Formula (IV-b) or pharmaceutically acceptable salts thereof, wherein: b4 is 0 or 1; and each R¹⁰ is independently selected from the group consisting of: -Cl, -F, -CN, and C_1-3 alkyl optionally substituted with 1-3 R^c. In some embodiments of Formula (IV-b), b4 is 0. In some embodiments of Formula (IV-b), R⁹ is NH₂. In some embodiments of Formula (IV), (IV-a), or (IV-b), X¹ is CH₂. In some embodiments of Formula (IV), (IV-a), or (IV-b), X² is CH₂; and X³ is CHR^L. In some embodiments of Formula (IV), (IV-a), or (IV-b), X² is -O-; and X³ is selected from the group consisting of: CHR^L and C(R^L)₂. In some embodiments of Formula (IV), (IV-a), or (IV-b), each R^L is independently selected from the group consisting of: CH₃, CF₃, CHF₂, and CH₂F. For example, each R^L can be CH3. In some embodiments of Formula (IV), (IV-a), or (IV-b), X¹ is CH₂; X² is CH₂; and X³ is CH(Me). In some embodiments, the compounds of Formula (IV) are compounds of Formula (IV- c): Formula (IV-c) or pharmaceutically acceptable salts thereof, wherein: b4 is 0 or 1; and each R¹⁰ is independently selected from the group consisting of: -Cl, -F, -CN, and C_1-3 alkyl optionally substituted with 1-3 R^c. In some embodiments of Formula (IV-c), R^L is CH₃. In some embodiments of Formula (IV-c), b4 is 0. In some embodiments of Formula (II) (e.g., Formula (II-a)), Formula (III), or Formula (IV) (e.g., Formula (IV-a), (IV-b), or (IV-c)), R¹ is -Z⁰–(Z¹)_m1-Z², wherein Z⁰ is -N(C_1-3 alkyl)- (e.g., -NMe-) or -NH-; and Z² is C_3-6 cycloalkyl optionally substituted with 1-3 R⁷, wherein each R⁷ is independently selected from the group consisting of: -F, -OH, -CN, and C_1- ₃ alkyl optionally substituted with 1-3 F. In some embodiments, each R⁷ is -F. In some embodiments, one R⁷ is -OH; and each remaining R⁷ if present is independently selected from the group consisting of: -F, -OH, -CN, and C_1-3 alkyl optionally substituted with 1-3 F. In some embodiments of Formula (II) (e.g., Formula (II-a)), Formula (III), or Formula (IV) (e.g., Formula (IV-a), (IV-b), or (IV-c)), m1 is 0; and Z² is cyclopropyl or cyclobutyl, each optionally substituted with 1-3 R⁷, wherein each R⁷ is independently selected from the group consisting of: -F, -OH, -CN, and C1-3 alkyl optionally substituted with 1-3 F. In some embodiments, each R⁷ is -F. In some embodiments, one R⁷ is -OH; and each remaining R⁷ if present is independently selected from the group consisting of: -F, -OH, -CN, and C_1-3 alkyl optionally substituted with 1-3 F. In some embodiments of Formula (II) (e.g., Formula (II-a)), Formula (III), or Formula (IV) (e.g., Formula (IV-a), (IV-b), or (IV-c)), R¹ is -N(H)-Z² or -N(C_1-3 alkyl)-Z², wherein Z² is C_3-6 cycloalkyl optionally substituted with 1-3 R⁷, wherein: one R⁷ is -OH; and each remaining R⁷, if present, is independently selected from the group consisting of: - F, -OH, -CN, and C_1-3 alkyl optionally substituted with 1-3 F. In some embodiments, Z² is C_3- ₆ cycloalkyl substituted with one -OH (e.g., Z² is or ). In some embodiments of Formula (II) (e.g., Formula (II-a)), Formula (III), or Formula (IV) (e.g., Formula (IV-a), (IV-b), or (IV-c)), R¹ is -N(R²)₂. In some embodiments of Formula (II) (e.g., Formula (II-a)), Formula (III), or Formula (IV) (e.g., Formula (IV-a), (IV-b), or (IV-c)), each R² is independently methyl or ethyl, each of which is optionally substituted with 1-3 R^c, wherein each R^c present on R² is independently selected from the group consisting of: -F, cyano, -OH, -C_1-6 alkoxy, and -C_1-6 haloalkoxy. In some embodiments of Formula (II) (e.g., Formula (II-a)), Formula (III), or Formula (IV) (e.g., Formula (IV-a), (IV-b), or (IV-c)), R¹ is -N(Me)₂, -N(Et)₂, or -N(Me)Et. In some embodiments of Formula (II) (e.g., Formula (II-a)), Formula (III), or Formula (IV) (e.g., Formula (IV-a), (IV-b), or (IV-c)), R¹ is -N(R²)2; one R² is a C2-6 alkyl substituted with -OH; and the other R² is -H or C_1-3 alkyl (e.g., -H or methyl). In some embodiments, one R² is or ; and the other R² is -H or methyl. In some embodiments of Formula (II) (e.g., Formula (II-a)), Formula (III), or Formula (IV) (e.g., Formula (IV-a), (IV-b), or (IV-c)), Y² is -CH₂-; and R³ is a 4-10 membered heterocyclyl having one ring nitrogen atom and 0-1 additional ring heteroatom selected from the group consisting of oxygen and nitrogen, wherein the heterocyclyl is optionally substituted with 1-6 R^a. In some embodiments of Formula (II) (e.g., Formula (II-a)), Formula (III), or Formula (IV) (e.g., Formula (IV-a), (IV-b), or (IV-c)), Y² is -CH₂-; and R³ is optionally substituted with 1-3 substituents independently selected from the group consisting of: -F, -C_1- ₃ alkoxy, -C_1-3 haloalkoxy, and -OH. In some embodiments of Formula (II) (e.g., Formula (II-a)), Formula (III), or Formula (IV) (e.g., Formula (IV-a), (IV-b), or (IV-c)), Y² is -CH₂-; and R³ is optionally substituted with 1-2 substituents independently selected from the group consisting of: -F, -C_1- ₆ alkoxy, and -C_1-6 haloalkoxy. In some embodiments of Formula (II) (e.g., Formula (II-a)), Formula (III), or Formula (IV) (e.g., Formula (IV-a), (IV-b), or (IV-c)), Y² is -CH₂-; and R³ is optionally substituted with 1-2 -F. For example, R³ can be (e.g., ). In some embodiments of Formula (II) (e.g., Formula (II-a)), Formula (III), or Formula (IV) (e.g., Formula (IV-a), (IV-b), or (IV-c)), the moiety is . In some embodiments, the compounds of Formula (II) are compound of Formula (II- 1): Formula (II-1) or pharmaceutically acceptable salts thereof, wherein: b1 is 1 or 2; each R¹⁰ is independently selected from the group consisting of: -Cl, -F, -CN, and C_1-3 alkyl optionally substituted with 1-3 R^c; X¹ is CH₂; and X² and X³ are independently selected from the group consisting of: O, CH₂, CHR^L, and C(R^L)₂. In some embodiments of Formula (II-1), b1 is 1. In some embodiments, the compounds of Formula (II-a) are compounds of Formula (II-a1): Formula (II-a1) or pharmaceutically acceptable salts thereof, wherein: b4 is 0 or 1; each R¹⁰ is independently selected from the group consisting of: -Cl, -F, -CN, and C_1-3 alkyl optionally substituted with 1-3 R^c; X¹ is CH₂; and X² and X³ are independently selected from the group consisting of: O, CH₂, CHR^L, and C(R^L)₂. In some embodiments of Formula (II-a1), b4 is 0. In some embodiments, the compounds of Formula (III) are compounds of Formula (III-1): Formula (III-1) or pharmaceutically acceptable salts thereof, wherein: b4 is 0 or 1; each R¹⁰ is independently selected from the group consisting of: -Cl, -F, -CN, and C_1-3 alkyl optionally substituted with 1-3 R^c; X¹ is CH₂; and X² and X³ are independently selected from the group consisting of: O, CH₂, CHR^L, and C(R^L)₂. In some embodiments of Formula (III-1), b4 is 0. In some embodiments of Formula (III-1), R⁹ is -NR^dR^e (e.g., -NH₂). In some embodiments, the compounds of Formula (IV-a) or (IV-b) are compounds of Formula (IV-a1) or (IV-b1): Formula (IV-a1) Formula (IV-b1) or pharmaceutically acceptable salts thereof, wherein: b1 is 0, 1, or 2; b4 is 0 or 1; each R¹⁰ is independently selected from the group consisting of: -Cl, -F, -CN, and C_1-3 alkyl optionally substituted with 1-3 R^c; X¹ is CH₂; one of X² and X³ is independently selected from the group consisting of: CHR^L and C(R^L)₂; and the other of X² and X³ is CH₂ or O. In some embodiments of Formula (IV-a1), b1 is 1; and the moiety is (e.g., ). In some embodiments of Formula (IV-b1), b4 is 0. In some embodiments of Formula (II-1), (II-a1), (III-1), (IV-a1), or (IV-b1), X² is CH₂; and X³ is CHR^L (e.g., CH(CH₃)). In some embodiments of Formula (II-1), (II-a1), or (III-1), X² is CH₂; and X³ is CH₂. In some embodiments of Formula (II-1), (II-a1), (III-1), (IV-a1), or (IV-b1), each R² is independently methyl or ethyl, each optionally substituted with 1-3 R^c, wherein each R^c present on R² is independently selected from the group consisting of: -F, cyano, -OH, -C_1-6 alkoxy, and -C_1-6 haloalkoxy. In some embodiments of Formula (II-1), (II-a1), (III-1), (IV-a1), or (IV-b1), each R² is independently methyl or ethyl. In some embodiments of Formula (II-1), (II-a1), (III-1), (IV-a1), or (IV-b1), one R² is a C_2-6 alkyl substituted with -OH; and the other R² is -H or C_1-3 alkyl. In some embodiments of Formula (II-1), (II-a1), (III-1), (IV-a1), or (IV-b1), Y² is - CH₂-; and R³ is a 4-10 membered heterocyclyl having one ring nitrogen atom and 0-1 additional ring heteroatom selected from the group consisting of oxygen and nitrogen, wherein the heterocyclyl is optionally substituted with 1-6 R^a. In some embodiments of Formula (II-1), (II-a1), (III-1), (IV-a1), or (IV-b1), Y² is - CH₂-; and R³ is optionally substituted with 1-2 -F. In some embodiments of Formula (II-1), (II-a1), (III-1), (IV-a1), or (IV-b1), R³ is (e.g., ). In some embodiments of Formula (II-1), (II-a1), (III-1), (IV-a1), or (IV-b1), the moiety is . In some embodiments, the compounds of Formula (II) or (II-a) are compounds of Formula (II-a2): Formula (II-a2) or pharmaceutically acceptable salts thereof, wherein: X³ is CH₂ or CHR^L, wherein R^L is C_1-3 alkyl optionally substituted with 1-3 -F; one R² is a C_2-6 alkyl substituted with -OH; the other R² is -H or C_1-3 alkyl; Y² is -CH₂-; and R³ is optionally substituted with 1-2 substituents independently selected from the group consisting of: -F, -C_1-6 alkoxy, and -C_1-6 haloalkoxy. In some embodiments of Formula (II-a2), one R² is a C_2-6 alkyl substituted with -OH (e.g., or ); and the other R² is -H or methyl. In some embodiments, the compounds of Formula (II) or (II-a) are compounds of Formula (II-a3): Formula (II-a3) or pharmaceutically acceptable salts thereof, wherein: X³ is CH₂ or CHR^L, wherein R^L is C_1-3 alkyl optionally substituted with 1-3 -F; R^f is -H or C_1-3 alkyl; Z² is a C_3-6 cycloalkyl optionally substituted with 1-3 R⁷, wherein: one R⁷ is -OH; each remaining R⁷ if present is independently selected from the group consisting of: - F, -OH, -CN, and C_1-3 alkyl optionally substituted with 1-3 F; Y² is -CH₂-; and R³ is optionally substituted with 1-2 substituents independently selected from the group consisting of: -F, -C_1-6 alkoxy, and -C_1-6 haloalkoxy. In some embodiments of Formula (II-a3), R^f is -H or methyl; and Z² is C_3-6 cycloalkyl substituted with one -OH (e.g., Z² is or ). In some embodiments of Formula (II-a2) or (II-a3), X³ is CH(Me). In some embodiments of Formula (II-a2) or (II-a3), R³ is (e.g., ). In some embodiments of Formula (II-a2) or (II-a3), the moiety is . In some embodiments of Formula (A) (e.g., Formula (I) (e.g., Formula (I-a1))), the compound is selected from the group consisting of compounds in Table C1, or a pharmaceutically acceptable salt thereof. Table C1 In certain compounds of Table C1, one or more stereogenic centers are denoted with the “V3000 enhanced stereochemical notation” (see: support.collaborativedrug.com/hc/en- us/articles/360020872171-Advanced-Stereochemistry-Registration-Atropisomers-Mixtures- Unknowns-and-Non-Tetrahedral-Chirality, accessed on November 29, 2023 and Accelrys Chemical Representation Guide, Accelrys Software Inc., 2014, each of which is incorporated by reference herein in its entirety). Using this stereochemical notation, certain stereogenic centers are denoted with “abs”, “&x”, or “orx”, wherein x is an integer (e.g., 1 or 2). For avoidance of doubt, the stereochemical notations in Table C1 have the following meaning: When a structure does not contain any wedged or hashed bonds (i.e., each stereogenic center is undefined), then each stereogenic center can independently adopt a (R) or (S) stereochemical configuration. For avoidance of doubt, such structures also encompass mixtures of stereoisomers. For example, represents , , or a mixture of and . When a structure contains a stereogenic center or a plurality of stereogenic centers that is depicted with wedges and hashes (i.e., one or more stereogenic center is defined), the following notations are used: (1) When a defined stereogenic center is denoted with “abs” or when the defined stereogenic center is not denoted with an enhanced stereochemical notation (e.g., “abs”, “&x”, or “orx”), the defined stereogenic center has the absolute configuration as depicted by the structural formula. For example, both of the structures and refer to (S)-(1-methylpyrrolidin-2-yl)methanol. (2) When a defined stereogenic center is denoted with “orx” in a structural formula, the defined stereogenic center has been resolved but the configuration at the defined s_{tereogenic center has not been determined. For example, the structure} refers to one stereoisomer selected from the group consisting of (S)-(1- methylpyrrolidin-2-yl)methanol and (R)-(1-methylpyrrolidin-2-yl)methanol. (3) When a defined stereogenic center is denoted with “&x” in a structural formula, a stereoisomeric mixture differing at this stereogenic center is represented. For example, the structure: represents a mixture of (S)-(1-methylpyrrolidin-2- yl)methanol and (R)-(1-methylpyrrolidin-2-yl)methanol. As another example, the structure: represents a mixture of ((2S,3S)-1,3-dimethylpyrrolidin-2- yl)methanol and ((2R,3S)-1,3-dimethylpyrrolidin-2-yl)methanol. (4) When two or more defined stereogenic centers are denoted with “orx” in a structural formula, each of these defined stereogenic centers has been resolved but the configurations at the defined stereogenic centers have not been determined. Specifically: a. For any pair of defined stereogenic centers denoted with “orx” in a structural formula, when the numerical parts in the notation are different (e.g., two defined stereogenic centers denoted with “or1” and “or2” respectively), each defined stereogenic center should be independently interpreted according to “(2)” supra. For example, the structure refers to one stereoisomer selected from the group consisting of: , , , and . b. For any pair of defined stereogenic centers denoted with “orx” in a structural formula, when the numerical part in the notation is identical (e.g., two defined stereogenic centers are each denoted with “or1”), the structural formula refers to one stereoisomer having the relative stereochemistry at these stereogenic centers as depicted in the structural formula, but the absolute configurations of these stereogenic centers have not been determined. For example, the structure refers to one of the two “syn” stereoisomers: or . As another example, the structure refers to one of the “anti” stereoisomers: or . (5) When two or more defined stereogenic centers are denoted with “&x” in a structural formula, the structural formula refers to a mixture of stereoisomers that differ in the configuration at the defined stereogenic centers. Specifically: a. For any pair of defined stereogenic centers denoted with “&x” in a structural formula, when the numerical parts in the notation are different (e.g., two defined stereogenic centers denoted with “&1” and “&2” respectively), the structural formula refers to a mixture of stereoisomers at these two defined stereogenic centers, wherein the configuration at each of the defined stereogenic centers can vary independently of one another. For example, the structure refers to a mixture of four stereoisomers: , , , and . b. For any pair of defined stereogenic centers denoted with “&x” in a structural formula, when the numerical part in the notation is identical (e.g., two defined stereogenic centers are each denoted with “&1”), the structural formula refers to a mixture of stereoisomers at these two defined stereogenic centers, wherein the relative configurations are as depicted in the structural formula. For example, the structure refers to a mixture of “syn” stereoisomers: and . As another example, the structure refers to a mixture of “anti” stereoisomers: and . In some embodiments, the compounds of Formula (AA), Formula (A), or Formula (I) are selected from the group consisting of the compounds depicted in Table C1 of U.S. Provisional Application Serial Nos. 63/650,229, filed May 21, 2024; and 63/757,623, filed February 12, 2025, each Table C1 is incorporated herein by reference in its entirety. Certain examples of Formula (AA) Formula (A), Formula (I) (e.g., Formula (I-a1)), Formula (II) (e.g., Formula (II-1), (II-a), (II-a1), (II-a2), or (II-a3)), Formula (III) (e.g., Formula (III-1)), Formula (IV) (e.g., Formula (IV-a), (IV-a1), (IV-b), (IV-b1), or (IV-c)), or Formula (B) (e.g., Formula (B-1)) compounds were synthesized using methods involving resolution of stereoisomeric mixture(s) (e.g., SFC separation of stereoisomers). In Table C1, the resolved stereogenic centers in these compounds are labelled with the “or1” and/or “or2” enhanced stereochemical notations. In some instances, the stereoisomeric resolutions were performed during the last step of the synthesis, thereby providing the individual stereoisomers of the compounds. Alternatively, in some other instances, the resolutions were performed on an intermediate or starting material, wherein each of the constituent stereoisomers of the intermediate or starting material could be separately subjected to the subsequent steps of the synthesis to provide the respective e.g., Formula (AA) compounds as separate stereoisomers. A person of ordinary skill in the art would understand that, under either approach for stereoisomeric resolution, stereoisomers having both (R)- and (S)-configurations at a resolved stereogenic center are provided. See Table C2, wherein Table C1 compounds whose stereoisomers contain the or1 and/or or2 stereochemical notations are provided in non- stereogenic form, followed by the respective stereoisomers having the (R)- and (S)- configurations. Table C2 Also provided herein are compounds of Formula (B): Formula (B) or pharmaceutically acceptable salts thereof, or prodrugs thereof, wherein: E¹ and E² are independently selected from the group consisting of: N, CH, and CR⁵, wherein each R⁵ is independently selected from the group consisting of: -CN, halo, C_1-3 alkyl, C_1-3 haloalkyl, and C_3-6 cycloalkyl, provided that at least one of E¹ and E² is N; R¹ is selected from the group consisting of: (a) -H; (b) -N(R²)₂; (c) –N(R²)C(=O)R²; (d) -O-C_1-3 alkyl optionally substituted with 1-3 R^c; (e) C_1-6 alkyl optionally substituted with 1-3 R^c; (f) -Z⁰–(Z¹)_m1-Z²; and (g) –Z¹-Z²; each R² is independently selected from the group consisting of: -H and C_1-6 alkyl optionally substituted with 1-3 R^c; Z⁰ is -N(R^f)- or -O-; m1 is 0 or 1; Z¹ is C1-4 alkylene optionally substituted with 1-3 R^c; Z² is selected from the group consisting of: C_3-10 cycloalkyl, 4-10 membered heterocyclyl, C6-10 aryl, and 5-10 membered heteroaryl, each of which is optionally substituted with 1-3 R⁷, wherein each R⁷ is independently selected from the group consisting of R^a and R^b; Ring B is wherein the * marks the ring carbon atom common to both Ring B and ; X¹ is selected from the group consisting of a bond, S(O)_0-2, CH₂, CHR^L, C(R^L)₂, and O; X² and X³ are independently selected from the group consisting of: CH₂, CHR^L, C(R^L)₂, O, and S(O)_0-2, provided that no more than one of X¹, X², and X³ is selected from the group consisting of: O and S(O)_0-2; b1 is 0, 1, 2, or 3; R⁹ is selected from the group consisting of: -H, -OH, -NR^dR^e, and halo; each R¹⁰ is independently selected from the group consisting of R^a and R^b; each R^L is independently selected from the group consisting of C_1-3 alkoxy, -F, -CN, and C_1-3 alkyl optionally substituted with 1-3 R^c; or a pair of R^L on the same or different ring carbon atom(s) taken together with the ring atom(s) connecting them form a C_3-6 cycloalkyl ring; y is 0 or 1; Y¹ is selected from the group consisting of: -O- and -N(R^d)-; Y² is a bond or a straight-chain C_1-6 alkylene optionally substituted with 1-6 R^Y; each R^Y is independently selected from the group consisting of: halo, -CN, -OH, oxo, C_1-6 alkoxy, C_1-6 haloalkoxy, C_1-6 alkyl, C_1-6 haloalkyl, and , or a pair of R^Y on the same or different carbon atom(s) taken together with the atom(s) connecting them forms a C_3-6 cycloalkyl ring or 4-6 membered heterocyclyl ring, each of which is optionally substituted with 1-3 substituents independently selected from the group consisting of F and C_1-3 alkyl; R³ is selected from the group consisting of: (a) 4-15 membered heterocyclyl optionally substituted with 1-6 substituents independently selected from the group consisting of: R^a, R^b, , and ; (b) -NR^dR^e; and (c) -NR^dR^b; each R^o is independently selected from the group consisting of: -H, -F, C_1-3 alkyl, and C_1-3 haloalkyl; R^ox is -H or C_1-3 alkyl; R^4a and R^4b are independently selected from the group consisting of: -H, R^b, and C_1-3 alkyl optionally substituted with 1-3 R^c; or R^4a and R^4b taken together with the ring carbon atom to which each is attached form a C_3-6 cycloalkyl ring or 4-6 membered heterocyclyl ring; R^4c and R^4d are independently selected from the group consisting of: -H, halo, -CN, R^b, and C_1-3 alkyl optionally substituted with 1-3 R^c; or R^4c and R^4d taken together with the ring carbon atom to which each is attached form a C_3-6 cycloalkyl ring or 4-6 membered heterocyclyl ring; each R^a is independently selected from the group consisting of: (a) halo; (b) -CN; (c) -OH; (d) oxo; (e) C_1-6 alkoxy; (f) C_1-6 haloalkoxy; (g) -NR^dR^e; (h) -C(=O)C1-6 alkyl; (i) -C(=O)C_1-6 haloalkyl; (j) -C(=O)OH; (k) -C(=O)OC_1-6 alkyl; (l) -C(=O)OC_1-6 haloalkyl; (m) -C(=O)N(R^f)₂; (n) -S(O)_0-2(C_1-6 alkyl); (o) -S(O)_0-2(C_1-6 haloalkyl); (p) -S(O)_1-2N(R^f)₂; and (q) C_1-6 alkyl, C_2-6 alkenyl, or C_2-6 alkynyl, each optionally substituted with 1-6 R^c; each R^b is independently selected from the group consisting of: -(L^b)b-R^b1 and R^b1, wherein: b is 1, 2, or 3; each -L^b is independently selected from the group consisting of: -O-, -N(H)-, -N(C_1-3 alkyl)-, -S(O)_0-2-, -C(=O)-, and C_1-3 alkylene; and each R^b1 is independently selected from the group consisting of: C_3-10 cycloalkyl, 4-10 membered heterocyclyl, C_6-10 aryl, and 5-10 membered heteroaryl, each of which is optionally substituted with 1-3 R^g; each R^c is independently selected from the group consisting of: halo, -CN, -OH, C_1-6 alkoxy, C_1-6 haloalkoxy, -NR^dR^e, -C(=O)C_1-6 alkyl, -C(=O)C_1-6 haloalkyl, -C(=O)OC_1-6 alkyl, -C(=O)OC_1-6 haloalkyl, -C(=O)OH, -C(=O)N(R^f)₂, -S(O)_0-2(C_1-6 alkyl), -S(O)_0-2(C_1-6 haloalkyl), and -S(O)_1-2N(R^f)₂; each R^d and R^e is independently selected from the group consisting of: -H, -C(=O)C_1-6 alkyl, -C(=O)C_1-6 haloalkyl, -C(=O)OC_1-6 alkyl, -C(=O)OC_1-6 haloalkyl, -C(=O)N(R^f)₂, - S(O)_1-2(C_1-6 alkyl), -S(O)_1-2(C_1-6 haloalkyl), -S(O)_1-2N(R^f)₂, and C_1-6 alkyl optionally substituted with 1-3 R^h; each R^f is independently selected from the group consisting of: -H and C_1-6 alkyl optionally substituted with 1-3 R^h; each R^g is independently selected from the group consisting of: R^h, C_1-3 alkyl, C_1-3 haloalkyl, C_3-5 cycloalkyl, and 4-5 membered heterocyclyl; and each R^h is independently selected from the group consisting of: halo, -CN, -OH, C_1-6 alkoxy, C1-6 haloalkoxy, -NH2, -N(H)(C1-3 alkyl), and -N(C1-3 alkyl)2. The term “prodrug” as used herein refers to a derivative of a compound of Formula (B) which releases the Formula (B) compound under appropriate conditions (e.g., under in vivo conditions) via non-enzymatic (e.g., chemical reduction, oxidation, or hydrolysis (e.g., acid catalyzed hydrolysis)) or enzymatic (e.g., esterase, nuclease, lipase, amidase, or protease catalyzed reactions) processes. A prodrug can be used to change the biological distribution of a compound of Formula (B) or its pharmacokinetics. A variety of groups have been used to modify compounds to form prodrugs, such as esters (e.g., benzoates, acetates, etc.), ethers, carbamates, carbonates, N,O-acetals, phosphate esters/salts, etc. A compound of Formula (B) may form prodrugs at -NH₂ (e.g., at R⁹ when R⁹ is -NH₂) or -OH functionalities. Further information on the use of prodrugs may be found in WO 2024/050640; ACS Omega 2023, 8, 7, 7211–7221, doi: 10.1021/acsomega.3c00329; Nat Rev Drug Discov 7, 255–270 (2008), doi: 10.1038/nrd246; Chem Biol Drug Des 82: 643-668 (2013), doi: 10.1111/cbdd.12224; Pro- drugs as Novel Delivery Systems, Vol.14, ACS Symposium Series; Bioreversible Carriers in Drug Design, Pergamon Press, 1987 (ed. E. B. Roche, American Pharmaceutical Association. In some embodiments, provided herein are compounds of Formula (B), or pharmaceutically acceptable salts thereof. In some embodiments of Formula (B), R^4c and R^4d are each -H. In some embodiments of Formula (B), R^4a and R^4b are each -H. In some embodiments of Formula (B), R^4b is -H; and R^4a is selected from the group consisting of: R^b14, -(C_1-3 alkylene)-R^b14, and C_1-3 alkyl optionally substituted with 1-3 R^c4, wherein R^b14 is selected from the group consisting of C_3-6 cycloalkyl and 4-6 membered heterocyclyl, each of which is optionally substituted with 1-3 substituents independently selected from the group consisting of: -F and C_1-3 alkyl; and each R^c4 is independently selected from the group consisting of: -F, -OH, C_1-3 alkoxy, and C_1-3 haloalkoxy. In some embodiments of Formula (B), R^4b is -H; and R^4a is C_1-3 alkyl optionally substituted with -OH or C_1-3 alkoxy. In some embodiments of Formula (B), E¹ and E² are both N. In some embodiments of Formula (B), Ring B is , wherein X³ is -CH₂- or -CHR^L-; and R^L is C_1-3 alkyl optionally substituted with 1-3 -F. In some embodiments R^L is methyl. In some embodiments of Formula (B), y is 1. In some embodiments of Formula (B), y is 1; and Y¹ is -O-. In some embodiments, the compounds of Formula (B) are compounds of Formula (B1): Formula (B1) or pharmaceutically acceptable salts thereof, wherein: X³ is -CH2- or -CHR^L-; R^L is C_1-3 alkyl optionally substituted with 1-3 -F; and R^4a is selected from the group consisting of: -H, R^b14, -(C1-3 alkylene)-R^b14, and C1-3 alkyl optionally substituted with 1-3 R^c4, wherein: R^b14 is selected from the group consisting of C_3-6 cycloalkyl and 4-6 membered heterocyclyl, each of which is optionally substituted with 1-3 substituents independently selected from the group consisting of: -F and C_1-3 alkyl; and each R^c4 is independently selected from the group consisting of: -F, -OH, C_1-3 alkoxy, and C_1-3 haloalkoxy. In some embodiments of Formula (B1), R^L is methyl. In some embodiments of Formula (B) or (B1), R^4a is -H. In some embodiments of Formula (B) or (B1), R³ is a 4-15 membered heterocyclyl optionally substituted with 1-6 substituents independently selected from the group consisting of: R^a, R^b, , and . In some embodiments of Formula (B) or (B1), each R^a present on R³ is independently selected from the group consisting of: (a) halo; (b) -CN; (c) -OH; (d) oxo; (e) -C_1-6 alkoxy; (f) -C_1-6 haloalkoxy; and (g) C_1-3 alkyl optionally substituted with 1-3 substituents independently selected from the group consisting of: halo, -CN, -OH, -C_1-6 alkoxy, and -C_1-6 haloalkoxy. In some embodiments of Formula (B) or (B1), each R^b present on R³ is independently selected from the group consisting of: R^b1, -CH₂-R^b1, -OCH₂R^b1, and -CH₂OC(=O)R^b1; and each R^b1 is independently selected from the group consisting of: C_3-8 cycloalkyl, 4-8 membered heterocyclyl, phenyl, and 5-6 membered heteroaryl, each of which is optionally substituted with 1-3 substituents independently selected from the group consisting of: C_1-3 alkyl, C1-3 haloalkyl, halo, -CN, -OH, -C1-6 alkoxy, and -C1-6 haloalkoxy. In some embodiments of Formula (B) or (B1), Y² is -CH₂- or -CD₂- (e.g., -CH₂-); and R³ is optionally substituted with 1-3 substituents independently selected from the group consisting of: R^a, R^b, and . In some embodiments of Formula (B) or (B1), Y² is -CH₂- or -CD₂- (e.g., -CH₂-); and R³ is optionally substituted with 1-2 substituents independently selected from the group consisting of: -F, -C_1-3 alkoxy, and -C_1-3 haloalkoxy. In some embodiments of Formula (B) or (B1), Y² is -CH₂- or -CD₂- (e.g., -CH₂-); and R³ is a 9-14 (e.g., 9-12) membered heterocyclyl optionally substituted with 1-3 substituents independently selected from the group consisting of: R^a, R^b, and . In some embodiments, R³ is a 9-12 membered heterocyclyl optionally substituted with 1-3 R^a. In some embodiments, R³ is a 9-12 membered heterocyclyl optionally substituted with 1-3 substituents independently selected from the group consisting of: -F, C_1-3 alkyl, and C_1-3 alkoxy. For example, R³ can be selected from the group consisting of: , , , , , , , , , , , , , , and . In some embodiments of Formula (B) or (B1), Y² is -CH₂- or -CD₂- (e.g., -CH₂-); and R³ is an 8-12 membered heterocyclyl substituted with 1-2 and further optionally substituted with 1-2 independently selected R^a. In some embodiments, R³ is selected from the group consisting of: , , and . In some embodiments, each R^a present on R³ is independently selected from the group consisting of: -F, C_1-3 alkyl, -OH, and C_1-3 alkoxy. For example, R³ can be selected from the group consisting of: , , , , , , , , , and . In some embodiments of Formula (B) or (B1), Y² is -CH₂- or -CD₂- (e.g., -CH₂-); and R³ is an 8-12 membered heterocyclyl substituted with R^b and further optionally substituted with 1-2 substituents independently selected from the group consisting of: R^a and . In some embodiments, R³ is selected from the group consisting of: , , , and . In some embodiments, the R^b substituent of R³ is selected from the group consisting of: R^b1, -OCH₂R^b1, and -CH₂OC(=O)R^b1. For example, R³ can be selected from the group consisting of: , , , , , , , , , , , , , , , , , , and . In some embodiments of Formula (B) or (B1), Y² is -CH₂- or -CD₂- (e.g., -CH₂-); and R³ is selected from the group consisting of: (e.g., ) or (e.g., ), wherein each R^a3 is an independently selected C_1-3 alkyl optionally substituted with 1-3 -F. For example, R³ can be selected from the group consisting of: , , and . In some embodiments of Formula (B) or (B1), Y² is -CH₂- or -CD₂- (e.g., -CH₂-); and R³ is selected from the group consisting of: , , , , , , , , , , , and , wherein each R^a3 is an independently selected C_1-3 alkyl optionally substituted with 1-3 -F. For example, R³ can be selected from the group consisting of: , , , , , , and . In some embodiments of Formula (B) or (B1), Y² is a straight-chain C_3-6 alkylene optionally substituted with 1-6 R^Y. In some embodiments, Y² is selected from the group consisting of: , , , and . In some embodiments of Formula (B) or (B1), Y² is a straight-chain C_3-6 alkylene optionally substituted with 1-6 R^Y; and R³ is -NR^dR^e. In some embodiments, Y² is selected from the group consisting of: , , , and ; and R³ is -N(C_1-3 alkyl)₂. For example, -O-Y²-R³ can be: , , , or . In some embodiments of Formula (B) or (B1), Y² is a straight-chain C_3-6 alkylene optionally substituted with 1-6 R^Y; and R³ is a 4-8 membered heterocyclyl optionally substituted with 1-3 substituents independently selected from the group consisting of: R^a, , and . In some embodiments, Y² is selected from the group consisting of: , , , and ; and R³ is selected from the group consisting of: , , , , , and . For example, -O-Y²-R³ can be: , , , , or . In some embodiments of Formula (B) or (B1), R¹ is -Z⁰–(Z¹)_m1-Z². In some embodiments, Z¹ is -N(R^f)-. In some embodiments of Formula (B) or (B1), Z⁰ is -N(C_1-3 alkyl)-, wherein the C_1-3 alkyl portion of -N(C_1-3 alkyl)- is optionally substituted with 1-3 R^h. In some embodiments, Z⁰ is -N(C_1-3 alkyl)- (e.g., -NMe-). In some embodiments of Formula (B) or (B1), Z⁰ is -NH-. In some embodiments of Formula (B) or (B1), m1 is 0; and Z² is C_3-10 cycloalkyl optionally substituted with 1-3 R⁷. In some embodiments, Z² is C_3-6 cycloalkyl optionally substituted with 1-3 R⁷, wherein each R⁷ is independently selected from the group consisting of: F, -OH, -CN, and C_1-3 alkyl optionally substituted with 1-3 F. In some embodiments, Z² is cyclopropyl optionally substituted with 1-3 R⁷, wherein each R⁷ is independently selected from the group consisting of: F, -OH, -CN, and C1-3 alkyl optionally substituted with 1-3 F. In some embodiments, Z² is cyclobutyl optionally substituted with 1-3 R⁷, wherein each R⁷ is independently selected from the group consisting of: F, -OH, -CN, and C1-3 alkyl optionally substituted with 1-3 F. In some embodiments of Formula (B) or (B1), m1 is 0; and Z² is cyclopropyl or cyclobutyl, each optionally substituted with 1-3 R⁷, wherein each R⁷ is independently selected from the group consisting of: -F, -OH, -CN, and C_1-3 alkyl optionally substituted with 1-3 F. In some embodiments of Formula (B) or (B1), Z² is (e.g., ). For example, Z² can be (e.g., ). In some embodiments of Formula (I), Z² is . In some embodiments of Formula (B) or (B1), Z² is , , or . In some embodiments, each R⁷ is -F. In some embodiments, one R⁷ is -OH; and each remaining R⁷ if present is independently selected from the group consisting of: -F, -OH, -CN, and C_1-3 alkyl optionally substituted with 1-3 F. In some embodiments of Formula (B) or (B1), Z⁰ is -N(C_1-3 alkyl)- (e.g., -NMe-) or - NH-; and Z² is C_3-6 cycloalkyl optionally substituted with 1-3 R⁷, wherein each R⁷ is independently selected from the group consisting of: -F, -OH, -CN, and C_1-3 alkyl optionally substituted with 1-3 F. In some embodiments, each R⁷ is -F. In some embodiments, one R⁷ is -OH; and each remaining R⁷ if present is independently selected from the group consisting of: -F, -OH, -CN, and C_1-3 alkyl optionally substituted with 1-3 F. In some embodiments of Formula (B) or (B1), m1 is 0; and Z² is cyclopropyl or cyclobutyl, each optionally substituted with 1-3 R⁷, wherein each R⁷ is independently selected from the group consisting of: -F, -OH, -CN, and C_1-3 alkyl optionally substituted with 1-3 F. In some embodiments, each R⁷ is -F. In some embodiments, one R⁷ is -OH; and each remaining R⁷ if present is independently selected from the group consisting of: -F, -OH, -CN, and C_1-3 alkyl optionally substituted with 1-3 F. In some embodiments of Formula (B) or (B1), Z¹ is C_1-3 alkylene optionally substituted with 1-2 R^c; and Z² is selected from the group consisting of: 4-10 membered heterocyclyl and 5-10 membered heteroaryl, each of which is optionally substituted with 1-3 R⁷. In some embodiments of Formula (B) or (B1), Z¹ is C_1-3 alkylene; and Z² is selected from the group consisting of: 4-6 membered heterocyclyl and 5-membered heteroaryl, each of which is optionally substituted with 1-2 R⁷. In some embodiments, Z² is selected from the group consisting of: tetrahydrofuranyl, piperidinyl, isoxazolyl, oxazolyl, and pyrazolyl, each of which is optionally substituted with 1-2 R⁷, wherein each R⁷ is independently selected from the group consisting of: -F, -OH, oxo, -CN, and C_1-3 alkyl optionally substituted with 1-3 F. For example, Z² can be selected from the group consisting of: tetrahydrofuranyl, isoxazolyl, and oxazolyl. In some embodiments of Formula (B) or (B1), Z⁰ is -N(C_1-3 alkyl)-, wherein the C_1-3 alkyl portion of -N(C_1-3 alkyl)- is optionally substituted with 1-3 R^h; m1 is 0; and Z² is C_3-6 cycloalkyl optionally substituted with 1-3 R⁷, wherein each R⁷ is independently selected from the group consisting of: F, -OH, -CN, and C_1-3 alkyl optionally substituted with 1-3 F. In some embodiments of Formula (B) or (B1), Z⁰ is -N(C_1-3 alkyl)-, wherein the C_1-3 alkyl portion of -N(C_1-3 alkyl)- is optionally substituted with 1-3 R^h; m1 is 0; and Z² is cyclopropyl optionally substituted with 1-3 R⁷, wherein each R⁷ is independently selected from the group consisting of: F, -OH, -CN, and C_1-3 alkyl optionally substituted with 1-3 F. In some embodiments of Formula (B) or (B1), Z⁰ is -N(C_1-3 alkyl)-, wherein the C_1-3 alkyl portion of -N(C_1-3 alkyl)- is optionally substituted with 1-3 R^h; m1 is 0; and Z² is (e.g., ). For example, Z² can be (e.g., ). In some embodiments of Formula (B) or (B1), m1 is 1; Z¹ is C_1-3 alkylene optionally substituted with 1-2 R^c; and Z² is 5-10 membered heteroaryl, which is optionally substituted with 1-3 R⁷. In some embodiments of Formula (B) or (B1), m1 is 1, Z¹ is C_1-3 alkylene (e.g., C_2-3 alkylene); and Z² is 6-membered heteroaryl, which is substituted with one NH₂ and further optionally substituted with 1-2 R⁷. In some embodiments of Formula (B) or (B1), m1 is 1, Z¹ is ; and Z² is pyridyl (e.g., 3-pyridyl), which is substituted with one NH₂ and further optionally substituted with 1-2 R⁷. For example, Z² can be . In some embodiments of Formula (B) or (B1), Z⁰ is -N(C_1-3 alkyl)-, wherein the C_1-3 alkyl portion of -N(C_1-3 alkyl)- is optionally substituted with 1-3 R^h; m1 is 1; Z¹ is C_1-3 alkylene (e.g., C_2-3 alkylene); and Z² is 6-membered heteroaryl, which is substituted with one NH₂ and further optionally substituted with 1-2 R⁷. In some embodiments of Formula (B) or (B1), Z⁰ is -N(C_1-3 alkyl)-, wherein the C_1-3 alkyl portion of -N(C_1-3 alkyl)- is optionally substituted with 1-3 R^h; m1 is 1; Z¹ is ; and Z² is pyridyl (e.g., 3-pyridyl), which is substituted with one NH₂ and further optionally substituted with 1-2 R⁷. For example, Z² can be . In some embodiments of Formula (B) or (B1), R¹ is -N(H)-Z² or -N(C_1-3 alkyl)-Z², wherein Z² is a C_3-6 cycloalkyl optionally substituted with 1-3 R⁷, wherein: one R⁷ is -OH; and each remaining R⁷ if present is independently selected from the group consisting of: - F, -OH, -CN, and C1-3 alkyl optionally substituted with 1-3 F. In some embodiments, Z² is C3- ₆ cycloalkyl substituted with one -OH (e.g., Z² is or ). In some embodiments of Formula (B) or (B1), R¹ is -N(R²)₂. In some embodiments of Formula (B) or (B1), each R² is an independently selected C_1- ₃ alkyl optionally substituted with 1-3 R^c. In some embodiments of Formula (B) or (B1), each R² is independently methyl or ethyl, each optionally substituted with 1-3 R^c, wherein each R^c present on R² is independently selected from the group consisting of: -F, -CN, -OH, -C_1-6 alkoxy, and -C_1-6 haloalkoxy. In some embodiments of Formula (B) or (B1), R¹ is -N(Me)₂, -N(Et)₂, or -N(Me)Et. In some embodiments of Formula (B) or (B1), R¹ is -N(R²)2; and one R² is a C2-6 alkyl substituted with -OH. In some embodiments, the other R² is -H or C_1-3 alkyl (e.g., -H or methyl). In some embodiments of Formula (B) or (B1), R¹ is -H. In some embodiments, the compounds of Formula (B) or (B1) are selected from the group consisting of compounds in Table C3, or pharmaceutically acceptable salts thereof. Table C3 Chemical definitions The term “halo” refers to fluoro (F), chloro (Cl), bromo (Br), or iodo (I). The term “oxo” refers to a divalent doubly bonded oxygen atom (i.e., “=O”). As used herein, oxo groups are attached to carbon atoms to form carbonyls. The term “alkyl” refers to a saturated acyclic hydrocarbon radical that may be a straight chain or branched chain, containing the indicated number of carbon atoms. For example, C_1-10 indicates that the group may have from 1 to 10 (inclusive) carbon atoms in it. Alkyl groups can either be unsubstituted or substituted with one or more substituents. Non-limiting examples include methyl, ethyl, iso-propyl, tert-butyl, n-hexyl. The term “saturated” as used in this context means only single bonds present between constituent carbon atoms and other available valences occupied by hydrogen and/or other substituents as defined herein. The term “haloalkyl” refers to an alkyl, in which one or more hydrogen atoms is/are replaced with an independently selected halo (e.g., -CF₃, -CHF₂, or -CH₂F). The term “alkoxy” refers to an -O-alkyl radical (e.g., -OCH₃). The term “haloalkoxy” refers to an -O-haloalkyl radical (e.g., -OCF_3, -OCHF₂, or -OCH₂F). The term “alkylene” refers to a divalent alkyl (e.g., -CH₂-). Similarly, terms such as “cycloalkylene” and “heterocyclylene” refer to divalent cycloalkyl and heterocyclyl respectively. For avoidance of doubt, in “cycloalkylene” and “heterocyclylene”, the two radicals can be on the same ring carbon atom (e.g., a geminal diradical such as or ) or on different ring atoms (e.g., ring carbon and/or nitrogen atoms (e.g., vicinal ring carbon and/or nitrogen atoms)) (e.g., , , , ). The term “alkenyl” refers to an acyclic hydrocarbon chain that may be a straight chain or branched chain having one or more carbon-carbon double bonds. The alkenyl moiety contains the indicated number of carbon atoms. For example, C_2-6 indicates that the group may have from 2 to 6 (inclusive) carbon atoms in it. Alkenyl groups can either be unsubstituted or substituted with one or more substituents. The term “alkynyl” refers to an acyclic hydrocarbon chain that may be a straight chain or branched chain having one or more carbon-carbon triple bonds. The alkynyl moiety contains the indicated number of carbon atoms. For example, C_2-6 indicates that the group may have from 2 to 6 (inclusive) carbon atoms in it. Alkynyl groups can either be unsubstituted or substituted with one or more substituents. The term “aryl” refers to a 6-20 carbon mono-, bi-, tri- or polycyclic group wherein at least one ring in the system is aromatic (e.g., 6-carbon monocyclic, 10-carbon bicyclic, or 14- carbon tricyclic aromatic ring system); and wherein 0, 1, 2, 3, or 4 atoms of each ring may be substituted by a substituent. Examples of aryl groups include phenyl, naphthyl, tetrahydronaphthyl, and the like. The term “cycloalkyl” as used herein refers to mono-, bi-, tri-, or polycyclic saturated or partially unsaturated hydrocarbon groups having, e.g., 3 to 20 ring carbons, preferably 3 to 15 ring carbons, and more preferably 3 to 12 ring carbons or 3-10 ring carbons or 3-6 ring carbons, wherein the cycloalkyl group may be optionally substituted. The term “saturated” as used in this context means only single bonds present between constituent carbon atoms. Examples of saturated cycloalkyl groups include, without limitation, cyclopropyl, cyclobutyl, cyclopentyl, cyclohexyl, cycloheptyl, and cyclooctyl. Partially unsaturated cycloalkyl may have any degree of unsaturation provided that one or more double bonds is present in the cycloalkyl, none of the rings in the ring system are aromatic, and the partially unsaturated cycloalkyl group is not fully saturated overall. Examples of partially unsaturated cycloalkyl include, without limitation, cyclopentenyl, cyclohexenyl, cycloheptenyl, and cyclooctenyl. Cycloalkyl may include multiple fused and/or bridged rings. Non-limiting examples of fused/bridged cycloalkyl includes: bicyclo[1.1.0]butyl, bicyclo[2.1.0]pentyl, bicyclo[1.1.1]pentyl, bicyclo[3.1.0]hexyl, bicyclo[2.1.1]hexyl, bicyclo[3.2.0]heptyl, bicyclo[4.1.0]heptyl, bicyclo[2.2.1]heptyl, bicyclo[3.1.1]heptyl, bicyclo[4.2.0]octyl, bicyclo[3.2.1]octyl, bicyclo[2.2.2]octyl, and the like. Cycloalkyl also includes spirocyclic rings (e.g., spirocyclic bicycle wherein two rings are connected through just one atom). Non-limiting examples of spirocyclic cycloalkyls include spiro[2.2]pentyl, spiro[2.5]octyl, spiro[3.5]nonyl, spiro[3.5]nonyl, spiro[3.5]nonyl, spiro[4.4]nonyl, spiro[2.6]nonyl, spiro[4.5]decyl, spiro[3.6]decyl, spiro[5.5]undecyl, and the like. The term “heteroaryl”, as used herein, means a mono-, bi-, tri- or polycyclic group having 5 to 20 ring atoms, alternatively 5, 6, 9, 10, or 15 ring atoms; wherein at least one ring in the system contains one or more heteroatoms independently selected from the group consisting of N, O, S (inclusive of oxidized forms such as: or ), and P (inclusive of oxidized forms such as: ) and at least one ring in the system is aromatic (but does not have to be a ring which contains a heteroatom, e.g. tetrahydroisoquinolinyl, e.g., tetrahydroquinolinyl). Heteroaryl groups can either be unsubstituted or substituted with one or more substituents. Examples of heteroaryl include thienyl, pyridinyl, furyl, oxazolyl, oxadiazolyl, pyrrolyl, imidazolyl, triazolyl, thiodiazolyl, pyrazolyl, isoxazolyl, thiadiazolyl, pyranyl, pyrazinyl, pyrimidinyl, pyridazinyl, triazinyl, thiazolyl benzothienyl, benzoxadiazolyl, benzofuranyl, benzimidazolyl, benzotriazolyl, cinnolinyl, indazolyl, indolyl, isoquinolinyl, isothiazolyl, naphthyridinyl, purinyl, thienopyridinyl, pyrido[2,3-d]pyrimidinyl, pyrrolo[2,3-b]pyridinyl, quinazolinyl, quinolinyl, thieno[2,3-c]pyridinyl, pyrazolo[3,4- b]pyridinyl, pyrazolo[3,4-c]pyridinyl, pyrazolo[4,3-c]pyridinyl, pyrazolo[4,3-b]pyridinyl, tetrazolyl, chromanyl, 2,3-dihydrobenzo[b][1,4]dioxinyl, benzo[d][1,3]dioxolyl, 2,3- dihydrobenzofuranyl, tetrahydroquinolinyl, 2,3-dihydrobenzo[b][1,4]oxathiinyl, isoindolinyl, and others. In some embodiments, the heteroaryl is selected from thienyl, pyridinyl, furyl, pyrazolyl, imidazolyl, isoindolinyl, pyranyl, pyrazinyl, and pyrimidinyl. For purposes of clarification, heteroaryl also includes aromatic lactams, aromatic cyclic ureas, or vinylogous analogs thereof, in which each ring nitrogen adjacent to a carbonyl is tertiary (i.e., all three valences are occupied by non-hydrogen substituents), such as one or more of pyridonyl (e.g., ,_{, , or ), pyrimidonyl (e.g., or ),} pyridazinonyl (e.g., or ), pyrazinonyl (e.g., or ), and imidazolonyl (e.g., ), wherein each ring nitrogen adjacent to a carbonyl is tertiary (i.e., the oxo group (i.e., “=O”) herein is a constituent part of the heteroaryl ring). The term “heterocyclyl” refers to a mono-, bi-, tri-, or polycyclic saturated or partially unsaturated ring system with 3-15 ring atoms (e.g., 5-8 membered monocyclic, 8-12 membered bicyclic, or 11-15 membered tricyclic ring system) having 1-3 heteroatoms if monocyclic, 1-6 heteroatoms if bicyclic, or 1-9 heteroatoms if tricyclic or polycyclic, said heteroatoms selected from O, N, S (inclusive of oxidized forms such as: or ), and P (inclusive of oxidized forms such as: ) (e.g., carbon atoms and 1-3, 1-6, or 1-9 heteroatoms of N, O, S, or P if monocyclic, bicyclic, or tricyclic, respectively), wherein 0, 1, 2 or 3 atoms of each ring may be substituted by a substituent. The term “saturated” as used in this context means only single bonds present between constituent ring atoms and other available valences occupied by hydrogen and/or other substituents as defined herein. Examples of saturated heterocyclyl groups include piperazinyl, pyrrolidinyl, dioxanyl, morpholinyl, tetrahydrofuranyl, and the like. Partially unsaturated heterocyclyl groups may have any degree of unsaturation provided that one or more double bonds is present in the heterocyclyl, none of the rings in the ring system are aromatic, and the partially unsaturated heterocyclyl group is not fully saturated overall. Examples of partially unsaturated heterocyclyl groups include, without limitation, tetrahydropyridyl, dihydropyrazinyl, dihydropyridyl, dihydropyrrolyl, dihydrofuranyl, dihydrothiophenyl. Heterocyclyl may include multiple fused and bridged rings. Non-limiting examples of fused/bridged heteorocyclyl includes: 2-azabicyclo[1.1.0]butyl, 2-azabicyclo[2.1.0]pentyl, 2- azabicyclo[1.1.1]pentyl, 3-azabicyclo[3.1.0]hexyl, 5-azabicyclo[2.1.1]hexyl, 3- azabicyclo[3.2.0]heptyl, octahydrocyclopenta[c]pyrrole, 3-azabicyclo[4.1.0]heptyl, 7- azabicyclo[2.2.1]heptyl, 6-azabicyclo[3.1.1]heptyl, 7-azabicyclo[4.2.0]octyl, 2- azabicyclo[2.2.2]octyl, 3-azabicyclo[3.2.1]octyl, 2-oxabicyclo[1.1.0]butyl, 2- oxabicyclo[2.1.0]pentyl, 2-oxabicyclo[1.1.1]pentyl, 3-oxabicyclo[3.1.0]hexyl, 5- oxabicyclo[2.1.1]hexyl, 3-oxabicyclo[3.2.0]heptyl, 3-oxabicyclo[4.1.0]heptyl, 7- oxabicyclo[2.2.1]heptyl, 6-oxabicyclo[3.1.1]heptyl, 7-oxabicyclo[4.2.0]octyl, 2- oxabicyclo[2.2.2]octyl, 3-oxabicyclo[3.2.1]octyl, and the like. Heterocyclyl also includes spirocyclic rings (e.g., spirocyclic bicycle wherein two rings are connected through just one atom). Non-limiting examples of spirocyclic heterocyclyls include 2-azaspiro[2.2]pentyl, 4- azaspiro[2.5]octyl, 1-azaspiro[3.5]nonyl, 2-azaspiro[3.5]nonyl, 7-azaspiro[3.5]nonyl, 2- azaspiro[4.4]nonyl, 6-azaspiro[2.6]nonyl, 1,7-diazaspiro[4.5]decyl, 7-azaspiro[4.5]decyl 2,5- diazaspiro[3.6]decyl, 3-azaspiro[5.5]undecyl, 2-oxaspiro[2.2]pentyl, 4-oxaspiro[2.5]octyl, 1- oxaspiro[3.5]nonyl, 2-oxaspiro[3.5]nonyl, 7-oxaspiro[3.5]nonyl, 2-oxaspiro[4.4]nonyl, 6- oxaspiro[2.6]nonyl, 1,7-dioxaspiro[4.5]decyl, 2,5-dioxaspiro[3.6]decyl, 1- oxaspiro[5.5]undecyl, 3-oxaspiro[5.5]undecyl, 3-oxa-9-azaspiro[5.5]undecyl and the like. As used herein, when a ring is described as being “partially unsaturated”, it means said ring has one or more additional degrees of unsaturation (in addition to the degree of unsaturation attributed to the ring itself; e.g., one or more double or triple bonds between constituent ring atoms), provided that the ring is not aromatic. Examples of such rings include: cyclopentene, cyclohexene, cycloheptene, dihydropyridine, tetrahydropyridine, dihydropyrrole, dihydrofuran, dihydrothiophene, and the like. For the avoidance of doubt, and unless otherwise specified, for rings and cyclic groups (e.g., aryl, heteroaryl, heterocyclyl, heterocycloalkenyl, cycloalkenyl, cycloalkyl, and the like described herein) containing a sufficient number of ring atoms to form bicyclic or higher order ring systems (e.g., tricyclic, polycyclic ring systems), it is understood that such rings and cyclic groups encompass those having fused rings, including those in which the points of fusion are located (i) on adjacent ring atoms (e.g., [x.x.0] ring systems, in which 0 represents a zero atom bridge (e.g., )); (ii) a single ring atom (spiro-fused ring systems) (e.g., , , or ), or (iii) a contiguous array of ring atoms (bridged ring systems having all bridge lengths > 0) (e.g., , , or ). In addition, atoms making up the compounds of the present embodiments are intended to include all isotopic forms of such atoms. Isotopes, as used herein, include those atoms having the same atomic number but different mass numbers. By way of general example and without limitation, isotopes of hydrogen include tritium and deuterium, and isotopes of carbon include ¹³C and ¹⁴C. In addition, the compounds generically or specifically disclosed herein are intended to include all tautomeric forms. Thus, by way of example, a compound containing the moiety: encompasses the tautomeric form containing the moiety: . Similarly, a pyridinyl or pyrimidinyl moiety that is described to be optionally substituted with hydroxyl encompasses pyridone or pyrimidone tautomeric forms. The compounds provided herein may encompass various stereochemical forms. The compounds also encompass diastereomers as well as optical isomers, e.g., mixtures of enantiomers including racemic mixtures, as well as individual enantiomers and diastereomers, which arise as a consequence of structural asymmetry in certain compounds. Unless otherwise indicated, when a disclosed compound is named or depicted by a structure without specifying the stereochemistry and has one or more chiral centers, it is understood to represent all possible stereoisomers of the compound. Certain combinations of heteroatoms (e.g., N, O, S, or halo) define compounds which are less stable under physiological conditions. Examples include (1) compounds containing acetal or aminal linkages; (2) compounds containing acyclic N-O, N-N, or N-S(O)₀ bonds; and (3) compounds containing O-O, O-S(O)_0-2, N-halo, O-halo, and S(O)_0-2-halo bonds. Accordingly, such compounds are less preferred. As used herein, “acyclic bonds” mean chemical bonds that are not part of a ring. Examples include the N-O bond in and . For avoidance of doubt, acyclic N-O, N-N, or N-S(O)₀ bonds (i.e., those bonds that are not part of a ring (e.g., in or )) are less preferred, but compounds provided herein can include N-O, N-N, or N-S(O)₀ bonds that form part of a ring (e.g., the N-N bond in ). Methods of Treatment Indications Provided herein are methods for inhibiting a KRas protein. For example, provided herein are inhibitors of a KRas protein (e.g., a dysregulated KRas protein (e.g., a mutant KRas protein (e.g., a KRas G12D mutant protein, a KRas G12R mutant protein, or a KRas G12V mutant protein))) useful for treating or preventing diseases or disorders associated with the KRas dysregulation (i.e., a KRas-associated disease or disorder), such as a cardiovascular disease, an inflammatory and/or autoimmune disease, or a cancer (e.g., a KRas-associated cancer). The term "KRas-associated disease or disorder" as used herein refers to diseases or disorders associated with or having a dysregulation of a KRAS gene, a KRas protein, or the expression or activity or level of any (e.g., one or more) of the same (e.g., any of the types of dysregulations of a KRAS gene, a KRas protein, or the expression or activity or level of any of the same described herein). Non-limiting examples of a KRas-associated disease or disorder include, for example, cancer, a cardiovascular disease (e.g., arteriovenous malformations), endometriosis, and an inflammatory and/or autoimmune disease (e.g., a nonmalignant syndrome of autoimmunity and abnormal leukocyte homeostasis). See, e.g., Adashek et al. Genome Med. 2020; 12: 16, doi: 10.1186/s13073-020-0714-y; Niemela et al. Blood. 2011; 117(10):2883-6, doi: 10.1182/blood-2010-07-295501; Nosan et al. Croat Med J.2013; 54(6): 574–578, doi: 10.3325/cmj.2013.54.574; and Messina et al. Small GTPases 11.5 (2020): 312- 319, 10.1080/21541248.2018.1502591. The term “mutant KRas-associated disease or disorder” as used herein refers to diseases or disorders associated with or having a KRas mutation (e.g., a KRAS gene having a mutation corresponding to a mutation in a KRas protein and/or a KRas protein having a mutation). Non- limiting examples of a mutant KRas-associated disease or disorder include, for example, cancer, a cardiovascular disease (e.g., arteriovenous malformations), endometriosis, and an inflammatory and/or autoimmune disease (e.g., a nonmalignant syndrome of autoimmunity and abnormal leukocyte homeostasis). See, e.g., Adashek et al. Genome Med. 2020; 12: 16, doi: 10.1186/s13073-020-0714-y; Niemela et al. Blood.2011; 117(10):2883-6, doi: 10.1182/blood- 2010-07-295501; Nosan et al. Croat Med J. 2013; 54(6): 574–578, doi: 10.3325/cmj.2013.54.574; and Messina et al. Small GTPases 11.5 (2020): 312-319, 10.1080/21541248.2018.1502591. The phrase “dysregulation of a KRAS gene, a KRas protein, or the expression or activity or level of any of the same” refers to a genetic mutation (e.g., a mutation in a KRAS gene that results in the expression of a KRas protein that includes a deletion of at least one amino acid as compared to a wild type KRas protein, a mutation in a KRAS gene that results in the expression of a KRas protein with one or more point mutations as compared to a wild type KRas protein, a mutation in a KRAS gene that results in the expression of a KRas protein with at least one inserted amino acid as compared to a wild type KRas protein, a gene duplication that results in an increased level of KRas protein in a cell, or a mutation in a regulatory sequence (e.g., a promoter and/or enhancer) that results in an increased level of KRas protein in a cell); an alternative spliced version of a KRas mRNA that results in a KRas protein having a deletion of at least one amino acid in the KRas protein as compared to the wild type KRas protein; or increased expression (e.g., increased levels) of a wild type KRas protein in a mammalian cell due to aberrant cell signaling and/or dysregulated autocrine/paracrine signaling (e.g., as compared to a control non-cancerous cell). As an example, a dysregulation of a KRAS gene, a KRas protein, or expression or activity, or level of any of the same, can be a mutation in a KRAS gene that encodes a KRas protein that has low GTPase activity and/or has increased signaling activity as compared to a protein encoded by a KRAS gene that does not include the mutation. As another example, a dysregulation of a KRAS gene, a KRas protein, or expression or activity, or level of any of the same, can be a KRas amplification. In some embodiments, a KRas amplification is an amplification of the wild type KRas. In some embodiments, a KRas amplification is an amplification of a mutant KRas. A “dysregulated KRas protein” as used herein refers to (i) a KRas protein having a mutation (e.g., a deletion of at least one amino acid as compared to a wild type KRas protein, one or more point mutations as compared to a wild type KRas protein, or an insertion of at least one amino acid as compared to a wild type KRas protein); (ii) a KRas protein resulting from a gene duplication event, e.g., of the gene encoding the KRas protein (e.g., the wild type KRas protein), thus resulting in an increased level and/or activity of the KRas protein (e.g., the wild type KRas protein) in a cell; (iii) a KRas protein resulting from a mutation in a regulatory sequence (e.g., a promoter and/or enhancer) that can also result in an increased level and/or activity of the KRas protein (e.g., the wild type KRas protein) in a cell); (iv) a KRas protein resulting from an alternative spliced version of a KRas mRNA that results in a KRas protein having a deletion of at least one amino acid in the KRas protein as compared to the wild type KRas protein); or (v) a KRas protein resulting from increased expression (e.g., increased levels) of a wild type KRas protein in a mammalian cell due to aberrant cell signaling and/or dysregulated autocrine/paracrine signaling (e.g., as compared to a control non-cancerous cell). In some embodiments, a dysregulated KRas protein is a dysregulated human KRas protein. A “mutant KRas protein” as used herein refers to a KRas protein including a substitution, an insertion, a deletion, a truncation and/or a fusion relative to the wild type human KRas sequence shown in SEQ ID NO:1. For example, a mutant human KRas protein includes a substitution at any amino acid position (relative to SEQ ID NO: 1). A “KRas G12X mutant protein” as used herein refers to a KRas protein including substitution of a glycine to any other amino acid at the twelfth amino acid position (relative to SEQ ID NO: 1). A “KRas G12A mutant protein” as used herein refers to a KRas protein including a glycine to alanine substitution at the twelfth amino acid position (relative to SEQ ID NO: 1). A “KRas G12C mutant protein” as used herein refers to a KRas protein including a glycine to cysteine substitution at the twelfth amino acid position (relative to SEQ ID NO: 1). A “KRas G12D mutant protein” as used herein refers to a KRas protein including a glycine to aspartic acid substitution at the twelfth amino acid position (relative to SEQ ID NO: 1). A “KRas G12R mutant protein” as used herein refers to a KRas protein including a glycine to arginine substitution at the twelfth amino acid position (relative to SEQ ID NO: 1). A “KRas G12S mutant protein” as used herein refers to a KRas protein including a glycine to serine substitution at the twelfth amino acid position (relative to SEQ ID NO: 1). A “KRas G12V mutant protein” as used herein refers to a KRas protein including a glycine to valine substitution at the twelfth amino acid position (relative to SEQ ID NO: 1). A “KRas G13X mutant protein” as used herein refers to a KRas protein including substitution of a glycine to any other amino acid at the thirteenth amino acid position (relative to SEQ ID NO: 1). A “KRas G13C mutant protein” as used herein refers to a KRas protein including a glycine to cysteine substitution at the thirteenth amino acid position (relative to SEQ ID NO: 1). A “KRas G13D mutant protein” as used herein refers to a KRas protein including a glycine to aspartic acid substitution at the thirteenth amino acid position (relative to SEQ ID NO: 1). A “KRas G13V mutant protein” as used herein refers to a KRas protein including a glycine to valine substitution at the thirteenth amino acid position (relative to SEQ ID NO: 1). A “KRas Q61X mutant protein” as used herein refers to a KRas protein including substitution of a glutamine to any other amino acid at the sixty-first amino acid position (relative to SEQ ID NO: 1). A “KRas Q61E mutant protein” as used herein refers to a KRas protein including a glutamine to glutamic acid substitution at the sixty-first amino acid position (relative to SEQ ID NO: 1). A “KRas Q61H mutant protein” as used herein refers to a KRas protein including a glutamine to histidine substitution at the sixty-first amino acid position (relative to SEQ ID NO: 1). A “KRas Q61K mutant protein” as used herein refers to a KRas protein including a glutamine to lysine substitution at the sixty-first amino acid position (relative to SEQ ID NO: 1). A “KRas Q61L mutant protein” as used herein refers to a KRas protein including a glutamine to leucine substitution at the sixty-first amino acid position (relative to SEQ ID NO: 1). A “KRas Q61P mutant protein” as used herein refers to a KRas protein including a glutamine to proline substitution at the sixty-first amino acid position (relative to SEQ ID NO: 1). A “KRas Q61R mutant protein” as used herein refers to a KRas protein including a glutamine to arginine substitution at the sixty-first amino acid position (relative to SEQ ID NO: 1). A “KRas inhibitor” as used herein includes any compound exhibiting KRas protein inactivation activity (e.g., inhibiting or decreasing KRas signaling activity). In some embodiments, a KRas inhibitor as described herein has an IC50 value of 1 μM or less in a nucleotide exchange assay as described herein, an IC₅₀ value of 1 μM or less in a Raf kinase interaction assay as described herein, or both. In some embodiments, a KRas inhibitor inhibits the signaling activity of a wild type KRas protein. In some embodiments, a KRas inhibitor inhibits the signaling activity of a dysregulated KRas protein, for example, resulting in a decrease in activated Raf or other downstream effectors, such as ERK. In some embodiments, a KRas inhibitor inhibits the signaling activity of a mutant KRas protein. In some embodiments, a KRas inhibitor inhibits both the signaling activity of a wild-type KRas protein and the signaling activity of one or more mutant KRas proteins and can be termed a “pan KRas inhibitor”. In some embodiments, a KRas inhibitor inhibits one or more mutant KRas proteins, and such a KRas inhibitor can be termed a “mutant KRas inhibitor”, and also termed by the mutant(s) it inhibits. For example, a KRas inhibitor that inhibits KRas G12R mutant protein could be termed a “KRas G12R inhibitor”. As another example, a KRas inhibitor that inhibits both KRas G12C mutant protein and KRas G12D mutant protein could be termed a “KRas G12C inhibitor” and/or a “KRas G12D inhibitor”. In some embodiments, a “mutant KRas inhibitor” inhibits two or more mutant KRas proteins and can be termed a “pan mutant KRas inhibitor”. In some embodiments, a pan mutant KRas inhibitor inhibits two or more mutant KRas proteins selected from the group consisting of: a KRas G12A mutant protein, a KRas G12C mutant protein, a KRas G12D mutant protein, a KRas G12R mutant protein, a KRas G12S mutant protein, a KRas G12V mutant protein, a KRas G13C mutant protein, a KRas G13D mutant protein, a KRas G13V mutant protein, a KRas Q61E mutant protein, a KRas Q61H mutant protein, a KRas Q61K mutant protein, a KRas Q61L mutant protein, a KRas Q61P mutant protein, and a KRas Q61R mutant protein. For example, a “KRas G12X inhibitor” can inhibit two or more mutant KRas proteins selected from the group consisting of: a KRas G12A mutant protein, a KRas G12C mutant protein, a KRas G12D mutant protein, a KRas G12R mutant protein, a KRas G12S mutant protein, and a KRas G12V mutant protein. As yet another example, a KRas inhibitor that inhibits a KRas G13D mutant protein could be termed a “KRas G13D inhibitor”. In some embodiments, a KRas inhibitor can inhibit a KRas protein having one or more mutations, and such a KRas inhibitor can be termed a “mutant KRas inhibitor” whether or not the mutant KRas inhibitor also inhibits wild type KRas protein. In some embodiments, a KRas inhibitor is a mutant KRas inhibitor. In some embodiments, a KRas inhibitor is an allosteric inhibitor. The term “compound(s) provided herein” refers to compound(s) of Formula (AA) Formula (A), Formula (I) (e.g., Formula (I-a1)), Formula (II) (e.g., Formula (II-1), (II-a), (II- a1), (II-a2), or (II-a3)), Formula (III) (e.g., Formula (III-1)), Formula (IV) (e.g., Formula (IV- a), (IV-a1), (IV-b), (IV-b1), or (IV-c)), or Formula (B) (e.g., Formula (B-1)) as disclosed herein. The compounds provided herein, or pharmaceutically acceptable salts thereof, are KRas inhibitors. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, is a mutant KRas inhibitor. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits two or more mutant KRas proteins selected from the group consisting of: a KRas G12A mutant protein, a KRas G12C mutant protein, a KRas G12D mutant protein, a KRas G12R mutant protein, a KRas G12S mutant protein, a KRas G12V mutant protein, a KRas G13C mutant protein, a KRas G13D mutant protein, a KRas G13V mutant protein, a KRas Q61E mutant protein, a KRas Q61H mutant protein, a KRas Q61K mutant protein, a KRas Q61L mutant protein, a KRas Q61P mutant protein, and a KRas Q61R mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits a KRas G12A mutant protein, a KRas G12C mutant protein, a KRas G12D mutant protein, a KRas G12R mutant protein, a KRas G12S mutant protein, a KRas G12V mutant protein, or a combination thereof. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits a KRas G12D mutant protein, a KRas G12R mutant protein, a KRas G12V mutant protein, or a combination thereof. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits a KRas G12D mutant protein, a KRas G12V mutant protein, or both. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits a KRas G12R mutant protein, a KRas G12V mutant protein, or both. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits a KRas G12A mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits a KRas G12C mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits a KRas G12D mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits a KRas G12R mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits a KRas G12S mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits a KRas G12V mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12X inhibitor. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits one or more mutant KRas proteins selected from the group consisting of: a KRas G12A mutant protein, a KRas G12C mutant protein, a KRas G12D mutant protein, a KRas G12R mutant protein, a KRas G12S mutant protein, and a KRas G12V mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits two or more mutant KRas proteins selected from the group consisting of: a KRas G12A mutant protein, a KRas G12C mutant protein, a KRas G12D mutant protein, a KRas G12R mutant protein, a KRas G12S mutant protein, and a KRas G12V mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits three or more mutant KRas proteins selected from the group consisting of: a KRas G12A mutant protein, a KRas G12C mutant protein, a KRas G12D mutant protein, a KRas G12R mutant protein, a KRas G12S mutant protein, and a KRas G12V mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits four or more mutant KRas proteins selected from the group consisting of: a KRas G12A mutant protein, a KRas G12C mutant protein, a KRas G12D mutant protein, a KRas G12R mutant protein, a KRas G12S mutant protein, and a KRas G12V mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits five or more mutant KRas proteins selected from the group consisting of: a KRas G12A mutant protein, a KRas G12C mutant protein, a KRas G12D mutant protein, a KRas G12R mutant protein, a KRas G12S mutant protein, and a KRas G12V mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits a KRas G12A mutant protein, a KRas G12C mutant protein, a KRas G12D mutant protein, a KRas G12R mutant protein, a KRas G12S mutant protein, and a KRas G12V mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits one or more mutant KRas proteins selected from the group consisting of: a KRas G12A mutant protein, a KRas G12D mutant protein, a KRas G12R mutant protein, a KRas G12S mutant protein, and a KRas G12V mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits two or more mutant KRas proteins selected from the group consisting of: a KRas G12A mutant protein, a KRas G12D mutant protein, a KRas G12R mutant protein, a KRas G12S mutant protein, and a KRas G12V mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits three or more mutant KRas proteins selected from the group consisting of: a KRas G12A mutant protein, a KRas G12D mutant protein, a KRas G12R mutant protein, a KRas G12S mutant protein, and a KRas G12V mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits four or more mutant KRas proteins selected from the group consisting of: a KRas G12A mutant protein, a KRas G12D mutant protein, a KRas G12R mutant protein, a KRas G12S mutant protein, and a KRas G12V mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits a KRas G12A mutant protein, a KRas G12D mutant protein, a KRas G12R mutant protein, a KRas G12S mutant protein, and a KRas G12V mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits a KRas G12D mutant protein, a KRAS G12V mutant protein, or both. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits a KRas G12A mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits a KRas G12C mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, does not inhibit a KRas G12C mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits a KRas G12D mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, does not inhibit a KRas G12D mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits a KRas G12R mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits a KRas G12S mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits a KRas G12V mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G13X inhibitor. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits one or more mutant KRas proteins selected from the group consisting of: a KRas G13C mutant protein, a KRas G13D mutant protein, and a KRas G13V mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits two or more mutant KRas proteins selected from the group consisting of: a KRas G13C mutant protein, a KRas G13D mutant protein, and a KRas G13V mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits a KRas G13C mutant protein, a KRas G13D mutant protein, and a KRas G13V mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits a KRas G13C mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits a KRas G13D mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits a KRas G13V mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas Q61X inhibitor. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits one or more mutant KRas proteins selected from the group consisting of: a KRas Q61E mutant protein, a KRas Q61H mutant protein, a KRas Q61K mutant protein, a KRas Q61L mutant protein, a KRas Q61P mutant protein, and a KRas Q61R mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits two or more mutant KRas proteins selected from the group consisting of: a KRas Q61E mutant protein, a KRas Q61H mutant protein, a KRas Q61K mutant protein, a KRas Q61L mutant protein, a KRas Q61P mutant protein, and a KRas mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits three or more mutant KRas proteins selected from the group consisting of: a KRas Q61E mutant protein, a KRas Q61H mutant protein, a KRas Q61K mutant protein, a KRas Q61L mutant protein, a KRas Q61P mutant protein, and a KRas Q61R mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits four or more mutant KRas proteins selected from the group consisting of: a KRas Q61E mutant protein, a KRas Q61H mutant protein, a KRas Q61K mutant protein, a KRas Q61L mutant protein, a KRas Q61P mutant protein, and a KRas Q61R mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits five or more mutant KRas proteins selected from the group consisting of: a KRas Q61E mutant protein, a KRas Q61H mutant protein, a KRas Q61K mutant protein, a KRas Q61L mutant protein, a KRas Q61P mutant protein, and a KRas Q61R mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits a KRas Q61E mutant protein, a KRas Q61H mutant protein, a KRas Q61K mutant protein, a KRas Q61L mutant protein, a KRas Q61P mutant protein, and a KRas Q61R mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits a KRas Q61E mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits a KRas Q61H mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits a KRas Q61K mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits a KRas Q61L mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits a KRas Q61P mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits a KRas Q61R mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits one or more mutant KRas proteins selected from the group consisting of: a KRas G12X mutant protein, a KRas G13X mutant protein, and a KRas Q61X mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits two or more mutant KRas proteins selected from the group consisting of: a KRas G12X mutant protein, a KRas G13X mutant protein, and a KRas Q61X mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits three or more mutant human KRas proteins selected from the group consisting of: a KRas G12X mutant protein, a KRas G13X mutant protein, and a KRas Q61X mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits a KRas G12X mutant protein, a KRas G13X mutant protein, and a KRas Q61X mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits one or more mutant KRas proteins selected from the group consisting of: a KRas G12A mutant protein, a KRas G12C mutant protein, a KRas G12D mutant protein, a KRas G12R mutant protein, a KRas G12S mutant protein, a KRas G12V mutant protein, a KRas G13C mutant protein, a KRas G13D mutant protein, a KRas G13V mutant protein, a KRas Q61E mutant protein, a KRas Q61H mutant protein, a KRas Q61K mutant protein, a KRas Q61L mutant protein, a KRas Q61P mutant protein, and a KRas Q61R mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits two or more mutant KRas proteins selected from the group consisting of: a KRas G12A mutant protein, a KRas G12C mutant protein, a KRas G12D mutant protein, a KRas G12R mutant protein, a KRas G12S mutant protein, a KRas G12V mutant protein, a KRas G13C mutant protein, a KRas G13D mutant protein, a KRas G13V mutant protein, a KRas Q61E mutant protein, a KRas Q61H mutant protein, a KRas Q61K mutant protein, a KRas Q61L mutant protein, a KRas Q61P mutant protein, and a KRas Q61R mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits three or more mutant KRas proteins selected from the group consisting of: a KRas G12A mutant protein, a KRas G12C mutant protein, a KRas G12D mutant protein, a KRas G12R mutant protein, a KRas G12S mutant protein, a KRas G12V mutant protein, a KRas G13C mutant protein, a KRas G13D mutant protein, a KRas G13V mutant protein, a KRas Q61E mutant protein, a KRas Q61H mutant protein, a KRas Q61K mutant protein, a KRas Q61L mutant protein, a KRas Q61P mutant protein, and a KRas Q61R mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits four or more mutant KRas proteins selected from the group consisting of: a KRas G12A mutant protein, a KRas G12C mutant protein, a KRas G12D mutant protein, a KRas G12R mutant protein, a KRas G12S mutant protein, a KRas G12V mutant protein, a KRas G13C mutant protein, a KRas G13D mutant protein, a KRas G13V mutant protein, a KRas Q61E mutant protein, a KRas Q61H mutant protein, a KRas Q61K mutant protein, a KRas Q61L mutant protein, a KRas Q61P mutant protein, and a KRas Q61R mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, five or more mutant KRas proteins selected from the group consisting of: a KRas G12A mutant protein, a KRas G12C mutant protein, a KRas G12D mutant protein, a KRas G12R mutant protein, a KRas G12S mutant protein, a KRas G12V mutant protein, a KRas G13C mutant protein, a KRas G13D mutant protein, a KRas G13V mutant protein, a KRas Q61E mutant protein, a KRas Q61H mutant protein, a KRas Q61K mutant protein, a KRas Q61L mutant protein, a KRas Q61P mutant protein, and a KRas Q61R mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits a KRas G12A mutant protein, a KRas G12C mutant protein, a KRas G12D mutant protein, a KRas G12R mutant protein, a KRas G12S mutant protein, a KRas G12V mutant protein, a KRas G13C mutant protein, a KRas G13D mutant protein, a KRas G13V mutant protein, a KRas Q61E mutant protein, a KRas Q61H mutant protein, a KRas Q61K mutant protein, a KRas Q61L mutant protein, a KRas Q61P mutant protein, and a KRas Q61R mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits a KRas G12A mutant protein, a KRas G12D mutant protein, a KRas G12R mutant protein, a KRas G12S mutant protein, a KRas G12V mutant protein, a KRas G13C mutant protein, a KRas G13D mutant protein, a KRas G13V mutant protein, a KRas Q61E mutant protein, a KRas Q61H mutant protein, a KRas Q61K mutant protein, a KRas Q61L mutant protein, a KRas Q61P mutant protein, and a KRas Q61R mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits one or more mutant KRas proteins selected from the group consisting of: a KRas G12C mutant protein, a KRas G12D mutant protein, a KRas G12R mutant protein, a KRas G12V mutant protein, a KRas G13D mutant protein, and a KRas Q61H mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits two or more mutant KRas proteins selected from the group consisting of: a KRas G12C mutant protein, a KRas G12D mutant protein, a KRas G12R mutant protein, a KRas G12V mutant protein, a KRas G13D mutant protein, and a KRas Q61H mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits three or more mutant KRas proteins selected from the group consisting of: a KRas G12C mutant protein, a KRas G12D mutant protein, a KRas G12R mutant protein, a KRas G12V mutant protein, a KRas G13D mutant protein, and a KRas Q61H mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits one or more mutant KRas proteins selected from the group consisting of: a KRas G12C mutant protein, a KRas G12D mutant protein, a KRas G12R mutant protein, and a KRas G12V mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits two or more mutant KRas proteins selected from the group consisting of: a KRas G12C mutant protein, a KRas G12D mutant protein, a KRas G12R mutant protein, and a KRas G12V mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits three or more mutant KRas proteins selected from the group consisting of: a KRas G12C mutant protein, a KRas G12D mutant protein, a KRas G12R mutant protein, and a KRas G12V mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits one or more mutant KRas proteins selected from the group consisting of: a KRas G12D mutant protein, a KRas G12R mutant protein, and a KRas G12V mutant protein. In some embodiments, compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits two or more mutant KRas proteins selected from the group consisting of: a KRas G12D mutant protein, a KRas G12R mutant protein, and a KRas G12V mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits a KRas G12D mutant protein, a KRas G12R mutant protein, and a KRas G12V mutant protein. In some such embodiments, the compounds provided herein, or pharmaceutically acceptable salts thereof, are useful for treating a bladder cancer. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits one or more mutant KRas proteins selected from the group consisting of: a KRas G12C mutant protein, a KRas G12D mutant protein, a KRas G12V mutant protein, and a KRas G13D mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits two or more mutant KRas proteins selected from the group consisting of: a KRas G12C mutant protein, a KRas G12D mutant protein, a KRas G12V mutant protein, and a KRas G13D mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits three or more mutant KRas proteins selected from the group consisting of: a KRas G12C mutant protein, a KRas G12D mutant protein, a KRas G12V mutant protein, and a KRas G13D mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits one or more mutant KRas proteins selected from the group consisting of: a KRas G12C mutant protein, a KRas G12D mutant protein, and a KRas G12V mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits two or more mutant KRas proteins selected from the group consisting of: a KRas G12C mutant protein, a KRas G12D mutant protein, and a KRas G12V mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits a KRas G12C mutant protein, a KRas G12D mutant protein, and a KRas G12V mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits a KRas G12D mutant protein, a KRas G12V mutant protein, or both. In some such embodiments, the compounds provided herein, or pharmaceutically acceptable salts thereof, are useful for treating a cervical cancer. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits one or more mutant KRas proteins selected from the group consisting of: a KRas G12A mutant protein, a KRas G12C mutant protein, a KRas G12D mutant protein, a KRas G12R mutant protein, a KRas G12S mutant protein, a KRas G12V mutant protein, a KRas G13C mutant protein, a KRas G13D mutant protein, a KRas G13V mutant protein, a KRas Q61E mutant protein, a KRas Q61H mutant protein, a KRas Q61K mutant protein, a KRas Q61L mutant protein, a KRas Q61P mutant protein, and a KRas Q61R mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits one or more mutant KRas proteins selected from the group consisting of: a KRas G12A mutant protein, a KRas G12C mutant protein, a KRas G12D mutant protein, a KRas G12R mutant protein, a KRas G12S mutant protein, and a KRas G12V mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits two or more mutant KRas proteins selected from the group consisting of: a KRas G12A mutant protein, a KRas G12C mutant protein, a KRas G12D mutant protein, a KRas G12R mutant protein, a KRas G12S mutant protein, and a KRas G12V mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits three or more mutant KRas proteins selected from the group consisting of: a KRas G12A mutant protein, a KRas G12C mutant protein, a KRas G12D mutant protein, a KRas G12R mutant protein, a KRas G12S mutant protein, and a KRas G12V mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits one or more mutant KRas proteins selected from the group consisting of: a KRas G12A mutant protein, a KRas G12D mutant protein, a KRas G12R mutant protein, and a KRas G12V mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits two or more mutant KRas proteins selected from the group consisting of: a KRas G12A mutant protein, a KRas G12D mutant protein, a KRas G12R mutant protein, and a KRas G12V mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits three or more mutant KRas proteins selected from the group consisting of: a KRas G12A mutant protein, a KRas G12D mutant protein, a KRas G12R mutant protein, and a KRas G12V mutant protein. In some such embodiments, the compounds provided herein, or pharmaceutically acceptable salts thereof, are useful for treating a colorectal cancer. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits one or more mutant KRas proteins selected from the group consisting of: a KRas G12A mutant protein, a KRas G12C mutant protein, a KRas G12D mutant protein, a KRas G12S mutant protein, a KRas G12V mutant protein, a KRas G13C mutant protein, a KRas G13D mutant protein, a KRas G13V mutant protein, a KRas Q61H mutant protein, and a KRas Q61L mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits two or more mutant KRas proteins selected from the group consisting of: a KRas G12A mutant protein, a KRas G12C mutant protein, a KRas G12D mutant protein, a KRas G12S mutant protein, a KRas G12V mutant protein, a KRas G13C mutant protein, a KRas G13D mutant protein, a KRas G13V mutant protein, a KRas Q61H mutant protein, and a KRas Q61L mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits three or more mutant KRas proteins selected from the group consisting of: a KRas G12A mutant protein, a KRas G12C mutant protein, a KRas G12D mutant protein, a KRas G12S mutant protein, a KRas G12V mutant protein, a KRas G13C mutant protein, a KRas G13D mutant protein, a KRas G13V mutant protein, a KRas Q61H mutant protein, and a KRas Q61L mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits one or more mutant KRas proteins selected from the group consisting of: a KRas G12A mutant protein, a KRas G12C mutant protein, a KRas G12D mutant protein, a KRas G12S mutant protein, and a KRas G12V mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits two or more mutant KRas proteins selected from the group consisting of: a KRas G12A mutant protein, a KRas G12C mutant protein, a KRas G12D mutant protein, a KRas G12S mutant protein, and a KRas G12V mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits three or more mutant KRas proteins selected from the group consisting of: a KRas G12A mutant protein, a KRas G12C mutant protein, a KRas G12D mutant protein, a KRas G12S mutant protein, and a KRas G12V mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits one or more mutant KRas proteins selected from the group consisting of: a KRas G12A mutant protein, a KRas G12D mutant protein, and a KRas G12V mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits two or more mutant KRas proteins selected from the group consisting of: a KRas G12A mutant protein, a KRas G12D mutant protein, and a KRas G12V mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits a KRas G12A mutant protein, a KRas G12D mutant protein, and a KRas G12V mutant protein. In some such embodiments, the compounds provided herein, or pharmaceutically acceptable salts thereof, are useful for treating an endometrial cancer. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits one or more mutant KRas proteins selected from the group consisting of: a KRas G12C mutant protein, a KRas G12D mutant protein, a KRas G12S mutant protein, a KRas G12V mutant protein, a KRas G13C mutant protein, a KRas G13D mutant protein, and a KRas Q61H mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits two or more mutant KRas proteins selected from the group consisting of: a KRas G12C mutant protein, a KRas G12D mutant protein, a KRas G12S mutant protein, a KRas G12V mutant protein, a KRas G13C mutant protein, a KRas G13D mutant protein, and a KRas Q61H mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits three or more mutant KRas proteins selected from the group consisting of: a KRas G12C mutant protein, a KRas G12D mutant protein, a KRas G12S mutant protein, a KRas G12V mutant protein, a KRas G13C mutant protein, a KRas G13D mutant protein, and a KRas Q61H mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits one or more mutant KRas proteins selected from the group consisting of: a KRas G12C mutant protein, a KRas G12D mutant protein, a KRas G12S mutant protein, and a KRas G12V mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits two or more mutant KRas proteins selected from the group consisting of: a KRas G12C mutant protein, a KRas G12D mutant protein, a KRas G12S mutant protein, and a KRas G12V mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits three or more mutant KRas proteins selected from the group consisting of: a KRas G12C mutant protein, a KRas G12D mutant protein, a KRas G12S mutant protein, and a KRas G12V mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits a KRas G12D mutant protein, a KRas G12V mutant protein, or both. In some such embodiments, the compounds provided herein, or pharmaceutically acceptable salts thereof, are useful for treating an esophageal or stomach cancer. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits one or more mutant KRas proteins selected from the group consisting of: a KRas G12A mutant protein, a KRas G12C mutant protein, a KRas G12D mutant protein, a KRas G12R mutant protein, a KRas G12S mutant protein, a KRas G12V mutant protein, a KRas G13C mutant protein, a KRas G13D mutant protein, a KRas G13V mutant protein, a KRas Q61E mutant protein, a KRas Q61H mutant protein, a KRas Q61K mutant protein, a KRas Q61L mutant protein, a KRas Q61P mutant protein, and a KRas Q61R mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits two or more mutant KRas proteins selected from the group consisting of: a KRas G12A mutant protein, a KRas G12C mutant protein, a KRas G12D mutant protein, a KRas G12R mutant protein, a KRas G12S mutant protein, a KRas G12V mutant protein, a KRas G13C mutant protein, a KRas G13D mutant protein, a KRas G13V mutant protein, a KRas Q61E mutant protein, a KRas Q61H mutant protein, a KRas Q61K mutant protein, a KRas Q61L mutant protein, a KRas Q61P mutant protein, and a KRas Q61R mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits three or more mutant KRas proteins selected from the group consisting of: a KRas G12A mutant protein, a KRas G12C mutant protein, a KRas G12D mutant protein, a KRas G12R mutant protein, a KRas G12S mutant protein, a KRas G12V mutant protein, a KRas G13C mutant protein, a KRas G13D mutant protein, a KRas G13V mutant protein, a KRas Q61E mutant protein, a KRas Q61H mutant protein, a KRas Q61K mutant protein, a KRas Q61L mutant protein, a KRas Q61P mutant protein, and a KRas Q61R mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits one or more mutant KRas proteins selected from the group consisting of: a KRas G12A mutant protein, a KRas G12C mutant protein, a KRas G12D mutant protein, a KRas G12R mutant protein, a KRas G12S mutant protein, and a KRas G12V mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits two or more mutant KRas proteins selected from the group consisting of: a KRas G12A mutant protein, a KRas G12C mutant protein, a KRas G12D mutant protein, a KRas G12R mutant protein, a KRas G12S mutant protein, and a KRas G12V mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits three or more mutant KRas proteins selected from the group consisting of: a KRas G12A mutant protein, a KRas G12C mutant protein, a KRas G12D mutant protein, a KRas G12R mutant protein, a KRas G12S mutant protein, and a KRas G12V mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits one or more mutant KRas proteins selected from the group consisting of: a KRas G12A mutant protein, a KRas G12D mutant protein, a KRas G12R mutant protein, and a KRas G12V mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits two or more mutant KRas proteins selected from the group consisting of: a KRas G12A mutant protein, a KRas G12D mutant protein, a KRas G12R mutant protein, and a KRas G12V mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits three or more mutant KRas proteins selected from the group consisting of: a KRas G12A mutant protein, a KRas G12D mutant protein, a KRas G12R mutant protein, and a KRas G12V mutant protein. In some such embodiments, the compounds provided herein, or pharmaceutically acceptable salts thereof, are useful for treating a leukemia. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits one or more mutant KRas proteins selected from the group consisting of: a KRas G12C mutant protein, a KRas G12D mutant protein, a KRas G12R mutant protein, a KRas G13D mutant protein, a KRas G13V mutant protein, a KRas a KRas Q61K mutant protein, a KRas Q61L mutant protein, and a KRas Q61R mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits two or more mutant KRas proteins selected from the group consisting of: a KRas G12C mutant protein, a KRas G12D mutant protein, a KRas G12R mutant protein, a KRas G13D mutant protein, a KRas G13V mutant protein, a KRas a KRas Q61K mutant protein, a KRas Q61L mutant protein, and a KRas Q61R mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits three or more mutant KRas proteins selected from the group consisting of: a KRas G12C mutant protein, a KRas G12D mutant protein, a KRas G12R mutant protein, a KRas G13D mutant protein, a KRas G13V mutant protein, a KRas a KRas Q61K mutant protein, a KRas Q61L mutant protein, and a KRas Q61R mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits one or more mutant KRas proteins selected from the group consisting of: a KRas G12C mutant protein, a KRas G12D mutant protein, and a KRas G12R mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits two or more mutant KRas proteins selected from the group consisting of: a KRas G12C mutant protein, a KRas G12D mutant protein, and a KRas G12R mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits a KRas G12C mutant protein, a KRas G12D mutant protein, and a KRas G12R mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits a KRas G12D mutant protein, and a KRas G12R mutant protein, or both. In some such embodiments, the compounds provided herein, or pharmaceutically acceptable salts thereof, are useful for treating a melanoma. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits one or more mutant KRas proteins selected from the group consisting of: a KRas G12A mutant protein, a KRas G12C mutant protein, a KRas G12D mutant protein, a KRas G12R mutant protein, a KRas G12S mutant protein, a KRas G13D mutant protein, and a KRas Q61L mutation. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits two or more mutant KRas proteins selected from the group consisting of: a KRas G12A mutant protein, a KRas G12C mutant protein, a KRas G12D mutant protein, a KRas G12R mutant protein, a KRas G12S mutant protein, a KRas G13D mutant protein, and a KRas Q61L mutation. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits three or more mutant KRas proteins selected from the group consisting of: a KRas G12A mutant protein, a KRas G12C mutant protein, a KRas G12D mutant protein, a KRas G12R mutant protein, a KRas G12S mutant protein, a KRas G13D mutant protein, and a KRas Q61L mutation. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits one or more mutant KRas proteins selected from the group consisting of: a KRas G12A mutant protein, a KRas G12C mutant protein, a KRas G12D mutant protein, a KRas G12R mutant protein, and a KRas G12S mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits two or more mutant KRas proteins selected from the group consisting of: a KRas G12A mutant protein, a KRas G12C mutant protein, a KRas G12D mutant protein, a KRas G12R mutant protein, and a KRas G12S mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits three or more mutant KRas proteins selected from the group consisting of: a KRas G12A mutant protein, a KRas G12C mutant protein, a KRas G12D mutant protein, a KRas G12R mutant protein, and a KRas G12S mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits a KRas G12C mutant protein, a KRas G12D mutant protein, and a KRas G12V mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits a KRas G12D mutant protein, a KRas G12V mutant protein, or both. In some such embodiments, the compounds provided herein, or pharmaceutically acceptable salts thereof, are useful for treating an ovarian cancer. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits one or more mutant KRas proteins selected from the group consisting of: a KRas G12A mutant protein, a KRas G12C mutant protein, a KRas G12D mutant protein, a KRas G12S mutant protein, a KRas G12V mutant protein, a KRas G13C mutant protein, a KRas G13D mutant protein, a KRas Q61H mutant protein, and a KRas Q61L mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits two or more mutant KRas proteins selected from the group consisting of: a KRas G12A mutant protein, a KRas G12C mutant protein, a KRas G12D mutant protein, a KRas G12S mutant protein, a KRas G12V mutant protein, a KRas G13C mutant protein, a KRas G13D mutant protein, a KRas Q61H mutant protein, and a KRas Q61L mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits three or more mutant KRas proteins selected from the group consisting of: a KRas G12A mutant protein, a KRas G12C mutant protein, a KRas G12D mutant protein, a KRas G12S mutant protein, a KRas G12V mutant protein, a KRas G13C mutant protein, a KRas G13D mutant protein, a KRas Q61H mutant protein, and a KRas Q61L mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits one or more mutant KRas proteins selected from the group consisting of: a KRas G12A mutant protein, a KRas G12C mutant protein, a KRas G12D mutant protein, a KRas G12S mutant protein, and a KRas G12V mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits two or more mutant KRas proteins selected from the group consisting of: a KRas G12A mutant protein, a KRas G12C mutant protein, a KRas G12D mutant protein, a KRas G12S mutant protein, and a KRas G12V mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits three or more mutant KRas proteins selected from the group consisting of: a KRas G12A mutant protein, a KRas G12C mutant protein, a KRas G12D mutant protein, a KRas G12S mutant protein, and a KRas G12V mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits one or more mutant KRas proteins selected from the group consisting of: a KRas G12A mutant protein, a KRas G12D mutant protein, and a KRas G12V mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits two or more mutant KRas proteins selected from the group consisting of: a KRas G12A mutant protein, a KRas G12D mutant protein, and a KRas G12V mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits a KRas G12A mutant protein, a KRas G12D mutant protein, and a KRas G12V mutant protein. In some such embodiments, the compounds provided herein, or pharmaceutically acceptable salts thereof, are useful for treating a lung cancer (e.g., non-small cell lung cancer). In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits one or more mutant KRas proteins selected from the group consisting of: a KRas G12A mutant protein, a KRas G12C mutant protein, a KRas G12D mutant protein, a KRas G12R mutant protein, a KRas G12S mutant protein, a KRas G12V mutant protein, a KRas G13C mutant protein, a KRas Q61H mutant protein, and a KRas Q61R mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits two or more mutant KRas proteins selected from the group consisting of: a KRas G12A mutant protein, a KRas G12C mutant protein, a KRas G12D mutant protein, a KRas G12R mutant protein, a KRas G12S mutant protein, a KRas G12V mutant protein, a KRas G13C mutant protein, a KRas Q61H mutant protein, and a KRas Q61R mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits three or more mutant KRas proteins selected from the group consisting of: a KRas G12A mutant protein, a KRas G12C mutant protein, a KRas G12D mutant protein, a KRas G12R mutant protein, a KRas G12S mutant protein, a KRas G12V mutant protein, a KRas G13C mutant protein, a KRas Q61H mutant protein, and a KRas Q61R mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits one or more mutant KRas proteins selected from the group consisting of: a KRas G12A mutant protein, a KRas G12C mutant protein, a KRas G12D mutant protein, a KRas G12R mutant protein, a KRas G12S mutant protein, and a KRas G12V mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits two or more mutant KRas proteins selected from the group consisting of: a KRas G12A mutant protein, a KRas G12C mutant protein, a KRas G12D mutant protein, a KRas G12R mutant protein, a KRas G12S mutant protein, and a KRas G12V mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits three or more mutant KRas proteins selected from the group consisting of: a KRas G12A mutant protein, a KRas G12C mutant protein, a KRas G12D mutant protein, a KRas G12R mutant protein, a KRas G12S mutant protein, and a KRas G12V mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits one or more mutant KRas proteins selected from the group consisting of: a KRas G12A mutant protein, a KRas G12D mutant protein, a KRas G12R mutant protein, and a KRas G12V mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits two or more mutant KRas proteins selected from the group consisting of: a KRas G12A mutant protein, a KRas G12D mutant protein, a KRas G12R mutant protein, and a KRas G12V mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits three or more mutant KRas proteins selected from the group consisting of: a KRas G12A mutant protein, a KRas G12D mutant protein, a KRas G12R mutant protein, and a KRas G12V mutant protein. In some such embodiments, the compounds provided herein, or pharmaceutically acceptable salts thereof, are useful for treating a pancreatic cancer. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits one or more mutant KRas proteins selected from the group consisting of: a KRas G12A mutant protein, a KRas G12R mutant protein, a KRas G12S mutant protein, a KRas G12V mutant protein, a KRas Q61L mutant protein, a KRas Q61P mutant protein, and a KRas Q61R mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits two or more mutant KRas proteins selected from the group consisting of: a KRas G12A mutant protein, a KRas G12R mutant protein, a KRas G12S mutant protein, a KRas G12V mutant protein, a KRas Q61L mutant protein, a KRas Q61P mutant protein, and a KRas Q61R mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits three or more mutant KRas proteins selected from the group consisting of: a KRas G12A mutant protein, a KRas G12R mutant protein, a KRas G12S mutant protein, a KRas G12V mutant protein, a KRas Q61L mutant protein, a KRas Q61P mutant protein, and a KRas Q61R mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits one or more mutant KRas proteins selected from the group consisting of: a KRas G12A mutant protein, a KRas G12R mutant protein, a KRas G12S mutant protein, and a KRas G12V mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits two or more mutant KRas proteins selected from the group consisting of: a KRas G12A mutant protein, a KRas G12R mutant protein, a KRas G12S mutant protein, and a KRas G12V mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits three or more mutant KRas proteins selected from the group consisting of: a KRas G12A mutant protein, a KRas G12R mutant protein, a KRas G12S mutant protein, and a KRas G12V mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits one or more mutant KRas proteins selected from the group consisting of: a KRas G12A mutant protein, a KRas G12R mutant protein, and a KRas G12V mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits two or more mutant KRas proteins selected from the group consisting of: a KRas G12A mutant protein, a KRas G12R mutant protein, and a KRas G12V mutant protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits a KRas G12A mutant protein, a KRas G12R mutant protein, and a KRas G12V mutant protein. In some such embodiments, the compounds provided herein, or pharmaceutically acceptable salts thereof, are useful for treating a testicular cancer (e.g., seminoma). In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, can bind to a KRas protein in the GTP-bound state. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, can bind selectively to a KRas protein in the GTP-bound state. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, can bind to a KRas protein in the GDP-bound state. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, can bind selectively to a KRas protein in the GDP-bound state. An exemplary sequence of mature human KRas protein is shown below (UniProtKB entry P01116) (SEQ ID NO: 1) MTEYKLVVVG AGGVGKSALT IQLIQNHFVD EYDPTIEDSY RKQVVIDGET CLLDILDTAG QEEYSAMRDQ YMRTGEGFLC VFAINNTKSF EDIHHYREQI KRVKDSEDVP MVLVGNKCDL PSRTVDTKQA QDLARSYGIP FIETSAKTRQ RVEDAFYTLV REIRQYRLKK ISKEEKTPGC VKIKKCIIM As used herein, “selective” or “selectively”, when referring to an assayed compound, indicates at least a 5-fold (e.g., at least a 10-fold, at least a 25-fold, at least a 50-fold, or at least a 100-fold) superior performance in an assay (e.g., binding affinity and/or potency) for a specified condition with reference to a comparator protein variant in the assay. For example, if a compound provided herein, or a pharmaceutically acceptable salt thereof, binds “selectively” to a KRas G12X mutant protein over the wild type KRas protein as determined by a surface plasmon resonance (SPR) assay, then the compound provided herein, or a pharmaceutically acceptable salt thereof, has at least a 5-fold (e.g., at least a 10-fold, at least a 25-fold, at least a 50-fold, or at least a 100-fold) smaller K_D value for any one or more KRas mutant proteins selected from the group consisting of the KRas G12X mutant proteins than for the wild type KRas protein when measured by the SPR assay. As a further example, if a compound provided herein, or a pharmaceutically acceptable salt thereof, “selectively” reduces the viability the KRas G12V mutant protein-expressing cells over the cells expressing KRas G12C protein as determined by a cell proliferation assay, then the compound has at least a 5-fold (e.g., at least a 10-fold, at least a 25-fold, at least a 50-fold, or at least a 100-fold) EC₅₀ value for the KRas G12V mutant protein-expressing cells than for the KRas G12C protein-expressing cells when measured by the cell proliferation assay. In another example, if a compound provided herein, or a pharmaceutically acceptable salt thereof, “selectively” inhibits a KRas G13X mutant protein over the wild type KRas protein as determined by a Raf kinase interaction assay, then the compound provided herein, or a pharmaceutically acceptable salt thereof, has at least a 5- fold (e.g., at least a 10-fold, at least a 25-fold, at least a 50-fold, or at least a 100-fold) smaller IC₅₀ value for the KRas G13X protein than for the wild type KRas protein when measured by the Raf kinase interaction assay. As a further example, if a compound provided herein, or a pharmaceutically acceptable salt thereof, “selectively” inhibits the KRas G12R mutant protein over the wild type KRas protein as determined by a nucleotide exchange assay, then the compound provided herein, or a pharmaceutically acceptable salt thereof, has at least a 5-fold (e.g., at least a 10-fold, at least a 25-fold, at least a 50-fold, or at least a 100-fold) smaller IC₅₀ value for the KRas G12R mutant protein than for the wild type KRas protein when measured by the nucleotide exchange assay. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, is a pan mutant KRas inhibitor (i.e., can inhibit two or more mutant KRas proteins (e.g., two or more of a KRas G12A mutant protein, a KRas G12D mutant protein, a KRas G12R mutant protein, and a KRas G12V mutant protein)). For example, such a compound can inhibit each mutant KRas protein (e.g., two or more mutant KRas proteins) with an IC₅₀ of less than 1 μM (e.g., less than 750 nM, less than 500 nM, or less than 200 nM). As another example, such a compound can inhibit ERK phosphorylation in cell lines each expressing a mutant KRas protein with an independent IC50 of less than 1 μM (e.g., less than 750 nM, less than 500 nM, or less than 200 nM) in at least of the two cell lines. For example, a compound provided herein, or a pharmaceutically acceptable salt thereof, can inhibit ERK phosphorylation in a cell line expressing a KRas G12R mutant protein with an IC₅₀ of less than 1 μM, and the compound provided herein, or a pharmaceutically acceptable salt thereof, can inhibit ERK phosphorylation in a cell line expressing a KRas G12V mutant protein with an IC₅₀ of less than 1 μM. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, is a pan KRas inhibitor (i.e., the compound can inhibit wild type KRas and one or more mutant KRas proteins). In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, does not inhibit certain KRas proteins (e.g., wild type KRas or one or more dysregulated KRas proteins). For example, such a compound can inhibit the interaction between a KRas protein it does not inhibit (e.g., a dysregulated KRas protein) and one or more Raf proteins with an IC₅₀ of 1 μM or greater than 1 μM (e.g., greater than 2 μM, greater than 5 μM, greater than 10 μM, or greater than 30 μM). As another example, such a compound can inhibit ERK phosphorylation in cell lines expressing the KRas protein it does not inhibit (e.g., a dysregulated KRas protein) with an IC₅₀ of 1 μM or greater than 1 μM (e.g., greater than 2 μM, greater than 5 μM, greater than 10 μM, or greater than 30 μM). In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits a KRas G12D mutant protein and a KRas G12V mutant protein. In some such embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits ERK phosphorylation in a cell line expressing a KRas G12D mutant protein (e.g., AGS, ASPC1, GP2D, LS180, Panc04.03, HPAFII, Panc02.03, A427, and HPAC) with an IC₅₀ that is within about 10-fold, i.e., within about 10-fold less or within about 10-fold more (e.g., within about 9-fold less or within about 9-fold more, within about 8-fold less or within about 8-fold more, within about 7-fold less or within about 7-fold more, within about 6-fold less or within about 6-fold more, within about 5-fold less or within about 5-fold more, or within about 2-fold less or within about 2-fold more) of the IC₅₀ measured for inhibition of ERK phosphorylation by the compound in a cell line expressing a KRas G12V mutant protein (e.g., SW620, H727, CFPAC1, CAPAN1, CAPAN2, RKN, H441, and SW480). For example, if the compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits ERK phosphorylation in a cell line expressing a KRas G12D mutant protein with an IC₅₀ of about 150 nM, then the IC₅₀ measured for inhibition of ERK phosphorylation by the compound in a cell line expressing a KRas G12V mutant protein would be within about 10-fold more than about 150 nM, thus ranging from about 150 nM to about 1500 nM, or within about 10-fold less than 150 nM, thus ranging from about 15 nM to about 150 nM. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, can inhibit ERK phosphorylation in a GP2d cell line with an IC₅₀ that is within about 10-fold, i.e., within about 10-fold less or within about 10-fold more (e.g., within about 9-fold less or within about 9-fold more, within about 8- fold less or within about 8-fold more, within about 7-fold less or within about 7-fold more, within about 6-fold less or within about 6-fold more, within about 5-fold less or within about 5-fold more, or within about 2-fold less or within about 2-fold more) of the IC₅₀ measured for inhibition of ERK phosphorylation by the compound in a SW620 cell line. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits ERK phosphorylation in a cell line expressing a KRas G12D mutant protein (e.g., AGS, ASPC1, GP2D, LS180, Panc04.03, HPAFII, Panc02.03, A427, and HPAC) with an IC₅₀ that is within about 10-fold less (e.g., within about 9-fold less, within about 8-fold less, within about 7-fold less, within about 6-fold less, within about 5-fold less, or within about 2-fold less) than the IC₅₀ measured for inhibition of ERK phosphorylation by the compound in a cell line expressing a KRas G12V mutant protein (e.g., SW620, H727, CFPAC1, CAPAN1, CAPAN2, RKN, H441, and SW480). For example, a compound provided herein, or a pharmaceutically acceptable salt thereof, can inhibit ERK phosphorylation in a GP2d cell line with an IC₅₀ that within about 10-fold less (e.g., within about 9-fold less, within about 8-fold less, within about 7-fold less, within about 6-fold less, within about 5-fold less, or within about 2-fold less) than the IC₅₀ measured for inhibition of ERK phosphorylation by the compound in a SW620 cell line. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits ERK phosphorylation in a cell line expressing a KRas G12D mutant protein (e.g., AGS, ASPC1, GP2D, LS180, Panc04.03, HPAFII, Panc02.03, A427, and HPAC ) with an IC₅₀ that is within about 10-fold more (e.g., within about 9-fold more, within about 8-fold more, within about 7-fold more, within about 6-fold more, within about 5-fold more, or within about 2-fold more) than the IC₅₀ measured for inhibition of ERK phosphorylation by the compound in a cell line expressing a KRas G12V mutant protein (e.g., SW620, H727, CFPAC1, CAPAN1, CAPAN2, RKN, H441, and SW480). For example, a compound provided herein, or a pharmaceutically acceptable salt thereof, can inhibit ERK phosphorylation in a GP2d cell line with an IC₅₀ that is within about 10-fold more (e.g., within about 9-fold more, within about 8-fold more, within about 7-fold more, within about 6-fold more, within about 5- fold more, or within about 2-fold more) than the IC₅₀ measured for inhibition of ERK phosphorylation by the compound in a SW620 cell line. In some such embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits ERK phosphorylation in a cell line expressing a KRas G12V mutant protein (e.g., SW620, H727, CFPAC1, CAPAN1, CAPAN2, RKN, H441, and SW480) with an IC₅₀ of less than 250 nM (e.g., less than 200 nM, less than 150 nM, less than 125 nM, less than 100 nM, less than 75 nM, less than 50 nM, less than 30 nM). For example, a compound provided herein, or a pharmaceutically acceptable salt thereof, can inhibit ERK phosphorylation in a SW620 cell line with an IC₅₀ of less than 250 nM (e.g., less than 200 nM, less than 150 nM, less than 125 nM, less than 100 nM, less than 75 nM, less than 50 nM, less than 30 nM). In some such further embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits ERK phosphorylation in a cell line expressing a KRas G12D mutant protein (e.g., AGS, ASPC1, GP2D, LS180, Panc04.03, HPAFII, Panc02.03, A427, and HPAC) with an IC₅₀ of less than 250 nM (e.g., less than 200 nM, less than 150 nM, less than 125 nM, less than 100 nM, less than 75 nM, less than 50 nM, less than 30 nM). For example, the compound provided herein, or a pharmaceutically acceptable salt thereof, can inhibit ERK phosphorylation in a GP2d cell line with an IC₅₀ of less than 250 nM (e.g., less than 200 nM, less than 150 nM, less than 125 nM, less than 100 nM, less than 75 nM, less than 50 nM, less than 30 nM). In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits ERK phosphorylation in a cell line expressing a KRas G12D mutant protein (e.g., AGS, ASPC1, GP2D, LS180, Panc04.03, HPAFII, Panc02.03, A427, and HPAC) with an IC₅₀ that is within about 10-fold, i.e., within about 10-fold less or within about 10-fold more (e.g., within about 9-fold less or within about 9-fold more, within about 8-fold less or within about 8-fold more, within about 7-fold less or within about 7-fold more, within about 6- fold less or within about 6-fold more, within about 5-fold less or within about 5-fold more, or within about 2-fold less or within about 2-fold more) of the IC₅₀ measured for inhibition of ERK phosphorylation by the compound in a cell line expressing a KRas G12V mutant protein (e.g., SW620, H727, CFPAC1, CAPAN1, CAPAN2, RKN, H441, and SW480), wherein the compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits ERK phosphorylation in the cell line expressing a KRas G12V mutant protein (e.g., SW620, H727, CFPAC1, CAPAN1, CAPAN2, RKN, H441, and SW480) with an IC₅₀ of less than 250 nM (e.g., less than 200 nM, less than 150 nM, less than 125 nM, less than 100 nM, less than 75 nM, less than 50 nM, less than 30 nM). In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits ERK phosphorylation in the cell line expressing a KRas G12D mutant protein (e.g., AGS, ASPC1, GP2D, LS180, Panc04.03, HPAFII, Panc02.03, A427, and HPAC) with an IC50 of less than 250 nM (e.g., less than 200 nM, less than 150 nM, less than 125 nM, less than 100 nM, less than 75 nM, less than 50 nM, less than 30 nM). For example, a compound provided herein, or a pharmaceutically acceptable salt thereof, can inhibit ERK phosphorylation in a GP2d cell line with an IC₅₀ that is within about 10-fold, i.e., within about 10-fold less or within about 10-fold more (e.g., within about 9-fold less or within about 9-fold more, within about 8-fold less or within about 8-fold more, within about 7-fold less or within about 7-fold more, within about 6-fold less or within about 6-fold more, within about 5-fold less or within about 5-fold more, or within about 2-fold less or within about 2-fold more) of the IC₅₀ measured for inhibition of ERK phosphorylation by the compound in a SW620 cell line, wherein the compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits ERK phosphorylation in a SW620 cell line with an IC₅₀ of less than 250 nM (e.g., less than 200 nM, less than 150 nM, less than 125 nM, less than 100 nM, less than 75 nM, less than 50 nM, less than 30 nM). In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits ERK phosphorylation in a GP2d cell line with an IC₅₀ of less than 250 nM (e.g., less than 200 nM, less than 150 nM, less than 125 nM, less than 100 nM, less than 75 nM, less than 50 nM, less than 30 nM). In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits ERK phosphorylation in a cell line expressing a KRas G12D mutant protein (e.g., AGS, ASPC1, GP2D, LS180, Panc04.03, HPAFII, Panc02.03, A427, and HPAC) with an IC₅₀ that is within about 10-fold less (e.g., within about 9-fold less, within about 8-fold less, within about 7-fold less, within about 6-fold less, within about 5-fold less, or within about 2- fold less) than the IC₅₀ measured for inhibition of ERK phosphorylation by the compound in a cell line expressing a KRas G12V mutant protein (e.g., SW620, H727, CFPAC1, CAPAN1, CAPAN2, RKN, H441, and SW480), wherein the compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits ERK phosphorylation in the cell line expressing a KRas G12V mutant protein (e.g., SW620, H727, CFPAC1, CAPAN1, CAPAN2, RKN, H441, and SW480) with an IC₅₀ of less than 250 nM (e.g., less than 200 nM, less than 150 nM, less than 125 nM, less than 100 nM, less than 75 nM, less than 50 nM, less than 30 nM). In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits ERK phosphorylation in the cell line expressing a KRas G12D mutant protein (e.g., AGS, ASPC1, GP2D, LS180, Panc04.03, HPAFII, Panc02.03, A427, and HPAC) with an IC₅₀ of less than 250 nM (e.g., less than 200 nM, less than 150 nM, less than 125 nM, less than 100 nM, less than 75 nM, less than 50 nM, less than 30 nM). For example, a compound provided herein, or a pharmaceutically acceptable salt thereof, can inhibit ERK phosphorylation in a GP2d cell line with an IC₅₀ that is within about 10-fold less (e.g., within about 9-fold less, within about 8-fold less, within about 7-fold less, within about 6-fold less, within about 5-fold less, or within about 2-fold less) than the IC₅₀ measured for inhibition of ERK phosphorylation by the compound in a SW620 cell line, wherein the compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits ERK phosphorylation in a SW620 cell line with an IC₅₀ of less than 250 nM (e.g., less than 200 nM, less than 150 nM, less than 125 nM, less than 100 nM, less than 75 nM, less than 50 nM, less than 30 nM). In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits ERK phosphorylation in a GP2d cell line with an IC₅₀ of less than 250 nM (e.g., less than 200 nM, less than 150 nM, less than 125 nM, less than 100 nM, less than 75 nM, less than 50 nM, less than 30 nM). In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits ERK phosphorylation in a cell line expressing a KRas G12D mutant protein (e.g., AGS, ASPC1, GP2D, LS180, Panc04.03, HPAFII, Panc02.03, A427, and HPAC) with an IC₅₀ that is within about 10-fold more (e.g., within about 9-fold more, within about 8- fold more, within about 7-fold more, within about 6-fold more, within about 5-fold more, or within about 2-fold more) than the IC₅₀ measured for inhibition of ERK phosphorylation by the compound in a cell line expressing a KRas G12V mutant protein (e.g., SW620, H727, CFPAC1, CAPAN1, CAPAN2, RKN, H441, and SW480), wherein the compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits ERK phosphorylation in the cell line expressing a KRas G12V mutant protein (e.g., SW620, H727, CFPAC1, CAPAN1, CAPAN2, RKN, H441, and SW480) with an IC₅₀ of less than 250 nM (e.g., less than 200 nM, less than 150 nM, less than 125 nM, less than 100 nM, less than 75 nM, less than 50 nM, less than 30 nM). In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits ERK phosphorylation in the cell line expressing a KRas G12D mutant protein (e.g., AGS, ASPC1, GP2D, LS180, Panc04.03, HPAFII, Panc02.03, A427, and HPAC) with an IC₅₀ of less than 250 nM (e.g., less than 200 nM, less than 150 nM, less than 125 nM, less than 100 nM, less than 75 nM, less than 50 nM, less than 30 nM). For example, a compound provided herein, or a pharmaceutically acceptable salt thereof, can inhibit ERK phosphorylation in a GP2d cell line with an IC50 that is within about 10-fold more (e.g., within about 9-fold more, within about 8-fold more, within about 7-fold more, within about 6-fold more, within about 5-fold more, or within about 2-fold more) than the IC₅₀ measured for inhibition of ERK phosphorylation by the compound in a SW620 cell line, wherein the compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits ERK phosphorylation in a SW620 cell line with an IC₅₀ of less than 250 nM (e.g., less than 200 nM, less than 150 nM, less than 125 nM, less than 100 nM, less than 75 nM, less than 50 nM, less than 30 nM). In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits ERK phosphorylation in a GP2d cell line with an IC₅₀ of less than 250 nM (e.g., less than 200 nM, less than 150 nM, less than 125 nM, less than 100 nM, less than 75 nM, less than 50 nM, less than 30 nM). The ability of a compound provided herein, or a pharmaceutically acceptable salt thereof, to bind to a KRas protein can be measured, for example, by a direct determination method (e.g., surface plasmon resonance or isothermal titration calorimetry); by radio labelling the compound prior to binding, isolating the compound/protein complex, and determining the amount of radio label bound; or by running a competition experiment where new compounds are incubated with the protein bound to known radioligands. As another example, the occupancy of a compound provided herein, or a pharmaceutically acceptable salt thereof, can be determined using a proximity-based technique, such as time-resolved Fluorescence Resonance Energy Transfer (FRET); for instance, using a labeled probe that binds mutually exclusively with the inhibitor, and using an antibody that binds to a position on the protein separate from where the compound provided herein, or a pharmaceutically acceptable salt thereof, binds (for example, an antibody that binds to an N-terminal tag). It will be understood that the antibody and probe can be tagged with any appropriate FRET pair. See, e.g., International Publication Nos. WO 2021/041671, WO 2021/120890, and U.S. Publication No. US 2021/0179633. In some cases, binding affinities (e.g., as measured by dissociation constant K_D) of the compounds provided herein, or pharmaceutically acceptable salts thereof with a KRas protein (e.g., a wild type KRas protein or a mutant KRas protein) in the GDP-bound and/or GTP-bound state can be measured using methods known in the art (e.g., using SPR (e.g., using one or more methods described herein (e.g., using the methods described in Example B1 or in Example B5 herein))). Binding affinity with the KRas protein in the GDP-bound state can be measured by loading the KRas protein with GDP (e.g., at the concentrations described in Example B1 or in Example B5). Binding affinity with the KRas protein in the GTP-bound state can be measured by loading the KRas protein with GMPPNP (e.g., at the concentrations described in Example B1). Another exemplary assay for determining the potency of a compound provided herein, or a pharmaceutically acceptable salt thereof, includes measuring the effect of the compound provided herein, or a pharmaceutically acceptable salt thereof, on cell proliferation. Cell proliferation assays can be performed in a number of formats, including 2D and 3D. Similarly, a cell proliferation assay can be performed with any appropriate cell line, including, for example, A375, A427, A549, AGS, ASPC1, CAL62, CALU1, CAPAN1, CAPAN2, CFPAC1, GP2D, H358, H441, H460, H727, HCT116, HKA1, HPAC, HPAFII, HTK, HUPT3, KMS20, KP2, LS123, LS180, MIAPaCa-2, MKN1, NCI-H1993, NCI-H211, NCI-H424, NCI-H526, Panc02.03, Panc04.03, PATC50, PC9, PK8, PSN1, RKN, SW480, SW620, and/or TCCPAN2. In some embodiments, the cell line can be AGS, A375, A427, ASPC1, H727, H441, RKN, and/or SW620. As an illustrative example, a 3D cell proliferation assay can include growing cells in a 3D medium, contacting the cells with a compound provided herein, or a pharmaceutically acceptable salt thereof, measuring the cellular proliferation using an appropriate reagent (e.g., CELLTITERGLO® 3D), and then comparing the signal from the experiment with the compound provided herein, or a pharmaceutically acceptable salt thereof, to the signal from a control experiment (e.g., lacking a compound provided herein). As another illustrative example, a 2D cell proliferation assay can include plating cells onto a growth surface, optionally letting the cells grow for a period of time, contacting the cells with a compound provided herein, or a pharmaceutically acceptable salt thereof, measuring the cellular proliferation using an appropriate reagent (e.g., CELLTITERGLO®), and then comparing the signal from the experiment with a compound provided herein, or a pharmaceutically acceptable salt thereof, to the signal from a control experiment (e.g., lacking a compound provided herein, or a pharmaceutically acceptable salt thereof). See, e.g., Example B7 herein. In some embodiments, cellular proliferation can be assessed using a platform for live cell imaging (e.g., an INCUCYTE® SX5 Live-Cell Analysis Instrument). See also, e.g., U.S. Publication No. US 2021/0179633, US 2021/0230142, and US 2019/0284144. As another example, the potency and/or efficacy of a compound provided herein, or a pharmaceutically acceptable salt thereof, can be evaluated in an animal model, for example, a xenograft model (e.g., using an established cancer cell line such as AGS, A375, A427, ASPC1, H727, H441, RKN, and/or SW620, or a patient-derived xenograft (PDX) model). See, e.g., U.S. Publication No. US 2021/0179633. In some embodiments, the potency and/or efficacy of a compound provided herein, or a pharmaceutically acceptable salt thereof can be evaluated in a cell-derived xenograft (CDX) model. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, is assessed in a CDX (e.g., H727, RKN, or SW620) mouse model. For example, mice can be implanted with a cell line of interest (e.g., H727, RKN, or SW620) and the tumor allowed to grow for a period of time, then the mice can be administered a compound provided herein, or a pharmaceutically acceptable salt thereof. The effect of the compound provided herein, or a pharmaceutically acceptable salt thereof, can be determined by measuring tumor growth (or regression). An exemplary protocol follows. All the procedures related to animal handling, care, and treatment in the efficacy study are performed according to guidelines approved by the Institutional Animal Care and Use Committee (IACUC) following the guidance of the Association for Assessment and Accreditation of Laboratory Animal Care (AAALAC). 6-8 week old BALB/c nude female mice are inoculated subcutaneously on the right flank with 5 × 10⁶ H727, RKN, or SW620 tumor cells in 0.1 mL of 1:1 medium/Matrigel for tumor development. Treatments start and groupings are assigned when the mean tumor volume reaches about 175-225 mm³. Based on the tumor volume, mice are randomly assigned to respective groups such that the average starting tumor size is the same for each treatment group. Tumor-bearing mice are treated orally twice daily with a compound provided herein, or a pharmaceutically acceptable salt thereof (e.g., a dose of about 1 mg/kg to about 200 mg/kg, such as 1 mg/kg, 3 mg/kg, 5 mg/kg, 10 mg/kg, 20 mg/kg, 30 mg/kg, 50 mg/kg, 75 mg/kg, 100 mg/kg, 150 mg/kg, or 200 mg/kg). The body weight of each animal is measured and recorded twice weekly throughout the study. The measurement of tumor size is conducted twice weekly with a caliper and recorded. The tumor volume (mm³) is estimated using the formula: TV=a × b²/2, where “a” and “b” are long and short diameters of a tumor, respectively. In some embodiments, the tumor volume is plotted as a function of time. Additional assays can include, for example, assays based on hydrogen exchange (HX) mass spectrometry. Such assays can be useful, for example, to evaluate whether a compound (e.g., a compound provided herein, or a pharmaceutically acceptable salt thereof) stabilizes the GTP-bound state or GDP-bound state of a KRas protein (e.g., a dysregulated KRas protein, e.g., a mutant KRas protein (e.g., a KRas G12D mutant protein, a KRas G12R mutant protein, or a KRas G12V mutant protein)). In such assays, the rate of hydrogen exchange of the backbone amide hydrogens can be measured for a KRas protein (e.g., a dysregulated KRas protein, e.g., a mutant KRas protein (e.g., a KRas G12D mutant protein, a KRas G12R mutant protein, or a KRas G12V mutant protein)) bound to a non-hydrolyzable GTP mimic (GMPPNP), GDP, or a compound provided herein, or a pharmaceutically acceptable salt thereof. See, e.g., Lim et al. Angew Chem Int Ed Engl. 2014; 53(1): 199–204, doi: 10.1002/anie.201307387. In some embodiments, potency of a compound provided herein, or a pharmaceutically acceptable salt thereof, as provided herein can be determined by EC₅₀ value. A compound with a lower EC₅₀ value, as determined under substantially similar conditions, is a more potent inhibitor relative to a compound with a higher EC₅₀ value. In some embodiments, an EC₅₀ value can be determined (e.g., using a KRas-dependent phosphorylation level (e.g., a phosphoERK level (sometimes called a “pERK” level)) or using a cell viability assay) in cells (e.g., in tumor cells, (e.g., cell lines such as A375, A427, A549, AGS, ASPC1, CAL62, CALU1, CAPAN1, CAPAN2, CFPAC1, GP2D, H358, H441, H460, H727, HCT116, HKA1, HPAC, HPAFII, HTK, HUPT3, KMS20, KP2, LS123, LS180, MIAPaCa-2, MKN1, NCI-H1993, NCI-H211, NCI-H424, NCI-H526, Panc02.03, Panc04.03, PATC50, PC9, PK8, PSN1, RKN, SW480, SW620, and/or TCCPAN2) expressing a KRas protein, such as a dysregulated KRas protein (e.g., a mutant KRas protein or an amplified KRas protein), or a fragment thereof). In some embodiments, potency of a compound provided herein, or a pharmaceutically acceptable salt thereof, as provided herein can also be determined by IC50 value. A compound with a lower IC₅₀ value, as determined under substantially similar conditions, is a more potent inhibitor relative to a compound with a higher IC₅₀ value. In some embodiments, an IC₅₀ value can be determined (e.g., using a KRas-dependent phosphorylation level (e.g., a phosphoERK level) or using a cell viability assay), in cells (e.g., in tumor cells, (e.g., cell lines such as A375, A427, A549, AGS, ASPC1, CAL62, CALU1, CAPAN1, CAPAN2, CFPAC1, GP2D, H358, H441, H460, H727, HCT116, HKA1, HPAC, HPAFII, HTK, HUPT3, KMS20, KP2, LS123, LS180, MIAPaCa-2, MKN1, NCI-H1993, NCI-H211, NCI-H424, NCI-H526, Panc02.03, Panc04.03, PATC50, PC9, PK8, PSN1, RKN, SW480, SW620, and/or TCCPAN2) expressing a KRas protein, such as a dysregulated KRas protein (e.g., a mutant KRas protein or an amplified KRas protein), or a fragment thereof). In some embodiments, measuring the potency of a compound provided herein, or a pharmaceutically acceptable salt thereof, includes measuring the phosphorylation of a downstream kinase, such as ERK (e.g., ERK1 and/or ERK2) or MEK. Such assays can be used to measure the inhibition of KRas signaling activity, for instance, in a cell line (e.g., A375, A427, A549, AGS, ASPC1, CAL62, CALU1, CAPAN1, CAPAN2, CFPAC1, GP2D, H358, H441, H460, H727, HCT116, HKA1, HPAC, HPAFII, HTK, HUPT3, KMS20, KP2, LS123, LS180, MIAPaCa-2, MKN1, NCI-H1993, NCI-H211, NCI-H424, NCI-H526, Panc02.03, Panc04.03, PATC50, PC9, PK8, PSN1, RKN, SW480, SW620, and/or TCCPAN2 (e.g., AGS, A375, A427, ASPC1, H727, H441, RKN, and/or SW620)). For example, cells can be contacted with a compound provided herein, or a pharmaceutically acceptable salt thereof for a period of time, then lysed or permeabilized, and total ERK or MEK and phosphoERK or phosphoMEK content can be determined (e.g., using antibodies, or a kit, such as Invitrogen InstantOne ERK1/ERK2 (Phospho) [pT202/pY204]/[pT185/pY187] ELISA, MesoScale Discovery p/t ERK1/2, AlphaScreen SUREFIRE® p-ERK1/2 (Thr202/Tyr204), or an HTRF® Phospho- ERK (Thr202/Tyr204) cellular kit (CisBio)). In some embodiments, multiple concentrations of a compound provided herein, or a pharmaceutically acceptable salt thereof can be used to construct a dose response curve. See, e.g., Example B6 herein. See, e.g., International Publication No. WO 2021/041671, U.S. Publication Nos. US 2021/0122764, US 2018/0334454, US 2021/0179633, US 2018/0334454, and US 2019/0144444. An exemplary ERK phosphorylation protocol follows. In some embodiments, an ERK phosphorylation assay can be carried out using the AlphaLisa SUREFIRE® Ultra Multiplex Phospho/Total ERK1/2 (Thr202/Tyr204) Assay Kit. In a plate (e.g., a white, opaque-bottom Perkin Elmer CulturPlate-384 (product number 6007680)), cells are seeded at the desired concentration one day prior to treatment with compounds provided herein, or pharmaceutically acceptable salts thereof, and incubated overnight in a standard 37 °C, 5% CO₂ humidified incubator. The cells can be any cells of interest, such as MIAPaCa-2 (KRas G12C), H358 (KRas G12C), AGS (KRas G12D), ASPC1 (KRas G12D), GP2D (KRas G12D), LS180 (KRas G12D), Panc04.03 (KRas G12D), HPAFII (KRas G12D), Panc02.03 (KRas G12D), A427 (KRas G12D), HPAC (KRas G12D), TCCPAN2 (KRas G12R), PSN1 (KRas G12R), KP2 (KRas G12R), LS123 (KRas G12S), SW620 (KRas G12V), H727 (KRas G12V), CFPAC1 (KRas G12V), CAPAN1 (KRas G12V), CAPAN2 (KRas G12V), RKN (KRas G12V), H441 (KRas G12V), SW480 (KRas G12V), PACADD159 (KRas G12V/G12S), HS766T (KRas Q61H), H460 (KRas Q61H), PANC0213 (KRas Q61R), or A3735 (KRas WT). The day after seeding, compounds provided herein, or pharmaceutically acceptable salts thereof, are dispensed into the treatment plates (e.g., using a Tecan D300e compound printer in 9-point _{DRC format (1:3 dilution), 10- M top concentration, in triplicate). Treatment plates are then} returned to a standard 37 °C, 5% CO₂ humidified incubator for the pre-determined treatment time. Following compound treatment, all media is removed from the treatment plate(s), and the cells are subsequently lysed (e.g., using 1X Lysis Buffer in accordance with manufacturer protocol). Next, the Acceptor Mix (prepared in accordance with manufacturer’s protocol) is added to each well of the assay plate and incubated on an orbital shaker at room temperature for 2 hours. Following incubation with the Acceptor Mix, the Donor Mix (prepared in accordance with manufacturer protocol) is added to each well of the assay plate, covered to protect from light, and incubated on an orbital shaker at room temperature overnight. Assay plates are read the following day (e.g., on a BMG Labtech PHERAstar FSX microplate reader). Data are then analyzed by calculating the ratio of ERK1/2-phosphorylation relative to Total ERK1/2 for each individual well. 1/2 The replicate ratios for each concentration are averaged and normalized to a DMSO control or other corresponding co-treatment before performing a variable slope (4-parameter), non-linear regression curve fit for each compound of interest. Data can be reported as IC₅₀ values. In some embodiments, the compounds provided herein, or pharmaceutically acceptable salts thereof, inhibit ERK phosphorylation in a cell line expressing a KRas protein (e.g., a dysregulated KRas protein (e.g., a mutant KRas protein (e.g., a KRas G12D mutant protein, a KRas G12R mutant protein, or a KRas G12V mutant protein))) with an IC₅₀ of less than 1 μM (e.g., less than 750 nM, less than 500 nM, or less than 200 nM). In some embodiments, the compounds inhibit ERK phosphorylation in a cell line expressing the KRas protein (e.g., a dysregulated KRas protein (e.g., a mutant KRas protein (e.g., a KRas G12D mutant protein, a KRas G12R mutant protein, or a KRas G12V mutant protein))) with an IC₅₀ of less than 200 nM (e.g., less than 150 nM, less than 200 nM, less than 100 nM, less than 10 nM, less than 1 nM). For example, the compounds can inhibit ERK phosphorylation in a cell line expressing the KRas protein (e.g., a dysregulated KRas protein (e.g., a mutant KRas protein (e.g., a KRas G12D mutant protein, a KRas G12R mutant protein, or a KRas G12V mutant protein))) with an IC₅₀ of 0.1 nM to 100 nM, 0.1 nM to 50 nM, 1 nM to 50 nM, or 1 nM to 20 nM. In some cases, a KRas A59G mutant protein (e.g., as a single mutant or as a double mutant with another mutation of interest, e.g., KRas G12X) can be used to “lock” the KRas protein in the GTP-bound state (e.g., by abrogating the GTPase activity of the protein); such an assay can be useful, for example, to determine the affinity of a compound provided herein, or a pharmaceutically acceptable salt thereof for the GTP-bound state and/or to determine the effect of the compound on downstream signaling (e.g., interaction with an RBD and/or the phosphorylation of a downstream kinase, such as ERK), potentially independent of the GTP cycling of the KRas protein. See, e.g., Hall, et al. Proceedings of the National Academy of Sciences 99.19 (2002): 12138-12142, doi: 10.1073/pnas.192453199; Lu, et al. Biochemistry 57.3 (2018): 324-333, doi: 10.1021/acs.biochem.7b00974; and Lim, Shuhui, et al. Chemical Science 12.48 (2021): 15975-15987, doi: 10.1039/D1SC05187C. In some embodiments, the potency of a compound provided herein, or a pharmaceutically acceptable salt thereof, as a KRas inhibitor can be evaluated by its effect on the nucleotide exchange of GDP for GTP. For example, nucleotide exchange can be measured via the increase in fluorescence of protein-bound N-methylanthraniloyl (MANT)-GDP upon the addition of an excess amount of a non-hydrolyzable GTP analog such as guanosine-5'- [(β,γ)-imido]triphosphate (GppNHp, sometimes also referred to as GMPPNP), when exchange is inhibited. See, e.g., Kanie and Jackson, Bio Protoc. 2018; 8(7): e2795, doi: 10.21769/BioProtoc.2795. As another example, nucleotide exchange can be measured via the decrease in fluorescence of an incubated mixture of KRas protein-bound fluorophore-tagged GDP (e.g., Bodipy-GDP (e.g., EDA-GTP-DY-647P1)) and a compound provided herein, or a pharmaceutically acceptable salt thereof, followed by treatment with unlabeled GTP. In such an assay, an exchange of fluorophore-tagged GDP (e.g., Bodipy-GDP) for unlabeled GTP results in a reduced TR-FRET signal. As another example, nucleotide exchange can be measured via the increase in fluorescence of an incubated mixture of KRas protein-bound GDP and a compound provided herein, or a pharmaceutically acceptable salt thereof, followed by treatment with labeled GTP. In such an assay, an exchange of GDP for labeled GTP results in an increased FRET signal. See, e.g., International Publication No. WO 2020/085493 and U.S. Publication Nos. US 2021/0122764, US 2021/0269434, and US 2018/0334454. In some embodiments of nucleotide exchange assays, a guanine nucleotide exchange factor (e.g., SOS1) can be added to accelerate nucleotide exchange. Inhibition of SOS1-catalyzed exchange of GDP for GTP on the KRas protein by compounds provided herein, or pharmaceutically acceptable salts thereof can be measured using methods known in the art (e.g., using one or more methods described herein (e.g., using methods described in Example B2 herein)). Additional examples of in vitro assays include assays that determine inhibition of the GTPase activity of KRas protein. In some embodiments, the potency of a compound provided herein, or a pharmaceutically acceptable salt thereof, can be evaluated by its effect on GTPase activity (or lack thereof, as a decrease in GTPase activity is generally believed to be associated with aberrant signaling). For example, GTPase activity of a KRas protein can be measured using a phosphate assay system that continuously measures phosphate release. In some embodiments, a purine nucleoside phosphorylase-based (PNP) assay can be used to measure GTPase activity of a KRas protein. See, e.g., Hunter et al. Mol Cancer Res. 2015; 13(9):1325-35, doi: 10.1158/1541-7786.MCR-15-0203. In some embodiments, an enzyme-linked immunosorbent assay (ELISA) can be used to measure the effect of a compound provided herein, or a pharmaceutically acceptable salt thereof, on the GTPase activity of a KRas protein (e.g., a dysregulated KRas protein, e.g., a mutant KRas protein (e.g., a KRas G12D mutant protein, a KRas G12R mutant protein, or a KRas G12V mutant protein)), for example, by detecting a change in the amount of GST-Ras-RBD that binds to the KRas protein following pull-down and antibody detection of the complex. See, e.g., US 2021/0179633. An exemplary SOS1-catalyzed nucleotide exchange assay protocol follows. GST-KRas G12R (1-169) loaded with GDP nucleotide is mixed with Anti-GST (Cisbio) antibody in assay buffer (20 mM HEPES pH 7.4, 150 mM NaCl, 5 mM MgCl₂, 1 mM DTT, 0.005% NP40, 1% DMSO) to produce a 1.5x solution.10 μL of the 1.5x KRas-Ab solution is added to wells of a black, low-volume 384-well assay plate. Compounds provided herein, or pharmaceutically acceptable salts thereof, are added to wells using acoustic transfer technology. A 10-point dose response of each compound is performed with a 30 μM top dose. The KRas/Ab-compound mixture is incubated 1 hour at room temperature. A 3x solution of SOS1 (564-1049) and EDA- GTP-DY-647P1 (Jena Bioscience) is prepared in assay buffer.5 μL of the SOS1-labeled GTP solution is added to the wells to initiate the nucleotide exchange reaction. The final concentration of KRas G12R and SOS1 are 10 nM and 200 nM, respectively. Time resolved fluorescence is read on a PHERAstar plate reader equipped with a filter module with excitation = 337 nm and emission 1 = 620 nm, emission 2 = 665 nm. The HTRF signal is calculated as the ratio of fluorescence intensity [emission 665 nm]/[emission 620 nm]. IC₅₀ values are calculated using a four-parameter, variable response sigmoidal dose response curve fit in Graphpad Prism software. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits SOS1-catalyzed exchange of GDP for GTP on the KRas protein with an IC₅₀ of less than 1 μM (e.g., less than 750 nM, less than 500 nM, or less than 200 nM). In some embodiments, the compound inhibits SOS1-catalyzed exchange of GDP for GTP on the KRas protein with an IC50 of less than 200 nM (e.g., less than 150 nM, less than 200 nM, less than 100 nM, less than 10 nM, less than 1 nM, less than 0.1 nM, or less than 0.01 nM). For example, the compound can inhibit SOS1-catalyzed exchange of GDP for GTP on the KRas protein with an IC₅₀ of 0.001 nM to 500 nM, 0.005 nM to 100 nM, 0.025 nM to 100 nM, 0.1 nM to 50 nM, or 0.1 nM to 10 nM. Additional assays for evaluating the potency of a compound provided herein, or a pharmaceutically acceptable salt thereof, can also include, for example, a RAF kinase interaction assay. Such assays can be used to measure the affinity of KRas:nucleotide complexes for the Ras Binding Domain (RBD) of a RAF protein kinase (e.g., as impacted by a compound provided herein, or a pharmaceutically acceptable salt thereof). For example, FLAG tagged KRas protein can be preloaded with the GTP analog GppNHp and then incubated with biotinylated Raf-RBD to form complexes. A competition assay can then be performed by adding untagged KRas protein preloaded with GppNHp, which had been preloaded with various test molecules, over a range of concentrations. The proximity-dependent signal after addition of streptavidin donor and anti-flag acceptor beads (e.g., ALPHASCREEN® beads) can be measured to determine the affinity of the KRas protein for the Raf kinase. See, e.g., Hunter et al. Mol Cancer Res. 2015; 13(9):1325-35, doi: 10.1158/1541-7786.MCR-15-0203; Lim et al. Angew Chem Int Ed Engl.2014; 53(1): 199–204, doi: 10.1002/anie.201307387; and Durrant, et al. Molecular Cancer Therapeutics 20.9 (2021): 1743-1754, doi: 10.1158/1535- 7163.MCT-21-0175. As another example, for compounds provided herein, or pharmaceutically acceptable salts thereof, that may bind selectively to the GTP-bound state, His-tagged KRas protein can be preloaded with the GTP analog GppNHp and then incubated with a compound provided herein, or a pharmaceutically acceptable salt thereof, to form complexes. A competition assay can then be performed by adding Raf-RBD. The proximity-dependent signal after addition of Alpha detection reagents, compared to the signal from the same experiment using GDP instead of GppNHP, can be used to determine an IC₅₀ value. See, e.g., International Publication No. WO 2021/085653. It will be understood that in many cases, tagging technologies (e.g., FLAG tag, His tag, biotinylation) may be altered in an assay by one of skill in the art. In some embodiments, a RAF kinase interaction assay can be coupled with a nucleotide exchange assay; for example, a compound provided herein, or a pharmaceutically acceptable salt thereof, can be incubated with a KRas protein (e.g., a dysregulated KRas protein, e.g., a mutant KRas protein (e.g., a KRas G12D mutant protein, a KRas G12R mutant protein, or a KRas G12V mutant protein)) and GDP, then GTP (and optionally, a GEF such as SOS1) can be introduced. Then, RAF (e.g., cRAF) acceptor beads (e.g., GST-tagged acceptor beads) can be incubated with the KRas mixture, followed by introduction of donor beads (e.g., glutathione donor beads) and measurement using ALPHASCREEN® technology. As an alternative to ALPHASCREEN® technology, any appropriate FRET pair can be used to perform homogenous time resolved fluorescence. See, e.g., U.S. Publication Nos. US 2018/0334454 and US 2021/0230142. Another exemplary assay to measure the affinity of KRas:nucleotide complex for a RBD is to incubate cells with a compound provided herein, or a pharmaceutically acceptable salt thereof, lyse the cells, then pull down non-RBD-bound KRas using an immobilized RBD. See, e.g., U.S. Publication No. US 2019/0233440. As another example, the effect of a compound provided herein, or a pharmaceutically acceptable salt thereof, on the interaction between KRas and Raf-RBD can be evaluated using HiBiT and/or NANOBIT™ technology, wherein two parts of an enzyme are fused to or inserted into two proteins of interest (e.g., KRas and Raf-RBD); when the two proteins of interest are in proximity, the two parts of the enzyme complement each other to complete an enzyme that has signaling activity (e.g., that produces luminescence). In some such assays, the affinity of the two parts of the enzyme can be tuned, for example, to reduce or eliminate signal based on proximity driven by the two parts of the enzyme. See, e.g., Schwinn, et al. ACS Chemical Biology 13.2 (2018): 467-474, doi: 10.1021/acschembio.7b00549. Similarly, the effect of a compound provided herein, or a pharmaceutically acceptable salt thereof, on the interaction between KRas and Raf-RBD can be evaluated using NANOBRET™ technology, wherein two parts of signaling system (e.g., a protein and a ligand) are fused to or inserted into two proteins of interest (e.g., KRas and Raf-RBD); when the two proteins of interest are in proximity, the two parts of the signaling system have signaling activity (e.g., producing fluorescence). See, e.g., Durrant, et al. Molecular Cancer Therapeutics 20.9 (2021): 1743-1754, doi: 10.1158/1535-7163.MCT-21-0175. In some embodiments, a RAF kinase interaction assay can be used to determine if a compound provided herein, or a pharmaceutically acceptable salt thereof, is selective for a KRas protein (e.g., a dysregulated KRas protein, e.g., a mutant KRas protein (e.g., a KRas G12D mutant protein, a KRas G12R mutant protein, or a KRas G12V mutant protein)) in the GDP-bound state or the GTP-bound state. Inhibition of the interaction between the KRas protein and Raf-RBD by compounds provided herein, or pharmaceutically acceptable salts thereof, can be measured using methods known in the art (e.g., using one or more methods described herein (e.g., using methods described in Example B3 or Example B4 herein)). In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, modulates the interaction between the KRas protein and one or more Raf proteins. In some embodiments, the compound inhibits the interaction between the KRas protein and Raf-RBD with an IC₅₀ of less than 1 μM (e.g., less than 750 nM, less than 500 nM, or less than 200 nM). In some embodiments, the compound inhibits the interaction between the KRas protein and Raf-RBD with an IC₅₀ of less than 200 nM (e.g., e.g., less than 150 nM, less than 200 nM, less than 100 nM, less than 10 nM, less than 1 nM, less than 0.1 nM, or less than 0.01 nM). For example, the compound inhibits the interaction between the KRas protein and Raf- RBD with an IC₅₀ from 0.001 nM to 500 nM, from 0.005 nM to 100 nM, from 0.025 nM to 100 nM, from 0.1 nM to 50 nM, or from 0.1 nM to 10 nM. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits the interaction between the KRas protein and Raf-RBD with an IC₅₀ of less than 1 μM in the absence of cyclophilin A (e.g., less than 750 nM, less than 500 nM, or less than 200 nM). In some embodiments, the compounds inhibit the interaction between the KRas protein and Raf-RBD with an IC₅₀ of less than 200 nM in the absence of cyclophilin A (e.g., e.g., less than 150 nM, less than 200 nM, less than 100 nM, less than 10 nM, less than 1 nM, less than 0.1 nM, or less than 0.01 nM). For example, the compounds inhibit the interaction between the KRas protein and Raf-RBD with an IC₅₀ from 0.001 nM to 500 nM, from 0.005 nM to 100 nM, from 0.025 nM to 100 nM, from 0.1 nM to 50 nM, or from 0.1 nM to 10 nM in the absence of cyclophilin A. Another exemplary assay for evaluating the potency of a compound provided herein, or a pharmaceutically acceptable salt thereof, includes measuring the phosphorylation of a downstream kinase, such as ERK (e.g., ERK1 and/or ERK2) or MEK. Such assays can be used to measure the inhibition of KRas signaling activity, for instance, in a cell line (e.g., A375, A427, A549, AGS, ASPC1, CAL62, CALU1, CAPAN1, CAPAN2, CFPAC1, GP2D, H358, H441, H460, H727, HCT116, HKA1, HPAC, HPAFII, HTK, HUPT3, KMS20, KP2, LS123, LS180, MIAPaCa-2, MKN1, NCI-H1993, NCI-H211, NCI-H424, NCI-H526, Panc02.03, Panc04.03, PATC50, PC9, PK8, PSN1, RKN, SW480, SW620, and/or TCCPAN2). For example, cells can be contacted with a compound provided herein, or a pharmaceutically acceptable salt thereof, for a period of time, then lysed or permeabilized, and total ERK or MEK and phosphoERK or phosphoMEK content can be determined (e.g., using antibodies, or a kit, such as Invitrogen InstantOne ERK1/ERK2 (Phospho) [pT202/pY204]/[pT185/pY187] ELISA or MesoScale Discovery p/t ERK1/2). In some embodiments, multiple concentrations of a compound provided herein, or a pharmaceutically acceptable salt thereof, can be used to construct a dose response curve. In some embodiments, the compounds provided herein, or pharmaceutically acceptable salts thereof, inhibit ERK phosphorylation in a cell line expressing a KRas protein (e.g., a mutant KRas protein (e.g., a KRas G12D mutant protein, a KRas G12R mutant protein, or a KRas G12V mutant protein)) with an IC₅₀ of less than 1 μM (e.g., less than 750 nM, less than 500 nM, or less than 200 nM). In some embodiments, the compounds inhibit ERK phosphorylation in a cell line expressing a KRas protein (e.g., a mutant KRas protein (e.g., a KRas G12D mutant protein, a KRas G12R mutant protein, or a KRas G12V mutant protein)) with an IC₅₀ of less than 200 nM (e.g., less than 150 nM, less than 200 nM, less than 100 nM, less than 10 nM, less than 1 nM). For example, the compounds can inhibit ERK phosphorylation in a cell line expressing a KRas protein (e.g., a mutant KRas protein (e.g., a KRas G12D mutant protein, a KRas G12R mutant protein, or a KRas G12V mutant protein)) with an IC₅₀ from 0.1 nM to 100 nM, from 0.1 nM to 50 nM, from 1 nM to 50 nM, or from 1 nM to 20 nM. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, can selectively inhibit one or more mutant KRas proteins over wild type KRas protein. The selectivity between wild type KRas protein and a mutant KRas protein as described herein can be measured using cellular proliferation assays where cell proliferation is dependent on signaling activity. For example, HEK293 cells transfected with a suitable version of wild type KRas, or HEK293 cells transfected with KRas containing one or more mutations as described herein (e.g., a G12D mutation, a G12R mutation, or a G12V mutation) can be used. Proliferation assays are performed at a range of inhibitor concentrations (e.g., 10 μM, 3 μM, 1.1 μM, 330 nM, 110 nM, 33 nM, 11 nM, 3 nM, 1 nM) and an EC₅₀ is calculated. See also the assays described in International Publication Nos. WO 2021/120890; WO 2021/041671; and U.S. Publication Nos. US 2021/0130369; US 2021/0179633; US 2018/0334454; and US 2021/0122764. The pharmacokinetic parameters of a compound provided herein, or a pharmaceutically acceptable salt thereof, can be evaluated in an animal model, for instance, a mouse model, a rat model, a dog model, or a nonhuman primate (e.g., cynomolgus monkey) model. Pharmacokinetics parameters, including clearance (CL), volume of distribution (V_d), maximum plasma concentration (C_max), time of maximum plasma concentration (t_max), half- life (t_1/2), area under the curve (AUC), and oral bioavailability (%F) can be calculated using, e.g., a non-compartmental model. In some embodiments, a reference compound (e.g., a first KRas inhibitor (e.g., MRTX1133)) may be used as a comparator. See, e.g., Example 3 (“Pharmacokinetic experiments in mice”) of International Publication No. WO 2023/098425. Certain pharmacokinetic parameters of a compound provided herein, or a pharmaceutically acceptable salt thereof, can be evaluated in hepatocytes, such as in mouse, rat, dog, nonhuman primate (e.g., cynomolgus monkey), or human hepatocytes. Pharmacokinetics parameters, including clearance (CL) and half-life (t_1/2), can be calculated. In some embodiments, a reference compound (e.g., a first KRas inhibitor (e.g., MRTX1133)) may be used as a comparator. See, e.g., Example VI (“Liver microsomal metabolically stability”) of International Publication No. WO 2023/284881. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof can be assessed for its pharmacokinetic parameters and/or its ability to cause toxicity (e.g., skin toxicity) in an animal model. For example, a compound provided herein, or a pharmaceutically acceptable salt thereof, can be administered to an animal (e.g., rat), and body fluid (e.g., blood) samples can be taken at various time points and analyzed for the amount of the compound provided herein, or a pharmaceutically acceptable salt thereof, remaining. As another example, a compound provided herein, or a pharmaceutically acceptable salt thereof, can be administered to an animal (e.g., rat), and the skin of the animal can be assessed for redness, scaling, and/or thickness. An exemplary protocol follows. Rats (e.g., male RNU Nude Rat or Sprague-Dawley IGS rats, 6-8 weeks of age) are dosed with a compound provided herein, or a pharmaceutically acceptable salt thereof, once per day orally (e.g., via gavage) for several days (e.g., 14 days). The compound provided herein, or a pharmaceutically acceptable salt thereof, is administered to the rat at a given dose level (e.g., 1, 3, 5, 10, 25, 30, 50, or 100 mg/kg) in a solution or suspension formulation (e.g., 10% DMSO/90% hydroxypropyl methylcellulose). The rats have access to food and water ad libitum. Blood samples (e.g., 200 μL per sample) from the rats are taken at predetermined intervals, such as 4, 8, or 24 hours after the first dose is administered. The blood is sampled via jugular vein puncture, then the blood samples (e.g., with K₂EDTA as anticoagulant) are temporarily put on ice and then centrifuged (e.g., at 4 °C and 4600 RPM for 5 minutes) within 30 minutes. Plasma samples can be diluted 1:1 v/v with acidified phosphate buffer and are put on dry ice. After the completion of the last sampling, all samples are stored at -80 °C or analyzed in a short time following collection. The concentration of the compound provided herein, or a pharmaceutically acceptable salt thereof, measured in an acidified plasma sample (e.g., diluted 1:1 v/v with pH 3 phosphate buffer) can be determined (e.g., via LC/MS/MS). For example, an acidified plasma sample is prepared for analysis using protein precipitation (e.g., by the addition of acetonitrile), and an internal standard is spiked in at a known concentration. The spiked sample is mixed, centrifuged, and the supernatant is used in an LC/MS/MS method. The LC/MS/MS method uses an ACQUITY UPLC BEH C18 1.7 μm (2.1*50 mm) column with a first mobile phase of 5 mM NH₄OAc (0.05% formic acid (FA) or 0.1% FA) and a second mobile phase of acetonitrile (0.1% FA). Multiple reaction monitoring is used to measure the analyte(s) of interest. Using the concentration of the compound provided herein, or a pharmaceutically acceptable salt thereof, in the plasma sample, pharmacokinetic parameters of t_1/2 (hr), t_max (hr), C_max (ng/mL), AUC_last (hr*ng/mL), AUC_Inf (hr*ng/mL), AUC_Extr (%), MRT_Inf (hr), AUC_Inf/D (hr*kg*ng/mL/mg), F (%), are determined. The clinical signs, body weight and food consumption of the rats are tracked during dosing. The potential for skin rash is tracked intermittently before and during dosing using one or more methodologies. A skin scoring system is used to evaluate skin redness (erythema) or skin scaling on a gradation of 0-4. Thickness of the back skin is measured using a micrometer (MITUTOYO ABSOLUTE Digimatic Micrometer Series 227-211). For the back skin, thickness measurement is performed by doing a skin folding of the applied area between the thumb and index fingers followed by measuring with the micrometer. The mice are then sacrificed and assessed for any abnormalities. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, can be tested for its potency in inhibiting hERG potassium channels. The cardiac potassium channel hERG is responsible for a rapid delayed rectifier current (I_Kr) in human ventricle, and inhibition of I_Kr is the most common cause of cardiac action potential prolongation by non-cardiac drugs. Increased action potential duration causes prolongation of the QT interval that has been associated with a dangerous ventricular arrhythmia, torsade de pointes. There are several methods of testing hERG inhibition potency, including SyncroPatch hERG and manual patch clamp experiments. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, is tested for its potency in inhibiting hERG potassium channels using a SyncroPatch hERG assay. For example, in some embodiments, solutions or suspension of a compound provided herein, or a pharmaceutically acceptable salt thereof, at several concentrations (0.30 μM, 1.00 μM, 3.00 μM, 10.00 μM and 30.00 μM) can be exposed to single CHO or HEK293 cells. The effect of the compound provided herein, or a pharmaceutically acceptable salt thereof, on the inhibition of hERG potassium channels can be measured in this system using an electrical pulse pattern, the data plotted, and an IC₅₀ value calculated for the inhibition of hERG by the compound provided herein, or a pharmaceutically acceptable salt thereof. An exemplary protocol follows. hERG potassium channels are expressed in a Chinese Hamster Ovarian (CHO (Sophian Biosciences)) cell line that lacks endogenous I_Kr. See, e.g., Brown, Arthur M., and David Rampe. Pharmaceutical News 7.4 (2000): 15-20; Weirich, Jörg, and H. Antoni, Basic Research in Cardiology 93 (1998): s125-s132, doi: 10.1007/s003950050236; Yap, Yee Guan, and A. J. Camm. Clinical & Experimental Allergy 29 (1999): 174-181, doi: 10.1046/j.1365- 2222.1999.0290s3174.x; Haraguchi, Yuji, et al. BMC Pharmacology and Toxicology 16 (2015): 1-6, doi: 10.1186/s40360-015-0042-9; and Walker, B. D., et al. British Journal of Pharmacology 127.1 (1999): 243-251, 10.1038/sj.bjp.0702502. All chemicals used in solution preparations are purchased from a commercial supplier (e.g., Sigma-Aldrich) and are of ACS reagent grade purity or higher. Stock solutions of the compound provided herein, or a pharmaceutically acceptable salt thereof, positive control compound(s), and reference substance(s) are prepared in dimethyl sulfoxide (DMSO) and stored frozen. Solutions of each tested compound provided herein, or a pharmaceutically acceptable salt thereof, positive control compound(s), and reference substance(s) are prepared fresh daily by diluting stock solutions into HEPES-buffered physiological saline solution (HB- PS; 140 mM NaCl, 4 mM KCl, 2.0 mM CaCl₂, 1 mM MgCl₂, 10 mM HEPES, and 5 mM glucose, pH 7.4). Since previous results have shown that ≤ 0.3% DMSO does not affect channel current, all test and control solutions can contain up to 0.3% DMSO. In some embodiments, a positive control compound can be included in the experiment. In some such embodiments, the positive control compound can be amitriptyline (Sigma- Aldrich), for example, in a HB-PS and 0.3% DMSO solution. In some embodiments, a positive control compound can be included in the experiment. In some such embodiments, the positive control compound can be E-4031 (4ʹ-[[1-[2-(6- Methyl-2-pyridinyl)ethyl-4-piperidinyl]carbonyl]methanesulfonanilide, 2HCl) (Sigma- Aldrich), for example, in a HB-PS and 0.3% DMSO solution. If necessary, solutions are sonicated to facilitate dissolution. Visible precipitate observed during preparation or exposure of formulations to the test system is noted for reference. The effect of compounds provided herein, or a pharmaceutically acceptable salt thereof, is initially evaluated at 1 μM. Subsequent concentrations are evaluated based on the inhibition observed at this initial concentration. The CHO cells, which are at least two days after plating and more than 75% confluent, are used for experiments. Before testing, cells are harvested using TrypLE and resuspended in HB-PBS at room temperature. The HB-PBS and external solution (80 mM NaCl, 4 mM KCl, 2 mM CaCl₂, 1 mM MgCl₂, 60 mM N-Methyl-D-glucamine (NMDG), 10 mM HEPES, and 5 mM glucose, pH 7.4) are prepared and stored up to 1 month. Voltage command protocol: From a holding potential of -80 mV, the voltage is first stepped to -50 mV for 80 ms for leak subtraction, and then stepped to +20 mV for 4800 ms to open hERG channels. After that, the voltage is stepped back down to -50 mV for 5000 ms, causing a "rebound" or tail current, which is measured and collected for data analysis. Finally, the voltage is stepped back to the holding potential (-80 mV, 1000 ms). This voltage command protocol is repeated every 20,000 msec. This command protocol is performed continuously during the experiment. The hERG SyncroPatch assay is conducted at room temperature. The Setup, Prime Chip, Catch and Seal Cells, Amplifier Settings, Voltage and Application Protocols are established with Biomek Software (Nanion). A single cell per well is clamped with the formation of a gigaseal. On one side of the seal, the cell is bathed in external solution. On the opposite side, addition of 40 μL of the vehicle (e.g., HB-PBS) is applied, followed by a 300 s pause to create a baseline period. Then a dose of a compound provided herein, or a pharmaceutically acceptable salt thereof, is added (40 μL), and the process is repeated for different concentrations. The exposure of a compound provided herein, or a pharmaceutically acceptable salt thereof, at each concentration is no less than 300 s. The recording for the whole process must pass quality control criteria (e.g., seal quality, rundown attributes) or the well is abandoned, and the compound is retested, all automatically set by exclusion criteria determined prior to experiment start. Five concentrations (0.30 μM, 1.00 μM, 3.00 μM, 10.00 μM, and 30.00 μM) are tested for each tested compound provided herein, or a pharmaceutically acceptable salt thereof. A minimum of 2 replicates per concentration are obtained. Data analysis is carried out using DataControl, Excel 2013 (Microsoft) and GraphPad Prism 5.0. Within each well recording, a percent of control values is calculated for each concentration of the compound provided herein, or a pharmaceutically acceptable salt thereof, with current response based on peak current in presence of a reference compound (e.g., E- 4031) (current response/peak current) ×100%. The Dose-Response curves are fit to the standard Hill equation as shown below: where X is the logarithm of concentration, I_{post compound}/I_{pre compound} is the normalized peak current amplitude, Top is 1, and Bottom is equal to 0. Curve-fitting and IC50 calculations are performed by GraphPad Prism 5.0. If the inhibition obtained at the lowest concentration tested is over 50%, or at the highest concentration tested is less than 50%, the IC₅₀ is reported as less than the lowest concentration, or higher than the highest concentration, respectively. In some embodiments, a positive control can be included in the experiment. In some such embodiments, the positive control compound can be cisapride (Tocris Bioscience), for example, in a 0.3% DMSO solution. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, is not a hERG inhibitor. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits hERG with an IC₅₀ of greater than 60 nM (e.g., greater than 100 nM, 300 nM, 500 nM, 1 μM, 3 μM, 5 μM, 10 μM, 20 μM, or 30 μM). For example, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits hERG with an IC₅₀ of greater than 500 nM (e.g., 1 μM, 3 μM, 5 μM, 10 μM, 20 μM, or 30 μM). In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits hERG with an IC₅₀ of greater than 1 μM (e.g., greater than 3 μM, 5 μM, 10 μM, 20 μM, or 30 μM). In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits hERG with an IC₅₀ of greater than 10 μM (e.g., greater than 20 μM or 30 μM). In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits hERG with an IC₅₀ of greater than 30 μM. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, can be assessed for its stability in hepatocytes (e.g., human hepatocytes). In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, is assessed for stability in human hepatocytes, yielding a value for intrinsic hepatocyte clearance (CL_int(hep)), from which intrinsic liver clearance (CL_int (liver)) can be estimated. For example, human hepatocytes can be incubated with a compound provided herein, or a pharmaceutically acceptable salt thereof, and aliquots at various time points can be removed and analyzed for the amount of the compound provided herein, or a pharmaceutically acceptable salt thereof, remaining. First-order kinetics equations can then be used to determine half-life (t1/2) and CL_int(hep)_. An exemplary protocol follows. A 1000X stock solution of a compound provided herein is prepared to a final concentration (e.g., 1 mM in DMSO). Similarly, 1000X stock solution(s) of positive control compound(s) (e.g., 7-ethoxycoumarin and/or 7-hydroxycoumarin) is prepared to a final concentration (e.g., 3 mM in DMSO). 100X stock solutions are then made by dilution with acetonitrile. To prepare a cell suspension (e.g., at 0.5 × 10⁶ cells/mL), cryopreserved hepatocytes (e.g., human hepatocytes) are thawed (e.g., in Williams’ Medium E containing 5% fetal bovine serum and 30% Percoll solution and other supplements), isolated, and suspended in incubation medium (e.g., Williams’ Medium E (no phenol red) containing 2 mM L-Glutamine and 25 mM HEPES), then diluted with pre-warmed incubation medium to 0.5 × 10⁶ cells/mL. Pre-warmed cell suspension (e.g., 198 μL) is added to a well in a testing plate (e.g., a 96-well plate). A quenching plate is prepared by transferring stop solution (e.g., acetonitrile containing tolbutamide and labetalol as internal standards) (e.g., 125 μL) to a set of pre-labeled 96-well plates, with one quenching plate for T₀ and one plate per time point to be tested. To begin the experiment, 2 μL of the 100X dosing solution of the compound provided herein, or a pharmaceutically acceptable salt thereof, or 2 μL of the 100X dosing solution of a control compound is added to a well of the testing plate. This is performed in duplicate. For T0 samples, the plate is mixed to achieve a homogenous suspension (e.g., mixed for about 1 min), then an aliquot (e.g., 25 μL) of each sample on the testing plates is immediately transferred into a well of a quenching plate containing ice-cold stop solution (e.g., 125 μL), followed by mixing. The testing plate is incubated (e.g., at 37 °C in a 95% humidified incubator at 5% CO₂ with constant shaking) to start the reactions. At each time point of 15, 30, 60 and 90 minutes, the plate is mixed and then an aliquot of each sample (e.g., 25 μL) is transferred to a well in a quenching plate containing ice-cold stop solution (e.g., 125 μL) followed by mixing. Medium Control (MC) sample plates (at least one for the first and last time point; additional time points are optional) are prepared in the same way as the testing plate except that incubation medium is used instead of cell suspension. At each corresponding time point as the testing plate, the reactions are stopped by removing the corresponding MC plate from the incubator and mixing with ice-cold stop solution (e.g., 125 μL). Immediately after addition of stop solution to each plate, the plate is immediately vortexed (e.g., on a plate shaker at 600 RPM for 10 minutes). Then the plate is centrifuged (e.g., at 3220 x g for 20 min at 4 °C). After centrifugation, supernatant from the plate (e.g., 80 μL/well) is transferred to another plate (e.g., a corresponding 96-well plate) which contains ultra pure water (240 μL per well) according to the plate map. This analytical plate is sealed and stored at 4 °C until LC- MS/MS analysis. The percent remaining of the compound provided herein, or a pharmaceutically acceptable salt thereof, after incubation is calculated by the following equations. The equation of first order kinetics is used to calculate t_1/2 and CL_int: Equation of first order kinetics: When , then CL_int (hep) = k / million cells per mL CL_int (liver) = CL_int (hep)* liver weight (g/kg body weight) x hepatocellularity Table 2 shows reference values for liver weight, liver blood flow, and hepatocellularity for various species. See, e.g., Sohlenius-Sternbeck, Anna-Karin Toxicology in vitro 20.8 (2006): 1582-1586, doi: 10.1016/j.tiv.2006.06.003; Davies, Brian, and Tim Morris Pharmaceutical Research 10.7 (1993): 1093-1095; and Obach, R. Scott, et al. Journal of Pharmacology and Experimental Therapeutics 283.1 (1997): 46-58. Table 2. Table 3 shows floor and ceiling values for the described assay. For example, if CL_int (hep) falls below 6.4 μL/min/10⁶ cells, an experimental value may not be able to be accurately determined. Table 3. Cut off Value in Hepatocyte Stability Assay In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof can be assessed for its stability in simulated human fluids (e.g., simulated gastric fluid or simulated intestinal fluid). For example, a compound provided herein, or a pharmaceutically acceptable salt thereof can be incubated in a simulated human fluid (e.g., simulated gastric fluid (e.g., fed or fasted state) or simulated intestinal fluid (e.g., fed or fasted state)), and aliquots at various time points can be removed and analyzed for the amount of the compound provided herein, or a pharmaceutically acceptable salt thereof, remaining. An exemplary protocol follows. Fasted state simulated gastric fluid (FaSSGF) is prepared (0.02 mM lecithin, 0.08 mM sodium taurocholate, 0.1 mg/mL pepsin, 34.2 mM sodium chloride, 25.1 mM hydrochloric acid, and deionized water, pH 1.6 ± 0.05). A working solution of a compound provided herein, or a pharmaceutically acceptable salt thereof is prepared (e.g., 2 μM in DMSO). Similarly, a working solution of a control compound (e.g., omeprazole) is prepared (e.g. 2 μM in DMSO). An aliquot (e.g., 2 μL) of either working solution is transferred to a deep-well plate, one plate per time condition to be tested (e.g., 0 minutes, 60 minutes, 120 minutes, 360 minutes, and 1440 minutes). To the plates corresponding to the later time points (e.g., T60, T120, T360, and T1440), an aliquot (e.g., 198 μL) of the FaSSGF is added, and the samples adjusted to have a final DMSO concentration of 1%. The plates are incubated at 37 °C with shaking at 600 RPM for the appointed amount of time. At the end of the appointed amount of time, the reaction is stopped by the addition of stop solution (e.g., 400 μL), and the resulting solution is mixed. A portion of this mixture (e.g., 200 μL) is removed and mixed with a further addition of stop solution (e.g., 400 μL). Similarly, the T₀ samples are prepared by adding stop solution (e.g., 400 μL), mixing, then adding the FaSSGF (e.g., 200 μL) and mixing again. The T₀ samples are further prepared by removing a portion of this mixture (e.g., 200 μL) and mixing with a further addition of stop solution (e.g., 400 μL). Following the second addition of stop solution at each time point, the samples are centrifuged (e.g., at 4000 RPM at 4 °C for 20 min). A portion of the supernatant (e.g., 60 μL) is removed and mixed with purified water (e.g., 180 μL) for LC-MS/MS analysis. The LC- MS/MS analysis is performed using an ACQUITY UPLC BEH C181.7 μm 2.1 * 50 mm (Part No.186002350) column, with a mobile phase A (0.1% formic acid in water) and a mobile phase B (0.1% formic acid in acetonitrile). The percent remaining of the compound provided herein, or a pharmaceutically acceptable salt thereof, at each incubation time is calculated based on peak area ratio of analyte to internal standard from the LC-MS/MS analysis using the equation below. Where PAR is the peak area ratio, the ratio of peak area of the analyte of interest and an internal standard; PAR_T is the peak area ratio at the appointed time; and PAR₀ is the peak area ratio at T₀. Fed state simulated intestinal fluid (FeSSIF) is prepared (0.282% (w/v) lecithin, 0.806% (w/v) sodium taurocholate, 0.865% (w/v) acetic acid, 1.52% (w/v) potassium chloride, and deionized water, pH 5.0 ± 0.05). A working solution of a compound provided herein, or a pharmaceutically acceptable salt thereof is prepared (e.g. 2 μM in DMSO). Similarly, a working solution of a control compound (e.g., chlorambucil) is prepared (e.g. 2 μM in DMSO). An aliquot (e.g., 2 μL) of either working solution is transferred to a deep-well plate, one plate per time condition to be tested (e.g., 0 minutes, 60 minutes, 120 minutes, 360 minutes, and 1440 minutes). To the plates corresponding to the later time points (e.g., T60, T120, T360, and T1440), an aliquot (e.g., 198 μL) of the FeSSIF is added, and the samples are adjusted to have a final DMSO concentration of 1%. The plates are incubated at 37 °C with shaking at 600 RPM for the appointed amount of time. At the end of the appointed amount of time, the reaction is stopped by the addition of stop solution (e.g., 400 μL), and the resulting solution is mixed. A portion of this mixture (e.g., 200 μL) is removed and mixed with a further addition of stop solution (e.g., 400 μL). Similarly, the T₀ samples are prepared by adding stop solution (e.g., 400 μL), mixing, then adding the FeSSIF (e.g., 200 μL) and mixing again. The T₀ samples are further prepared by removing a portion of this mixture (e.g., 200 μL) and mixing with a further addition of stop solution (e.g., 400 μL). Following the second addition of stop solution at each time point, the samples are centrifuged (e.g., at 4000 RPM at 4 °C for 20 min). A portion of the supernatant (e.g., 60 μL) is removed and mixed with purified water (e.g., 180 μL) for LC-MS/MS analysis. The LC-MS/MS analysis is performed using an ACQUITY UPLC HSS T31.8 μm 2.1 * 50 mm, (Part No.186003538) column, with a mobile phase A (0.1% formic acid in water) and a mobile phase B (0.1% formic acid in acetonitrile). The percent remaining of the compound provided herein, or a pharmaceutically acceptable salt thereof, at each incubation time is calculated based on peak area ratio of analyte to internal standard from the LC-MS/MS analysis using the equation below. Where PAR is the peak area ratio, the ratio of peak area of the analyte of interest and an internal standard; PAR_T is the peak area ratio at the appointed time; and PAR₀ is the peak area ratio at T₀. Fasted state simulated intestinal fluid (FaSSIF) is prepared (0.056% (w/v) lecithin, 0.161% (w/v) sodium taurocholate, 0.39% (w/v) monobasic potassium phosphate, 0.77% (w/v) potassium chloride, and deionized water, pH 6.5 ± 0.05). A working solution of a compound provided herein, or a pharmaceutically acceptable salt thereof is prepared (e.g. 2 μM in DMSO). Similarly, a working solution of a control compound (e.g., chlorambucil) is prepared (e.g. 2 μM in DMSO). An aliquot (e.g., 2 μL) of either working solution is transferred to a deep-well plate, one plate per time condition to be tested (e.g., 0 minutes, 60 minutes, 120 minutes, 360 minutes, and 1440 minutes). To the plates corresponding to the later time points (e.g., T60, T120, T360, and T1440), an aliquot (e.g., 198 μL) of the FaSSIF is added, and the samples adjusted to have a final DMSO concentration of 1%. The plates are incubated at 37 °C with shaking at 600 RPM for the appointed amount of time. At the end of the appointed amount of time, the reaction is stopped by the addition of stop solution (e.g., 400 μL), and the resulting solution is mixed. A portion of this mixture (e.g., 200 μL) is removed and mixed with a further addition of stop solution (e.g., 400 μL). Similarly, the T₀ samples are prepared by adding stop solution (e.g., 400 μL), mixing, then adding the FaSSIF (e.g., 200 μL) and mixing again. The T₀ samples are further prepared by removing a portion of this mixture (e.g., 200 μL) and mixing with a further addition of stop solution (e.g., 400 μL). Following the second addition of stop solution at each time point, the samples are centrifuged (e.g., at 4000 RPM at 4 °C for 20 min). A portion of the supernatant (e.g., 60 μL) is removed and mixed with purified water (e.g., 180 μL) for LC-MS/MS analysis. The LC-MS/MS analysis is performed using an ACQUITY UPLC HSS T31.8 μm 2.1 * 50mm, (Part No.186003538) column, with a mobile phase A (0.1% formic acid in water) and a mobile phase B (0.1% formic acid in acetonitrile). The percent remaining of the compound provided herein, or a pharmaceutically acceptable salt thereof, at each incubation time is calculated based on peak area ratio of analyte to internal standard from the LC-MS/MS analysis using the equation below. Where PAR is the peak area ratio, the ratio of peak area of the analyte of interest and an internal standard; PAR_T is the peak area ratio at the appointed time; and PAR₀ is the peak area ratio at T₀. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof can be assessed for its solubility in simulated human fluids (e.g., simulated gastric fluid or simulated intestinal fluid) or aqueous solutions (e.g., water or pH 3.0 citrate buffer). For example, a compound provided herein, or a pharmaceutically acceptable salt thereof can be incubated in a simulated human fluid (e.g., simulated gastric fluid or simulated intestinal fluid) or an aqueous solution (e.g., water or pH 3.0 citrate buffer). For example, a compound provided herein, or a pharmaceutically acceptable salt thereof can be incubated in a simulated human fluid (e.g., simulated gastric fluid (e.g., fed or fasted state) or simulated intestinal fluid (e.g., fed or fasted state)) or an aqueous solution (e.g., water or pH 3.0 citrate buffer) , and aliquots at various time points can be removed and analyzed for the amount of the compound provided herein, or a pharmaceutically acceptable salt thereof, remaining. An exemplary protocol follows. Fasted state simulated gastric fluid (FaSSGF) is prepared (0.02 mM lecithin, 0.08 mM sodium taurocholate, 0.1 mg/mL pepsin, 34.2 mM sodium chloride, 25.1 mM hydrochloric acid, and deionized water, pH 1.6 ± 0.05). The FaSSGF is equilibrated at 37 °C. Fed state simulated intestinal fluid (FeSSIF) is prepared (0.282% (w/v) lecithin, 0.806% (w/v) sodium taurocholate, 0.865% (w/v) acetic acid, 1.52% (w/v) potassium chloride, and deionized water, pH 5.0 ± 0.05). The FeSSIF is equilibrated at 37 °C. Fasted state simulated intestinal fluid (FaSSIF) is prepared (0.056% (w/v) lecithin, 0.161% (w/v) sodium taurocholate, 0.39% (w/v) monobasic potassium phosphate, 0.77% (w/v) potassium chloride, and deionized water, pH 6.5 ± 0.05). The FaSSIF is equilibrated at 37 °C. Citrate buffer is prepared (100 mM sodium citrate, pH 3.07). Solubility in citrate buffer and water is determined at room temperature. A compound provided herein, or a pharmaceutically acceptable salt thereof, (e.g., 6 mg) is combined with FaSSGF, FeSSIF, FaSSIF, citrate buffer, or water (e.g., 3 mL). The vials are stirred (at 37 °C for simulated human fluid or room temperature for citrate buffer and water), and at 30 minutes, 3 hours, and 24 hours, an aliquot is removed and filtered (e.g., using a 0.2 μm syringe filter), then analyzed with HPLC (e.g., HPLC is conducted using an Agilent 1290 Infinity LC System equipped with a VWD (Variable Wavelength Detector) and an Agilent 1260 ELSD (Evaporative Light Scattering Detector). Flow rate range of the instrument is 0.2– 5.0 mL/min, operating pressure range is 0–1300 bar, temperature range is 5 °C above ambient to 60 °C, and wavelength range is 190–600 nm; mobile phase A of 0.1% trifluoroacetic acid (TFA) in distilled water; mobile phase B of 0.1% TFA in acetonitrile; column Waters Acuity UPLC CSH C-18, 2.1 x 150 mm, 1.7 μm) to determine the dissolved concentration of the compound provided herein, or a pharmaceutically acceptable salt thereof. In some embodiments, the kinetic solubility of a compound provided herein, or a pharmaceutically acceptable salt thereof can be determined. In some embodiments, the kinetic solubility of a compound provided herein, or a pharmaceutically acceptable salt thereof, is determined at a physiologically relevant pH (e.g., 7.4). For example, a stock solution of a compound provided herein, or a pharmaceutically acceptable salt thereof, can be prepared, and any solids separated (e.g., by centrifugation). The resulting mixture (e.g., supernatant) can be subsequently filtered, and the dissolved concentration of the compound provided herein, or a pharmaceutically acceptable salt thereof, can be determined via liquid chromatography. An exemplary protocol follows. A stock solution (e.g., a 200 μM stock solution) of a compound provided herein, or a pharmaceutically acceptable salt thereof, is diluted with buffer (e.g., phosphate buffer, pH 7.4) (e.g., 10 μL of the stock solution with 490 uL of the buffer). The diluted sample is vortexed for at least two minutes and then shaken (e.g., at 800 RPM) on a shaker for 24 hours at room temperature. The sample is then centrifuged (e.g., at 4000 RPM for 10 minutes at 25 °C). The supernatant is filtered (e.g., in a plate format by centrifugation for 5 minutes), and the concentration of the compound provided herein, or a pharmaceutically acceptable salt thereof, is determined by an LC-UV system (e.g., with a mobile phase A of 0.1% TFA and 5 mM NH₄OAc in water/MeCN (v:v, 95:5) and a mobile phase B of 0.1% TFA and 5 mM NH₄OAc in water/MeCN (v:v, 5:95)). In some embodiments, the chemical stability of a compound provided herein, or a pharmaceutically acceptable salt thereof, can be determined. For example, an aliquot of a solution of a compound provided herein, or a pharmaceutically acceptable salt thereof, is added to an acidic solution (e.g., pH 1.5 or pH 5) and incubated for a period of time. A sample of the incubation mixture can be taken, and the remaining amount of the compound provided herein, or a pharmaceutically acceptable salt thereof, can be determined via liquid chromatography- mass spectrometry (LCMS) and/or nuclear magnetic resonance (NMR). Exemplary protocols follow. To prepare a pH 1.5 HCl solution, 1 N hydrogen chloride solution (1 mL) is added to deionized water (99 mL) and stirred for 5 minutes. The pH is adjusted, while stirring and monitoring by pH meter, to the desired pH using concentrated hydrochloric acid. To prepare a pH 5 HCl solution, 1 N hydrogen chloride solution (1 mL) is added to deionized water. (99 mL) and stirred for 5 minutes. The pH is adjusted, while stirring and monitoring by pH meter, to the desired pH using 1N sodium hydroxide. A portion (e.g., 10 μL) of a stock solution (e.g., 10 mM) of a compound provided herein, or a pharmaceutically acceptable salt thereof, is added the HCl solution at pH of 1.5 or pH 5 (e.g., 90 μL) in separate vials denoted for each timepoint (e.g., T₀, T_30m, T_60m, T_90m, T_240m, and T_3d). The samples are incubated at 37 °C for the desired timeframe and then immediately neutralized with 10 μL of HEPES buffer to pH of 7. The T₀ timepoint is neutralized immediately upon preparation of the sample. The samples are then analyzed by LCMS to determine the amount of the compound provided herein, or a pharmaceutically acceptable salt thereof, remaining. To prepare pH 1.5 and pH 5 DCl solutions, deuterium oxide (5 mL) is adjusted to the desired pH of 1.5 or 5, monitoring by pH meter, using 20% DCl in D₂O and stirred at room temperature for 5 minutes. A compound provided herein, or a pharmaceutically acceptable salt thereof, is dissolved in the pH 1.5 or pH 5 DCl solution to achieve a 3 mg/mL solution. The resulting solution is incubated at 37 °C to the desired timepoint (T₀, T_90m, T_240m, T_5d) then an aliquot (e.g., 0.3 mL) is taken and analyzed by ¹H NMR to determine the amount of the compound provided herein, or a pharmaceutically acceptable salt thereof, remaining and/or to determine the presence of a compound that is not the compound provided herein. At the same timepoints, 30 μL of the solution was neutralized with HEPES buffer to pH of 7 and analyzed by LCMS to determine the amount of the compound provided herein, or a pharmaceutically acceptable salt thereof, remaining and/or to determine the presence of a compound that is not the compound provided herein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, can be assessed as a potential substrate for efflux (e.g., as a potential substrate for p-glycoprotein (P-gp)). In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, is assessed as a substrate for efflux using efflux pump-expressing cells, such as MDCKII cells. For example, a compound provided herein, or a pharmaceutically acceptable salt thereof, can be applied to one side of a cell monolayer, incubated, and then the recovery of the compound on the opposite side of the cell monolayer can be measured to determine the permeability of the compound to the cell monolayer in that direction. An exemplary protocol follows. MDCKⅡ cells (e.g., obtained from the Netherlands Cancer Institute) are seeded onto polycarbonate membranes (PC) in 96-well insert systems at 2.33 x 10⁵ cells/cm² for 4-7 days for confluent cell monolayer formation. A solution of a compound provided herein, or a pharmaceutically acceptable salt thereof, is diluted with transport buffer (e.g., Hank’s Balanced Salt Solution (HBSS) with 10 mM HEPES, pH 7.4) from a DMSO stock solution to a final concentration (e.g., of 2.00 μM (DMSO < 1%)) and applied to the apical or basolateral side of the cell monolayer. Permeation of the compound provided herein, or a pharmaceutically acceptable salt thereof, from the A to B direction and the B to A direction is determined in duplicate. For control data, digoxin is tested at 10.0 μM from A to B direction or B to A direction, while nadolol and metoprolol are tested (e.g., at 2.00 μM) in A to B direction in duplicate. The plate is incubated (e.g., for 2.5 hours in an incubator at 37.0 °C, with 5% CO2 at saturated humidity without shaking). The efflux ratio of each compound is then determined. The compound provided herein, or pharmaceutically acceptable salt thereof, and control compounds are quantified by LC-MS/MS analysis based on the peak area ratio of analyte/internal standard (IS). The apparent permeability coefficient P_app (cm/s) is calculated using the equation: P_app = (dC_r/dt) x V_r / (A x C₀) Where dC_r/dt is the cumulative concentration of compound in the receiver chamber as a function of time; V_r is the solution volume in the receiver chamber (0.075 mL on the apical side, 0.25 mL on the basolateral side); A is the surface area for the transport (e.g., 0.143 cm² for the area of the monolayer); and C₀ is the initial concentration in the donor chamber. The efflux ratio was calculated using the equation: Efflux Ratio = P_app (BA) / P_app (AB) Without being bound by any particular theory, it is believed that the Efflux Ratio indicates how efficiently a tested compound is removed from the tested cell. Percent recovery was calculated using the equation: %Solution Recovery = 100 x [(V_r x C_r) + (V_d x C_d)] / (V_d x C₀) Where V_d is the volume in the donor chamber (0.075 mL on the apical side, 0.25 mL on the basolateral side); Cd and Cr are the final concentrations of transport compound in donor and receiver chambers, respectively. Without being bound by any particular theory, it is believed that the percent recovery is informative of whether the tested compound could have a solubility issue, is stuck in the cellular membrane, metabolized, or a combination thereof. After the transport assay, a Lucifer yellow rejection assay is used to determine the cell monolayer integrity (e.g., to determine whether the cell monolayer from the efflux study is intact). Buffers are removed from both apical and basolateral chambers, followed by the addition of lucifer yellow dye (e.g., 75 μL of a 100 μM solution in transport buffer) and transport buffer (e.g., 250 μL) in the apical and basolateral chambers, respectively. The plate is incubated (e.g., for 30 minutes at 37 °C with 5% CO₂ and 95% relative humidity without shaking). After incubation, a lucifer yellow (e.g., 20 μL) sample is taken from the apical side, and transport buffer (e.g., 60 μL) is added. A lucifer yellow sample (e.g., 80 μL) is taken from the basolateral side. The relative fluorescence unit (RFU) of lucifer yellow is measured at 425/528 nm (excitation/emission) with an Envision plate reader. Percent of lucifer yellow in the basolateral well is calculated using the equation: where RFU_Apical and RFU_Basolateral are the relative fluorescence unit values of lucifer yellow in the apical and basolateral wells, respectively; V_Apical and V_Basolateral are the volume of apical and basolateral wells (0.075 mL and 0.25 mL), respectively. The %Lucifer Yellow should be less than 2.0 to indicate an intact cell monolayer. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, can be assessed for formation of metabolites. For example, a compound provided herein, or a pharmaceutically acceptable salt thereof can be incubated with hepatocytes (e.g., rat hepatocytes, dog hepatocytes, or human hepatocytes), and at the end of incubation, the sample can be analyzed for the amount of the compound provided herein, or a pharmaceutically acceptable salt thereof, remaining, as well as for the amount of any metabolite from Phase 1 metabolism, Phase 2 metabolism, or a combination thereof. An exemplary protocol follows. A working solution of a compound provided herein, or a pharmaceutically acceptable salt thereof, is prepared (e.g. 10 μM in DMSO). Similarly, a working solution of a control compound (e.g., 7-ethoxycoumarin) is prepared (e.g. 30 μM in DMSO). An aliquot of each working solution of a compound provided herein, or a pharmaceutically acceptable salt thereof, or the working solution of the control compound is incubated with hepatocytes (e.g., 1.0 × 10⁶ cells/mL) (e.g., rat hepatocytes, dog hepatocytes, or human hepatocytes) in incubation medium (e.g., Williams’ Medium E with HEPES (e.g., 5.958 g/L) glutamine (e.g., 0.292 g/L)), to a total volume of 200 μL, for 0 minutes or 120 minutes at 37 °C in 5% CO₂/saturated humidity. After incubation, MeCN (800 μL) is added to each sample, and the samples are centrifuged. The supernatants are dried under N₂ gas, and the residue is reconstituted (e.g., with 200 μL of 10% MeCN with 0.1% FA). The reconstituted residue of the compound provided herein, or a pharmaceutically acceptable salt thereof, is subjected to LC-UV-MS (e.g., LC with a Mobile Phase A of 0.1% FA and 2 mM NH₄FA in H₂O/MeCN (v : v = 95 : 5), a Mobile Phase B of 0.1% FA and 2 mM NH₄FA in H₂O/MeCN (v : v = 5 : 95) using an ACQUITY UPLC® HSS T32.1 × 100 mm, 1.8 μm column; a UV detector with λ: 190~500 nm; and MS with a Xevo G2 Q-TOF instrument in ESI⁺ mode with a scanning mode of MS^E/MS²). The reconstituted residue of the control compound is subjected to LC-UV-MS (e.g., LC with a Mobile Phase A of 0.1% FA in H₂O, a Mobile Phase B of 0.1% FA in MeCN using an ACQUITY UPLC® HSS T32.1 × 100 mm, 1.8 μm column; a UV detector with λ: 190~500 nm; and MS with a Xevo G2 Q-TOF instrument in ESI⁺ mode with a scanning mode of MS^E). The data is then analyzed to identify and, if desired, quantify the metabolites. In some embodiments, the compounds provided herein, or pharmaceutically acceptable salts thereof, can exhibit potent and selective inhibition of a dysregulated KRas protein (e.g., a wild-type KRas protein and/or a mutant KRas protein (e.g., a KRas G12D mutant protein, a KRas G12R mutant protein, and/or a KRas G12V mutant protein (e.g., a KRas G12D mutant protein and/or a KRas G12V mutant protein))). In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, can selectively inhibit a dysregulated KRas protein (e.g., a wild-type KRas protein and/or a mutant KRas protein (e.g., a KRas G12D mutant protein, a KRas G12R mutant protein, and/or a KRas G12V mutant protein (e.g., a KRas G12D mutant protein and/or a KRas G12V mutant protein))) over another GTPase or non-GTPase target. In some embodiments, the compounds provided herein can exhibit nanomolar potency against a KRas protein (e.g., a wild-type KRas protein and/or a mutant KRas protein (e.g., a KRas G12D mutant protein, a KRas G12R mutant protein, and/or a KRas G12V mutant protein (e.g., a KRas G12D mutant protein and/or a KRas G12V mutant protein))) with minimal activity against related GTPases (e.g., wild type NRas protein, and/or wild type HRas protein). In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, can exhibit greater inhibition of a KRas protein (e.g., a wild-type KRas protein and/or a mutant KRas protein (e.g., a KRas G12D mutant protein, a KRas G12R mutant protein, and/or a KRas G12V mutant protein (e.g., a KRas G12D mutant protein and/or a KRas G12V mutant protein))) relative to inhibition of a related GTPase (e.g., wild type NRas protein, and/or wild type HRas protein). In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, can exhibit at least 2-fold, 3-fold, 5-fold, 10-fold, 25- fold, 50-fold, or 100-fold greater inhibition of a KRas protein (e.g., a wild-type KRas protein and/or a mutant KRas protein (e.g., a KRas G12D mutant protein, a KRas G12R mutant protein, and/or a KRas G12V mutant protein (e.g., a KRas G12D mutant protein and/or a KRas G12V mutant protein))) relative to inhibition of a related GTPase (e.g., wild type NRas protein, and/or wild type HRas protein). In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, can exhibit up to 10000-fold greater inhibition of a KRas protein (e.g., a wild-type KRas protein and/or a mutant KRas protein (e.g., a KRas G12D mutant protein, a KRas G12R mutant protein, and/or a KRas G12V mutant protein (e.g., a KRas G12D mutant protein and/or a KRas G12V mutant protein))) relative to inhibition of a related GTPase (e.g., wild type NRas protein, and/or wild type HRas protein). In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, can exhibit from about 2-fold to about 10-fold greater inhibition of a KRas protein (e.g., a wild-type KRas protein and/or a mutant KRas protein (e.g., a KRas G12D mutant protein, a KRas G12R mutant protein, and/or a KRas G12V mutant protein (e.g., a KRas G12D mutant protein and/or a KRas G12V mutant protein))) relative to inhibition of a related GTPase (e.g., wild type NRas protein, and/or wild type HRas protein). In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, can exhibit from about 10-fold to about 100-fold greater inhibition of a KRas protein (e.g., a wild-type KRas protein and/or a mutant KRas protein (e.g., a KRas G12D mutant protein, a KRas G12R mutant protein, and/or a KRas G12V mutant protein (e.g., a KRas G12D mutant protein and/or a KRas G12V mutant protein))) relative to inhibition of a related GTPase (e.g., wild type NRas protein, and/or wild type HRas protein). In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, can exhibit from about 100-fold to about 1000-fold greater inhibition of a KRas protein (e.g., a wild-type KRas protein and/or a mutant KRas protein (e.g., a KRas G12D mutant protein, a KRas G12R mutant protein, and/or a KRas G12V mutant protein (e.g., a KRas G12D mutant protein and/or a KRas G12V mutant protein))) relative inhibition of a related GTPase (e.g., wild type NRas protein, and/or wild type HRas protein). In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, can exhibit from about 1000-fold to about 10000-fold greater inhibition of a KRas protein (e.g., a wild-type KRas protein and/or a mutant KRas protein (e.g., a KRas G12D mutant protein, a KRas G12R mutant protein, and/or a KRas G12V mutant protein (e.g., a KRas G12D mutant protein and/or a KRas G12V mutant protein))) relative to inhibition of a related GTPase (e.g., wild type NRas protein, and/or wild type HRas protein). In some embodiments, the compounds provided herein, or pharmaceutically acceptable salts thereof, can exhibit potent and selective inhibition of a dysregulated KRas protein (e.g., a mutant KRas protein (e.g., a KRas G12D mutant protein, a KRas G12R mutant protein, and/or a KRas G12V mutant protein (e.g., a KRas G12D mutant protein and/or a KRas G12V mutant protein))). In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutically acceptable salt thereof, can selectively inhibit a dysregulated KRas protein (e.g., a mutant KRas protein (e.g., a KRas G12D mutant protein, a KRas G12R mutant protein, and/or a KRas G12V mutant protein (e.g., a KRas G12D mutant protein and/or a KRas G12V mutant protein))) over another GTPase or non-GTPase target. In some embodiments, the compounds provided herein can exhibit nanomolar potency against a mutant KRas protein (e.g., a KRas G12D mutant protein, a KRas G12R mutant protein, and/or a KRas G12V mutant protein (e.g., a KRas G12D mutant protein and/or a KRas G12V mutant protein))) with minimal activity against related GTPases (e.g., wild type KRas protein, wild type NRas protein, and/or wild type HRas protein). In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, can exhibit greater inhibition of a mutant KRas protein (e.g., a KRas G12D mutant protein, a KRas G12R mutant protein, and/or a KRas G12V mutant protein (e.g., a KRas G12D mutant protein and/or a KRas G12V mutant protein)) relative to inhibition of wild type KRas protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, can exhibit at least 2-fold, 3-fold, 5-fold, 10-fold, 25-fold, 50-fold, or 100-fold greater inhibition of a mutant KRas protein (e.g., a KRas G12D mutant protein, a KRas G12R mutant protein, and/or a KRas G12V mutant protein (e.g., a KRas G12D mutant protein and/or a KRas G12V mutant protein)) relative to inhibition of wild type KRas protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, can exhibit up to 10000-fold greater inhibition of a mutant KRas protein (e.g., a KRas G12D mutant protein, a KRas G12R mutant protein, and/or a KRas G12V mutant protein (e.g., a KRas G12D mutant protein and/or a KRas G12V mutant protein)) relative to inhibition of wild type KRas protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, can exhibit from about 2-fold to about 10-fold greater inhibition of a mutant KRas protein (e.g., a KRas G12D mutant protein, a KRas G12R mutant protein, and/or a KRas G12V mutant protein (e.g., a KRas G12D mutant protein and/or a KRas G12V mutant protein)) relative to inhibition of wild type KRas protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, can exhibit from about 10-fold to about 100-fold greater inhibition of a mutant KRas protein (e.g., a KRas G12D mutant protein, a KRas G12R mutant protein, and/or a KRas G12V mutant protein (e.g., a KRas G12D mutant protein and/or a KRas G12V mutant protein)) relative to inhibition of wild type KRas protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, can exhibit from about 100-fold to about 1000-fold greater inhibition of a mutant KRas protein (e.g., a KRas G12D mutant protein, a KRas G12R mutant protein, and/or a KRas G12V mutant protein (e.g., a KRas G12D mutant protein and/or a KRas G12V mutant protein)) relative to inhibition of wild type KRas protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, can exhibit from about 1000-fold to about 10000-fold greater inhibition of a mutant KRas protein (e.ga KRas G12D mutant protein, a KRas G12R mutant protein, and/or a KRas G12V mutant protein (e.g., a KRas G12D mutant protein and/or a KRas G12V mutant protein)) relative to inhibition of wild type KRas protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, can exhibit nanomolar potency against a dysregulated KRas protein (e.g., a mutant KRas protein (e.g., a KRas G12D mutant protein, a KRas G12R mutant protein, and/or a KRas G12V mutant protein (e.g., a KRas G12D mutant protein and/or a KRas G12V mutant protein))) with minimal activity against wild type NRas protein and/or wild type HRas protein In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, can exhibit greater inhibition of a dysregulated KRas protein (e.g., a mutant KRas protein (e.g., a KRas G12D mutant protein, a KRas G12R mutant protein, and/or a KRas G12V mutant protein (e.g., a KRas G12D mutant protein and/or a KRas G12V mutant protein))) relative to inhibition of wild type NRas protein and/or wild type HRas protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, can exhibit at least 2-fold, 3-fold, 5-fold, 10-fold, 25-fold, 50-fold or 100-fold greater inhibition of a dysregulated KRas protein (e.g., a mutant KRas protein (e.g., a KRas G12D mutant protein, a KRas G12R mutant protein, and/or a KRas G12V mutant protein (e.g., a KRas G12D mutant protein and/or a KRas G12V mutant protein))) relative to inhibition of wild type NRas protein and/or wild type HRas protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, can exhibit up to 1000-fold greater inhibition of a dysregulated KRas protein (e.g., a mutant KRas protein (e.g., a KRas G12D mutant protein, a KRas G12R mutant protein, and/or a KRas G12V mutant protein (e.g., a KRas G12D mutant protein and/or a KRas G12V mutant protein))) relative to inhibition of wild type NRas protein and/or wild type HRas protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, can exhibit up to 10000-fold greater inhibition of a dysregulated KRas protein (e.g., a mutant KRas protein (e.g., a KRas G12D mutant protein, a KRas G12R mutant protein, and/or a KRas G12V mutant protein (e.g., a KRas G12D mutant protein and/or a KRas G12V mutant protein))) relative to inhibition of wild type NRas protein and/or wild type HRas protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, can exhibit from about 2-fold to about 10-fold greater inhibition of a dysregulated KRas protein (e.g., a mutant KRas protein (e.g., a KRas G12D mutant protein, a KRas G12R mutant protein, and/or a KRas G12V mutant protein (e.g., a KRas G12D mutant protein and/or a KRas G12V mutant protein))) relative to inhibition of wild type NRas protein and/or wild type HRas protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, can exhibit from about 10-fold to about 100-fold greater inhibition of a dysregulated KRas protein (e.g., a mutant KRas protein (e.g., a KRas G12D mutant protein, a KRas G12R mutant protein, and/or a KRas G12V mutant protein (e.g., a KRas G12D mutant protein and/or a KRas G12V mutant protein))) relative to inhibition of wild type HRas protein and/or wild type NRas protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, can exhibit from about 100-fold to about 1000-fold greater inhibition of a dysregulated KRas protein (e.g., a mutant KRas protein (e.g., a KRas G12D mutant protein, a KRas G12R mutant protein, and/or a KRas G12V mutant protein (e.g., a KRas G12D mutant protein and/or a KRas G12V mutant protein))) relative to inhibition of wild type NRas protein and/or wild type HRas protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, can exhibit from about 1000- fold to about 10000-fold greater inhibition of a dysregulated KRas protein (e.g., a mutant KRas protein (e.g., a KRas G12D mutant protein, a KRas G12R mutant protein, and/or a KRas G12V mutant protein (e.g., a KRas G12D mutant protein and/or a KRas G12V mutant protein))) relative to inhibition of wild type NRas protein and/or wild type HRas protein. Compounds provided herein, or pharmaceutically acceptable salts thereof, are useful for treating diseases and disorders including cardiovascular disease (e.g., arteriovenous malformations or Noonan syndrome), endometriosis, an inflammatory and/or autoimmune disease (e.g., a nonmalignant syndrome of autoimmunity and abnormal leukocyte homeostasis), proliferative disorders such as cancers, including hematological cancers and solid tumors (e.g., advanced solid tumors), and disorders of the MAPK pathway (e.g., neurofibromatosis type 1). In some embodiments, the diseases and disorders are KRas- associated diseases and disorders (e.g., mutant KRas-associated diseases or disorders (e.g., KRas G12D-, KRas G12R-, or G12V-associated diseases or disorders)). In certain embodiments, compounds provided herein, or pharmaceutically acceptable salts thereof, are useful for preventing diseases and disorders as defined herein (for example, a cardiovascular disease, endometriosis, and an inflammatory and/or autoimmune disease, or cancer). In some embodiments of any of the methods or uses described herein, the inflammatory and/or autoimmune disease is RAS-associated autoimmune leukoproliferative disease. See, e.g., Niemela et al. Blood.2011; 117(10):2883-6, doi: 10.1182/blood-2010-07-295501. In some embodiments, the subject has been identified or diagnosed as having a cancer with a KRas dysregulation (e.g., a KRas mutation or amplification) (e.g., as determined using a regulatory agency-approved, e.g., FDA-approved, assay or kit). In some embodiments, the subject has a cancer (e.g., a tumor sample) that has a KRas dysregulation (e.g., a KRas mutation or amplification) (e.g., as determined using a regulatory agency-approved assay or kit). The subject can be a subject with a cancer (e.g., one or more tumor samples) that is positive for a KRas dysregulation (e.g., a KRas mutation or amplification) (e.g., identified as positive using a regulatory agency-approved, e.g., FDA-approved, assay or kit). The subject can be a subject whose cancer (e.g., a tumor sample) has a KRas dysregulation (e.g., a KRas mutation or amplification) (e.g., where the cancer (e.g., tumor sample) is identified as such using a regulatory agency-approved, e.g., FDA-approved, kit or assay). In some embodiments, the subject is suspected of having a mutant KRas-associated cancer. In some embodiments, the subject has a clinical record indicating that the subject has a cancer (e.g., a tumor sample) that has a KRas dysregulation (e.g., a KRas mutation or amplification) (and optionally the clinical record indicates that the subject should be treated with any of the compounds and/or compositions provided herein). In some such embodiments, the cancer (e.g., a tumor sample) has a KRas mutation selected from the group consisting of: a KRas G12X mutation, a KRas G13X mutation, and a KRas Q61X mutation. In some embodiments, a KRas mutation is selected from the group consisting of: a KRas G12A mutation, a KRas G12C mutation, a KRas G12D mutation, a KRas G12R mutation, a KRas G12S mutation, a KRas G12V mutation, a KRas G13C mutation, a KRas G13D mutation, a KRas G13V mutation, a KRas Q61E mutation, a KRas Q61H mutation, a KRas Q61K mutation, a KRas Q61L mutation, a KRas Q61P mutation, and a KRas Q61R mutation. In some embodiments, a KRas mutation is selected from the group consisting of: a KRas G12A mutation, a KRas G12C mutation, a KRas G12D mutation, a KRas G12R mutation, a KRas G12S mutation, and a KRas G12V mutation. In some embodiments, the cancer (e.g., a tumor sample) has a KRas mutation selected from the group consisting of: a KRas G12A mutation, a KRas G12D mutation, a KRas G12R mutation, and a KRas G12V mutation. In some embodiments, the cancer (e.g., a tumor sample) has a KRas G12A mutation. In some embodiments, the cancer (e.g., a tumor sample) has a KRas G12C mutation. In some embodiments, the cancer (e.g., a tumor sample) has a KRas G12D mutation. In some embodiments, the cancer (e.g., a tumor sample) has a KRas G12R mutation. In some embodiments, the cancer (e.g., a tumor sample) has a KRas G12S mutation. In some embodiments, the cancer (e.g., a tumor sample) has a KRas G12Vmutation. In some embodiments, the cancer (e.g., a tumor sample) has a KRas G12D mutation, a KRas G12R mutation, or KRas G12V mutation (e.g., a KRas G12D mutation or a KRas G12V mutation). In some embodiments, the cancer (e.g., a tumor sample) has a KRas G12D mutation or a KRas G12V mutation. In some embodiments, the cancer (e.g., a tumor sample) has a KRas G12D mutation. In some embodiments, the cancer (e.g., a tumor sample) has a KRas G12R mutation. In some embodiments, the cancer (e.g., a tumor sample) has a KRas G12V mutation. The term “KRas-associated cancer” as used herein refers to cancers associated with or having a dysregulation of a KRAS gene, a KRas protein, or the expression or activity or level of any (e.g., one or more) of the same (e.g., any of the types of dysregulations of a KRAS gene, a KRas protein, or the expression or activity or level of any of the same described herein). Non- limiting examples of a KRas-associated cancer are described herein. The term “mutant KRas-associated cancer” as used herein refers to cancers associated with or having a KRas mutation (e.g., a KRAS gene having a mutation corresponding to a mutation in a KRas protein and/or a KRas protein having a mutation). Non-limiting examples of a mutant KRas-associated cancer are described herein. The term “KRas G12X-associated cancer” as used herein refers to cancers associated with or having a KRas G12X mutation (e.g., a KRAS gene having a mutation corresponding to a G12X mutation in a KRas protein and/or a KRas protein having a G12X mutation). Non- limiting examples of a KRas G12X-associated cancer are described herein. The term “KRas G12A-associated cancer” as used herein refers to cancers associated with or having a KRas G12A mutation (e.g., a KRAS gene having a mutation corresponding to a G12A mutation in a KRas protein and/or a KRas protein having a G12A mutation). Non- limiting examples of a KRas G12A-associated cancer are described herein. The term “KRas G12C-associated cancer” as used herein refers to cancers associated with or having a KRas G12C mutation (e.g., a KRAS gene having a mutation corresponding to a G12C mutation in a KRas protein and/or a KRas protein having a G12C mutation). Non- limiting examples of a KRas G12C-associated cancer are described herein. The term “KRas G12D-associated cancer” as used herein refers to cancers associated with or having a KRas G12D mutation (e.g., a KRAS gene having a mutation corresponding to a G12D mutation in a KRas protein and/or a KRas protein having a G12D mutation). Non- limiting examples of a KRas G12D-associated cancer are described herein. The term “KRas G12R-associated cancer” as used herein refers to cancers associated with or having a KRas G12R mutation (e.g., a KRAS gene having a mutation corresponding to a G12R mutation in a KRas protein and/or a KRas protein having a G12R mutation). Non- limiting examples of a KRas G12R-associated cancer are described herein. The term “KRas G12S-associated cancer” as used herein refers to cancers associated with or having a KRas G12S mutation (e.g., a KRAS gene having a mutation corresponding to a G12S mutation in a KRas protein and/or a KRas protein having a G12S mutation). Non- limiting examples of a KRas G12S-associated cancer are described herein. The term “KRas G12V-associated cancer” as used herein refers to cancers associated with or having a KRas G12V mutation (e.g., a KRAS gene having a mutation corresponding to a G12V mutation in a KRas protein and/or a KRas protein having a G12V mutation). Non- limiting examples of a KRas G12V-associated cancer are described herein. The term “KRas G13X-associated cancer” as used herein refers to cancers associated with or having a KRas G13X mutation (e.g., a KRAS gene having a mutation corresponding to a G13X mutation in a KRas protein and/or a KRas protein having a G13X mutation). Non- limiting examples of a KRas G13X-associated cancer are described herein. The term “KRas G13C-associated cancer” as used herein refers to cancers associated with or having a KRas G13C mutation (e.g., a KRAS gene having a mutation corresponding to a G13C mutation in a KRas protein and/or a KRas protein having a G13C mutation). Non- limiting examples of a KRas G13C-associated cancer are described herein. The term “KRas G13D-associated cancer” as used herein refers to cancers associated with or having a KRas G13D mutation (e.g., a KRAS gene having a mutation corresponding to a G13D mutation in a KRas protein and/or a KRas protein having a G13D mutation). Non- limiting examples of a KRas G13D-associated cancer are described herein. The term “KRas G13V-associated cancer” as used herein refers to cancers associated with or having a KRas G13V mutation (e.g., a KRAS gene having a mutation corresponding to a G13V mutation in a KRas protein and/or a KRas protein having a G13V mutation). Non- limiting examples of a KRas G13V-associated cancer are described herein. The term “KRas Q61X-associated cancer” as used herein refers to cancers associated with or having a KRas Q61X mutation (e.g., a KRAS gene having a mutation corresponding to a Q61X mutation in a KRas protein and/or a KRas protein having a Q61X mutation). Non- limiting examples of a KRas Q61X-associated cancer are described herein. The term “KRas Q61E-associated cancer” as used herein refers to cancers associated with or having a KRas Q61E mutation (e.g., a KRAS gene having a mutation corresponding to a Q61E mutation in a KRas protein and/or a KRas protein having a Q61E mutation). Non- limiting examples of a KRas Q61E-associated cancer are described herein. The term “KRas Q61H-associated cancer” as used herein refers to cancers associated with or having a KRas Q61H mutation (e.g., a KRAS gene having a mutation corresponding to a Q61H mutation in a KRas protein and/or a KRas protein having a Q61H mutation). Non- limiting examples of a KRas Q61H-associated cancer are described herein. The term “KRas Q61K-associated cancer” as used herein refers to cancers associated with or having a KRas Q61K mutation (e.g., a KRAS gene having a mutation corresponding to a Q61K mutation in a KRas protein and/or a KRas protein having a Q61K mutation). Non- limiting examples of a KRas Q61K-associated cancer are described herein. The term “KRas Q61L-associated cancer” as used herein refers to cancers associated with or having a KRas Q61L mutation (e.g., a KRAS gene having a mutation corresponding to a Q61L mutation in a KRas protein and/or a KRas protein having a Q61L mutation). Non- limiting examples of a KRas Q61L-associated cancer are described herein. The term “KRas Q61P-associated cancer” as used herein refers to cancers associated with or having a KRas Q61P mutation (e.g., a KRAS gene having a mutation corresponding to a Q61P mutation in a KRas protein and/or a KRas protein having a Q61P mutation). Non- limiting examples of a KRas Q61P-associated cancer are described herein. The term “KRas Q61R-associated cancer” as used herein refers to cancers associated with or having a KRas Q61R mutation (e.g., a KRAS gene having a mutation corresponding to a Q61R mutation in a KRas protein and/or a KRas protein having a Q61R mutation). Non- limiting examples of a KRas Q61R-associated cancer are described herein. Such mutations can be associated with the development of a variety of cancers. See, e.g., Hunter et al. Mol Cancer Res. 2015;13(9):1325-35, doi: 10.1158/1541-7786.MCR-15- 0203. Provided herein are methods of treating a cancer in a subject in need of such treatment, the methods comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition thereof. In some embodiments, the subject is treatment naïve with respect to the cancer. In some embodiments, the subject has received one or more lines of previous therapy for the cancer. Also provided herein are methods of treating a cancer in a subject in need thereof, the methods comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition thereof, as a monotherapy. In some embodiments, the subject is treatment naïve with respect to the cancer. In some embodiments, the subject has received one or more lines of previous therapy for the cancer. In some embodiments, the subject has received one or more lines of previous therapy for the cancer prior to administration of a compound provided herein. In some such embodiments, the subject has received previous chemotherapy for the cancer prior to administration of a compound provided herein. In some embodiments, the subject has received first- or second- line chemotherapy prior to administration of a compound provided herein. In some embodiments, the subject has received standard of care chemotherapy prior to administration of a compound provided herein. In some embodiments, a subject with colorectal cancer has previously received one or more of capecitabine, fluorouracil (5-FU), leucovorin, and oxaliplatin. In some embodiments, a subject with colorectal cancer has previously received FOLFOX (fluorouracil, leucovorin, and oxaliplatin). In some embodiments, a subject with colorectal cancer has previously received FOLFIRI (fluorouracil, leucovorin, and irinotecan). In some embodiments, a subject with a colorectal cancer has previously received FOLFIRINOX (fluorouracil, leucovorin (e.g., leucovorin calcium), irinotecan (e.g., irinotecan hydrochloride), and oxaliplatin). In some embodiments, a subject with colorectal cancer has previously received CAPEOX (capecitabine and oxaliplatin). In some embodiments, a subject with colorectal cancer has previously received FOLFIRI and one or more of bevacizumab, ziv-aflibercept, and ramucirumab. In some embodiments, a subject with colorectal cancer has previously received FOLFIRI and one or more of cetuximab or panitumumab. In some embodiments, a subject with colorectal cancer has previously received FOLFOX and one or more of bevacizumab, ziv-aflibercept, and ramucirumab. In some embodiments, a subject with colorectal cancer has previously received FOLFOX and one or more of cetuximab or panitumumab. In some embodiments, a subject with colorectal cancer has previously received FOLFIRINOX and one or more of bevacizumab, ziv-aflibercept, and ramucirumab. In some embodiments, a subject with colorectal cancer has previously received FOLFIRINOX and one or more of cetuximab or panitumumab. In some embodiments, a subject with colorectal cancer has previously received CAPEOX and one or more of bevacizumab, ziv-aflibercept, and ramucirumab. In some embodiments, a subject with colorectal cancer has previously received CAPEOX and one or more of cetuximab or panitumumab. In some embodiments, a subject with endometrial cancer has previously received one or more of cisplatin, carboplatin, paclitaxel, capecitabine, mitomycin, and gemcitabine. In some embodiments, a subject with endometrial cancer has previously received cisplatin and radiation therapy. In some embodiments, a subject with endometrial cancer has previously received cisplatin and radiation therapy followed by carboplatin and paclitaxel. In some embodiments, a subject with endometrial cancer has previously received capecitabine and mitomycin. In some embodiments, a subject with endometrial cancer has previously received gemcitabine. In some embodiments, a subject with endometrial cancer has previously received paclitaxel. In some embodiments, a subject with endometrial cancer has previously received carboplatin and paclitaxel. In some embodiments, a subject with endometrial cancer has previously received carboplatin, paclitaxel, and pembrolizumab. In some embodiments, a subject with endometrial cancer has previously received carboplatin, paclitaxel, and dostarlimab (e.g., dostarlimab-gxly). In some embodiments, a subject with endometrial cancer has previously received carboplatin, paclitaxel, and trastuzumab. In some embodiments, a subject with endometrial cancer has previously received carboplatin, paclitaxel, and bevacizumab. In some embodiments, a subject with endometrial carcinoma has previously received megestrol acetate and tamoxifen. In some embodiments, a subject with endometrial carcinoma has previously received everolimus and letrozole. In some embodiments, a subject with lung cancer (e.g., NSCLC) has previously received one or more of pembrolizumab, atezolizumab, cemiplimab (e.g., cemiplimiab-rwlc), durvalumab, nivolumab, ipilimumab, tremelimumab (e.g., tremelimumab-actl), carboplatin, cisplatin, pemetrexed, paclitaxel (e.g., albumin-bound paclitaxel), and bevacizumab. In some embodiments, a subject with lung cancer (e.g., NSCLC) has previously received pembrolizumab. In some embodiments, a subject with lung cancer (e.g., NSCLC) has previously received carboplatin, pemetrexed, and pembrolizumab. In some embodiments, a subject with lung cancer (e.g., NSCLC) has previously received cisplatin, pemetrexed, and pembrolizumab. In some embodiments, a subject with lung cancer (e.g., NSCLC) has previously received cemiplimab. In some embodiments, a subject with lung cancer (e.g., NSCLC) has previously received cemiplimab, pemetrexed, and carboplatin. In some embodiments, a subject with lung cancer (e.g., NSCLC) has previously received cemiplimab, pemetrexed, and cisplatin. In some embodiments, a subject with lung cancer (e.g., NSCLC) has previously received carboplatin, paclitaxel, bevacizumab, and atezolizumab. In some embodiments, a subject with lung cancer (e.g., NSCLC) has previously received carboplatin, paclitaxel (e.g., albumin-bound paclitaxel), and atezolizumab. In some embodiments, a subject with lung cancer (e.g., NSCLC) has previously received cemiplimab, paclitaxel, and carboplatin. In some embodiments, a subject with lung cancer (e.g., NSCLC) has previously received cemiplimab, paclitaxel, and cisplatin. In some embodiments, a subject with lung cancer (e.g., NSCLC) has previously received tremelimumab, durvalumab, carboplatin, and paclitaxel (e.g., albumin-bound paclitaxel). In some embodiments, a subject with lung cancer (e.g., NSCLC) has previously received tremelimumab, durvalumab, carboplatin, and pemetrexed. In some embodiments, a subject with lung cancer (e.g., NSCLC) has previously received tremelimumab, durvalumab, cisplatin, and pemetrexed. In some embodiments, a subject with lung cancer (e.g., NSCLC) has previously received tremelimumab, durvalumab, carboplatin, and paclitaxel (e.g., albumin-bound paclitaxel). In some embodiments, a subject with lung cancer (e.g., NSCLC) has previously received tremelimumab, durvalumab, carboplatin, and gemcitabine. In some embodiments, a subject with lung cancer (e.g., NSCLC) has previously received tremelimumab, durvalumab, cisplatin, and gemcitabine. In some embodiments, a subject with lung cancer (e.g., NSCLC) has previously received nivolumab and ipilimumab. In some embodiments, a subject with lung cancer (e.g., NSCLC) has previously received carboplatin, paclitaxel (e.g., albumin-bound paclitaxel), and pembrolizumab. In some embodiments, a subject with lung cancer (e.g., NSCLC) has previously received nivolumab, ipilimumab, paclitaxel, and carboplatin. In some embodiments, a subject with ovarian cancer has previously received one or more of paclitaxel, carboplatin, fluorouracil, leucovorin, oxaliplatin, capecitabine, docetaxel, and doxorubicin (e.g., liposomal doxorubicin). In some embodiments, a subject with ovarian cancer has previously received paclitaxel and carboplatin. In some embodiments, a subject with ovarian cancer has previously received fluorouracil, leucovorin, and oxaliplatin. In some embodiments, a subject with ovarian cancer has previously received hormone therapy (e.g., an aromatase inhibitor such as anastrozole, letrozole, or exemestane). In some embodiments, a subject with ovarian cancer has previously received docetaxel and carboplatin. In some embodiments, a subject with ovarian cancer has previously received carboplatin and doxorubicin (e.g., liposomal doxorubicin). In some embodiments, a subject with ovarian cancer has previously received paclitaxel, carboplatin, and bevacizumab. In some embodiments, a subject with ovarian cancer has previously received fluorouracil, leucovorin, oxaliplatin, and bevacizumab. In some embodiments, a subject with ovarian cancer has previously received capecitabine, oxaliplatin, and bevacizumab. In some embodiments, a subject with pancreatic cancer has previously received one or more of capecitabine, fluorouracil, gemcitabine, irinotecan, leucovorin, paclitaxel (e.g., albumin-bound paclitaxel), and oxaliplatin. In some embodiments, a subject with pancreatic cancer has previously received FOLFIRINOX. In some embodiments, a subject with pancreatic cancer has previously received GEMOX (gemcitabine and oxaliplatin). In some embodiments, a subject with pancreatic cancer has previously received gemcitabine. In some embodiments, a subject with pancreatic cancer has previously received gemcitabine and paclitaxel (e.g., albumin-bound paclitaxel). In some embodiments, a subject with pancreatic cancer has previously received NALIRIFOX (liposomal irinotecan, fluorouracil, leucovorin, and oxaliplatin). Provided herein is use of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition thereof, for the treatment of cancer, for example, any of the cancers provided herein. Provided herein is use of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition thereof, as a medicament for the treatment of cancer, for example, any of the cancers provided herein. Provided herein is use of a compound provided herein, or a pharmaceutically acceptable salt thereof, in the manufacture of a medicament for the treatment of cancer, for example, any of the cancers provided herein. Provided herein is a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition thereof, for use as a medicament. Also provided herein is a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition thereof, for use as a medicament for the treatment of cancer, for example, any of the cancers provided herein. Provided herein is a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition thereof, for use in treating a cancer, for example, any of the cancers provided herein. As used herein, “monotherapy”, when referring to a compound provided herein, or a pharmaceutically acceptable salt thereof, means that the compound provided herein, or a pharmaceutically acceptable salt thereof, is the only therapeutic agent or therapy (e.g., anticancer agent or therapy) administered to the subject during the treatment cycle (e.g., no additional targeted therapeutics, anticancer agents, chemotherapeutics, or checkpoint inhibitors are administered to the subject during the treatment cycle). As a person of ordinary skill in the art would understand, monotherapy does not exclude the co-administration of medicaments for the treatment of side effects or general symptoms associated with the cancer or treatment, such as pain, rash, edema, photosensitivity, pruritis, skin discoloration, hair brittleness, hair loss, brittle nails, cracked nails, discolored nails, swollen cuticles, fatigue, weight loss, general malaise, shortness of breath, infection, anemia, or gastrointestinal symptoms, including nausea, diarrhea, and lack of appetite. As used herein, “the subject has previously received one or lines of previous therapy” means that the subject has been previously administered one or more therapeutic agents or therapies (e.g., anticancer agent or therapy, such as chemotherapy, radiation, or surgery) for the cancer other than a compound provided herein, or a pharmaceutically acceptable salt thereof, during a treatment cycle prior to administration of a compound provided herein. In some embodiments, the subject cannot tolerate the one or more therapeutic agents or therapies previously administered for the cancer. In some embodiments, the subject did not respond to the one or more therapeutic agents or therapies previously administered for the cancer. In some embodiments, the subject did not adequately respond to one or more therapeutic agents or therapies previously administered for the cancer. In some embodiments, the subject has stopped responding to the one or more therapeutic agents or therapies previously administered for the cancer. In some embodiments, a lack of response, an inadequate response, or a discontinued response can be determined by objective criteria (e.g., tumor volume, or by criteria such as RECIST 1.1). In some embodiments, a lack of response, an inadequate response, or a discontinued response can be determined by the subject’s physician. As used herein, “the subject is treatment naïve with respect to the cancer” means that the subject has not been previously administered one or more therapeutic agents or therapies for the cancer. For any of the solid tumors described herein, the solid tumors can be primary tumors or metastatic (or secondary) tumors. As used herein, “primary” tumors are those located at the site where the tumor began to grow (i.e., where it originated). As used herein, “metastatic” (or “secondary”) tumors are those that have spread to other parts of body from the original tumor site. In some embodiments, the metastatic or secondary tumors are the same type of cancer as the primary tumor. In some embodiments, the metastatic or secondary tumors are not genetically identical to the primary tumor. Provided herein is a method of treating a cancer in a in a subject in need of such treatment, the method comprising a) detecting a KRas dysregulation (e.g., a KRas mutation (e.g., a KRas G12A mutation, a KRas G12C mutation, a KRas G12D mutation, a KRas G12R mutation, a KRas G12S mutation, or a KRas G12V mutation (e.g., a KRas G12D mutation or a KRas G12V mutation)) or amplification) in a sample from the subject (e.g., detecting a KRAS gene having a mutation corresponding to a mutation in KRas protein and/or detecting a KRas protein having a mutation, a KRAS gene copy number increase, and/or an increase in KRas mRNA or protein expression); and b) administering a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof. Provided herein is a method of treating a cancer in a subject in need of such treatment, the method comprising a) detecting a KRas dysregulation (e.g., a KRas mutation (e.g., a KRas G12X mutation)) or amplification) in a sample from the subject (e.g., detecting a KRAS gene having a mutation corresponding to a mutation in KRas protein and/or detecting a KRas protein having a mutation, a KRAS gene copy number increase, and/or an increase in KRas mRNA or protein expression); and b) administering a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof. Also provided herein is a method of treating a KRas-associated cancer (e.g., a mutant KRas-associated cancer (e.g., a KRas G12A- associated cancer, a KRas G12C-associated cancer, a KRas G12D-associated cancer, a KRas G12R-associated cancer, a KRas G12S-associated cancer, or a KRas G12V-associated cancer (e.g., a KRas G12D-associated cancer or a KRas G12V-associated cancer))) in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Also provided herein is a method of treating a KRas-associated cancer (e.g., a mutant KRas-associated cancer (e.g., a KRas G12X- associated cancer)) in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. For example, provided herein are methods for treating a KRas-associated cancer (e.g., a mutant KRas-associated cancer (e.g., a KRas G12A-associated cancer, a KRas G12C-associated cancer, a KRas G12D-associated cancer, a KRas G12R-associated cancer, a KRas G12S- associated cancer, or a KRas G12V-associated cancer (e.g., a KRas G12D-associated cancer or a KRas G12V-associated cancer))) in a subject in need of such treatment, the methods comprising a) detecting a KRas dysregulation (e.g., a KRas mutation (e.g., a KRas G12A mutation, a KRas G12C mutation, a KRas G12D mutation, a KRas G12R mutation, a KRas G12S mutation, or a KRas G12V mutation (e.g., a KRas G12D mutation or a KRas G12V mutation)) or amplification) in a sample from the subject (e.g., detecting a KRAS gene having a mutation corresponding to a mutation in KRas protein and/or detecting a KRas protein having a mutation, a KRAS gene copy number increase, and/or an increase in KRas mRNA or protein expression); and b) administering a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof. For example, provided herein are methods for treating a KRas-associated cancer (e.g., a mutant KRas-associated cancer (e.g., a KRas G12X-associated cancer)) in a subject in need of such treatment, the methods comprising a) detecting a KRas dysregulation (e.g., a KRas mutation (e.g., a KRas G12X mutation) or amplification) in a sample from the subject (e.g., detecting a KRAS gene having a mutation corresponding to a mutation in KRas protein and/or detecting a KRas protein having a mutation, a KRAS gene copy number increase, and/or an increase in KRas mRNA or protein expression); and b) administering a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof. In some embodiments of any of the methods or uses described herein, the cancer (e.g., KRas-associated cancer (e.g., mutant KRas-associated cancer (e.g., a KRas G12A-associated cancer, a KRas G12C-associated cancer, a KRas G12D-associated cancer, a KRas G12R- associated cancer, a KRas G12S-associated cancer, or a KRas G12V-associated cancer (e.g., a KRas G12D-associated cancer or a KRas G12V-associated cancer)))) is breast cancer (e.g., breast invasive carcinoma, breast invasive ductal carcinoma), central or peripheral nervous system tissue cancer (e.g., brain cancer (e.g., astrocytoma, glioblastoma, glioma, oligoastrocytoma)), endocrine or neuroendocrine cancer (e.g., adrenal cancer (e.g., adrenocortical carcinoma, pheochromocytoma, paraganglioma), multiple neuroendocrine type I and type II tumors, parathyroid cancer, pituitary tumors, thyroid cancer (e.g., papillary thyroid cancer)), eye cancer (e.g., uveal cancer (e.g., uveal melanoma)), gastrointestinal cancer (e.g., anal cancer, bile duct cancer (e.g., cholangiocarcinoma), colorectal cancer (e.g., colon adenocarcinoma, rectal adenocarcinoma, mucinous adenocarcinoma, mucinous carcinoma), esophageal cancer (e.g., esophageal adenocarcinoma), gallbladder cancer, gastrointestinal carcinoid tumor, gastrointestinal stromal tumor, liver cancer (e.g., hepatocellular carcinoma, intrahepatic bile duct cancer), pancreatic cancer (e.g., pancreatic adenocarcinoma, pancreatic islet cell cancer), small intestine cancer, or stomach cancer (e.g., stomach adenocarcinoma, signet ring cell carcinoma of the stomach)), genitourinary cancer (e.g., bladder cancer (e.g., bladder urothelial carcinoma), kidney cancer (e.g., renal clear cell carcinoma, renal papillary cell carcinoma, kidney chromophobe), prostate cancer (e.g., prostate adenocarcinoma), testicular cancer (e.g., testicular germ cell tumors, seminoma), or ureter cancer), gynecologic cancer (e.g., cervical cancer (e.g., cervical squamous cell carcinoma, endocervical adenocarcinoma, mucinous carcinoma), ovarian cancer (e.g., serous ovarian cancer, ovarian serous cystadenocarcinoma), uterine cancer (e.g., uterine carcinosarcoma, uterine endometrioid carcinoma, uterine serous carcinoma, uterine papillary serous carcinoma, uterine corpus endometrial carcinoma), or vulvar cancer), head and neck cancer (e.g., ear cancer (e.g., middle ear cancer), head and neck squamous cell carcinoma, nasal cavity cancer, oral cancer, pharynx cancer (e.g., hypopharynx cancer, nasopharynx cancer, oropharyngeal cancer), hematological cancer (e.g., leukemia (e.g., chronic lymphocytic leukemia (CLL), acute lymphocytic leukemia (ALL) (e.g., Philadelphia chromosome positive ALL), acute myeloid leukemia (AML) (e.g., acute promyelocytic leukemia (APL)), chronic myeloid leukemia (CML)), lymphoma (e.g., Hodgkin lymphoma (e.g., nodular lymphocyte predominant Hodgkin lymphoma (NLPHL)), non-Hodgkin lymphoma (e.g., Burkitt lymphoma (BL), diffuse large B- cell lymphoma (DLBCL), diffuse histiocytic lymphoma (DHL), follicular lymphoma (FL), intravascular large B-cell lymphoma (IVLBCL), mantle cell lymphoma (MCL), small lymphocytic lymphoma (SLL))), or myeloma (e.g., multiple myeloma)), Li-Fraumeni tumors, mesentery cancer (e.g., omentum cancer, peritoneal cancer), pleural cancer, respiratory cancer (e.g., larynx cancer, lung cancer (e.g., lung squamous cell carcinoma, lung adenocarcinoma, mesothelioma, non-small cell lung cancer (NSCLC)), tracheal cancer), sarcoma (e.g., bone cancer (e.g., osteosarcoma, chondrosarcoma) or soft tissue sarcoma (Ewing sarcoma, leiomyosarcoma, myxofibrosarcoma, rhabdomyosarcoma)), skin cancer (e.g., melanoma), thymus cancer (e.g., thymoma), or a combination thereof. In some embodiments, the cancer (e.g., KRas-associated cancer (e.g., mutant KRas- associated cancer)) is a hematological cancer, a soft tissue cancer, bile duct cancer, bladder cancer, brain cancer, breast cancer, cervical cancer, colon cancer, endometrial cancer, esophageal cancer, kidney cancer, liver cancer, lung cancer, mucinous carcinoma, rectal cancer, ovarian cancer, pancreatic cancer, prostate cancer, rectal cancer, skin cancer, stomach cancer, testicular cancer, thymus cancer, thyroid cancer, urothelial cancer, or uterine cancer. In some embodiments, the cancer (e.g., KRas-associated cancer (e.g., mutant KRas- associated cancer)) is colorectal cancer (e.g., a colon cancer or a rectal cancer), endometrial cancer, lung cancer (e.g., NSCLC), ovarian cancer, or pancreatic cancer. In some embodiments, the cancer (e.g., KRas-associated cancer (e.g., mutant KRas- associated cancer)) is colon cancer, endometrial cancer, lung cancer, pancreatic cancer, and uterine cancer. In some embodiments, the cancer is a colorectal cancer (e.g., a colon cancer or a rectal cancer). In some such embodiments, the colorectal cancer has a KRas dysregulation (e.g., a KRas mutation (e.g., a KRas G12X mutation)) or amplification). In some embodiments, the cancer is an endometrial cancer. In some such embodiments, the endometrial cancer has a KRas dysregulation (e.g., a KRas mutation (e.g., a KRas G12X mutation)) or amplification). In some embodiments, the cancer is a lung cancer (e.g., NSCLC). In some such embodiments, the lung cancer (e.g., NSCLC) has a KRas dysregulation (e.g., a KRas mutation (e.g., a KRas G12X mutation)) or amplification). In some embodiments, the cancer is an ovarian cancer. In some such embodiments, the ovarian cancer has a KRas dysregulation (e.g., a KRas mutation (e.g., a KRas G12X mutation)) or amplification). In some embodiments, the cancer is a pancreatic cancer. In some such embodiments, the pancreatic cancer has a KRas dysregulation (e.g., a KRas mutation (e.g., a KRas G12X mutation)) or amplification). In some embodiments, the cancer (e.g., a KRas-associated cancer (e.g., a mutant KRas- associated cancer (e.g., a KRas G12X-associated cancer))) is a hematological cancer, bile duct cancer, brain cancer, breast cancer, cervical cancer, colon cancer, endometrial cancer, esophageal cancer, kidney cancer, liver cancer, lung cancer, mucinous carcinoma, pancreatic cancer, prostate cancer, rectal cancer, testicular cancer (e.g., seminoma), skin cancer, stomach cancer, thymus cancer, thyroid cancer, urothelial cancer, or uterine cancer. In some embodiments, the cancer is brain cancer, colon cancer, lung cancer, pancreatic cancer, rectal cancer, testicular cancer (e.g., seminoma), or uterine cancer. In some embodiments, the cancer is a KRas G12A-associated cancer. In some embodiments, the cancer is bladder cancer, breast cancer, cervical cancer, colon cancer, lung cancer, kidney cancer, liver cancer, or rectal cancer. In some embodiments, the cancer is a KRas G12C-associated cancer. In some embodiments, the cancer is a hematological cancer, brain cancer, cervical cancer, colon cancer, endometrial cancer, esophageal cancer, kidney cancer, liver cancer, lung cancer, mucinous carcinoma, ovarian cancer, pancreatic cancer, prostate cancer, rectal cancer, skin cancer, stomach cancer, thymus cancer, urothelial cancer, or uterine cancer. In some embodiments, the cancer is a KRas G12D-associated cancer. In some embodiments, the cancer is a hematological cancer, bladder cancer, bile duct cancer, colon cancer, ovarian cancer, pancreatic cancer, prostate cancer, rectal cancer, skin cancer, or testicular cancer. In some embodiments, the cancer is a KRas G12R-associated cancer. In some embodiments, the cancer is colon cancer, lung cancer, pancreatic cancer, rectal cancer, stomach cancer, testicular cancer (e.g., seminoma), or uterine cancer. In some embodiments, the cancer is a KRas G12S-associated cancer. In some embodiments, the cancer is a hematological cancer, bladder cancer, bile duct cancer, brain cancer, breast cancer, cervical cancer, colon cancer, endometrial cancer, esophageal cancer, kidney cancer, liver cancer, lung cancer, mucinous carcinoma, ovarian cancer, pancreatic cancer, rectal cancer, skin cancer, stomach cancer, testicular cancer (e.g., seminoma), thymus cancer, or uterine cancer. In some embodiments, the cancer is a G12V- associated cancer. In some embodiments, the cancer (e.g., a KRas-associated cancer (e.g., a mutant KRas- associated cancer (e.g., a KRas G13X-associated cancer))) is a hematological cancer, a soft tissue cancer, cervical cancer, colon cancer, endometrial cancer, liver cancer, lung cancer, pancreatic cancer, rectal cancer, skin cancer, stomach cancer, or urothelial cancer. In some embodiments, the cancer (e.g., a KRas-associated cancer (e.g., a mutant KRas-associated cancer (e.g., a KRas Q61X-associated cancer)) is bladder cancer, colon cancer, lung cancer, ovarian cancer, rectal cancer, thyroid cancer, or uterine cancer. In some embodiments, the cancer (e.g., a KRas-associated cancer (e.g., a cancer associated with KRas amplification (e.g., a cancer associated with wild-type KRas amplification)) is colorectal cancer, gastric cancer, gastroesophageal cancer, head and neck squamous carcinoma, or lung cancer (e.g., NSCLC). See, e.g., the public database cBioPortal. In some such embodiments, the cancer is a lung cancer. For example, the lung cancer non-small cell lung cancer (NSCLC). In some embodiments, the lung cancer is relapsed or refractory. For example, the subject has received at least one prior systemic therapy for the lung cancer. In some embodiments, the at least one prior systemic therapy is selected from the group consisting of chemotherapy (e.g., docetaxel, pemetrexed, and gemcitabine), immunotherapy (e.g., anti-PD- 1 therapy), kinase inhibitor (e.g., an ALK inhibitor, a ROS1 inhibitor, a BRAF inhibitor, a RET inhibitor, a MET inhibitor, an NTRK inhibitor, a KRas inhibitor, and a HER2 inhibitor), and combinations thereof. In some embodiments, the cancer (e.g., a KRas-associated cancer (e.g., mutant KRas- associated cancer)) is pancreatic cancer or metastatic pancreatic cancer. In some embodiments, the cancer (e.g., a KRas-associated cancer (e.g., mutant KRas-associated cancer)) is pancreatic ductal adenocarcinoma (PDAC). In some such embodiments, the pancreatic cancer is a KRas G12R-associated cancer. In some embodiments, the pancreatic cancer (e.g., PDAC) is relapsed or refractory. In some embodiments, the subject has received at least one prior systemic therapy for the pancreatic cancer. For example, the at least one prior systemic therapy is selected from the group consisting of chemotherapy (e.g., FOLFIRNOX, gemcitabine (e.g., combined with abraxane (e.g., nab-paclitaxel))), immunotherapy (e.g., anti-PD-1 therapy (e.g., pembrolizumab)), a PARP inhibitor (e.g., olaparib), and combinations thereof. In some embodiments, the cancer is a colorectal cancer. In some embodiments, the colorectal cancer is relapsed or refractory. In some embodiments, the subject has received at least one prior systemic therapy for the colorectal cancer. For example, the at least one prior systemic therapy is selected from the group consisting of chemotherapy (e.g., FOLFIRI, FOLFOX, FOLFIRNOX, or FOLFOXIRI), anti-VEGF therapy, anti-PD-1 therapy (e.g., pembrolizumab), an EGFR inhibitor (e.g., cetuximab), and combinations thereof. In some embodiments, the cancer (e.g., a KRas-associated cancer (e.g., mutant KRas- associated cancer)) is advanced-stage lung adenocarcinoma. In some embodiments, the cancer is a solid tumor. In some embodiments, the solid tumor has a KRas dysregulation (e.g., a KRas mutation or amplification). For example, the solid tumor has a KRas mutation selected from the group consisting of: a KRas G12A mutation, a KRas G12C mutation, a KRas G12D mutation, a KRas G12R mutation, a KRas G12S mutation, and a KRas G12V mutation. In some embodiments, the solid tumor has a KRas G12D mutation, a KRas G12R mutation, or a KRas G12V mutation. In some embodiments, the solid tumor has a KRas G12D mutation or a KRas G12V mutation. In some embodiments, the solid tumor has a KRas G12A mutation. In some embodiments, the solid tumor has a KRas G12C mutation. In some embodiments, the solid tumor has a KRas G12D mutation. In some embodiments, the solid tumor has a KRas G12R mutation. In some embodiments, the solid tumor has a KRas G12S mutation. In some embodiments, the solid tumor has a KRas G12V mutation. Also provided herein is a method of treating a solid tumor in a subject in need thereof, the method comprising: (a) detecting a KRas dysregulation (e.g., a KRas mutation or amplification) in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Also provided herein is a method of treating a solid tumor in a subject in need thereof, the method comprising: (a) detecting a KRas G12A mutation, a KRas G12C mutation, a KRas G12D mutation, a KRas G12R mutation, a KRas G12S mutation, or a KRas G12V mutation in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Additionally provided herein is a method of treating a solid tumor in a subject in need thereof, the method comprising: (a) detecting a KRas G12D or a KRas G12V mutation in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Additionally provided herein is a method of treating a solid tumor in a subject in need thereof, the method comprising: (a) detecting a KRas G12A mutation in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Additionally provided herein is a method of treating a solid tumor in a subject in need thereof, the method comprising: (a) detecting a KRas G12C mutation in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Additionally provided herein is a method of treating a solid tumor in a subject in need thereof, the method comprising: (a) detecting a KRas G12D mutation in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Additionally provided herein is a method of treating a solid tumor in a subject in need thereof, the method comprising: (a) detecting a KRas G12R mutation in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Additionally provided herein is a method of treating a solid tumor in a subject in need thereof, the method comprising: (a) detecting a KRas G12S mutation in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Additionally provided herein is a method of treating a solid tumor in a subject in need thereof, the method comprising: (a) detecting a KRas G12V mutation in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Also provided herein is a method of treating an advanced solid tumor in a subject in need thereof, the method comprising: (a) detecting a KRas dysregulation (e.g., a KRas mutation or amplification) in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Also provided herein is a method of treating an advanced solid tumor in a subject in need thereof, the method comprising: (a) detecting a KRas G12A mutation, a KRas G12C mutation, a KRas G12D mutation, a KRas G12R mutation, a KRas G12S mutation, or a KRas G12V mutation in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Additionally provided herein is a method of treating an advanced solid tumor in a subject in need thereof, the method comprising: (a) detecting a KRas G12D or a KRas G12V mutation in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Additionally provided herein is a method of treating an advanced solid tumor in a subject in need thereof, the method comprising: (a) detecting a KRas G12A mutation in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Additionally provided herein is a method of treating an advanced solid tumor in a subject in need thereof, the method comprising: (a) detecting a KRas G12C mutation in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Additionally provided herein is a method of treating an advanced solid tumor in a subject in need thereof, the method comprising: (a) detecting a KRas G12D mutation in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Additionally provided herein is a method of treating an advanced solid tumor in a subject in need thereof, the method comprising: (a) detecting a KRas G12R mutation in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Additionally provided herein is a method of treating an advanced solid tumor in a subject in need thereof, the method comprising: (a) detecting a KRas G12S mutation in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Additionally provided herein is a method of treating an advanced solid tumor in a subject in need thereof, the method comprising: (a) detecting a KRas G12V mutation in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. As used herein, an “advanced solid tumor” is a solid tumor that has spread extensively to other anatomic sites and/or that is no longer responding to treatment. In some embodiments, classification of an advanced solid tumor can be made by the subject’s physician. In some embodiments, the cancer is a bladder cancer. In some embodiments, the bladder cancer has a KRas dysregulation (e.g., a KRas mutation or amplification). For example, the bladder cancer has a KRas mutation selected from the group consisting of: a KRas G12C mutation, a KRas G12D mutation, a KRas G12R mutation, a KRas G12V mutation, a KRas G13D mutation, and a KRas Q61H mutation. As another example, the bladder cancer has a KRas mutation selected from the group consisting of: a KRas G12C mutation, a KRas G12D mutation, a KRas G12R mutation, and a KRas G12V mutation. In some embodiments, the bladder cancer has a KRas G12D mutation, a KRas G12R mutation, or a KRas G12V mutation. In some embodiments, the bladder cancer has a KRas G12D mutation or a KRas G12V mutation. In some embodiments, the bladder cancer has a KRas G12D mutation. In some embodiments, the bladder cancer has a KRas G12R mutation. In some embodiments, the bladder cancer has a KRas G12V mutation. Also provided herein is a method of treating a bladder cancer in a subject in need thereof, the method comprising: (a) detecting a KRas dysregulation (e.g., a KRas mutation or amplification) in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Also provided herein is a method of treating a bladder cancer in a subject in need thereof, the method comprising: (a) detecting a KRas G12C mutation, a KRas G12D mutation, a KRas G12R mutation, a KRas G12V mutation, a KRas G13D mutation, or a KRas Q61H mutation in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Also provided herein is a method of treating a bladder cancer in a subject in need thereof, the method comprising: (a) detecting a KRas G12C mutation, a KRas G12D mutation, a KRas G12R mutation, or a KRas G12V mutation in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Additionally provided herein is a method of treating a bladder cancer in a subject in need thereof, the method comprising: (a) detecting a KRas G12D or a KRas G12V mutation in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Additionally provided herein is a method of treating a bladder cancer in a subject in need thereof, the method comprising: (a) detecting a KRas G12C mutation in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Additionally provided herein is a method of treating a bladder cancer in a subject in need thereof, the method comprising: (a) detecting a KRas G12D mutation in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Additionally provided herein is a method of treating a bladder cancer in a subject in need thereof, the method comprising: (a) detecting a KRas G12R mutation in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Additionally provided herein is a method of treating a bladder cancer in a subject in need thereof, the method comprising: (a) detecting a KRas G12V mutation in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some embodiments, the cancer is a cervical cancer. In some embodiments, the cervical cancer has a KRas dysregulation (e.g., a KRas mutation or amplification). For example, the cervical cancer has a KRas mutation selected from the group consisting of: a KRas G12C mutation, a KRas G12D mutation, a KRas G12V mutation, and a KRas G13D mutation. As another example, the cervical cancer has a KRas mutation selected from the group consisting of: a KRas G12C mutation, a KRas G12D mutation, and a KRas G12V mutation. In some embodiments, the cervical cancer has a KRas G12D mutation or a KRas G12V mutation. In some embodiments, the cervical cancer has a KRas G12C mutation. In some embodiments, the cervical cancer has a KRas G12D mutation. In some embodiments, the cervical cancer has a KRas G12V mutation. Also provided herein is a method of treating a cervical cancer in a subject in need thereof, the method comprising: (a) detecting a KRas dysregulation (e.g., a KRas mutation or amplification) in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Also provided herein is a method of treating a cervical cancer in a subject in need thereof, the method comprising: (a) detecting a KRas G12C mutation, a KRas G12D mutation, a KRas G12V mutation, or a KRas G13D mutation in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Also provided herein is a method of treating a cervical cancer in a subject in need thereof, the method comprising: (a) detecting a KRas G12C mutation, a KRas G12D mutation, or a KRas G12V mutation in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Additionally provided herein is a method of treating a cervical cancer in a subject in need thereof, the method comprising: (a) detecting a KRas G12D mutation or a KRas G12V mutation in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Additionally provided herein is a method of treating a cervical cancer in a subject in need thereof, the method comprising: (a) detecting a KRas G12C mutation in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Additionally provided herein is a method of treating a cervical cancer in a subject in need thereof, the method comprising: (a) detecting a KRas G12D mutation in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Additionally provided herein is a method of treating a cervical cancer in a subject in need thereof, the method comprising: (a) detecting a KRas G12V mutation in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some embodiments, the cancer is a colorectal cancer. In some embodiments, the colorectal cancer has a KRas dysregulation (e.g., a KRas mutation or amplification). For example, the colorectal cancer has a KRas mutation selected from the group consisting of: a KRas G12A mutation, a KRas G12C mutation, a KRas G12D mutation, a KRas G12R mutation, a KRas G12S mutation, a KRas G12V mutation, a KRas G13C mutation, a KRas G13D mutation, a KRas G13V mutation, a KRas Q61E mutation, a KRas Q61H mutation, a KRas Q61K mutation, a KRas Q61L mutation, a KRas Q61P mutation, and a KRas Q61R mutation. As another example, the colorectal cancer has a KRas mutation selected from the group consisting of: a KRas G12A mutation, a KRas G12C mutation, a KRas G12D mutation, a KRas G12R mutation, a KRas G12S mutation, and a KRas G12V mutation. In some embodiments, the colorectal cancer has a KRas G12D mutation, a KRas G12R mutation, or a KRas G12V mutation. In some embodiments, the colorectal cancer has a KRas G12D mutation or a KRas G12V mutation. In some embodiments, the colorectal cancer has a KRas G12C mutation. In some embodiments, the colorectal cancer has a KRas G12D mutation. In some embodiments, the colorectal cancer has a KRas G12S mutation. In some embodiments, the colorectal cancer has a KRas G12V mutation. Also provided herein is a method of treating a colorectal cancer in a subject in need thereof, the method comprising: (a) detecting a KRas dysregulation (e.g., a KRas mutation or amplification) in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Also provided herein is a method of treating a colorectal cancer in a subject in need thereof, the method comprising: (a) detecting a KRas G12A mutation, a KRas G12C mutation, a KRas G12D mutation, a KRas G12R mutation, a KRas G12S mutation, a KRas G12V mutation, a KRas G13C mutation, a KRas G13D mutation, a KRas G13V mutation, a KRas Q61E mutation, a KRas Q61H mutation, a KRas Q61K mutation, a KRas Q61L mutation, a KRas Q61P mutation, or a KRas Q61R mutation in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Also provided herein is a method of treating a colorectal cancer in a subject in need thereof, the method comprising: (a) detecting a KRas G12A mutation, a KRas G12C mutation, a KRas G12D mutation, a KRas G12R mutation, a KRas G12S mutation, or a KRas G12V mutation, in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Additionally provided herein is a method of treating a colorectal cancer in a subject in need thereof, the method comprising: (a) detecting a KRas G12D mutation or a KRas G12V mutation in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Additionally provided herein is a method of treating a colorectal cancer in a subject in need thereof, the method comprising: (a) detecting a KRas G12C mutation in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Additionally provided herein is a method of treating a colorectal cancer in a subject in need thereof, the method comprising: (a) detecting a KRas G12D mutation in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Additionally provided herein is a method of treating a colorectal cancer in a subject in need thereof, the method comprising: (a) detecting a KRas G12R mutation in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Additionally provided herein is a method of treating a colorectal cancer in a subject in need thereof, the method comprising: (a) detecting a KRas G12S mutation in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Additionally provided herein is a method of treating a colorectal cancer in a subject in need thereof, the method comprising: (a) detecting a KRas G12V mutation in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some embodiments, the cancer is an endometrial cancer. In some embodiments, the endometrial cancer has a KRas dysregulation (e.g., a KRas mutation or amplification). For example, the endometrial cancer has a KRas mutation selected from the group consisting of: a KRas G12A mutation, a KRas G12C mutation, a KRas G12D mutation, a KRas G12S mutation, a KRas G12V mutation, a KRas G13C mutation, a KRas G13D mutation, a KRas G13V mutation, a KRas Q61H mutation, and a KRas Q61L mutation. As another example, the endometrial cancer has a KRas mutation selected from the group consisting of: a KRas G12A mutation, a KRas G12C mutation, a KRas G12D mutation, a KRas G12S mutation, and a KRas G12V mutation. In some embodiments, the endometrial cancer has a KRas G12D mutation or a KRas G12V mutation. In some embodiments, the endometrial cancer has a KRas G12A mutation. In some embodiments, the endometrial cancer has a KRas G12C mutation. In some embodiments, the endometrial cancer has a KRas G12D mutation. In some embodiments, the endometrial cancer has a KRas G12S mutation. In some embodiments, the endometrial cancer has a KRas G12V mutation. Also provided herein is a method of treating an endometrial cancer in a subject in need thereof, the method comprising: (a) detecting a KRas dysregulation (e.g., a KRas mutation or amplification) in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Also provided herein is a method of treating an endometrial cancer in a subject in need thereof, the method comprising: (a) detecting a KRas G12A mutation, a KRas G12C mutation, a KRas G12D mutation, a KRas G12S mutation, a KRas G12V mutation, a KRas G13C mutation, a KRas G13D mutation, a KRas G13V mutation, a KRas Q61H mutation, or a KRas Q61L mutation in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Also provided herein is a method of treating an endometrial cancer in a subject in need thereof, the method comprising: (a) detecting a KRas G12A mutation, a KRas G12C mutation, a KRas G12D mutation, a KRas G12S mutation, or a KRas G12V mutation in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Additionally provided herein is a method of treating an endometrial cancer in a subject in need thereof, the method comprising: (a) detecting a KRas G12D mutation or a KRas G12V mutation in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Additionally provided herein is a method of treating an endometrial cancer in a subject in need thereof, the method comprising: (a) detecting a KRas G12A mutation in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Additionally provided herein is a method of treating an endometrial cancer in a subject in need thereof, the method comprising: (a) detecting a KRas G12C mutation in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Additionally provided herein is a method of treating an endometrial cancer in a subject in need thereof, the method comprising: (a) detecting a KRas G12D mutation in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Additionally provided herein is a method of treating an endometrial cancer in a subject in need thereof, the method comprising: (a) detecting a KRas G12S mutation in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Additionally provided herein is a method of treating an endometrial cancer in a subject in need thereof, the method comprising: (a) detecting a KRas G12V mutation in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some embodiments, the cancer is an esophageal or stomach cancer. In some embodiments, the esophageal or stomach cancer has a KRas dysregulation (e.g., a KRas mutation or amplification). For example, the esophageal or stomach cancer has a KRas mutation selected from the group consisting of: a KRas G12C mutation, a KRas G12D mutation, a KRas G12S mutation, a KRas G12V mutation, a KRas G13C mutation, a KRas G13D mutation, and a KRas Q61H mutation. As another example, the esophageal or stomach cancer has a KRas mutation selected from the group consisting of: a KRas G12C mutation, a KRas G12D mutation, a KRas G12S mutation, and a KRas G12V mutation. In some embodiments, the esophageal or stomach cancer has a KRas G12D mutation or a KRas G12V mutation. In some embodiments, the esophageal or stomach cancer has a KRas G12C mutation. In some embodiments, the esophageal or stomach cancer has a KRas G12D mutation. In some embodiments, the esophageal or stomach cancer has a KRas G12S mutation. In some embodiments, the esophageal or stomach cancer has a KRas G12V mutation. Also provided herein is a method of treating an esophageal or stomach cancer in a subject in need thereof, the method comprising: (a) detecting a KRas dysregulation (e.g., a KRas mutation or amplification) in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Also provided herein is a method of treating an esophageal or stomach cancer in a subject in need thereof, the method comprising: (a) detecting a KRas G12C mutation, a KRas G12D mutation, a KRas G12S mutation, a KRas G12V mutation, a KRas G13C mutation, a KRas G13D mutation, or a KRas Q61H mutation in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Also provided herein is a method of treating an esophageal or stomach cancer in a subject in need thereof, the method comprising: (a) detecting a KRas G12C mutation, a KRas G12D mutation, a KRas G12S mutation, or a KRas G12V mutation in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Additionally provided herein is a method of treating an esophageal or stomach cancer in a subject in need thereof, the method comprising: (a) detecting a KRas G12C mutation or a KRas G12V mutation in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Additionally provided herein is a method of treating an esophageal or stomach cancer in a subject in need thereof, the method comprising: (a) detecting a KRas G12D mutation or a KRas G12V mutation in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Additionally provided herein is a method of treating an esophageal or stomach cancer in a subject in need thereof, the method comprising: (a) detecting a KRas G12D mutation in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Additionally provided herein is a method of treating an esophageal or stomach cancer in a subject in need thereof, the method comprising: (a) detecting a KRas G12S mutation or a KRas G12V mutation in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Additionally provided herein is a method of treating an esophageal or stomach cancer in a subject in need thereof, the method comprising: (a) detecting a KRas G12V mutation in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some embodiments, the cancer is a leukemia. In some embodiments, the leukemia has a KRas dysregulation (e.g., a KRas mutation or amplification). For example, the leukemia has a KRas mutation selected from the group consisting of: a KRas G12A mutation, a KRas G12C mutation, a KRas G12D mutation, a KRas G12R mutation, a KRas G12S mutation, a KRas G12V mutation, a KRas G13C mutation, a KRas G13D mutation, a KRas G13V mutation, a KRas Q61E mutation, a KRas Q61H mutation, a KRas Q61K mutation, a KRas Q61L mutation, a KRas Q61P mutation, and a KRas Q61R mutation. For example, the leukemia has a KRas mutation selected from the group consisting of: a KRas G12A mutation, a KRas G12C mutation, a KRas G12D mutation, a KRas G12R mutation, a KRas G12S mutation, and a KRas G12V mutation. In some embodiments, the leukemia has a KRas G12D mutation, a KRas G12R mutation, or a KRas G12V mutation. In some embodiments, the leukemia has a KRas G12D mutation or a KRas G12V mutation. In some embodiments, the leukemia has a KRas G12A mutation. In some embodiments, the leukemia has a KRas G12C mutation. In some embodiments, the leukemia has a KRas G12D mutation. In some embodiments, the leukemia has a KRas G12R mutation. In some embodiments, the leukemia has a KRas G12S mutation. In some embodiments, the leukemia has a KRas G12V mutation. Also provided herein is a method of treating a leukemia in a subject in need thereof, the method comprising: (a) detecting a KRas dysregulation (e.g., a KRas mutation or amplification) in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Also provided herein is a method of treating a leukemia in a subject in need thereof, the method comprising: (a) detecting a KRas G12A mutation, a KRas G12C mutation, a KRas G12D mutation, a KRas G12R mutation, a KRas G12S mutation, a KRas G12V mutation, a KRas G13C mutation, a KRas G13D mutation, a KRas G13V mutation, a KRas Q61E mutation, a KRas Q61H mutation, a KRas Q61K mutation, a KRas Q61L mutation, a KRas Q61P mutation, or a KRas Q61R mutation in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Also provided herein is a method of treating a leukemia in a subject in need thereof, the method comprising: (a) detecting a KRas G12A mutation, a KRas G12C mutation, a KRas G12D mutation, a KRas G12R mutation, a KRas G12S mutation, or a KRas G12V mutation in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Additionally provided herein is a method of treating a leukemia in a subject in need thereof, the method comprising: (a) detecting a KRas G12A mutation or a KRas G12V mutation in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Additionally provided herein is a method of treating a leukemia in a subject in need thereof, the method comprising: (a) detecting a KRas G12D mutation or a KRas G12C mutation in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Additionally provided herein is a method of treating a leukemia in a subject in need thereof, the method comprising: (a) detecting a KRas G12D mutation or a KRas G12V mutation in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Additionally provided herein is a method of treating a leukemia in a subject in need thereof, the method comprising: (a) detecting a KRas G12D mutation in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Additionally provided herein is a method of treating a leukemia in a subject in need thereof, the method comprising: (a) detecting a KRas G12R mutation in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Additionally provided herein is a method of treating a leukemia in a subject in need thereof, the method comprising: (a) detecting a KRas G12S mutation or a KRas G12V mutation in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Additionally provided herein is a method of treating a leukemia in a subject in need thereof, the method comprising: (a) detecting a KRas G12V mutation in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some embodiments, the cancer is a melanoma. In some embodiments, the melanoma has a KRas dysregulation (e.g., a KRas mutation or amplification). For example, the melanoma has a KRas mutation selected from the group consisting of: a KRas G12C mutation, a KRas G12D mutation, a KRas G12R mutation, a KRas G13D mutation, a KRas G13V mutation, a KRas a KRas Q61K mutation, a KRas Q61L mutation, and a KRas Q61R mutation. As another example, the melanoma has a KRas mutation selected from the group consisting of: a KRas G12C mutation, a KRas G12D mutation, and a KRas G12R mutation. In some embodiments, the melanoma has a KRas G12D mutation or a KRas G12R mutation. In some embodiments, the melanoma has a KRas G12C mutation. In some embodiments, the melanoma has a KRas G12D mutation. In some embodiments, the melanoma has a KRas G12R mutation. Also provided herein is a method of treating a melanoma in a subject in need thereof, the method comprising: (a) detecting a KRas dysregulation (e.g., a KRas mutation or amplification) in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Also provided herein is a method of treating a melanoma in a subject in need thereof, the method comprising: (a) detecting a KRas G12C mutation, a KRas G12D mutation, a KRas G12R mutation, a KRas G13D mutation, a KRas G13V mutation, a KRas a KRas Q61K mutation, a KRas Q61L mutation, or a KRas Q61R mutation in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Also provided herein is a method of treating a melanoma in a subject in need thereof, the method comprising: (a) detecting a KRas G12C mutation, a KRas G12D mutation, a KRas G12R mutation in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Additionally provided herein is a method of treating a melanoma in a subject in need thereof, the method comprising: (a) detecting a KRas G12C mutation in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Additionally provided herein is a method of treating a melanoma in a subject in need thereof, the method comprising: (a) detecting a KRas G12D mutation in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Additionally provided herein is a method of treating a melanoma in a subject in need thereof, the method comprising: (a) detecting a KRas G12R mutation in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some embodiments, the cancer is a lung cancer (e.g., non-small cell lung cancer). In some embodiments, the lung cancer (e.g., non-small cell lung cancer) has a KRas dysregulation (e.g., a KRas mutation or amplification). For example, the lung cancer (e.g., non-small cell lung cancer) has a KRas mutation selected from the group consisting of: a KRas G12A mutation, a KRas G12C mutation, a KRas G12D mutation, a KRas G12S mutation, a KRas G12V mutation, a KRas G13C mutation, a KRas G13D mutation, a KRas Q61H mutation, and a KRas Q61L mutation. For example, the lung cancer (e.g., non-small cell lung cancer) has a KRas mutation selected from the group consisting of: a KRas G12A mutation, a KRas G12C mutation, a KRas G12D mutation, a KRas G12S mutation, and a KRas G12V mutation. In some embodiments, the lung cancer has a KRas G12D mutation or a KRas G12V mutation. In some embodiments, the lung cancer has a KRas G12A mutation. In some embodiments, the lung cancer has a KRas G12C mutation. In some embodiments, the lung cancer has a KRas G12D mutation. In some embodiments, the lung cancer has a KRas G12S mutation. In some embodiments, the lung cancer has a KRas G12V mutation. Also provided herein is a method of treating a lung cancer (e.g., non-small cell lung cancer) in a subject in need thereof, the method comprising: (a) detecting a KRas dysregulation (e.g., a KRas mutation or amplification) in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Also provided herein is a method of treating a lung cancer (e.g., non-small cell lung cancer) in a subject in need thereof, the method comprising: (a) detecting a KRas G12A mutation, a KRas G12C mutation, a KRas G12D mutation, a KRas G12S mutation, a KRas G12V mutation, a KRas G13C mutation, a KRas G13D mutation, a KRas Q61H mutation, or a KRas Q61L mutation in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Also provided herein is a method of treating a lung cancer (e.g., non-small cell lung cancer) in a subject in need thereof, the method comprising: (a) detecting a KRas G12A mutation, a KRas G12C mutation, a KRas G12D mutation, a KRas G12S mutation, or a KRas G12V mutation in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Additionally provided herein is a method of treating a lung cancer in a subject in need thereof, the method comprising: (a) detecting a KRas G12D mutation or a KRas G12V mutation in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Additionally provided herein is a method of treating a lung cancer in a subject in need thereof, the method comprising: (a) detecting a KRas G12A mutation in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Additionally provided herein is a method of treating a lung cancer in a subject in need thereof, the method comprising: (a) detecting a KRas G12C mutation in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Additionally provided herein is a method of treating a lung cancer in a subject in need thereof, the method comprising: (a) detecting a KRas G12D mutation in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Additionally provided herein is a method of treating a lung cancer in a subject in need thereof, the method comprising: (a) detecting a KRas G12S mutation in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Additionally provided herein is a method of treating a lung cancer in a subject in need thereof, the method comprising: (a) detecting a KRas G12V mutation in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some embodiments, the cancer is a pancreatic cancer. In some embodiments, the pancreatic cancer has a KRas dysregulation (e.g., a KRas mutation or amplification). For example, the pancreatic cancer has a KRas mutation selected from the group consisting of: a KRas G12A mutation, a KRas G12C mutation, a KRas G12D mutation, a KRas G12R mutation, a KRas G12S mutation, a KRas G12V mutation, a KRas G13C mutation, a KRas Q61H mutation, and a KRas Q61R mutation. For example, the pancreatic cancer has a KRas mutation selected from the group consisting of: a KRas G12A mutation, a KRas G12C mutation, a KRas G12D mutation, a KRas G12R mutation, a KRas G12S mutation, and a KRas G12V mutation. In some embodiments, the pancreatic cancer has a KRas G12D mutation, a KRas G12R mutation, or a KRas G12V mutation. In some embodiments, the pancreatic cancer has a KRas G12D mutation or a KRas G12V mutation. In some embodiments, the pancreatic cancer has a KRas G12A mutation. In some embodiments, the pancreatic cancer has a KRas G12C mutation. In some embodiments, the pancreatic cancer has a KRas G12D mutation. In some embodiments, the pancreatic cancer has a KRas G12R mutation. In some embodiments, the pancreatic cancer has a KRas G12S mutation. In some embodiments, the pancreatic cancer has a KRas G12V mutation. Also provided herein is a method of treating a pancreatic cancer in a subject in need thereof, the method comprising: (a) detecting a KRas dysregulation (e.g., a KRas mutation or amplification) in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Also provided herein is a method of treating a pancreatic cancer in a subject in need thereof, the method comprising: (a) detecting a KRas G12A mutation, a KRas G12C mutation, a KRas G12D mutation, a KRas G12R mutation, a KRas G12S mutation, a KRas G12V mutation, a KRas G13C mutation, a KRas Q61H mutation, or a KRas Q61R mutation in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Additionally provided herein is a method of treating a pancreatic cancer in a subject in need thereof, the method comprising: (a) detecting a KRas G12D mutation, a KRas G12R mutation, or a KRas G12V mutation in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Also provided herein is a method of treating a pancreatic cancer in a subject in need thereof, the method comprising: (a) detecting a KRas G12A mutation, a KRas G12C mutation, a KRas G12D mutation, a KRas G12R mutation, a KRas G12S mutation, or a KRas G12V mutation in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Additionally provided herein is a method of treating a pancreatic cancer in a subject in need thereof, the method comprising: (a) detecting a KRas G12D mutation or a KRas G12V mutation in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Additionally provided herein is a method of treating a pancreatic cancer in a subject in need thereof, the method comprising: (a) detecting a KRas G12A mutation in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Additionally provided herein is a method of treating a pancreatic cancer in a subject in need thereof, the method comprising: (a) detecting a KRas G12C mutation in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Additionally provided herein is a method of treating a pancreatic cancer in a subject in need thereof, the method comprising: (a) detecting a KRas G12D mutation in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Additionally provided herein is a method of treating a pancreatic cancer in a subject in need thereof, the method comprising: (a) detecting a KRas G12R mutation in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Additionally provided herein is a method of treating a pancreatic cancer in a subject in need thereof, the method comprising: (a) detecting a KRas G12S mutation in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Additionally provided herein is a method of treating a pancreatic cancer in a subject in need thereof, the method comprising: (a) detecting a KRas G12V mutation in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some embodiments, the cancer is a testicular cancer (e.g., seminoma). In some embodiments, the testicular cancer (e.g., seminoma) has a KRas dysregulation (e.g., a KRas mutation or amplification). For example, the testicular cancer (e.g., seminoma) has a KRas mutation selected from the group consisting of: a KRas G12A mutation, a KRas G12R mutation, a KRas G12S mutation, a KRas G12V mutation, a KRas Q61L mutation, a KRas Q61P mutation, and a KRas Q61R mutation. As another example, the testicular cancer (e.g., seminoma) has a KRas mutation selected from the group consisting of: a KRas G12A mutation, a KRas G12R mutation, a KRas G12S mutation, and a KRas G12V mutation. In some embodiments, the testicular cancer (e.g., seminoma) cancer has a KRas G12R mutation or a KRas G12V mutation. In some embodiments, the testicular cancer (e.g., seminoma) cancer has a KRas G12A mutation. In some embodiments, the testicular cancer (e.g., seminoma) cancer has a KRas G12R mutation. In some embodiments, the testicular cancer (e.g., seminoma) cancer has a KRas G12S mutation. In some embodiments, the testicular cancer (e.g., seminoma) cancer has a KRas G12V mutation. Also provided herein is a method of treating a testicular cancer (e.g., seminoma) in a subject in need thereof, the method comprising: (a) detecting a KRas dysregulation (e.g., a KRas mutation or amplification) in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Also provided herein is a method of treating a testicular cancer (e.g., seminoma) in a subject in need thereof, the method comprising: (a) detecting a KRas G12A mutation, a KRas G12R mutation, a KRas G12S mutation, a KRas G12V mutation, a KRas Q61L mutation, a KRas Q61P mutation, or a KRas Q61R mutation in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Also provided herein is a method of treating a testicular cancer (e.g., seminoma) in a subject in need thereof, the method comprising: (a) detecting a KRas G12A mutation, a KRas G12R mutation, a KRas G12S mutation, or a KRas G12V mutation in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Additionally provided herein is a method of treating a testicular cancer (e.g., seminoma) in a subject in need thereof, the method comprising: (a) detecting a KRas G12A mutation in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Additionally provided herein is a method of treating a testicular cancer (e.g., seminoma) in a subject in need thereof, the method comprising: (a) detecting a KRas G12R mutation in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Additionally provided herein is a method of treating a testicular cancer (e.g., seminoma) in a subject in need thereof, the method comprising: (a) detecting a KRas G12S mutation in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Additionally provided herein is a method of treating a testicular cancer (e.g., seminoma) in a subject in need thereof, the method comprising: (a) detecting a KRas G12V mutation in a sample from the subject, and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Also provided herein is a method of treating a bladder cancer in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some embodiments, the method further comprises determining that the bladder cancer has a KRas mutation selected from the group consisting of: a KRas G12C mutation, a KRas G12D mutation, a KRas G12R mutation, a KRas G12V mutation, a KRas G13D mutation, and a KRas Q61H mutation. In some embodiments, the method further comprises determining that the bladder cancer has a KRas mutation selected from the group consisting of: a KRas G12C mutation, a KRas G12D mutation, a KRas G12R mutation, and a KRas G12V mutation. In some such embodiments, the cancer is a KRas G12C- associated cancer, a KRas G12D-associated cancer, a KRas G12R-associated cancer, a KRas G12V-associated cancer, a KRas G13D-associated cancer, or a KRas Q61H-associated cancer. In some such embodiments, the cancer is a KRas G12C-associated cancer, a KRas G12D- associated cancer, a KRas G12R-associated cancer, or a KRas G12V-associated cancer. In some aspects of this embodiment, the cancer is a KRas G12D-associated cancer, a KRas G12R- associated cancer, or a KRas G12V-associated cancer. In some embodiments, the cancer is a KRas G12C-associated cancer. In some embodiments, the cancer is a KRas G12D-associated cancer. In some embodiments, the cancer is a KRas G12R-associated cancer. In some embodiments, the cancer is a KRas G12V-associated cancer. In some embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12C inhibitor, a KRas G12D inhibitor, a KRas G12R inhibitor, a KRas G12V inhibitor, a KRas G13D inhibitor, a KRas Q61H inhibitor, or two or more thereof. In some embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12C inhibitor, a KRas G12D inhibitor, a KRas G12R inhibitor, a KRas G12V inhibitor, or two or more thereof. In some aspects of this embodiment, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12D inhibitor, a KRas G12R inhibitor, and/or a KRas G12V inhibitor. In some aspects of this embodiment, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12D inhibitor, a KRas G12V inhibitor, or both. Also provided herein is a method of treating a cervical cancer in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some embodiments, the method further comprises determining that the cervical cancer has a KRas mutation selected from the group consisting of: a KRas G12C mutation, a KRas G12D mutation, a KRas G12V mutation, and a KRas G13D mutation. In some embodiments, the method further comprises determining that the cervical cancer has a KRas mutation selected from the group consisting of: a KRas G12C mutation, a KRas G12D mutation, and a KRas G12V mutation. In some embodiments, the cancer is a KRas G12C-associated cancer, a KRas G12D-associated cancer, a KRas G12V- associated cancer, or a KRas G13D-associated cancer. In some embodiments, the cancer is a KRas G12C-associated cancer, a KRas G12D-associated cancer, or a KRas G12V-associated cancer. In some embodiments, the cancer is a KRas G12D-associated cancer or a KRas G12V- associated cancer. In some embodiments, the cancer is a KRas G12C-associated cancer. In some embodiments, the cancer is a KRas G12D-associated cancer. In some embodiments, the cancer is a KRas G12V-associated cancer. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12C inhibitor, a KRas G12D inhibitor, a KRas G12V inhibitor, a KRas G13D inhibitor, or two or more thereof. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12C inhibitor, a KRas G12D inhibitor, a KRas G12V inhibitor, or two or more thereof. In some aspects of this embodiment, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12D inhibitor, a KRas G12V inhibitor, or both. Also provided herein is a method of treating a colorectal cancer in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some embodiments, the method further comprises determining that the colorectal cancer has a KRas mutation selected from the group consisting of: a KRas G12A mutation, a KRas G12C mutation, a KRas G12D mutation, a KRas G12R mutation, a KRas G12S mutation, a KRas G12V mutation, a KRas G13C mutation, a KRas G13D mutation, a KRas G13V mutation, a KRas Q61E mutation, a KRas Q61H mutation, a KRas Q61K mutation, a KRas Q61L mutation, a KRas Q61P mutation, and a KRas Q61R mutation. In some embodiments, the method further comprises determining that the colorectal cancer has a KRas mutation selected from the group consisting of: a KRas G12A mutation, a KRas G12C mutation, a KRas G12D mutation, a KRas G12R mutation, a KRas G12S mutation, and a KRas G12V mutation. In some embodiments, the cancer is a KRas G12A-associated cancer, a KRas G12C-associated cancer, a KRas G12D-associated cancer, a KRas G12R-associated cancer, a KRas G12S-associated cancer, a KRas G12V-associated cancer, a KRas G13C-associated cancer, a KRas G13D-associated cancer, a KRas G13V- associated cancer, a KRas Q61E-associated cancer, a KRas Q61H-associated cancer, a KRas Q61K-associated cancer, a KRas Q61L-associated cancer, a KRas Q61P-associated cancer, or a KRas Q61R-associated cancer. In some embodiments, the cancer is a KRas G12A-associated cancer, a KRas G12C-associated cancer, a KRas G12D-associated cancer, a KRas G12R- associated cancer, a KRas G12S-associated cancer, or a KRas G12V-associated cancer. In some aspects of this embodiment, the cancer is a KRas G12D-associated cancer, a KRas G12R- associated cancer, or a KRas G12V-associated cancer. In some embodiments, the cancer is a KRas G12D-associated cancer or a KRas G12V-associated cancer. In some embodiments, the cancer is a KRas G12A-associated cancer. In some embodiments, the cancer is a KRas G12C- associated cancer. In some embodiments, the cancer is a KRas G12D-associated cancer. In some embodiments, the cancer is a KRas G12R-associated cancer. In some embodiments, the cancer is a KRas G12S-associated cancer. In some embodiments, the cancer is a KRas G12V- associated cancer. In some embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12A inhibitor, a KRas G12C inhibitor, a KRas G12D inhibitor, a KRas G12R inhibitor, a KRas G12S inhibitor, a KRas G12V inhibitor, a KRas G13C inhibitor, a KRas G13D inhibitor, a KRas G13V inhibitor, a KRas Q61E inhibitor, a KRas Q61H inhibitor, a KRas Q61K inhibitor, a KRas Q61L inhibitor, a KRas Q61P inhibitor, a KRas Q61R inhibitor, or two or more thereof. In some embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12A inhibitor, a KRas G12C inhibitor, a KRas G12D inhibitor, a KRas G12R inhibitor, a KRas G12S inhibitor, a KRas G12V inhibitor, or two or more thereof. In some aspects of this embodiment, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12D inhibitor, a KRas G12R inhibitor, and/or a KRas G12V inhibitor. In some aspects of this embodiment, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12D inhibitor, a KRas G12V inhibitor, or both. Also provided herein is a method of treating an endometrial cancer in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some embodiments, the method further comprises determining that the endometrial cancer has a KRas mutation selected from the group consisting of: a KRas G12A mutation, a KRas G12C mutation, a KRas G12D mutation, a KRas G12S mutation, a KRas G12V mutation, a KRas G13C mutation, a KRas G13D mutation, a KRas G13V mutation, a KRas Q61H mutation, and a KRas Q61L mutation. In some embodiments, the method further comprises determining that the endometrial cancer has a KRas mutation selected from the group consisting of: a KRas G12A mutation, a KRas G12C mutation, a KRas G12D mutation, a KRas G12S mutation, and a KRas G12V mutation. In some embodiments, the cancer is a KRas G12A-associated cancer, a KRas G12C-associated cancer, a KRas G12D-associated cancer, a KRas G12S-associated cancer, a KRas G12V- associated cancer, a KRas G13C-associated cancer, a KRas G13D-associated cancer, a KRas G13V-associated cancer, a KRas Q61H-associated cancer, or a KRas Q61L-associated cancer. In some embodiments, the cancer is a KRas G12A-associated cancer, a KRas G12C-associated cancer, a KRas G12D-associated cancer, a KRas G12S-associated cancer, or a KRas G12V- associated cancer. In some embodiments, the cancer is a KRas G12D-associated cancer or a KRas G12V-associated cancer. In some embodiments, the cancer is a KRas G12A-associated cancer. In some embodiments, the cancer is a KRas G12C-associated cancer. In some embodiments, the cancer is a KRas G12D-associated cancer. In some embodiments, the cancer is a KRas G12S-associated cancer. In some embodiments, the cancer is a KRas G12V- associated cancer. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12A inhibitor, a KRas G12C inhibitor, a KRas G12D inhibitor, a KRas G12S inhibitor, a KRas G12V inhibitor, a KRas G13C inhibitor, a KRas G13D inhibitor, a KRas G13V inhibitor, a KRas Q61H inhibitor, a KRas Q61L inhibitor, or two or more thereof. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12A inhibitor, a KRas G12C inhibitor, a KRas G12D inhibitor, a KRas G12S inhibitor, a KRas G12V inhibitor, or two or more thereof. In some aspects of this embodiment, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12D inhibitor, a KRas G12V inhibitor, or both. Also provided herein is a method of treating an esophageal or stomach cancer in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some embodiments, the method further comprises determining that the esophageal or stomach cancer has a KRas mutation selected from the group consisting of: a KRas G12C mutation, a KRas G12D mutation, a KRas G12S mutation, a KRas G12V mutation, a KRas G13C mutation, a KRas G13D mutation, and a KRas Q61H mutation. In some embodiments, the method further comprises determining that the esophageal or stomach cancer has a KRas mutation selected from the group consisting of: a KRas G12C mutation, a KRas G12D mutation, a KRas G12S mutation, and a KRas G12V mutation. In some embodiments, the cancer is a KRas G12C- associated cancer, a KRas G12D-associated cancer, a KRas G12S-associated cancer, a KRas G12V-associated cancer, a KRas G13C-associated cancer, a KRas G13D-associated cancer, or a KRas Q61H-associated cancer. In some embodiments, the cancer is a KRas G12C-associated cancer, a KRas G12D-associated cancer, a KRas G12S-associated cancer, or a KRas G12V- associated cancer. In some embodiments, the cancer is a KRas G12D-associated cancer or a KRas G12V-associated cancer. In some embodiments, the cancer is a KRas G12C-associated cancer. In some embodiments, the cancer is a KRas G12D-associated cancer. In some embodiments, the cancer is a KRas G12S-associated cancer. In some embodiments, the cancer is a KRas G12V-associated cancer. In some embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12C inhibitor, a KRas G12D inhibitor, a KRas G12S inhibitor, a KRas G12V inhibitor, a KRas G13C inhibitor, a KRas G13D inhibitor, a KRas Q61H inhibitor, or two or more thereof. In some embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12C inhibitor, a KRas G12D inhibitor, a KRas G12S inhibitor, a KRas G12V inhibitor, or two or more thereof. In some aspects of this embodiment, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12D inhibitor, a KRas G12V inhibitor, or both. Also provided herein is a method of treating a leukemia in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some embodiments, the method further comprises determining that the leukemia has a KRas mutation selected from the group consisting of: a KRas G12A mutation, a KRas G12C mutation, a KRas G12D mutation, a KRas G12R mutation, a KRas G12S mutation, a KRas G12V mutation, a KRas G13C mutation, a KRas G13D mutation, a KRas G13V mutation, a KRas Q61E mutation, a KRas Q61H mutation, a KRas Q61K mutation, a KRas Q61L mutation, a KRas Q61P mutation, and a KRas Q61R mutation. In some embodiments, the method further comprises determining that the leukemia has a KRas mutation selected from the group consisting of: a KRas G12A mutation, a KRas G12C mutation, a KRas G12D mutation, a KRas G12R mutation, a KRas G12S mutation, and a KRas G12V mutation. In some embodiments, the cancer is a KRas G12A- associated cancer, a KRas G12C-associated cancer, a KRas G12D-associated cancer, a KRas G12R-associated cancer, a KRas G12S-associated cancer, a KRas G12V-associated cancer, a KRas G13C-associated cancer, a KRas G13D-associated cancer, a KRas G13V-associated cancer, a KRas Q61E-associated cancer, a KRas Q61H-associated cancer, a KRas Q61K- associated cancer, a KRas Q61L-associated cancer, a KRas Q61P-associated cancer, or a KRas Q61R-associated cancer. In some embodiments, the cancer is a KRas G12A-associated cancer, a KRas G12C-associated cancer, a KRas G12D-associated cancer, a KRas G12R-associated cancer, a KRas G12S-associated cancer, and a KRas G12V-associated cancer. In some aspects of this embodiment, the cancer is a KRas G12D-associated cancer, a KRas G12R-associated cancer, or a KRas G12V-associated cancer. In some embodiments, the cancer is a KRas G12D- associated cancer or a KRas G12V-associated cancer. In some embodiments, the cancer is a KRas G12A-associated cancer. In some embodiments, the cancer is a KRas G12C-associated cancer. In some embodiments, the cancer is a KRas G12D-associated cancer. In some embodiments, the cancer is a KRas G12R-associated cancer. In some embodiments, the cancer is a KRas G12S-associated cancer. In some embodiments, the cancer is a KRas G12V- associated cancer. In some embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12A inhibitor, a KRas G12C inhibitor, a KRas G12D inhibitor, a KRas G12R inhibitor, a KRas G12S inhibitor, a KRas G12V inhibitor, a KRas G13C inhibitor, a KRas G13D inhibitor, a KRas G13V inhibitor, a KRas Q61E inhibitor, a KRas Q61H inhibitor, a KRas Q61K inhibitor, a KRas Q61L inhibitor, a KRas Q61P inhibitor, a KRas Q61R inhibitor, or two or more thereof. In some embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12A inhibitor, a KRas G12C inhibitor, a KRas G12D inhibitor, a KRas G12R inhibitor, a KRas G12S inhibitor, a KRas G12V inhibitor, or two or more thereof. In some aspects of this embodiment, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12D inhibitor, a KRas G12R inhibitor, and/or a KRas G12V inhibitor. In some aspects of this embodiment, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12D inhibitor, a KRas G12V inhibitor, or both. Also provided herein is a method of treating a melanoma in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some embodiments, the method further comprises determining that the melanoma has a KRas mutation selected from the group consisting of: a KRas G12C mutation, a KRas G12D mutation, a KRas G12R mutation, a KRas G13D mutation, a KRas G13V mutation, a KRas Q61K mutation, a KRas Q61L mutation, and a KRas Q61R mutation. In some embodiments, the method further comprises determining that the melanoma has a KRas mutation selected from the group consisting of: a KRas G12C mutation, a KRas G12D mutation, and a KRas G12R mutation. In some embodiments, the cancer is a KRas G12C-associated cancer, a KRas G12D-associated cancer, a KRas G12R- associated cancer, a KRas G13D-associated cancer, a KRas G13V-associated cancer, a KRas Q61K-associated cancer, a KRas Q61L-associated cancer, or a KRas Q61R-associated cancer. In some embodiments, the cancer is a KRas G12C-associated cancer, a KRas G12D-associated cancer, or a KRas G12R-associated cancer. In some embodiments, the cancer is a KRas G12D- associated cancer or a KRas G12R-associted cancer. In some embodiments, the cancer is a KRas G12C-associated cancer. In some embodiments, the cancer is a KRas G12D-associated cancer. In some embodiments, the cancer is a KRas G12R-associated cancer. In some embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12C inhibitor, a KRas G12D inhibitor, a KRas G12R inhibitor, a KRas G13D inhibitor, a KRas G13V inhibitor, a KRas Q61K inhibitor, a KRas Q61L inhibitor, a KRas Q61R inhibitor, or two or more thereof. In some embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12C inhibitor, a KRas G12D inhibitor, a KRas G12R inhibitor, or two or more thereof. In some aspects of this embodiment, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12D inhibitor, a KRas G12R inhibitor, or both. Also provided herein is a method of treating a lung cancer (e.g., NSCLC) in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some embodiments, the method further comprises determining that the lung cancer (e.g., NSCLC) has a KRas mutation selected from the group consisting of: KRas G12A mutation, a KRas G12C mutation, a KRas G12D mutation, a KRas G12S mutation, a KRas G12V mutation, a KRas G13C-asociated cancer, a KRas G13D mutation, a KRas Q61H mutation, and a KRas Q61L mutation. In some embodiments, the method further comprises determining that the lung cancer (e.g., NSCLC) has a KRas mutation selected from the group consisting of: KRas G12A mutation, a KRas G12C mutation, a KRas G12D mutation, a KRas G12S mutation, and a KRas G12V mutation. In some embodiments, the cancer is a KRas G12A-associated cancer, a KRas G12C-associated cancer, a KRas G12D- associated cancer, a KRas G12S-associated cancer, a KRas G12V-associated cancer, a KRas G13C-asociated cancer, a KRas G13D-associated cancer, a KRas Q61H-associated cancer, or a KRas Q61L-associated cancer. In some embodiments, the cancer is a KRas G12A-associated cancer, a KRas G12C-associated cancer, a KRas G12D-associated cancer, a KRas G12S- associated cancer, or a KRas G12V-associated cancer. In some embodiments, the cancer is a KRas G12D-associated cancer or a KRas G12V-associated cancer. In some embodiments, the cancer is a KRas G12A-associated cancer. In some embodiments, the cancer is a KRas G12C- associated cancer. In some embodiments, the cancer is a KRas G12D-associated cancer. In some embodiments, the cancer is a KRas G12S-associated cancer. In some embodiments, the cancer is a KRas G12V-associated cancer. In some embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12A inhibitor, a KRas G12C inhibitor, a KRas G12D inhibitor, a KRas G12S inhibitor, a KRas G12V inhibitor, a KRas G13C-asociated cancer, a KRas G13D inhibitor, a KRas Q61H inhibitor, a KRas Q61L inhibitor, or two or more thereof. In some embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12A inhibitor, a KRas G12C inhibitor, a KRas G12D inhibitor, a KRas G12S inhibitor, a KRas G12V inhibitor, or two or more thereof. In some aspects of this embodiment, the compound provided herein, or a pharmaceutically acceptable salt thereof, a KRas G12D inhibitor, a KRas G12V inhibitor, or both. Also provided herein is a method of treating a pancreatic cancer in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some embodiments, the method further comprises determining that the pancreatic cancer has a KRas mutation selected from the group consisting of: a KRas G12A mutation, a KRas G12C mutation, a KRas G12D mutation, a KRas G12R mutation, a KRas G12S mutation, a KRas G12V mutation, a KRas G13C-asociated cancer, and a KRas Q61H mutation. In some embodiments, the method further comprises determining that the pancreatic cancer has a KRas mutation selected from the group consisting of: a KRas G12A mutation, a KRas G12C mutation, a KRas G12D mutation, a KRas G12R mutation, a KRas G12S mutation, and a KRas G12V mutation. In some embodiments, the cancer is a KRas G12A-associated cancer, a KRas G12C-associated cancer, a KRas G12D- associated cancer, a KRas G12R-associated cancer, a KRas G12S-associated cancer, a KRas G12V-associated cancer, a KRas G13C-asociated cancer, or a KRas Q61H-associated cancer. In some embodiments, the cancer is a KRas G12A-associated cancer, a KRas G12C-associated cancer, a KRas G12D-associated cancer, a KRas G12R-associated cancer, a KRas G12S- associated cancer, or a KRas G12V-associated cancer. In some aspects of this embodiment, the cancer is a KRas G12D-associated cancer, a KRas G12R-associated cancer, or a KRas G12V- associated cancer. In some embodiments, the cancer is a KRas G12D-associated cancer or a KRas G12V-associated cancer. In some embodiments, the cancer is a KRas G12A-associated cancer. In some embodiments, the cancer is a KRas G12C-associated cancer. In some embodiments, the cancer is a KRas G12D-associated cancer. In some embodiments, the cancer is a KRas G12R-associated cancer. In some embodiments, the cancer is a KRas G12S- associated cancer. In some embodiments, the cancer is a KRas G12V-associated cancer. In some embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12A inhibitor, a KRas G12C inhibitor, a KRas G12D inhibitor, a KRas G12R inhibitor, a KRas G12S inhibitor, a KRas G12V inhibitor, a KRas G13C inhibitor, a KRas Q61H inhibitor, or two or more thereof. In some embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12A inhibitor, a KRas G12C inhibitor, a KRas G12D inhibitor, a KRas G12R inhibitor, a KRas G12S inhibitor, a KRas G12V inhibitor, or two or more thereof. In some aspects of this embodiment, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12D inhibitor, a KRas G12R inhibitor, and/or a KRas G12V inhibitor. In some aspects of this embodiment, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12D inhibitor, a KRas G12V inhibitor, or both. Also provided herein is a method of treating a testicular cancer (e.g., seminoma) in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some embodiments, the method further comprises determining that the testicular cancer (e.g., seminoma) has a KRas mutation selected from the group consisting of: a KRas G12A mutation, a KRas G12R mutation, a KRas G12S mutation, a KRas G12V mutation, a KRas Q61L mutation, a KRas Q61P mutation, and a KRas Q61R mutation. In some embodiments, the method further comprises determining that the testicular cancer (e.g., seminoma) has a KRas mutation selected from the group consisting of: a KRas G12A mutation, a KRas G12R mutation, a KRas G12S mutation, and a KRas G12V mutation. In some embodiments, the cancer is a KRas G12A-associated cancer, a KRas G12R-associated cancer, a KRas G12S- associated cancer, a KRas G12V-associated cancer, a KRas Q61L-associated cancer, a KRas Q61P-associated cancer, or a KRas Q61R-associated cancer. In some embodiments, the cancer is a KRas G12A-associated cancer, a KRas G12R-associated cancer, a KRas G12S-associated cancer, or a KRas G12V-associated cancer. In some aspects of this embodiment, the cancer is a KRas G12R-associated cancer or a KRas G12V-associated cancer. In some embodiments, the cancer is a KRas G12A-associated cancer. In some embodiments, the cancer is a KRas G12R-associated cancer. In some embodiments, the cancer is a KRas G12S-associated cancer. In some embodiments, the cancer is a KRas G12V-associated cancer. In some embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12A inhibitor, a KRas G12R inhibitor, a KRas G12S inhibitor, a KRas G12V inhibitor, a KRas Q61L inhibitor, a KRas Q61P inhibitor, a KRas Q61R inhibitor, or two or more thereof. In some embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12A inhibitor, a KRas G12R inhibitor, a KRas G12S inhibitor, a KRas G12V inhibitor, or two or more thereof. In some aspects of this embodiment, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12R inhibitor, a KRas G12V inhibitor, or both. In some embodiments, the KRas-associated cancer is bladder cancer, breast cancer, cervical cancer, colorectal cancer, endometrial cancer, esophageal or stomach cancer, liver cancer, skin cancer (e.g., melanoma), lung cancer (e.g., NSCLC), or pancreatic cancer. In some embodiments, the cancer has a KRas G12C mutation or a KRas G12D mutation. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12C inhibitor, a KRas G12D inhibitor, or both. Also provided herein is a method of treating a KRas G12C-associated cancer or a KRas G12D-associated cancer in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some such embodiments, the cancer is bladder cancer, breast cancer, cervical cancer, colorectal cancer, endometrial cancer, esophageal or stomach cancer, liver cancer, skin cancer (e.g., melanoma), lung cancer (e.g., NSCLC), or pancreatic cancer. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12C inhibitor, a KRas G12D inhibitor, or both. Also provided herein is a method of treating bladder cancer, breast cancer, cervical cancer, colorectal cancer, endometrial cancer, esophageal or stomach cancer, liver cancer, skin cancer (e.g., melanoma), lung cancer (e.g., NSCLC), or pancreatic cancer in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some such embodiments, the cancer is a KRas G12C-associated cancer or a KRas G12D-associated cancer, or both. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12C inhibitor, a KRas G12D inhibitor, or both. In some embodiments, the KRas-associated cancer is bladder cancer, breast cancer, cervical cancer, colorectal cancer, endometrial cancer, esophageal or stomach cancer, leukemia, lung cancer (e.g., NSCLC), pancreatic cancer, or kidney cancer. In some embodiments, the cancer has a KRas G12D mutation or a KRas G12V mutation. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12D inhibitor, a KRas G12V inhibitor, or both. Also provided herein is a method of treating a KRas G12D-associated cancer or a KRas G12V-associated cancer in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some such embodiments, the cancer is bladder cancer, breast cancer, cervical cancer, colorectal cancer, endometrial cancer, esophageal or stomach cancer, leukemia, lung cancer (e.g., NSCLC), pancreatic cancer, or kidney cancer. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12D inhibitor, a KRas G12V inhibitor, or both. Also provided herein is a method of treating bladder cancer, breast cancer, cervical cancer, colorectal cancer, endometrial cancer, esophageal or stomach cancer, leukemia, lung cancer (e.g., NSCLC), pancreatic cancer, or kidney cancer in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some such embodiments, the cancer is a KRas G12D-associated cancer or a KRas G12V-associated cancer. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12D inhibitor, a KRas G12V inhibitor, or both. In some embodiments, the KRas-associated cancer is bladder cancer, cervical cancer, colorectal cancer, endometrial cancer, esophageal or stomach cancer, liver cancer, leukemia, skin cancer (e.g., melanoma), or lung cancer (e.g., NSCLC). In some embodiments, the cancer has a KRas G12D mutation or a KRas G13D mutation. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12D inhibitor, a KRas G13D inhibitor, or both. Also provided herein is a method of treating a KRas G12D-associated cancer or a KRas G13D-associated cancer in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some such embodiments, the cancer is bladder cancer, cervical cancer, colorectal cancer, endometrial cancer, esophageal or stomach cancer, liver cancer, leukemia, skin cancer (e.g., melanoma), or lung cancer (e.g., NSCLC). In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12D inhibitor, a KRas G13D inhibitor, or both. Also provided herein is a method of treating bladder cancer, cervical cancer, colorectal cancer, endometrial cancer, esophageal or stomach cancer, liver cancer, leukemia, skin cancer (e.g., melanoma), or lung cancer (e.g., NSCLC) in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some such embodiments, the cancer is a KRas G12D- associated cancer or a KRas G13D-associated cancer. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12D inhibitor, a KRas G13D inhibitor, or both. In some embodiments, the KRas-associated cancer is bladder cancer, breast cancer, cervical cancer, colorectal cancer, endometrial cancer, esophageal or stomach cancer, lung cancer (e.g., NSCLC), or pancreatic cancer. In some embodiments, the cancer has a KRas G12C mutation or a KRas G12V mutation. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12C inhibitor, a KRas G12V inhibitor, or both. Also provided herein is a method of treating a KRas G12C-associated cancer or a KRas G12V-associated cancer in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some such embodiments, the cancer is bladder cancer, breast cancer, cervical cancer, colorectal cancer, endometrial cancer, esophageal or stomach cancer, lung cancer (e.g., NSCLC), or pancreatic cancer. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12C inhibitor, a KRas G12V inhibitor, or both. Also provided herein is a method of treating bladder cancer, breast cancer, cervical cancer, colorectal cancer, endometrial cancer, esophageal or stomach cancer, lung cancer (e.g., NSCLC), or pancreatic cancer in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some such embodiments, the cancer is a KRas G12C-associated cancer or a KRas G12V-associated cancer. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12C inhibitor, a KRas G12V inhibitor, or both. In some embodiments, the KRas-associated cancer is bladder cancer, cervical cancer, colorectal cancer, endometrial cancer, esophageal or stomach cancer, liver cancer, skin cancer (e.g., melanoma), or lung cancer (e.g., NSCLC). In some embodiments, the cancer has a KRas G12C mutation or a KRas G13D mutation. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12C inhibitor, a KRas G13D inhibitor, or both. Also provided herein is a method of treating a KRas G12C-associated cancer or a KRas G13D-associated cancer in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some such embodiments, the cancer is bladder cancer, cervical cancer, colorectal cancer, endometrial cancer, esophageal or stomach cancer, liver cancer, skin cancer (e.g., melanoma), or lung cancer (e.g., NSCLC). In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12C inhibitor, a KRas G13D inhibitor, or both. Also provided herein is a method of treating bladder cancer, cervical cancer, colorectal cancer, endometrial cancer, esophageal or stomach cancer, liver cancer, skin cancer (e.g., melanoma), or lung cancer (e.g., NSCLC) in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some such embodiments, the cancer is a KRas G12C-associated cancer or a KRas G13D-associated cancer. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12C inhibitor, a KRas G13D inhibitor, or both. In some embodiments, the KRas-associated cancer is bladder cancer, colorectal cancer, endometrial cancer, esophageal or stomach cancer, leukemia, lung cancer (e.g., NSCLC), or pancreatic cancer. In some embodiments, the cancer has a KRas G12D mutation or a KRas Q61H mutation. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12D inhibitor, a KRas Q61H inhibitor, or both. Also provided herein is a method of treating a KRas G12D-associated cancer or a KRas Q61H-associated cancer in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some such embodiments, the cancer is bladder cancer, colorectal cancer, endometrial cancer, esophageal or stomach cancer, leukemia, lung cancer (e.g., NSCLC), or pancreatic cancer. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12D inhibitor, a KRas Q61H inhibitor, or both. Also provided herein is a method of treating bladder cancer, colorectal cancer, endometrial cancer, esophageal or stomach cancer, leukemia, lung cancer (e.g., NSCLC), or pancreatic cancer in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some such embodiments, the cancer is a KRas G12D-associated cancer or a KRas Q61H- associated cancer. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12D inhibitor, a KRas Q61H inhibitor, or both. In some embodiments, the KRas-associated cancer is bladder cancer, cervical cancer, colorectal cancer, endometrial cancer, esophageal or stomach cancer, leukemia, or lung cancer (e.g., NSCLC). In some embodiments, the cancer has a KRas G12V mutation or a KRas G13D mutation. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12V inhibitor, a KRas G13D inhibitor, or both. Also provided herein is a method of treating a KRas G12V-associated cancer or a KRas G13D-associated cancer in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some such embodiments, the cancer is bladder cancer, cervical cancer, colorectal cancer, endometrial cancer, esophageal or stomach cancer, leukemia, or lung cancer (e.g., NSCLC). In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12V inhibitor, a KRas G13D inhibitor, or both. Also provided herein is a method of treating bladder cancer, cervical cancer, colorectal cancer, endometrial cancer, esophageal or stomach cancer, leukemia, or lung cancer (e.g., NSCLC) in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some such embodiments, the cancer is a KRas G12V-associated cancer or a KRas G13V- associated cancer. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12V inhibitor, a KRas G13D inhibitor, or both. In some embodiments, the KRas-associated cancer is bladder cancer, colorectal cancer, endometrial cancer, esophageal or stomach cancer, leukemia, lung cancer (e.g., NSCLC), or pancreatic cancer. In some embodiments, the cancer has a KRas G12V mutation or a KRas Q61H mutation. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12V inhibitor, a KRas Q61H inhibitor, or both. Also provided herein is a method of treating a KRas G12V-associated cancer or a KRas Q61H-associated cancer in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some such embodiments, the cancer is bladder cancer, colorectal cancer, endometrial cancer, esophageal or stomach cancer, leukemia, lung cancer (e.g., NSCLC), or pancreatic cancer. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12V inhibitor, a KRas Q61H inhibitor, or both. Also provided herein is a method of treating bladder cancer, colorectal cancer, endometrial cancer, esophageal or stomach cancer, leukemia, lung cancer (e.g., NSCLC), or pancreatic cancer in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some such embodiments, the cancer is a KRas G12V-associated cancer or a KRas Q61H- associated cancer. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12V inhibitor, a KRas Q61H inhibitor, or both. In some embodiments, the KRas-associated cancer is bladder cancer, colorectal cancer, endometrial cancer, esophageal or stomach cancer, lung cancer (e.g., NSCLC), or pancreatic cancer. In some embodiments, the cancer has a KRas G12C mutation or a KRas Q61H mutation. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12C inhibitor, a KRas Q61H inhibitor, or both. Also provided herein is a method of treating a KRas G12C-associated cancer or a KRas Q61H-associated cancer in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some such embodiments, the cancer is bladder cancer, colorectal cancer, endometrial cancer, esophageal or stomach cancer, lung cancer (e.g., NSCLC), or pancreatic cancer. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12C inhibitor, a KRas Q61H inhibitor, or both. Also provided herein is a method of treating bladder cancer, colorectal cancer, endometrial cancer, esophageal or stomach cancer, lung cancer (e.g., NSCLC), or pancreatic cancer in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some such embodiments, the cancer is a KRas G12C-associated cancer or a KRas Q61H- associated cancer. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12C inhibitor, a KRas Q61H inhibitor, or both. In some embodiments, the KRas-associated cancer is colorectal cancer, endometrial cancer, esophageal or stomach cancer, lung cancer (e.g., NSCLC), pancreatic cancer, or testicular cancer (e.g., seminoma). In some embodiments, the cancer has a KRas G12S mutation or a KRas G12V mutation. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12S inhibitor, a KRas G12V inhibitor, or both. Also provided herein is a method of treating a KRas G12S-associated cancer or a KRas G12V-associated cancer in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some such embodiments, the cancer is colorectal cancer, endometrial cancer, esophageal or stomach cancer, lung cancer (e.g., NSCLC), pancreatic cancer, or testicular cancer (e.g., seminoma). In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12S inhibitor, a KRas G12V inhibitor, or both. Also provided herein is a method of treating colorectal cancer, endometrial cancer, esophageal or stomach cancer, lung cancer (e.g., NSCLC), pancreatic cancer, or testicular cancer (e.g., seminoma) in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some such embodiments, the cancer is a KRas G12S-associated cancer or a KRas G12V-associated cancer. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12S inhibitor, a KRas G12V inhibitor, or both. In some embodiments, the KRas-associated cancer is colorectal cancer, endometrial cancer, lung cancer (e.g., NSCLC), pancreatic cancer, or testicular cancer (e.g., seminoma). In some embodiments, the cancer has a KRas G12A mutation or a KRas G12S mutation. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12A inhibitor, a KRas G12S inhibitor, or both. Also provided herein is a method of treating a KRas G12A-associated cancer or a KRas G12S-associated cancer in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some such embodiments, the cancer is colorectal cancer, endometrial cancer, lung cancer (e.g., NSCLC), pancreatic cancer, or testicular cancer (e.g., seminoma). In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12A inhibitor, a KRas G12S inhibitor, or both. Also provided herein is a method of treating colorectal cancer, endometrial cancer, lung cancer (e.g., NSCLC), pancreatic cancer, or testicular cancer (e.g., seminoma) in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some such embodiments, the cancer is a KRas G12A-associated cancer or a KRas G12S-associated cancer. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12A inhibitor, a KRas G12S inhibitor, or both. In some embodiments, the KRas-associated cancer is colorectal cancer, endometrial cancer, lung cancer (e.g., NSCLC), pancreatic cancer, or testicular cancer (e.g., seminoma). In some embodiments, the cancer has a KRas G12A mutation or a KRas G12V mutation. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12A inhibitor, a KRas G12V inhibitor, or both. Also provided herein is a method of treating a KRas G12A-associated cancer or a KRas G12V-associated cancer in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some such embodiments, the cancer is colorectal cancer, endometrial cancer, lung cancer (e.g., NSCLC), pancreatic cancer, or testicular cancer (e.g., seminoma). In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12A inhibitor, a KRas G12V inhibitor, or both. Also provided herein is a method of treating colorectal cancer, endometrial cancer, lung cancer (e.g., NSCLC), pancreatic cancer, or testicular cancer (e.g., seminoma) in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some such embodiments, the cancer is a KRas G12A-associated cancer or a KRas G12V-associated cancer. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12A inhibitor, a KRas G12V inhibitor, or both. In some embodiments, the KRas-associated cancer is colorectal cancer, endometrial cancer, esophageal or stomach cancer, lung cancer (e.g., NSCLC), or pancreatic cancer. In some embodiments, the cancer has a KRas G12C mutation or a KRas G12S mutation. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12C inhibitor, a KRas G12S inhibitor, or both. Also provided herein is a method of treating a KRas G12C-associated cancer or a KRas G12S-associated cancer in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some such embodiments, the cancer is colorectal cancer, endometrial cancer, esophageal or stomach cancer, lung cancer (e.g., NSCLC), or pancreatic cancer. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12C inhibitor, a KRas G12S inhibitor, or both. Also provided herein is a method of treating colorectal cancer, endometrial cancer, esophageal or stomach cancer, lung cancer (e.g., NSCLC), or pancreatic cancer in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some such embodiments, the cancer is a KRas G12C-associated cancer or a KRas G12S-associated cancer. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12C inhibitor, a KRas G12S inhibitor, or both. In some embodiments, the KRas-associated cancer is bladder cancer, colorectal cancer, skin cancer (e.g., melanoma), pancreatic cancer, or prostate cancer. In some embodiments, the cancer has a KRas G12D mutation or a KRas G12R mutation. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12D inhibitor, a KRas G12R inhibitor, or both. Also provided herein is a method of treating a KRas G12D-associated cancer or a KRas G12R-associated cancer in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some such embodiments, the cancer is bladder cancer, colorectal cancer, skin cancer (e.g., melanoma), pancreatic cancer, or prostate cancer. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12D inhibitor, a KRas G12R inhibitor, or both. Also provided herein is a method of treating bladder cancer, colorectal cancer, skin cancer (e.g., melanoma), pancreatic cancer, or prostate cancer in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some such embodiments, the cancer is a KRas G12D-associated cancer or a KRas G12R-associated cancer. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12D inhibitor, a KRas G12R inhibitor, or both. In some embodiments, the KRas-associated cancer is colorectal cancer, endometrial cancer, esophageal or stomach cancer, lung cancer (e.g., NSCLC), or pancreatic cancer. In some embodiments, the cancer has a KRas G12D mutation or a KRas G12S mutation. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12D inhibitor, a KRas G12S inhibitor, or both. Also provided herein is a method of treating a KRas G12D-associated cancer or a KRas G12S-associated cancer in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some such embodiments, the cancer is colorectal cancer, endometrial cancer, esophageal or stomach cancer, lung cancer (e.g., NSCLC), or pancreatic cancer. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12D inhibitor, a KRas G12S inhibitor, or both. Also provided herein is a method of treating colorectal cancer, endometrial cancer, esophageal or stomach cancer, lung cancer (e.g., NSCLC), or pancreatic cancer in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some such embodiments, the cancer is a KRas G12D-associated cancer or a KRas G12S-associated cancer. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12D inhibitor, a KRas G12S inhibitor, or both. In some embodiments, the KRas-associated cancer is bladder cancer, colorectal cancer, ovarian cancer, pancreatic cancer, or testicular cancer (e.g., seminoma). In some embodiments, the cancer has a KRas G12R mutation or a KRas G12V mutation. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12R inhibitor, a KRas G12V inhibitor, or both. Also provided herein is a method of treating a KRas G12R-associated cancer or a KRas G12V-associated cancer in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some such embodiments, the cancer is bladder cancer, colorectal cancer, ovarian cancer, pancreatic cancer, or testicular cancer (e.g., seminoma). In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12R inhibitor, a KRas G12V inhibitor, or both. Also provided herein is a method of treating bladder cancer, colorectal cancer, ovarian cancer, pancreatic cancer, or testicular cancer (e.g., seminoma) in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some such embodiments, the cancer is a KRas G12R-associated cancer or a KRas G12V-associated cancer. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12R inhibitor, a KRas G12V inhibitor, or both. In some embodiments, the KRas-associated cancer is colorectal cancer, endometrial cancer, esophageal or stomach cancer, lung cancer (e.g., NSCLC), or pancreatic cancer. In some embodiments, the cancer has a KRas G12S mutation or a KRas Q61H mutation. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12S inhibitor, a KRas Q61H inhibitor, or both. Also provided herein is a method of treating a KRas G12S-associated cancer or a KRas Q61H-associated cancer in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some such embodiments, the cancer is colorectal cancer, endometrial cancer, esophageal or stomach cancer, lung cancer (e.g., NSCLC), or pancreatic cancer. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12S inhibitor, a KRas Q61H inhibitor, or both. Also provided herein is a method of treating colorectal cancer, endometrial cancer, esophageal or stomach cancer, lung cancer (e.g., NSCLC), or pancreatic cancer in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some such embodiments, the cancer is a KRas G12S-associated cancer or a KRas Q61H-associated cancer. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12S inhibitor, a KRas Q61H inhibitor, or both. In some embodiments, the KRas-associated cancer is colorectal cancer, endometrial cancer, lung cancer (e.g., NSCLC), ovarian cancer, or testicular cancer (e.g., seminoma). In some embodiments, the cancer has a KRas G12V mutation or a KRas Q61L mutation. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12V inhibitor, a KRas Q61L inhibitor, or both. Also provided herein is a method of treating a KRas G12V-associated cancer or a KRas Q61L-associated cancer in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some such embodiments, the cancer is colorectal cancer, endometrial cancer, lung cancer (e.g., NSCLC), ovarian cancer, or testicular cancer (e.g., seminoma). In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12V inhibitor, a KRas Q61L inhibitor, or both. Also provided herein is a method of treating colorectal cancer, endometrial cancer, lung cancer (e.g., NSCLC), ovarian cancer, or testicular cancer (e.g., seminoma) in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some such embodiments, the cancer is a KRas G12V-associated cancer or a KRas Q61L-associated cancer. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12V inhibitor, a KRas Q61L inhibitor, or both. In some embodiments, the KRas-associated cancer is colorectal cancer, endometrial cancer, lung cancer (e.g., NSCLC), or pancreatic cancer. In some embodiments, the cancer has a KRas G12A mutation or a KRas G12C mutation. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12A inhibitor, a KRas G12C inhibitor, or both. Also provided herein is a method of treating a KRas G12A-associated cancer or a KRas G12C-associated cancer in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some such embodiments, the cancer is colorectal cancer, endometrial cancer, lung cancer (e.g., NSCLC), or pancreatic cancer. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12A inhibitor, a KRas G12C inhibitor, or both. Also provided herein is a method of treating colorectal cancer, endometrial cancer, lung cancer (e.g., NSCLC), or pancreatic cancer in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some such embodiments, the cancer is a KRas G12A-associated cancer or a KRas G12C-associated cancer. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12A inhibitor, a KRas G12C inhibitor, or both. In some embodiments, the KRas-associated cancer is colorectal cancer, endometrial cancer, lung cancer (e.g., NSCLC), or pancreatic cancer. In some embodiments, the cancer has a KRas G12A mutation or a KRas G12D mutation. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12A inhibitor, a KRas G12D inhibitor, or both. Also provided herein is a method of treating a KRas G12A-associated cancer or a KRas G12D-associated cancer in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some such embodiments, the cancer is colorectal cancer, endometrial cancer, lung cancer (e.g., NSCLC), or pancreatic cancer. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12A inhibitor, a KRas G12D inhibitor, or both. Also provided herein is a method of treating colorectal cancer, endometrial cancer, lung cancer (e.g., NSCLC), or pancreatic cancer in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some such embodiments, the cancer is a KRas G12A-associated cancer or a KRas G12D-associated cancer. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12A inhibitor, a KRas G12D inhibitor, or both. In some embodiments, the KRas-associated cancer is colorectal cancer, endometrial cancer, lung cancer (e.g., NSCLC), or pancreatic cancer. In some embodiments, the cancer has a KRas G12A mutation or a KRas G13C mutation. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12A inhibitor, a KRas G13C inhibitor, or both. Also provided herein is a method of treating a KRas G12A-associated cancer or a KRas G13C-associated cancer in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some such embodiments, the cancer is colorectal cancer, endometrial cancer, lung cancer (e.g., NSCLC), or pancreatic cancer. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12A inhibitor, a KRas G13C inhibitor, or both. Also provided herein is a method of treating colorectal cancer, endometrial cancer, lung cancer (e.g., NSCLC), or pancreatic cancer in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some such embodiments, the cancer is a KRas G12A-associated cancer or a KRas G13C-associated cancer. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12A inhibitor, a KRas G13C inhibitor, or both. In some embodiments, the KRas-associated cancer is colorectal cancer, endometrial cancer, lung cancer (e.g., NSCLC), or pancreatic cancer. In some embodiments, the cancer has a KRas G12A mutation or a KRas Q61H mutation. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12A inhibitor, a KRas Q61H inhibitor, or both. Also provided herein is a method of treating a KRas G12A-associated cancer or a KRas Q61H-associated cancer in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some such embodiments, the cancer is colorectal cancer, endometrial cancer, lung cancer (e.g., NSCLC), or pancreatic cancer. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12A inhibitor, a KRas Q61H inhibitor, or both. Also provided herein is a method of treating colorectal cancer, endometrial cancer, lung cancer (e.g., NSCLC), or pancreatic cancer in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some such embodiments, the cancer is a KRas G12A-associated cancer or a KRas Q61H-associated cancer. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12A inhibitor, a KRas Q61H inhibitor, or both. In some embodiments, the KRas-associated cancer is colorectal cancer, endometrial cancer, lung cancer (e.g., NSCLC), or testicular cancer (e.g., seminoma). In some embodiments, the cancer has a KRas G12A mutation or a KRas Q61L mutation. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12A inhibitor, a KRas Q61L inhibitor, or both. Also provided herein is a method of treating a KRas G12A-associated cancer or a KRas Q61L-associated cancer in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some such embodiments, the cancer is colorectal cancer, endometrial cancer, lung cancer (e.g., NSCLC), or testicular cancer (e.g., seminoma). In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12A inhibitor, a KRas Q61L inhibitor, or both. Also provided herein is a method of treating colorectal cancer, endometrial cancer, lung cancer (e.g., NSCLC), or testicular cancer (e.g., seminoma) in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some such embodiments, the cancer is a KRas G12A-associated cancer or a KRas Q61L-associated cancer. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12A inhibitor, a KRas Q61L inhibitor, or both. In some embodiments, the KRas-associated cancer is bladder cancer, colorectal cancer, skin cancer (e.g., melanoma), or pancreatic cancer. In some embodiments, the cancer has a KRas G12C mutation or a KRas G12R mutation. In some such embodiments, the compound provided herein, or pharmaceutically acceptable salt thereof, is a KRas G12C inhibitor, a KRas G12R inhibitor, or both. Also provided herein is a method of treating a KRas G12C-associated cancer or a KRas G12R-associated cancer in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some such embodiments, the cancer is bladder cancer, colorectal cancer, skin cancer (e.g., melanoma), or pancreatic cancer. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12C inhibitor, a KRas G12R inhibitor, or both. Also provided herein is a method of treating bladder cancer, colorectal cancer, skin cancer (e.g., melanoma), or pancreatic cancer in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some such embodiments, the cancer is a KRas G12C-associated cancer or a KRas G12R-associated cancer. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12C inhibitor, a KRas G12R inhibitor, or both. In some embodiments, the KRas-associated cancer is colorectal cancer, endometrial cancer, lung cancer (e.g., NSCLC), or pancreatic cancer. In some embodiments, the cancer has a KRas G12C mutation or a KRas G13C mutation. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12C inhibitor, a KRas G13C inhibitor, or both. Also provided herein is a method of treating a KRas G12C-associated cancer or a KRas G13C-associated cancer in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some such embodiments, the cancer is colorectal cancer, endometrial cancer, lung cancer (e.g., NSCLC), or pancreatic cancer. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12C inhibitor, a KRas G13C inhibitor, or both. Also provided herein is a method of treating colorectal cancer, endometrial cancer, lung cancer (e.g., NSCLC), or pancreatic cancer in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some such embodiments, the cancer is a KRas G12C-associated cancer or a KRas G13C-associated cancer. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12C inhibitor, a KRas G13C inhibitor, or both. In some embodiments, the KRas-associated cancer is colorectal cancer, endometrial cancer, skin cancer (e.g., melanoma), or lung cancer (e.g., NSCLC). In some embodiments, the cancer has a KRas G12C mutation or a KRas Q61L mutation. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12C inhibitor, a KRas Q61L inhibitor, or both. Also provided herein is a method of treating a KRas G12C-associated cancer or a KRas Q61L-associated cancer in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some such embodiments, the cancer is colorectal cancer, endometrial cancer, skin cancer (e.g., melanoma), or lung cancer (e.g., NSCLC). In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12C inhibitor, a KRas Q61L inhibitor, or both. Also provided herein is a method of treating colorectal cancer, endometrial cancer, skin cancer (e.g., melanoma), or lung cancer (e.g., NSCLC) in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some such embodiments, the cancer is a KRas G12C- associated cancer or a KRas Q61L-associated cancer. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12C inhibitor, a KRas Q61L inhibitor, or both. In some embodiments, the KRas-associated cancer is colorectal cancer, endometrial cancer, lung cancer (e.g., NSCLC), or pancreatic cancer. In some embodiments, the cancer has a KRas G12D mutation or a KRas G13C mutation. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12D inhibitor, a KRas G13C inhibitor, or both. Also provided herein is a method of treating a KRas G12D-associated cancer or a KRas G13C-associated cancer in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some such embodiments, the cancer is colorectal cancer, endometrial cancer, lung cancer (e.g., NSCLC), or pancreatic cancer. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12D inhibitor, a KRas G13C inhibitor, or both. Also provided herein is a method of treating colorectal cancer, endometrial cancer, lung cancer (e.g., NSCLC), or pancreatic cancer in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some such embodiments, the cancer is a KRas G12D-associated cancer or a KRas G13C-associated cancer. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12D inhibitor, a KRas G13C inhibitor, or both. In some embodiments, the KRas-associated cancer is colorectal cancer, endometrial cancer, skin cancer (e.g., melanoma), or lung cancer (e.g., NSCLC). In some embodiments, the cancer has a KRas G12D mutation or a KRas Q61L mutation. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12D inhibitor, a KRas Q61L inhibitor, or both. Also provided herein is a method of treating a KRas G12D-associated cancer or a KRas Q61L-associated cancer in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some such embodiments, the cancer is colorectal cancer, endometrial cancer, skin cancer (e.g., melanoma), or lung cancer (e.g., NSCLC). In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12D inhibitor, a KRas Q61L inhibitor, or both. Also provided herein is a method of treating colorectal cancer, endometrial cancer, skin cancer (e.g., melanoma), or lung cancer (e.g., NSCLC) in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some such embodiments, the cancer is a KRas G12D- associated cancer or a KRas Q61L-associated cancer. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12D inhibitor, a KRas Q61L inhibitor, or both. In some embodiments, the KRas-associated cancer is colorectal cancer, skin cancer (e.g., melanoma), ovarian cancer, or testicular cancer (e.g., seminoma). In some embodiments, the cancer has a KRas G12R mutation or a KRas Q61L mutation. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12R inhibitor, a KRas Q61L inhibitor, or both. Also provided herein is a method of treating a KRas G12R-associated cancer or a KRas Q61L-associated cancer in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some such embodiments, the cancer is colorectal cancer, skin cancer (e.g., melanoma), ovarian cancer, or testicular cancer (e.g., seminoma). In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12R inhibitor, a KRas Q61L inhibitor, or both. Also provided herein is a method of treating colorectal cancer, skin cancer (e.g., melanoma), ovarian cancer, or testicular cancer (e.g., seminoma) in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some such embodiments, the cancer is a KRas G12R-associated cancer or a KRas Q61L-associated cancer. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12R inhibitor, a KRas Q61L inhibitor, or both. In some embodiments, the KRas-associated cancer is colorectal cancer, skin cancer (e.g., melanoma), pancreatic cancer, or testicular cancer (e.g., seminoma). In some embodiments, the cancer has a KRas G12R mutation or a KRas Q61R mutation. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12R inhibitor, a KRas Q61R inhibitor, or both. Also provided herein is a method of treating a KRas G12R-associated cancer or a KRas Q61R-associated cancer in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some such embodiments, the cancer is colorectal cancer, skin cancer (e.g., melanoma), pancreatic cancer, or testicular cancer (e.g., seminoma). In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12R inhibitor, a KRas Q61R inhibitor, or both. Also provided herein is a method of treating colorectal cancer, skin cancer (e.g., melanoma), pancreatic cancer, or testicular cancer (e.g., seminoma) in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some such embodiments, the cancer is a KRas G12R-associated cancer or a KRas Q61R-associated cancer. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12R inhibitor, a KRas Q61R inhibitor, or both. In some embodiments, the KRas-associated cancer is colorectal cancer, endometrial cancer, lung cancer (e.g., NSCLC), or pancreatic cancer. In some embodiments, the cancer has a KRas G12S mutation or a KRas G13C mutation. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12S inhibitor, a KRas G13C inhibitor, or both. Also provided herein is a method of treating a KRas G12S-associated cancer or a KRas G13C-associated cancer in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some such embodiments, the cancer is colorectal cancer, endometrial cancer, lung cancer (e.g., NSCLC), or pancreatic cancer. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12S inhibitor, a KRas G13C inhibitor, or both. Also provided herein is a method of treating colorectal cancer, endometrial cancer, lung cancer (e.g., NSCLC), or pancreatic cancer in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some such embodiments, the cancer is a KRas G12S-associated cancer or a KRas G13C-associated cancer. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12S inhibitor, a KRas G13C inhibitor, or both. In some embodiments, the KRas-associated cancer is colorectal cancer, endometrial cancer, esophageal or stomach cancer, or lung cancer (e.g., NSCLC). In some embodiments, the cancer has a KRas G12S mutation or a KRas G13D mutation. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12S inhibitor, a KRas G13D inhibitor, or both. Also provided herein is a method of treating a KRas G12S-associated cancer or a KRas G13D-associated cancer in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some such embodiments, the cancer is colorectal cancer, endometrial cancer, esophageal or stomach cancer, or lung cancer (e.g., NSCLC). In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12S inhibitor, a KRas G13D inhibitor, or both. Also provided herein is a method of treating colorectal cancer, endometrial cancer, esophageal or stomach cancer, or lung cancer (e.g., NSCLC) in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some such embodiments, the cancer is a KRas G12S-associated cancer or a KRas G13D-associated cancer. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12S inhibitor, a KRas G13D inhibitor, or both. In some embodiments, the KRas-associated cancer is colorectal cancer, endometrial cancer, lung cancer (e.g., NSCLC), or testicular cancer (e.g., seminoma). In some embodiments, the cancer has a KRas G12S mutation or a KRas Q61L mutation. In some such embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12S inhibitor, a KRas Q61L inhibitor, or both. Also provided herein is a method of treating a KRas G12S-associated cancer or a KRas Q61L-associated cancer in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some such embodiments, the cancer is colorectal cancer, endometrial cancer, lung cancer (e.g., NSCLC), or testicular cancer (e.g., seminoma). In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12S inhibitor, a KRas Q61L inhibitor, or both. Also provided herein is a method of treating colorectal cancer, endometrial cancer, lung cancer (e.g., NSCLC), or testicular cancer (e.g., seminoma) in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some such embodiments, the cancer is a KRas G12S-associated cancer or a KRas Q61L-associated cancer. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12S inhibitor, a KRas Q61L inhibitor, or both. In some embodiments, the KRas-associated cancer is colorectal cancer, endometrial cancer, lung cancer (e.g., NSCLC), or pancreatic cancer. In some embodiments, the cancer has a KRas G12V mutation or a KRas G13C mutation. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12V inhibitor, a KRas G13C inhibitor, or both. Also provided herein is a method of treating a KRas G12V-associated cancer or a KRas G13C-associated cancer in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some such embodiments, the cancer is colorectal cancer, endometrial cancer, lung cancer (e.g., NSCLC), or pancreatic cancer. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12V inhibitor, a KRas G13C inhibitor, or both. Also provided herein is a method of treating colorectal cancer, endometrial cancer, lung cancer (e.g., NSCLC), or pancreatic cancer in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some such embodiments, the cancer is a KRas G12V-associated cancer or a KRas G13C-associated cancer. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12V inhibitor, a KRas G13C inhibitor, or both. In some embodiments, the KRas-associated cancer is colorectal cancer, pancreatic cancer, testicular cancer (e.g., seminoma), or thyroid cancer. In some embodiments, the cancer has a KRas G12V mutation or a KRas Q61R mutation. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12V inhibitor, a KRas Q61R inhibitor, or both. Also provided herein is a method of treating a KRas G12V-associated cancer or a KRas Q61R-associated cancer in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some such embodiments, the cancer is colorectal cancer, pancreatic cancer, testicular cancer (e.g., seminoma), or thyroid cancer. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12V inhibitor, a KRas Q61R inhibitor, or both. Also provided herein is a method of treating colorectal cancer, pancreatic cancer, testicular cancer (e.g., seminoma), or thyroid cancer in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some such embodiments, the cancer is a KRas G12V- associated cancer or a KRas Q61R-associated cancer. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12V inhibitor, a KRas Q61R inhibitor, or both. In some embodiments, the KRas-associated cancer is colorectal cancer, pancreatic cancer, or testicular cancer (e.g., seminoma). In some embodiments, the cancer has a KRas G12A mutation or a KRas G12R mutation. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12A inhibitor, a KRas G12R inhibitor, or both. Also provided herein is a method of treating a KRas G12A-associated cancer or a KRas G12R-associated cancer in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some such embodiments, the cancer is colorectal cancer, pancreatic cancer, or testicular cancer (e.g., seminoma). In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12A inhibitor, a KRas G12R inhibitor, or both. Also provided herein is a method of treating colorectal cancer, pancreatic cancer, or testicular cancer (e.g., seminoma) in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some such embodiments, the cancer is a KRas G12A-associated cancer or a KRas G12R-associated cancer. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12A inhibitor, a KRas G12R inhibitor, or both. In some embodiments, the KRas-associated cancer is colorectal cancer, endometrial cancer, or lung cancer (e.g., NSCLC). In some embodiments, the cancer has a KRas G12A mutation or a KRas G13D mutation. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12A inhibitor, a KRas G13D inhibitor, or both. Also provided herein is a method of treating a KRas G12A-associated cancer or a KRas G13D-associated cancer in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some such embodiments, the cancer is colorectal cancer, endometrial cancer, or lung cancer (e.g., NSCLC). In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12A inhibitor, a KRas G13D inhibitor, or both. Also provided herein is a method of treating colorectal cancer, endometrial cancer, or lung cancer (e.g., NSCLC) in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some such embodiments, the cancer is a KRas G12A-associated cancer or a KRas G13D-associated cancer. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12A inhibitor, a KRas G13D inhibitor, or both. In some embodiments, the KRas-associated cancer is colorectal cancer, pancreatic cancer, or testicular cancer (e.g., seminoma). In some embodiments, the cancer has a KRas G12A mutation or a KRas Q61R mutation. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12A inhibitor, a KRas Q61R inhibitor, or both. Also provided herein is a method of treating a KRas G12A-associated cancer or a KRas Q61R-associated cancer in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some such embodiments, the cancer is colorectal cancer, pancreatic cancer, or testicular cancer (e.g., seminoma). In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12A inhibitor, a KRas Q61R inhibitor, or both. Also provided herein is a method of treating colorectal cancer, pancreatic cancer, or testicular cancer (e.g., seminoma) in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some such embodiments, the cancer is a KRas G12A-associated cancer or a KRas Q61R-associated cancer. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12A inhibitor, a KRas Q61R inhibitor, or both. In some embodiments, the KRas-associated cancer is colorectal cancer, skin cancer (e.g., melanoma), or pancreatic cancer. In some embodiments, the cancer has a KRas G12C mutation or a KRas Q61R mutation. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12C inhibitor, a KRas Q61R inhibitor, or both. Also provided herein is a method of treating a KRas G12C-associated cancer or a KRas Q61R-associated cancer in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some such embodiments, the cancer is colorectal cancer, skin cancer (e.g., melanoma), or pancreatic cancer. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12C inhibitor, a KRas Q61R inhibitor, or both. Also provided herein is a method of treating colorectal cancer, skin cancer (e.g., melanoma), or pancreatic cancer in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some such embodiments, the cancer is a KRas G12C-associated cancer or a KRas Q61R-associated cancer. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12C inhibitor, a KRas Q61R inhibitor, or both. In some embodiments, the KRas-associated cancer is colorectal cancer, skin cancer (e.g., melanoma), or pancreatic cancer. In some embodiments, the cancer has a KRas G12D mutation or a KRas Q61R mutation. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12D inhibitor, a KRas Q61R inhibitor, or both. Also provided herein is a method of treating a KRas G12D-associated cancer or a KRas Q61R-associated cancer in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some such embodiments, the cancer is colorectal cancer, skin cancer (e.g., melanoma), or pancreatic cancer. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12D inhibitor, a KRas Q61R inhibitor, or both. Also provided herein is a method of treating colorectal cancer, skin cancer (e.g., melanoma), or pancreatic cancer in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some such embodiments, the cancer is a KRas G12D-associated cancer or a KRas Q61R-associated cancer. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12D inhibitor, a KRas Q61R inhibitor, or both. In some embodiments, the KRas-associated cancer is colorectal cancer, pancreatic cancer, or testicular cancer (e.g., seminoma). In some embodiments, the cancer has a KRas G12R mutation or a KRas G12S mutation. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12R inhibitor, a KRas G12S inhibitor, or both. Also provided herein is a method of treating a KRas G12R-associated cancer or a KRas G12S-associated cancer in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some such embodiments, the cancer is colorectal cancer, pancreatic cancer, or testicular cancer (e.g., seminoma). In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12R inhibitor, a KRas G12S inhibitor, or both. Also provided herein is a method of treating colorectal cancer, pancreatic cancer, or testicular cancer (e.g., seminoma) in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some such embodiments, the cancer is a KRas G12R-associated cancer or a KRas G12S-associated cancer. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12R inhibitor, a KRas G12S inhibitor, or both. In some embodiments, the KRas-associated cancer is bladder cancer, colorectal cancer, or skin cancer (e.g., melanoma). In some embodiments, the cancer has a KRas G12R mutation or a KRas G13D mutation. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12R inhibitor, a KRas G13D inhibitor, or both. Also provided herein is a method of treating a KRas G12R-associated cancer or a KRas G13D-associated cancer in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some such embodiments, the cancer is bladder cancer, colorectal cancer, or skin cancer (e.g., melanoma). In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12R inhibitor, a KRas G13D inhibitor, or both. Also provided herein is a method of treating bladder cancer, colorectal cancer, or skin cancer (e.g., melanoma) in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some such embodiments, the cancer is a KRas G12R-associated cancer or a KRas G13D-associated cancer. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12R inhibitor, a KRas G13D inhibitor, or both. In some embodiments, the KRas-associated cancer is bladder cancer, colorectal cancer, or pancreatic cancer. In some embodiments, the cancer has a KRas G12R mutation or a KRas Q61H mutation. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12R inhibitor, a KRas Q61H inhibitor, or both. Also provided herein is a method of treating a KRas G12R-associated cancer or a KRas Q61H-associated cancer in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some such embodiments, the cancer is bladder cancer, colorectal cancer, or pancreatic cancer. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12R inhibitor, a KRas Q61H inhibitor, or both. Also provided herein is a method of treating bladder cancer, colorectal cancer, or pancreatic cancer in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some such embodiments, the cancer is a KRas G12R-associated cancer or a KRas Q61H- associated cancer. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12R inhibitor, a KRas Q61H inhibitor, or both. In some embodiments, the KRas-associated cancer is bile duct cancer (e.g., cholangiocarcinoma), colorectal cancer, or skin cancer (e.g., melanoma). In some embodiments, the cancer has a KRas G12R mutation or a KRas Q61K mutation. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12R inhibitor, a KRas Q61K inhibitor, or both. Also provided herein is a method of treating a KRas G12R-associated cancer or a KRas Q61K-associated cancer in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some such embodiments, the cancer is bile duct cancer (e.g., cholangiocarcinoma), colorectal cancer, or skin cancer (e.g., melanoma). In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12R inhibitor, a KRas Q61K inhibitor, or both. Also provided herein is a method of treating bile duct cancer (e.g., cholangiocarcinoma), colorectal cancer, or skin cancer (e.g., melanoma) in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some such embodiments, the cancer is a KRas G12R-associated cancer or a KRas Q61K-associated cancer. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12R inhibitor, a KRas Q61K inhibitor, or both. In some embodiments, the KRas-associated cancer is colorectal cancer, pancreatic cancer, or testicular cancer (e.g., seminoma). In some embodiments, the cancer has a KRas G12S mutation or a KRas Q61R mutation. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12S inhibitor, a KRas Q61R inhibitor, or both. Also provided herein is a method of treating a KRas G12S-associated cancer or a KRas Q61R-associated cancer in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some such embodiments, the cancer is colorectal cancer, pancreatic cancer, or testicular cancer (e.g., seminoma). In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12S inhibitor, a KRas Q61R inhibitor, or both. Also provided herein is a method of treating colorectal cancer, pancreatic cancer, or testicular cancer (e.g., seminoma) in a subject in need of such treatment, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. In some such embodiments, the cancer is a KRas G12S-associated cancer or a KRas Q61R-associated cancer. In some such embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, is a KRas G12S inhibitor, a KRas Q61R inhibitor, or both. Also provided herein is a method for treating a subject diagnosed with or identified as having a KRas-associated cancer, e.g., any of the exemplary mutant KRas-associated cancers disclosed herein, comprising administering to the subject a therapeutically effective amount of a compound provided herein or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition thereof, as defined herein. Also provided herein is a method for treating a subject diagnosed with or identified as having a cancer with a KRas dysregulation (e.g., a KRas mutation or amplification) comprising administering to the subject a therapeutically effective amount of a compound provided herein or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition thereof, as defined herein. Accordingly, provided herein are methods for treating a subject diagnosed with (or identified as having) a KRas-associated cancer (e.g., a mutant KRas-associated cancer (e.g., a KRas G12D-associated cancer, a KRas G12R-associated cancer, or a KRas G12V-associated cancer (e.g., a KRas G12D-associated cancer or a KRas G12V-associated cancer))) that include administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof. In some embodiments, the subject that has been identified or diagnosed as having a KRas-associated cancer (e.g., a mutant KRas-associated cancer (e.g., a KRas G12D-associated cancer, a KRas G12R-associated cancer, or a KRas G12V-associated cancer (e.g., a KRas G12D-associated cancer or a KRas G12V-associated cancer))) through the use of a regulatory agency-approved, e.g., FDA-approved test or assay for identifying a dysregulation associated with KRas (e.g., a KRAS gene having a mutation corresponding to a mutation in a KRas protein and/or a KRas protein having a mutation, a KRAS gene copy number increase, and/or an increase in KRas mRNA or protein expression), in a subject or a biopsy sample from the subject or by performing any of the non-limiting examples of assays described herein. Accordingly, provided herein are methods for treating a subject diagnosed with (or identified as having) a cancer having a KRas dysregulation (e.g., a KRas mutation or amplification) that include administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof. In some embodiments, the subject that has been identified or diagnosed as having a cancer with a KRas dysregulation (e.g., a KRas mutation or amplification) through the use of a regulatory agency-approved, e.g., FDA-approved test or assay for identifying a dysregulation associated with KRas (e.g., a KRAS gene having a mutation corresponding to a mutation in a KRas protein and/or a KRas protein having a mutation, a KRAS gene copy number increase, and/or an increase in KRas mRNA or protein expression), in a subject or a biopsy sample from the subject or by performing any of the non-limiting examples of assays described herein. In some embodiments, the subject that has been identified or diagnosed as having a KRas-associated cancer through the use of a regulatory agency-approved, e.g., FDA-approved test or assay for identifying a KRas dysregulation (e.g., KRas mutation) in a subject or a biopsy sample from the subject or by performing any of the non-limiting examples of assays described herein. In some embodiments, the test or assay is provided as a kit. Also provided are methods for treating cancer in a subject in need thereof, the methods comprising: (a) detecting a KRas-associated cancer (e.g., a mutant KRas-associated cancer (e.g., a KRas G12D-associated cancer, a KRas G12R-associated cancer, or a KRas G12V- associated cancer (e.g., a KRas G12D-associated cancer or a KRas G12V-associated cancer))) in the subject; and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition thereof. Also provided are methods for treating cancer in a subject in need thereof, the method comprising: (a) detecting a cancer having a KRas dysregulation (e.g., a KRas mutation or amplification) in the subject; and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition thereof. Some embodiments of these methods further include administering to the subject another anticancer agent (e.g., a second compound provided herein, or a pharmaceutically acceptable salt thereof, an immunotherapy, or any of the other anticancer agents described herein). In some embodiments, the subject was previously treated with another anticancer treatment, e.g., chemotherapy or a kinase inhibitor (e.g., an EGFR inhibitor), at least partial resection of the tumor, radiation therapy, or a combination thereof. In some embodiments, the cancer in the subject is determined to have a KRas dysregulation (e.g., a KRas mutation (e.g., a KRas G12A mutation, a KRas G12C mutation, a KRas G12D mutation, a KRas G12R mutation, a KRas G12S mutation, or a KRas G12V mutation (e.g., a KRas G12D mutation or a KRas G12V mutation))) through the use of a regulatory agency- approved, e.g., FDA-approved test or assay for identifying a KRas mutation (e.g., a KRAS gene having a mutation corresponding to a mutation in a KRas protein and/or a KRas protein having a mutation, a KRAS gene copy number increase, and/or an increase in KRas mRNA or protein expression), in a subject or a sample (e.g., a tumor sample or blood sample) from the subject or by performing any of the non-limiting examples of assays described herein. In some embodiments, the subject that has been identified or diagnosed as having a cancer with a KRas dysregulation (e.g., a KRas mutation (e.g., a KRas G12D mutation, a KRas G12R mutation, or a KRas G12V mutation (e.g., a KRas G12D mutation or a KRas G12V mutation))) through the use of a regulatory agency-approved, e.g., FDA-approved test or assay for identifying a KRas dysregulation in a subject or a biopsy sample from the subject or by performing any of the non- limiting examples of assays described herein. In some embodiments, the test or assay is provided as a kit. Also provided are methods of treating a subject that include performing an assay on a sample (e.g., a tumor sample or a blood sample) obtained from the subject to determine whether the cancer in the subject has a KRas dysregulation (e.g., a KRas mutation (e.g., a KRas G12A mutation, a KRas G12C mutation, a KRas G12D mutation, a KRas G12R mutation, a KRas G12S mutation, or a KRas G12V mutation (e.g., a KRas G12D mutation or a KRas G12V mutation))), and administering (e.g., specifically or selectively administering) a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition thereof, to the subject determined a cancer having a KRas dysregulation (e.g., a KRas mutation (e.g., a KRas G12A mutation, a KRas G12C mutation, a KRas G12D mutation, a KRas G12R mutation, a KRas G12S mutation, or a KRas G12V mutation (e.g., a KRas G12D mutation or a KRas G12V mutation))). In some embodiments, provided are methods of treating a subject that include performing an assay on a sample (e.g., a tumor sample or a blood sample) obtained from the subject to determine whether the cancer in the subject has a KRas dysregulation (e.g., a KRAS gene having a mutation corresponding to a mutation in a KRas protein and/or a KRas protein having a mutation, a KRAS gene copy number increase, and/or an increase in KRas mRNA or protein expression), and administering (e.g., specifically or selectively administering) a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition thereof, to the subject having a cancer determined to have a KRas dysregulation. Some embodiments of these methods further include administering to the subject another anticancer agent (e.g., a second compound provided herein, or a pharmaceutically acceptable salt thereof, chemotherapy, or immunotherapy). In some embodiments of these methods, the subject was previously treated with another anticancer treatment, e.g., a first KRas inhibitor, chemotherapy, a kinase inhibitor (e.g., an EGFR inhibitor), at least partial resection of a tumor, radiation therapy, or a combination thereof. In some embodiments, the subject is a subject suspected of having a KRas-associated cancer (e.g., a mutant KRas-associated cancer (e.g., a KRas G12A-associated cancer, a KRas G12C-associated cancer, a KRas G12D-associated cancer, a KRas G12R-associated cancer, a KRas G12S-assoicated cancer, or a KRas G12V- associated cancer (e.g., a KRas G12D-associated cancer or a KRas G12V-associated cancer))), a subject presenting with one or more symptoms of a KRas-associated cancer (e.g., a mutant KRas-associated cancer (e.g., a KRas G12A-associated cancer, a KRas G12C-associated cancer, a KRas G12D-associated cancer, a KRas G12R-associated cancer, a KRas G12S- associated cancer, or a KRas G12V-associated cancer (e.g., a KRas G12D-associated cancer or a KRas G12V-associated cancer))), or a subject having an elevated risk of developing a KRas- associated cancer (e.g., a mutant KRas-associated cancer (e.g., a KRas G12A-associated cancer, a KRas G12C-associated cancer, a KRas G12D-associated cancer, a KRas G12R- associated cancer, a KRas G12S-associated or a KRas G12V-associated cancer (e.g., a KRas G12D-associated cancer or a KRas G12V-associated cancer))). In some embodiments, the assay utilizes next generation sequencing, pyrosequencing, or immunohistochemistry. In some embodiments, the assay is a regulatory agency-approved assay, e.g., FDA-approved kit. In some embodiments, the assay is a liquid biopsy. Additional, non-limiting assays that may be used in these methods are described herein. Additional assays are also known in the art. Also provided is a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition thereof, for use in treating a KRas-associated cancer (e.g., a mutant KRas-associated cancer (e.g., a KRas G12A-associated cancer, a KRas G12C-associated cancer, a KRas G12D-associated cancer, a KRas G12R-associated cancer, a KRas G12S- associated cancer, or a KRas G12V-associated cancer (e.g., a KRas G12D-associated cancer or a KRas G12V-associated cancer))) in a subject identified or diagnosed as having a KRas- associated cancer (e.g., a mutant KRas-associated cancer (e.g., a KRas G12A-associated cancer, a KRas G12C-associated cancer, a KRas G12D-associated cancer, a KRas G12R- associated cancer, a KRas G12S-associated cancer or a KRas G12V-associated cancer (e.g., a KRas G12D-associated cancer or a KRas G12V-associated cancer))) through a step of performing an assay (e.g., an in vitro assay) on a sample (e.g., a tumor sample or a blood sample) obtained from the subject to determine whether the cancer in the subject has a KRas dysregulation, where the presence of a KRas dysregulation (e.g., a KRAS gene having a mutation corresponding to a mutation in a KRas protein and/or a KRas protein having a mutation, a KRAS gene copy number increase, and/or an increase in KRas mRNA or protein expression), identifies that the cancer in the subject has a KRas-associated cancer (e.g., a mutant KRas-associated cancer (e.g., a KRas G12D-associated cancer, a KRas G12R- associated cancer, or a KRas G12V-associated cancer (e.g., a KRas G12D-associated cancer or a KRas G12V-associated cancer))). Also provided is a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition thereof, for use in treating a cancer having a KRas dysregulation (e.g., a KRas mutation or amplification) in a subject identified or diagnosed as having a cancer having a KRas dysregulation (e.g., a KRas mutation or amplification) through a step of performing an assay (e.g., an in vitro assay) on a sample (e.g., a tumor sample or a blood sample) obtained from the subject to determine whether the cancer in the subject has a KRas dysregulation, where the presence of a KRas dysregulation (e.g., a KRAS gene having a mutation corresponding to a mutation in a KRas protein and/or a KRas protein having a mutation, a KRAS gene copy number increase, and/or an increase in KRas mRNA or protein expression), identifies that the cancer in the subject has a KRas dysregulation. In some cases, the level (e.g., the protein expression level, the mRNA expression level, and/or the ctDNA level) of a biomarker of response can be determined following administration of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition comprising a compound provided herein, or a pharmaceutically acceptable salt thereof. For example, following administration of one or more doses (e.g., one dose, two doses, three doses, four doses, five doses, or more) of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition comprising a compound provided herein, or a pharmaceutically acceptable salt thereof, to a subject, a tumor sample (e.g., a biopsy) or a blood sample (e.g., a sample containing circulating tumor DNA (ctDNA), circulating cell-free tumor RNA (cfRNA), and/or circulating tumor cells (CTCs)) can be obtained from the subject, and an assay can be performed to determine the level (e.g., the protein expression level, the mRNA expression level, and/or the ctDNA level) of a biomarker of response. Any appropriate biomarker of response can be used, for instance, a mutant KRas protein (e.g., a KRas G12A mutant protein, a KRas G12C mutant protein, a KRas G12D mutant protein, a KRas G12R mutant protein, a KRas G12S mutant protein, or a KRas G12V mutant protein (e.g., a KRas G12D mutant protein or a KRas G12V mutant protein)), ERK1 and/or ERK2 (e.g., phosphoERK1 and/or phosphoERK2), DUSP6 (dual specificity protein phosphatase 6), and/or SPRY4 (protein sprouty homolog 4). See, e.g., Riely, Gregory J., et al. Journal of Thoracic Oncology 16.4 (2021): S751-S752, doi: 10.1016/S1556- 0864(21)01941-9; and Hallin, Jill, et al. Molecular Cancer Research 21.5_Supplement (2023): B012-B012, doi: 10.1158/1557-3125.RAS23-B012. Determining the level (e.g., the protein expression level, the mRNA expression level, and/or the ctDNA level) of a biomarker of response can be performed using any appropriate method, including consulting the subject’s medical record (i.e., if a level (e.g., a baseline level) of the biomarker of response was previously determined), and/or performing an assay, such as an immunohistochemical (IHC) assay, an immunofluorescence assay, a PCR assay (e.g., RT-qPCR assay or a digital droplet PCR assay), and/or a sequencing assay (e.g., a next-generation sequencing (NGS) assay). In some embodiments, the biomarker of response is a mutant KRas protein (e.g., a KRas G12D mutant protein, a KRas G12R mutant protein, or a KRas G12V mutant protein (e.g., a KRas G12D mutant protein or a KRas G12V mutant protein)), and the assay is an IHC assay, a PCR assay (e.g., RT-qPCR assay or a digital droplet PCR assay), or a sequencing assay (e.g., a next- generation sequencing assay). In some embodiments, the biomarker of response is ERK1 and/or ERK2 (e.g., phosphoERK1 and/or phosphoERK2), and the assay is an IHC assay or an immunofluorescence assay. In some embodiments, the biomarker of response is DUSP6, and the assay is a PCR assay (e.g., RT-qPCR assay or a digital droplet PCR assay). In some embodiments, the biomarker of response is SPRY4, and the assay is a PCR assay (e.g., RT- qPCR assay or a digital droplet PCR assay). See, e.g., Holm, Matilda, et al. PLoS One 15.11 (2020): e0239819, doi: 10.1371/journal.pone.0239819; Li, Jun, et al. Oncotarget 7.3 (2016): 2646, doi: 10.18632/oncotarget.6104; Van Herpen, Carla ML, et al. Oncotarget 10.19 (2019): 1850, doi: 10.18632/oncotarget.26753; Raez, L., et al. Journal of Thoracic Oncology 13.9 (2018): S153-S154, doi: 10.1016/j.jtho.2018.07.024; and Thatikonda, Venu, et al. bioRxiv (2023), doi: 10.1101/2023.01.23.525210. Accordingly, in some embodiments of the methods provided herein, the method includes (a) administering a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition comprising a compound provided herein, or a pharmaceutically acceptable salt thereof, to a subject; and (b) determining the level (e.g., the protein expression level, the mRNA expression level, and/or the ctDNA level) of a biomarker of response (e.g., a mutant KRas protein (e.g., a KRas G12A mutant protein, a KRas G12C mutant protein, a KRas G12D mutant protein, a KRas G12R mutant protein, a KRas G12S mutant protein, or a KRas G12V mutant protein (e.g., a KRas G12D mutant protein or a KRas G12V mutant protein)), ERK1 and/or ERK2 (e.g., phosphoERK1 and/or phosphoERK2), DUSP6, and/or SPRY4). In some embodiments, determining the level (e.g., the protein expression level, the mRNA expression level, and/or the ctDNA level) of a biomarker of response includes performing an assay on a sample (e.g., a tumor sample or a blood sample) obtained from the subject. In some embodiments, prior to administering a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition comprising a compound provided herein, or a pharmaceutically acceptable salt thereof, to a subject, the level (e.g., the protein expression level, the mRNA expression level, and/or the ctDNA level) of a biomarker of response (e.g., a mutant KRas protein (e.g., a KRas G12A mutant protein, a KRas G12C mutant protein, a KRas G12D mutant protein, a KRas G12R mutant protein, a KRas G12S mutant protein, or a KRas G12V mutant protein (e.g., a KRas G12D mutant protein or a KRas G12V mutant protein)), ERK1 and/or ERK2 (e.g., phosphoERK1 and/or phosphoERK2), DUSP6, and/or SPRY4) is determined (e.g., by performing an assay or by consulting the subject’s medical record); in some cases, this can be referred to as a baseline level. Thus, in some embodiments of the methods provided herein, the method includes (a) administering a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition comprising a compound provided herein, or a pharmaceutically acceptable salt thereof, to a subject; (b) after (a) determining the level (e.g., the protein expression level, the mRNA expression level, and/or the ctDNA level) of a biomarker of response (e.g., a mutant KRas protein (e.g., a KRas G12A mutant protein, a KRas G12C mutant protein, a KRas G12D mutant protein, a KRas G12R mutant protein, a KRas G12S mutant protein, or a KRas G12V mutant protein (e.g., a KRas G12D mutant protein or a KRas G12V mutant protein)), ERK1 and/or ERK2 (e.g., phosphoERK1 and/or phosphoERK2), DUSP6, and/or SPRY4; and (c) comparing the level of the biomarker(s) of response to a baseline level of the biomarker(s) of response. In some embodiments of the methods provided herein, the method includes (a) determining a first (e.g., baseline) level (e.g., the protein expression level, the mRNA expression level, and/or the ctDNA level) of a biomarker of response (e.g., a mutant KRas protein (e.g., a KRas G12A mutant protein, a KRas G12C mutant protein, a KRas G12D mutant protein, a KRas G12R mutant protein, a KRas G12S mutant protein, or a KRas G12V mutant protein (e.g., a KRas G12D mutant protein or a KRas G12V mutant protein)), ERK1 and/or ERK2 (e.g., phosphoERK1 and/or phosphoERK2), DUSP6, and/or SPRY4; (b) after (a), administering a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition comprising a compound provided herein, or a pharmaceutically acceptable salt thereof, to a subject; (c) after (b), determining a second level (e.g., the protein expression level, the mRNA expression level, and/or the ctDNA level) of the biomarker of response (e.g., a mutant KRas protein (e.g., a KRas G12A mutant protein, a KRas G12C mutant protein, a KRas G12D mutant protein, a KRas G12R mutant protein, a KRas G12S mutant protein or a KRas G12V mutant protein (e.g., a KRas G12D mutant protein or a KRas G12V mutant protein)), ERK1 and/or ERK2 (e.g., phosphoERK1 and/or phosphoERK2), DUSP6, and/or SPRY4; and (d) comparing the second level of the biomarker(s) of response to the first level of the biomarker(s) of response. In some such embodiments, step (a) is performed before the subject has received any doses of the compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition comprising a compound provided herein, or a pharmaceutically acceptable salt thereof. In some embodiments, the method includes (e) after (c), administering a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition comprising a compound provided herein, or a pharmaceutically acceptable salt thereof, to the subject; (f) after (e), determining a third level (e.g., the protein expression level, the mRNA expression level, and/or the ctDNA level) of the biomarker of response (e.g., a mutant KRas protein (e.g., a KRas G12A mutant protein, a KRas G12C mutant protein, a KRas G12D mutant protein, a KRas G12R mutant protein, a KRas G12S mutant protein, or a KRas G12V mutant protein (e.g., a KRas G12D mutant protein or a KRas G12V mutant protein)), ERK1 and/or ERK2 (e.g., phosphoERK1 and/or phosphoERK2), DUSP6, and/or SPRY4; and (g) comparing the third level of the biomarker(s) of response to a previous level of the biomarker(s) of response (e.g., the first level of the biomarker(s) of response and/or the second level of the biomarker(s) of response). In some embodiments, steps (e) through (g) are repeated one or more times (e.g., two or more times, three or more times, four or more times, five or more times, or more). In some embodiments, administering a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition comprising a compound provided herein, or a pharmaceutically acceptable salt thereof, to a subject comprises administration of one or more doses (e.g., one dose, two doses, three doses, four doses, five doses, or more) of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition comprising a compound provided herein, or a pharmaceutically acceptable salt thereof to the subject. Also provided is the use of a compound provided herein, or a pharmaceutically acceptable salt thereof, for the manufacture of a medicament for treating a KRas-associated cancer (e.g., a mutant KRas-associated cancer (e.g., a KRas G12A-associated cancer, a KRas G12C-associated cancer, a KRas G12D-associated cancer, a KRas G12R-associated cancer, a KRas G12S-associated cancer, or a KRas G12V-associated cancer (e.g., a KRas G12D- associated cancer or a KRas G12V-associated cancer))) in a subject identified or diagnosed as having a KRas-associated cancer (e.g., a mutant KRas-associated cancer (e.g., a KRas G12A- associated cancer, a KRas G12C-associated cancer, a KRas G12D-associated cancer, a KRas G12R-associated cancer, a KRas G12S-associated cancer or a KRas G12V-associated cancer (e.g., a KRas G12D-associated cancer or a KRas G12V-associated cancer))) through a step of performing an assay on a sample obtained from the subject to determine whether the cancer in the subject has a KRas dysregulation (e.g., a KRAS gene having a mutation corresponding to a mutation in a KRas protein and/or a KRas protein having a mutation, a KRAS gene copy number increase, and/or an increase in KRas mRNA or protein expression) where the presence of a KRas dysregulation (e.g., a KRAS gene having a mutation corresponding to a mutation in a KRas protein and/or a KRas protein having a mutation, a KRAS gene copy number increase, and/or an increase in KRas mRNA or protein expression), identifies that the subject has a KRas- associated cancer (e.g., a mutant KRas-associated cancer (e.g., a KRas G12A-associated cancer, a KRas G12C-associated cancer, a KRas G12D-associated cancer, a KRas G12R- associated cancer, a KRas G12S-associated cancer, or a KRas G12V-associated cancer (e.g., a KRas G12D-associated cancer or a KRas G12V-associated cancer))). Also provided is the use of a compound provided herein, or a pharmaceutically acceptable salt thereof, for the manufacture of a medicament for treating a cancer having a KRas dysregulation (e.g., a KRas mutation or amplification) in a subject identified or diagnosed as having a cancer having a KRas dysregulation (e.g., a KRas mutation or amplification) through a step of performing an assay on a sample obtained from the subject to determine whether the cancer in the subject has a KRas dysregulation (e.g., a KRAS gene having a mutation corresponding to a mutation in a KRas protein and/or a KRas protein having a mutation, a KRAS gene copy number increase, and/or an increase in KRas mRNA or protein expression) where the presence of a KRas dysregulation (e.g., a KRAS gene having a mutation corresponding to a mutation in a KRas protein and/or a KRas protein having a mutation, a KRAS gene copy number increase, and/or an increase in KRas mRNA or protein expression), identifies that the subject has a cancer having a KRas dysregulation. Some embodiments of any of the methods or uses described herein further include recording in the subject’s clinical record (e.g., a computer readable medium) that the subject is determined to have a KRas dysregulation (e.g., a KRAS gene having a mutation corresponding to a mutation in a KRas protein and/or a KRas protein having a mutation, a KRAS gene copy number increase, and/or an increase in KRas mRNA or protein expression), through the performance of the assay, should be administered a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition thereof. In some embodiments, the assay utilizes next generation sequencing, pyrosequencing, or immunohistochemistry. In some embodiments, the assay is a regulatory agency-approved assay, e.g., FDA-approved kit. In some embodiments, the assay is a liquid biopsy. Also provided is a compound provided herein, or a pharmaceutically acceptable salt thereof, for use in the treatment of a cancer in a subject in need thereof, or a subject identified or diagnosed as having a KRas-associated cancer (e.g., a mutant KRas-associated cancer (e.g., a KRas G12A-associated cancer, a KRas G12C-associated cancer, a KRas G12D-associated cancer, a KRas G12R-associated cancer, a KRas G12S-associated cancer, or a KRas G12V- associated cancer (e.g., a KRas G12D-associated cancer or a KRas G12V-associated cancer))) (e.g., any of the KRas-associated cancers described herein). Also provided is a compound provided herein, or a pharmaceutically acceptable salt thereof, for use in the treatment of a cancer in a subject in need thereof, or a subject identified or diagnosed as having a cancer having a KRas dysregulation (e.g., a KRas mutation or amplification). Also provided is the use of a compound provided herein, or a pharmaceutically acceptable salt thereof, for the manufacture of a medicament for treating a cancer in a subject identified or diagnosed as having a KRas-associated cancer (e.g., a mutant KRas-associated cancer (e.g., a KRas G12A- associated cancer, a KRas G12C-associated cancer, a KRas G12D-associated cancer, a KRas G12R-associated cancer, a KRas G12S-associated cancer, or a KRas G12V-associated cancer (e.g., a KRas G12D-associated cancer or a KRas G12V-associated cancer))) (e.g., any of the KRas-associated cancers described herein). Also provided is the use of a compound provided herein, or a pharmaceutically acceptable salt thereof, for the manufacture of a medicament for treating a cancer in a subject identified or diagnosed as having a cancer having a KRas dysregulation (e.g., a KRas mutation or amplification) In some embodiments, a mutant KRas- associated cancer is a cancer that was previously identified as having no KRas mutation (e.g., KRas wild-type), for example, in a cancer that was previously identified as having no KRas mutation and then, later, a KRas mutation (e.g., a resistance mutation) was identified. In some embodiments, a subject is identified or diagnosed as having a KRas-associated cancer (e.g., a mutant KRas-associated cancer (e.g., a KRas G12A-associated cancer, a KRas G12C- associated cancer, a KRas G12D-associated cancer, a KRas G12R-associated cancer, a KRas G12S-associated cancer, or a KRas G12V-associated cancer (e.g., a KRas G12D-associated cancer or a KRas G12V-associated cancer))) through the use of a regulatory agency-approved, e.g., FDA-approved, kit for identifying a KRas dysregulation, in a subject or a biopsy sample from the subject. In some embodiments, a subject is identified or diagnosed as having a cancer having a KRas dysregulation (e.g., a KRas mutation or amplification) through the use of a regulatory agency-approved, e.g., FDA-approved, kit for identifying a KRas dysregulation, in a subject or a biopsy sample from the subject. As provided herein, a KRas-associated cancer (e.g., a mutant KRas-associated cancer (e.g., a KRas G12A-associated cancer, a KRas G12C- associated cancer, a KRas G12D-associated cancer, a KRas G12R-associated cancer, a KRas G12S-associated cancer, or a KRas G12V-associated cancer (e.g., a KRas G12D-associated cancer or a KRas G12V-associated cancer))) includes those described herein and known in the art. In some embodiments of any of the methods or uses described herein, the subject has been identified or diagnosed as having a cancer with a KRas dysregulation (e.g., a KRas mutation (e.g., a KRas G12A mutation, a KRas G12C mutation, a KRas G12D mutation, a KRas G12R mutation, a KRas G12S mutation, or a KRas G12V mutation (e.g., a KRas G12D mutation or a KRas G12V mutation)) or amplification). In some embodiments of any of the methods or uses described herein, the subject has a cancer (e.g., a tumor sample) that is positive for a KRas dysregulation (e.g., a KRas mutation (e.g., a KRas G12A mutation, a KRas G12C mutation, a KRas G12D mutation, a KRas G12R mutation, a KRas G12S mutation or a KRas G12V mutation (e.g., a KRas G12D mutation or a KRas G12V mutation)) or amplification). In some embodiments of any of the methods or uses described herein, the subject can be a subject with a cancer (e.g., one or more tumor samples) that is positive for a KRas dysregulation (e.g., KRas mutation (e.g., a KRas G12A mutation, a KRas G12C mutation, a KRas G12D mutation, a KRas G12R mutation, a KRas G12S mutation, or a KRas G12V mutation (e.g., a KRas G12D mutation or a KRas G12V mutation))). In some embodiments of any of the methods or uses described herein, the subject is suspected of having a mutant KRas-associated cancer (e.g., a cancer that was previously identified a cancer having no KRas mutation (e.g., KRas wild type)). In some embodiments, provided herein are methods for treating a KRas-associated cancer (e.g., a mutant KRas-associated cancer (e.g., a KRas G12A-associated cancer, a KRas G12C- associated cancer, a KRas G12D-associated cancer, a KRas G12R-associated cancer, a KRas G12S-associated cancer, or a KRas G12V-associated cancer (e.g., a KRas G12D-associated cancer or a KRas G12V-associated cancer))) in a subject in need of such treatment, the method comprising a) detecting a KRas dysregulation (e.g., a KRAS gene having a mutation corresponding to a mutation in a KRas protein and/or a KRas protein having a mutation, a KRAS gene copy number increase, and/or an increase in KRas mRNA or protein expression) in a sample from the subject; and b) administering a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof. In some embodiments, provided herein are methods for treating cancer having a KRas dysregulation in a subject in need of such treatment, the method comprising a) detecting a KRas dysregulation (e.g., a KRAS gene having a mutation corresponding to a mutation in a KRas protein and/or a KRas protein having a mutation, a KRAS gene copy number increase, and/or an increase in KRas mRNA or protein expression) in a sample from the subject; and b) administering a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof. In some embodiments, a mutant KRas-associated cancer is characterized by a mutation that arises from treatment with a first KRas inhibitor; for example, a mutant KRas-associated cancer as described herein can include one or more KRas mutations that confer resistance to treatment with a first KRas inhibitor. For example, a subject can acquire one or more of the following KRas mutations as a resistance mutation to a KRas G12C inhibitor: G12D, G12R, G12V, G12W, G13D, Q61H, R68S, H95D, H95Q, H95R, or Y96C. See, e.g., Awad et al. N Engl J Med.2021 Jun 24;384(25):2382-2393, doi: 10.1056/NEJMoa2105281. As used herein, a “first inhibitor of KRas” or “first KRas inhibitor” is a KRas inhibitor as defined herein, but which does not include a compound provided herein, or a pharmaceutically acceptable salt thereof, as defined herein. As used herein, a “second inhibitor of KRas” or a “second KRas inhibitor” is a KRas inhibitor as defined herein, but which does not include a compound provided herein, or a pharmaceutically acceptable salt thereof. When both a first and a second inhibitor of KRas are present in a method provided herein, the first and second inhibitors of KRas are different. In some embodiments, the first and/or second inhibitor of KRas bind in a different location than a compound provided herein, or a pharmaceutically acceptable salt thereof. Exemplary first and second inhibitors of KRas are described herein. In some embodiments, a first or a second inhibitor of KRas can be a KRas G12C inhibitor. In some embodiments, a first or second inhibitor of KRas can be selected from the group consisting of sotorasib, adragrasib, ARS-853, ARS-1620, ARS-3248, ATG-012, BI 1823911, D-1553, ERAS-3490, GDC-6036, GFH925, JAB-21822, JDQ-443, LY3537982, MRTX-1257, RMC- 6291, and combinations thereof. In some embodiments, a first or second inhibitor of KRas can be selected from the group consisting of sotorasib, adragrasib, ARS-853, ARS-1620, ARS- 3248, ATG-012, BI 1823911, D-1553, ERAS-3490, GDC-6036, GFH925, JAB-21822, JDQ- 443, LY3537982, MRTX-1133, MRTX-1257, RMC-6291, RMC-6236, and combinations thereof. In some embodiments, the methods provided herein include performing an assay on a sample (e.g., a tumor sample or a blood sample) obtained from the subject to determine whether the cancer in the subject has a KRas dysregulation (e.g., a KRas mutation (e.g., a KRas G12A mutation, a KRas G12C mutation, a KRas G12D mutation, a KRas G12R mutation, a KRas G12S mutation or a KRas G12V mutation (e.g., a KRas G12D mutation or a KRas G12V mutation)) or amplification). In some such embodiments, the method also includes administering to a subject determined to have a KRas dysregulation (e.g., a KRas mutation (e.g., a KRas G12A mutation, a KRas G12C mutation, a KRas G12D mutation, a KRas G12R mutation, a KRas G12S mutation or a KRas G12V mutation (e.g., a KRas G12D mutation or a KRas G12V mutation)) or amplification) a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof. In some embodiments, the method includes determining that a cancer in a subject has a KRas dysregulation (e.g., a KRas mutation (e.g., a KRas G12A mutation, a KRas G12C mutation, a KRas G12D mutation, a KRas G12R mutation, a KRas G12S mutation, or a KRas G12V mutation (e.g., a KRas G12D mutation or a KRas G12V mutation)) or amplification) via an assay performed on a sample obtained from the subject. In such embodiments, the method also includes administering to a subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof. Some embodiments of these methods further include administering to the subject another anticancer agent (e.g., a second compound provided herein, or a pharmaceutically acceptable salt thereof, or immunotherapy). In some embodiments of any of the methods or uses described herein, an assay is used to determine whether the cancer in the subject has a KRas dysregulation (e.g., a KRas mutation (e.g., a KRas G12A mutation, a KRas G12C mutation, a KRas G12D mutation, a KRas G12R mutation, a KRas G12S mutation, or a KRas G12V mutation (e.g., a KRas G12D mutation or a KRas G12V mutation)) or amplification), using a sample (e.g., a tumor sample or a blood sample) from a subject can include, for example, next generation sequencing, immunohistochemistry, fluorescence microscopy, Southern blotting, Western blotting, FACS analysis, Northern blotting, and PCR-based amplification (e.g., RT-PCR and quantitative real- time RT-PCR). As is well-known in the art, the assays are typically performed, e.g., with at least one labelled nucleic acid probe or at least one labelled antibody or antigen-binding fragment thereof. Assays can utilize other detection methods known in the art for detecting a KRas dysregulation (e.g., a KRas mutation (e.g., a KRas G12A mutation, a KRas G12C mutation, a KRas G12D mutation, a KRas G12R mutation, a KRas G12S mutation, or a KRas G12V mutation (e.g., a KRas G12D mutation or a KRas G12V mutation)) or amplification) (see, e.g., the references cited herein). In some embodiments, the sample is tumor biopsy sample (e.g., a paraffin-embedded biopsy sample) from the subject. In some embodiments, the subject is a subject suspected of having a KRas-associated cancer (e.g., mutant KRas- associated cancer (e.g., a KRas G12A-associated cancer, a KRas G12C-associated cancer, a KRas G12D-associated cancer, a KRas G12R-associated cancer, a KRas G12S-associateion, or a KRas G12V-associated cancer (e.g., a KRas G12D-associated cancer or a KRas G12V- associated cancer))), a subject having one or more symptoms of a KRas-associated cancer (e.g., mutant KRas-associated cancer (e.g., a KRas G12A-associated cancer, a KRas G12C- associated cancer, a KRas G12D-associated cancer, a KRas G12R-associated cancer, a KRas G12S-associated cancer, or a KRas G12V-associated cancer (e.g., a KRas G12D-associated cancer or a KRas G12V-associated cancer))), and/or a subject that has an increased risk of developing a KRas-associated cancer (e.g., mutant KRas-associated cancer (e.g., a KRas G12A-associated cancer, a KRas G12C-associated cancer, a KRas G12D-associated cancer, a KRas G12R-associated cancer, a KRas G12S-associated cancer, or a KRas G12V-associated cancer (e.g., a KRas G12D-associated cancer or a KRas G12V-associated cancer))). In some embodiments, the subject is a subject suspected of having a cancer having a KRas dysregulation (e.g., a KRas mutation or amplification), a subject having one or more symptoms of a cancer having a KRas dysregulation (e.g., a KRas mutation or amplification), and/or a subject that has an increased risk of developing a cancer having a KRas dysregulation (e.g., a KRas mutation or amplification). In some embodiments, a KRas dysregulation (e.g., a KRas mutation (e.g., a KRas G12A mutation, a KRas G12C mutation, a KRas G12D mutation, a KRas G12R mutation, a KRas G12S mutation, or a KRas G12V mutation (e.g., a KRas G12D mutation or a KRas G12V mutation)) or amplification) can be identified using a liquid biopsy (variously referred to as a fluid biopsy or fluid phase biopsy). See, e.g., Karachialiou et al., “Real-time liquid biopsies become a reality in cancer treatment”, Ann. Transl. Med., 3(3):36, 2016, doi: 10.3978/j.issn.2305-5839.2015.01.16. Liquid biopsy methods can be used to detect total tumor burden and/or the KRas dysregulation (e.g., the KRas mutation or amplification). Liquid biopsies can be performed on biological samples obtained relatively easily from a subject (e.g., via a simple blood draw) and are generally less invasive than traditional methods used to detect tumor burden and/or KRas dysregulation (e.g., a KRas mutation (e.g., a KRas G12A mutation, a KRas G12C mutation, a KRas G12D mutation, a KRas G12R mutation, a KRas G12S mutation, or a KRas G12V mutation (e.g., a KRas G12D mutation or a KRas G12V mutation)) or amplification). In some embodiments, liquid biopsies can be used to detect the presence of a KRas dysregulation (e.g., a KRas mutation or amplification) at an earlier stage than traditional methods. In some embodiments, the biological sample to be used in a liquid biopsy can include, blood, plasma, urine, cerebrospinal fluid, saliva, sputum, broncho-alveolar lavage, bile, lymphatic fluid, cyst fluid, stool, ascites, and combinations thereof. In some embodiments, a liquid biopsy can be used to detect circulating tumor cells (CTCs). In some embodiments, a liquid biopsy can be used to detect cell-free DNA. In some embodiments, cell-free DNA detected using a liquid biopsy is circulating tumor DNA (ctDNA) that is derived from tumor cells. Analysis of ctDNA (e.g., using sensitive detection techniques such as, without limitation, next-generation sequencing (NGS), traditional PCR, digital PCR, or microarray analysis) can be used to identify a KRas dysregulation (e.g., KRas mutation (e.g., a KRas G12A mutation, a KRas G12C mutation, a KRas G12D mutation, a KRas G12R mutation, a KRas G12S mutation, or a KRas G12V mutation (e.g., a KRas G12D mutation or a KRas G12V mutation))). Also provided is a method for modulating (e.g., decreasing) KRas protein activity (e.g., dysregulated KRas protein activity (e.g., mutant KRas protein activity (e.g., KRas G12R mutant protein activity or G12V mutant protein activity))) in a cell, comprising contacting the cell with a compound provided herein, or a pharmaceutically acceptable salt thereof. In some embodiments, the contacting is in vitro. In some embodiments, the contacting is in vivo. In some embodiments, the contacting is ex vivo. In some embodiments, the contacting is in vivo, wherein the method comprises administering an effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, to a subject having a cell having a KRas protein (e.g., a dysregulated KRas protein (e.g., a mutant KRas protein (e.g., a KRas G12A mutant protein, a KRas G12C mutant protein, a KRas G12D mutant protein, a KRas G12R mutant protein, a KRas G12S mutant protein, or a KRas G12V mutant protein (e.g., a KRas G12D mutant protein or a KRas G12V mutant protein)))). In some embodiments, the contacting is ex vivo, wherein the method comprises contacting a cell from a subject having a KRas protein (e.g., a dysregulated KRas protein (e.g., a mutant KRas protein (e.g., a KRas G12A mutant protein, a KRas G12C mutant protein, a KRas G12D mutant protein, a KRas G12R mutant protein, a KRas G12S mutant protein, or a KRas G12V mutant protein (e.g., a KRas G12D mutant protein or a KRas G12V mutant protein)))) with a compound provided herein, or a pharmaceutically acceptable salt thereof. In some embodiments, the cell is a cancer cell. In some embodiments, the cell is a mammalian cell. In some embodiments, the cell is a mammalian cancer cell. In some embodiments, the cancer cell is any cancer as described herein. In some embodiments, the cancer cell is a KRas-associated cancer cell (e.g., a mutant KRas-associated cancer cell (e.g., a KRas G12A-associated cancer cell, a KRas G12C- associated cancer cell, a KRas G12D-associated cancer cell, a KRas G12R-associated cancer cell, a KRas G12S-associated cancer cell, or a KRas G12V-associated cancer cell (e.g., a KRas G12D-associated cancer cell or a KRas G12V-associated cancer cell))). As used herein, the term “contacting” refers to the bringing together of indicated moieties in an in vitro system, an in vivo system, or an ex vivo system. For example, “contacting” a KRas protein with a compound provided herein includes the administration of a compound provided herein to an individual or subject, such as a human, having a KRas protein, as well as, for example, introducing a compound provided herein into a sample containing a cellular or purified preparation containing the KRas protein. Also provided herein is a method of inhibiting cell proliferation, in vitro, in vivo, or ex vivo, the method comprising contacting a cell with an effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition thereof as defined herein. In some embodiments, the cell has a KRas dysregulation. In some embodiments, the cell has a KRas mutation. In some embodiments, the cell has a KRas G12D mutation or a KRas G12V mutation. In some embodiments, the cell has a KRas G12A mutation. In some embodiments, the cell has a KRas G12C mutation. In some embodiments, the cell has a KRas G12D mutation. In some embodiments, the cell has a KRas G12R mutation. In some embodiments, the cell has a KRas G12S mutation. In some embodiments, the cell has a KRas G12V mutation. In some embodiments, the cell has a KRas amplification. Further provided herein is a method of increasing cell death, in vitro, in vivo, or ex vivo, the method comprising contacting a cell with an effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition thereof as defined herein. Also provided herein is a method of increasing tumor cell death in a subject. The method comprises administering to the subject a compound provided herein, or a pharmaceutically acceptable salt thereof, in an amount effective to increase tumor cell death. In some embodiments, the cell has a KRas dysregulation. In some embodiments, the cell has a KRas mutation. In some embodiments, the cell has a KRas G12D mutation or a KRas G12V mutation. In some embodiments, the cell has a KRas G12A mutation. In some embodiments, the cell has a KRas G12C mutation. In some embodiments, the cell has a KRas G12D mutation. In some embodiments, the cell has a KRas G12R mutation. In some embodiments, the cell has a KRas G12S mutation. In some embodiments, the cell has a KRas G12V mutation. In some embodiments, the cell has a KRas amplification. When employed as pharmaceuticals, the compounds provided herein, or pharmaceutically acceptable salts thereof, can be administered in the form of pharmaceutical compositions as described herein. Also provided herein is a method for inhibiting a KRas protein in a mammalian cell, the method comprising contacting the mammalian cell with an effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof. Also provided herein is a method for inhibiting a dysregulated KRas protein (e.g., a mutant KRas protein (e.g., a KRas G12A mutant protein, a KRas G12C mutant protein, a KRas G12D mutant protein, a KRas G12R mutant protein, a KRas G12S mutant protein, or a KRas G12V mutant protein (e.g., a KRas G12D mutant protein or a KRas G12V mutant protein))) in a mammalian cell, the method comprising contacting the mammalian cell with an effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof. In some embodiments, the mammalian cell is ex vivo. Also provided herein is a method of treating a subject having a cancer, wherein the method comprises: administering a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, as a monotherapy or in conjunction with a first anticancer agent to the subject who has been administered one or more doses of the first anticancer agent to the subject for a period of time. Also provided herein is a method of treating a subject having a cancer, wherein the method comprises: (a) administering one or more doses of a first anticancer agent to the subject for a period of time; (b) after (a), determining whether a cancer cell in a sample (e.g., a tumor sample or a blood sample) obtained from the subject has a KRas dysregulation (e.g., a KRas mutation (e.g., a KRas G12A mutation, a KRas G12C mutation, a KRas G12D mutation, a KRas G12R mutation, a KRas G12S mutation, or a KRas G12V mutation (e.g., a KRas G12D mutation or a KRas G12V mutation)) or amplification); and (c) administering a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, as a monotherapy or in conjunction with a second anticancer agent to the subject if the subject has been determined to have a cancer cell that has a KRas dysregulation (e.g., a KRas mutation or amplification); or (d) administering additional doses of the first anticancer agent of step (a) to the subject if the subject has not been determined to have a cancer cell that has a KRas dysregulation (e.g., a KRas mutation (e.g., a KRas G12A mutation, a KRas G12C mutation, a KRas G12D mutation, a KRas G12R mutation, a KRas G12S mutation, or a KRas G12V mutation (e.g., a KRas G12D mutation or a KRas G12V mutation)) or amplification). Further provided herein is a method of treating a subject having a cancer, wherein the method comprises: (a) determining whether a cancer cell in a sample (e.g., a tumor sample or a blood sample) obtained from a subject having a cancer and previously administered one or more doses of a first anticancer agent has a KRas dysregulation (e.g., a KRas mutation (e.g., a KRas G12A mutation, a KRas G12C mutation, a KRas G12D mutation, a KRas G12R mutation, a KRas G12S mutation, or a KRas G12V mutation (e.g., a KRas G12D mutation or a KRas G12V mutation)) or amplification); and (b) administering a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, as a monotherapy or in conjunction with a second anticancer agent to the subject if the subject has been determined to have a cancer cell that has a KRas dysregulation (e.g., a KRas mutation (e.g., a KRas G12A mutation, a KRas G12C mutation, a KRas G12D mutation, a KRas G12R mutation, a KRas G12S mutation, or a KRas G12V mutation (e.g., a KRas G12D mutation or a KRas G12V mutation)) or amplification); or (c) administering additional doses of the first anticancer agent to the subject if the subject has not been determined to have a cancer cell that has a KRas dysregulation (e.g., KRas mutation (e.g., a KRas G12A mutation, a KRas G12C mutation, a KRas G12D mutation, a KRas G12R mutation, a KRas G12S mutation, or a KRas G12V mutation (e.g., a KRas G12D mutation or a KRas G12V mutation)) or amplification). Also provided herein is a method of treating a subject having a cancer, wherein the method comprises: (a) determining that a cancer cell in a sample (e.g., a tumor sample or a blood sample) obtained from a subject having a cancer and previously administered one or more doses of a first anticancer agent has a KRas dysregulation (e.g., a KRas mutation (e.g., a KRas G12A mutation, a KRas G12C mutation, a KRas G12D mutation, a KRas G12R mutation, a KRas G12S mutation, or a KRas G12V mutation (e.g., a KRas G12D mutation or a KRas G12V mutation)) or amplification); and (b) administering a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, as a monotherapy or in conjunction with a second anticancer agent to the subject. In some embodiments of any of the methods described herein, the first anticancer agent can be a first KRas inhibitor. When employed as pharmaceuticals, the compounds provided herein, or pharmaceutically acceptable salts thereof, can be administered in the form of pharmaceutical compositions as described herein. Combinations In any of the indications described herein, a compound provided herein, or a pharmaceutically acceptable salt thereof, can be used as a monotherapy. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, can be used prior to administration of an additional therapeutic agent or additional therapy. For example, a subject in need thereof can be administered one or more doses of a compound provided herein, or a pharmaceutically acceptable salt thereof, for a period of time and then undergo at least partial resection of the tumor. In some embodiments, the treatment with one or more doses of a compound provided herein, or a pharmaceutically acceptable salt thereof, reduces the size of the tumor (e.g., the tumor burden) prior to the at least partial resection of the tumor. In some embodiments, a subject in need thereof can be administered one or more doses of a compound provided herein, or a pharmaceutically acceptable salt thereof, for a period of time and under one or more rounds of radiation therapy. In some embodiments, the treatment with one or more doses of a compound provided herein, or a pharmaceutically acceptable salt thereof, reduces the size of the tumor (e.g., the tumor burden) prior to the one or more rounds of radiation therapy. In some embodiments, a subject has a cancer (e.g., a locally advanced or metastatic tumor) that is refractory or intolerant to standard therapy (e.g., administration of a chemotherapeutic agent, such as a first KRas inhibitor, a kinase inhibitor, immunotherapy, or radiation. In some embodiments, a subject has a cancer (e.g., a locally advanced or metastatic tumor) that is refractory or intolerant to prior therapy (e.g., administration of a chemotherapeutic agent, such as a first KRas inhibitor, a kinase inhibitor, immunotherapy, or radiation). In some embodiments, a subject has a cancer (e.g., a locally advanced or metastatic tumor) that has no standard therapy. In some embodiments, a subject is KRas inhibitor naïve. In some embodiments, a subject is not KRas inhibitor naïve. In some embodiments, a subject has undergone prior therapy. For example, treatment with surgery, radiation, a chemotherapeutic agent, an immunotherapy, a multi-kinase inhibitor (MKI), a KRas inhibitor, a RAF/MEK/PI3K pathway inhibitor, a MEK inhibitor, a Raf inhibitor, a YAP inhibitor, a proteasome inhibitor, a PI3K-AKT-mTOR pathway inhibitor, an ERK inhibitor, a pan-ErbB inhibitor, a MET inhibitor, a farnesyl transferase inhibitor, a FAK inhibitor, a HSP90 inhibitor, or a combination thereof. In some embodiments of any the methods described herein, the compound provided herein, or a pharmaceutically acceptable salt thereof, is administered in combination with a therapeutically effective amount of at least one additional therapeutic agent selected from one or more additional therapies or therapeutic (e.g., chemotherapeutic) agents. Non-limiting examples of additional therapeutic agents include: Ras pathway targeted therapeutic agents (e.g., Ras/RAF/MEK/PI3K pathway inhibitors or degraders, (e.g., Ras inhibitors or degraders, KRas-targeted therapeutic agents, SOS1 inhibitors or degraders, SOS1/Ras protein-protein interaction inhibitors, SHP2 inhibitors or degraders, PI3K-AKT- mTOR pathway inhibitors or degraders)), kinase-targeted therapeutics (e.g., MEK inhibitors or degraders, ERK inhibitors or degraders, Raf inhibitors or degraders (e.g., BRaf inhibitors or degraders), PI3K inhibitors or degraders, AKT inhibitors or degraders, mTOR inhibitors or degraders, CDK4/5 inhibitors or degraders, CDK4/6 inhibitors or degraders, MET inhibitors or degraders, FAK inhibitors or degraders, ErbB family inhibitors or degraders (e.g., EGFR inhibitors or degraders, HER2 inhibitors or degraders), Src inhibitors or degraders), Bcl-XL inhibitors or degraders, mTORC1 inhibitors or degraders, YAP inhibitors or degraders, TEAD inhibitors or degraders, proteasome inhibitors or degraders, farnesyl transferase inhibitors or degraders, HSP90 inhibitors or degraders, PTEN inhibitors or degraders, signal transduction pathway inhibitors or degraders, checkpoint inhibitors, modulators of the apoptosis pathway (e.g., venetoclax, navitoclax, obataclax), chemotherapeutics, angiogenesis-targeted therapies, immune-targeted agents including immunomodulatory imide drugs (sometimes called “IMiDs” or “CELMoDs”), immunotherapy (e.g., anti-PD1, anti-PD-L1, anti-CTLA4, anti-LAG3, anti- TIM3, anti-B7-H3, anti-VISTA therapies, including antibodies (e.g., single-targeted antibodies targeting one or more of PD1, PD-L1, CTLA4, LAG3, TIM3, B7-H3, or VISTA; bispecific antibodies (including bispecific T cell engagers (BiTEs)) targeting one or more of PD1, PD- L1, CTLA4, LAG3, TIM3, B7-H3, or VISTA; and antibody-drug conjugates (ADCs) incorporating one or more of PD1, PD-L1, CTLA4, LAG3, TIM3, B7-H3, or VISTA) or antigen-binding fragments thereof, a PD-1 inhibitor, a PD-L1 inhibitor, or an ADORA2A inhibitor), cell-based therapeutics (e.g., adoptive cell therapy (e.g., CAR T therapy, cytokine- induced killer cells (CIKs), natural killer cells (e.g., CAR-modified NK cells)) or antibody- armed cell therapy), and radiotherapy. See also, e.g., the therapeutic agents listed in U.S. Publication No. US 2021/0130303. A “degrader” as used herein is a heterobifunctional molecule that induces degradation of a target protein, the degrader including a moiety that binds to the target protein and a moiety that binds to a ubiquitin E3 ligase (sometimes referred to as an E3 ligase or simply an E3), these two moieties being optionally separated by a linker. Such degraders are sometimes known as “PROTACs”. A “Ras pathway targeted therapeutic agent” as used herein includes any compound exhibiting inactivation activity of any protein in a Ras pathway (e.g., kinase inhibition, allosteric inhibition, inhibition of dimerization, and/or induction of degradation). Non-limiting examples of a protein in a Ras pathway include any one of the proteins in the Ras-RAF-MAPK pathway or PI3K/AKT pathway such as Ras (e.g., KRas, HRas, and NRas), RAF, BRAF, MEK, ERK, PI3K, AKT, and mTOR. In some embodiments, a Ras pathway modulator can be selective for a protein in a Ras pathway, e.g., the Ras pathway modulator can be selective for Ras (also referred to as a Ras modulator). In some embodiments, a Ras modulator is a covalent inhibitor. In some embodiments, a Ras pathway targeted therapeutic agent is a “KRas pathway modulator.” A KRas pathway modulator includes any compound exhibiting inactivation activity of any protein in a KRas pathway (e.g., kinase inhibition, allosteric inhibition, inhibition of dimerization, and/or induction of degradation). Non-limiting examples of a protein in a KRas pathway include any one of the proteins in the KRas-RAF-MAPK pathway or PI3K/AKT pathway such as KRas, RAF, BRAF, MEK, ERK, PI3K, AKT, and mTOR. In some embodiments, a KRas pathway modulator is a KRas-targeted therapeutic agent. In some embodiments, the Ras pathway targeted therapeutic agent is a SOS1 inhibitor or a SHP2 inhibitor. Non-limiting examples of SOS1 inhibitors include MRTX-0902 and RMC-5845. Non-limiting examples of SHP2 inhibitors include batoprotafib (TNO-155), vociprotafib (RMC-4630), ARRY-558, BBP-398, ENT-03, ERAS-601, ET-0038, GDC-1971 (RLY-1971), GH-21, HS-10381, ICP-189, JAB-3068, JAB-3312, and SH-3809. Non-limiting examples of KRas-targeted therapeutic agents (e.g., a first KRas inhibitor or a second KRas inhibitor) include a KRas-selective inhibitor, a Ras inhibitor, and an anti- KRas antibody. In some embodiments, the KRas inhibitor is a covalent inhibitor. In some embodiments, the KRas-targeted therapeutic agent is adagrasib, divarasib (GDC-6036), garsorasib (D-1553), glecirasib (JAB-21822), olomorasib (LY-3537982), sotorasib, ARS- 1620, ARS-3248, ARS-853, ASP-3082, ATG-012, BI-1701963, BI-1823911, BPI-421286, ERAS-3490, GFH-925, GH-35, JDQ-443, MK-1084, MRTX-1133, MRTX-1257, RMC-6236, RMC-6291, RMC-7977, RMC-9805, RSC-1255, SHR-1127, or a combination thereof. In some embodiments, the KRas-targeted therapeutic agent is an agent that inhibits the interaction between KRas and SOS1 or SHP2. Non-limiting examples of an agent that inhibits the interaction between SOS1 and KRas include BI-3406, BI-1701963, and BAY 293. Additional KRas-targeted therapeutic agents (e.g., a first KRas inhibitor or a second KRas inhibitor) include those disclosed in International Publication Nos. WO 2021/104431; WO WO2021/119343; WO2021/113595; WO 2021/107160; WO 2016/161361; WO 2016/17262; WO 2020/035031; WO 2021/041671; WO 2016/077793; WO 2020/180768; WO 2021/092115; WO 2020/180770; U.S. Patent Nos. US 10,898,487; US 10,829,487; US 10,858,359; US 10,561,655; US 10,532,042; U.S. Publication Nos. US 2021/0101870; US 2019/0231805; US 2020/0017517; US 2020/0017511; US 2020/0147058; US 2021/0009577; and Hillig et al. PNAS.2019; 116(7): 2551-2560, doi: 10.1073/pnas.1812963116. Further non-limiting examples of Ras pathway-targeted therapeutic agents include BRAF inhibitors, MEK inhibitors, ERK inhibitors, PI3K inhibitors, AKT inhibitors, and mTOR inhibitors. In some embodiments, the BRAF inhibitor is avutometinib, dabrafenib (e.g., dabrafenib mesylate, TAFINLAR®), encorafenib (BRAFTOVI™), naporafenib, sorafenib (e.g., sorafenib tosylate), vemurafenib (ZELBORAF®), ARQ 736, AZ304, BMS-908662 (XL281), C17071479-F, CHIR-265, FORE-8394, GDC-0879, GSK2118436, HLX-208, HM95573, LGX818, LXH254, PLX-3603, PLX-4720, PLX-8394, RAF265, RO5126766, RO5185426, or a combination thereof. In some embodiments, the BRAF inhibitor is avutometinib, dabrafenib (e.g., dabrafenib mesylate), encorafenib, naporafenib, sorafenib (e.g., sorafenib tosylate), vemurafenib, C17071479-F, CHIR-265, FORE-8394, HLX-208, or a combination thereof. In some embodiments, the MEK inhibitor is avutometinib, binimetinib (MEKTOVI®, MEK162), cobimetinib (e.g., cobimetinib fumarate, COTELLIC®), mirdametinib, pimasertib, refametinib, selumetinib (e.g., selumetinib sulfate, AZD6244), trametinib (e.g., trametinib dimethyl sulfoxide, GSK-1120212 MEKINIST®), zapnometinib, hypothemycin, CI1040 (PD184352), CS3006, FCN-159, MSC1936369B, NFX-179, PD0325901, PD98059,RO5126766, SHR7390, TAK-733, WX-554, or a combination thereof. In some embodiments, the MEK inhibitor is avutometinib, binimetinib, cobimetinib (e.g., cobimetinib fumarate), mirdametinib, nedometinib, pimasertib, refametinib, selumetinib (e.g., selumetinib sulfate), trametinib (e.g., trametinib dimethyl sulfoxide, GSK-1120212), tunlametinib, zapnometinib, FCN-159, NFX-179, TAK-733, or a combination thereof. In some embodiments, the MEK inhibitor is a MEK-Raf protein-protein interaction stabilizer, such as NST-628 or avutometinib (VS6766). In some embodiments, the ERK inhibitor is 25-OH-D3-3-BE (B3CD, bromoacetoxycalcidiol), 5-7-Oxozeaenol, 5-iodotubercidin, AEZ-131 (AEZS-131), AEZS- 136, ASN007, AZ-13767370, BL-EI-001, CC-90003, FR148083, FR-180204, FRI-20 (ON- 01060), GDC0994, GDC-0994 (RG-7482), KO-947, KO-947, LTT-462, LY-3214996, MK- 8353 (SCH900353), ONC201SCH772984, ulixertinib (BVD-523), VTX-11e, or a combination thereof. In some embodiments, the ERK inhibitor is rineterkib, ulixertinib, or a combination thereof. In some embodiments, PI3K inhibitor is alpelisib (BYL719), apitolisib (GDC-0980), buparlisib (BKM120), copanlisib (ALIQOPA™, BAY80-6946), dactolisib (NVP-BEZ235, BEZ-235), gedatolisib (PF-05212384, PKI-587), omipalisib (GSK2126458, GSK458), pictilisib (GDC-0941), pilaralisib (XL147, SAR245408), rigosertib, serabelisib (TAK-117, MLN1117, INK 1117), sonolisib (PX-866), taselisib (GDC-0032, RG7604), voxtalisib (XL756, SAR245409), wortmannin, AMG 511, AMG319, ASN003, AZD8835, BGT-226 (NVP-BGT226), CH5132799, CUDC-907, GDC-0077, GDC-0084 (RG7666), GS-9820, GSK1059615, GSK2636771, KIN-193 (AZD-6428), LY2023414, LY294002, PF-04691502, PI-103, PKI-402, PQR309, SAR260301, SF1126, VS-5584 (SB2343), WX-037, XL-765, ZSTK474, or a combination thereof. In some embodiments, the PI3K inhibitor is alpelisib, amdizalisib, apitolisib, bimiralisib, buparlisib, copanlisib (e.g., copanlisib dihydrochloride or a hydrate of copanlisib dihydrochloride), dactolisib, dezapelisib, dordaviprone, duvelisib (e.g., a hydrate of duvelisib), eganelisib, fimepinostat, gedatolisib, idelalisib, inavolisib, leniolisib (e.g., leniolisib phosphate), linperlisib, parsaclisib, paxalisib, risovalisib, seletalisib, serabelisib, sonolisib, tenalisib, umbralisib (e.g., umbralisib tosylate), zandelisib, PF- 04691502, SHC-014748-M, TQ-B-3525, or a combination thereof. In some embodiments, the AKT inhibitor is 2-[4-(2-aminoprop-2-yl)phenyl]-3- phenylquinoxaline, 3-oxo-tirucallic acid, A-443654, A-674563, afuresertib, API-1, ARQ092, AT13148, AT7867, AZD5363, BAY 1125976, boc-Phe-vinyl ketone, CCT128930, DC120, DM-PIT-1, edelfosine, erucylphophocholine, erufosine, GSK2141795, GSK690693, H-89, ipatasertib (GDC-0068, RG7440), lactoquinomycin, miltefosine (IMPADIVO®), MK-2206, N-(4-(5-(3-acetamidophenyl)-2-(2-aminopyridin-3-yl)-3H-imidazo[4,5-b] pyridin-3- yl)benzyl)-3-fluorobenzamide, NL-71-101, ONC201, OSU-A9, Perifosine (D-21266), PH- 316, PHT-427, PIT-1, SR13668, TCN, TCN-P, triciribine (Triciribine Phosphate Monohydrate), uprosertib, wortmannin, or a combination thereof. In some embodiments, the AKT inhibitor is afuresertib, capivasertib (AZD-5363), miransertib (e.g., miransertib mesylate), pifusertib, uprosertib, MK-2206, SM-020, or a combination thereof. In some embodiments, the mTOR inhibitor is MLN0128, AZD-2014, CC-223, AZD2014, CC-115, everolimus (RAD001), temsirolimus (CCI-779), ridaforolimus (AP- 23573), sirolimus (rapamycin), or a combination thereof. In some embodiments, the mTOR inhibitor is apitolisib, bimiralisib, dactolisib, everolimus, fosciclopirox (e.g., fosciclopirox sodium), gedatolisib, onatasertib, paxalisib, sapanisertib, sirolimus, sodium 2- hydroxylinoleate, temsirolimus, umirolimus, zandelisib, zotarolimus, BI-860585, CC-115, PF- 04691502, or a combination thereof. In some embodiments, the mTOR inhibitor is everolimus, sirolimus, temsirolimus, umirolimus, zotarolimus, or a combination thereof. In some embodiments, the mTOR inhibitor is everolimus, sirolimus, temsirolimus, umirolimus, zotarolimus, RMC5552, or a combination thereof. In some embodiments, the farnesyl transferase inhibitor is lonafarnib, tipifarnib, BMS- 214662, L778123, L744832, FTI-277, or a combination thereof. In some embodiments, the farnesyl transferase inhibitor is lonafarnib, tipifarnib, BMS-214662, or a combination thereof. In some embodiments, a chemotherapeutic agent includes a DNA replication inhibitor (e.g., a DNA intercalator (e.g., an anthracycline)), a DNA crosslinker (e.g., cyclophosphamide, a mitomycin (e.g., mitomycin C), a platinum complex), a ribonucleotide-diphosphate reductase inhibitor (e.g., gemcitabine), or a topoisomerase inhibitor), an anti-microtubule agent (e.g., a taxane a vinca alkaloid, or eribulin), or a combination thereof. Non-limiting examples of a taxane include paclitaxel, docetaxel, abraxane, and taxotere. In some embodiments, the anthracycline is selected from daunorubicin, doxorubicin, epirubicin, idarubicin, and combinations thereof. In some embodiments, the platinum-based agent is selected from carboplatin, cisplatin, oxaliplatin, nedplatin, triplatin tetranitrate, phenanthriplatin, picoplatin, satraplatin and combinations thereof. In some embodiments, the chemotherapy is a platinum complex, a microtubule inhibitor (e.g., a microtubule destabilizer or a microtubule stabilizer), a topoisomerase inhibitor, or an antibody-drug conjugate including any thereof. In some embodiments, the platinum complex is carboplatin, cisplatin, lobaplatin, miriplatin, oxaliplatin, or a combination thereof. In some embodiments, the microtubule inhibitor is cabazitaxel, colchicine, desoxyepothilone B, docetaxel, eribulin, ixabepilone, nab-paclitaxel, paclitaxel, plinabulin, sabizabulin, tirbanibulin, vinblastine, vinflunine, vinorelbine, or a combination thereof. In some embodiments, the microtubule inhibitor is cabazitaxel, docetaxel, nab-paclitaxel, paclitaxel, or a combination thereof. In some embodiments, the topoisomerase inhibitor is aclarubicin, amsacrine, belotecan, camptothecin, daunorubicin, dexrazoxane, elliptinium, epirubicin, etoposide, gepotidacin, idarubicin, mitoxantrone, nemonoxacin, pirarubicin, pixantrone, razoxane, rubitecan, sobuzoxane, temozolomide, teniposide, topotecan, SN-38, or a combination thereof. In some embodiments, the hypomethylating agent is azacitidine, decitabine, or a combination thereof. In some embodiments, the chemotherapy is a platinum complex and a topoisomerase inhibitor (e.g., cisplatin and etoposide). In some embodiments, the antibody-drug conjugate including the microtubule inhibitor is belantamab mafodotin, brentuximab vedotin, cofetuzumab pelidotin, disitamab vedotin, enfortumab vedotin (e.g., enfortumab vedotin-ejfv, or a biosimilar thereof), mirvetuximab soravtansine (e.g., mirvetuximab soravtansine-gynx, or a biosimilar thereof), polatuzumab vedotin, telisotuzumab vedotin, tisotumab vedotin, trastuzumab emtansine (e.g., ado-trastuzumab emtansine, or a biosimilar thereof), tusamitamab ravtansine, upifitamab rilsodotin, zilovertamab vedotin, Alpha-Her2-pAF1-AS-269, BAT-8001, TAA-013, biosimilars thereof, or a combination thereof. In some embodiments, the antibody-drug conjugate including the microtubule inhibitor is enfortumab vedotin (e.g., enfortumab vedotin-ejfv, or a biosimilar thereof). In some embodiments, the antibody-drug conjugate including the microtubule inhibitor is mirvetuximab soravtansine (e.g., mirvetuximab soravtansine-gynx, or a biosimilar thereof). In some embodiments, the antibody-drug conjugate including the microtubule inhibitor is trastuzumab emtansine (e.g., ado-trastuzumab emtansine, or a biosimilar thereof). In some embodiments, the antibody-drug conjugate including the topoisomerase inhibitor is datopotamab deruxtecan, patritumab deruxtecan, sacituzumab govitecan (e.g., sacituzumab govitecan-hziy, or a biosimilar thereof), trastuzumab deruxtecan (fam-trastuzumab deruxtecan- nxki, or a biosimilar thereof), or a combination thereof. In some embodiments, the antibody- drug conjugate including the topoisomerase inhibitor is sacituzumab govitecan (e.g., sacituzumab govitecan-hziy, or a biosimilar thereof). In some embodiments, the antibody-drug conjugate including the topoisomerase inhibitor is trastuzumab deruxtecan (e.g., fam- trastuzumab deruxtecan-nxki, or a biosimilar thereof). In some embodiments, the chemotherapy includes one or more of capecitabine, carboplatin, cisplatin, docetaxel, doxorubicin (e.g., liposomal doxorubicin), fluorouracil, gemcitabine, leucovorin, mitomycin, oxaliplatin, paclitaxel (e.g., albumin-bound paclitaxel), and pemetrexed. In some embodiments, the chemotherapy is FOLFOX. In some embodiments, the chemotherapy is FOLFIRI. In some embodiments, the chemotherapy is FOLFIRINOX. In some embodiments, the chemotherapy is CAPEOX. In some embodiments, the chemotherapy is GEMOX. In some embodiments, the chemotherapy is NALIRIFOX. In some embodiments, the chemotherapy is carboplatin and paclitaxel. In some embodiments, the chemotherapy is capecitabine and mitomycin. In some embodiments, the chemotherapy is fluorouracil, leucovorin, and oxaliplatin. In some embodiments, the chemotherapy is carboplatin and doxorubicin (e.g., liposomal doxorubicin). In some embodiments, the chemotherapy is gemcitabine. In some embodiments, the chemotherapy is gemcitabine and paclitaxel. In some embodiments, the BCL-X_L inhibitor or degrader is foselutoclax (UBX-1325), , navitoclax, obatoclax, pelcitoclax, mirzotamab clezutoclax (ABBV-155), ABBV-637, APG- 1252-12A, AZD-0466, DT-2216, PA-15227, UBX-1967, XZ-739, 753-B, or a combination thereof. In some embodiments, the CDK4/6 inhibitor is abemaciclib, birociclib, dalpiciclib, lerociclib, milciclib, palbociclib, ribociclib (e.g., ribociclib succinate), riviciclib, roniciclib, trilaciclib (e.g., trilaciclib dihydrochloride), BPI-16350, FCN-437, SPH-4336, or a combination thereof. In some embodiments, the CDK4/6 inhibitor is palbociclib or ribociclib (e.g., ribociclib succinate). In some embodiments, the EGFR inhibitor, or a pharmaceutically acceptable salt thereof, is abivertinib, afatinib (e.g., afatinib dimaleate), alflutinib (e.g., alflutinib mesylate), almonertinib (e.g., almonertinib mesylate), befotertinib, brigatinib, canertinib, dacomitinib (e.g., dacomitinib monohydrate), dovitinib, erlotinib (e.g., erlotinib hydrochloride), gefitinib, icotinib (e.g., icotinib hydrochloride), lapatinib (e.g., lapatinib ditosylate monohydrate), larotinib, lazertinib, limertinib, mobocertinib (e.g., mobocertinib succinate), nazartinib, neratinib (e.g., neratinib maleate), olmutinib, osimertinib (e.g., osimertinib mesylate), pelitinib, poziotinib, pyrotinib (e.g., pyrotinib maleate), ruserontinib (SKLB-1028), sacibertinib, sapitinib, sunvozertinib, sutetinib, tesevatinib, vandetanib, varlitinib, zipalertinib, zorifertinib, BAY-2927088, BEBT-109, BIBW-2948, BPI-7711, FHND-9041, HA-121-28, PLB-1004, SH-1028, or a combination thereof. In some embodiments, the EGFR inhibitor, or a pharmaceutically acceptable salt thereof, is ametumumab, amivantamab (e.g., amivantamab-vmjw, or a biosimilar thereof), becotatug, cetuximab (e.g., ERBITUX® (cetuximab), or a biosimilar thereof (e.g., CMAB- 009, CPGJ-602, or KL-140)), cetuximab sarotalocan (AKALUX® (cetuximab sarotalocan), or a biosimilar thereof), dalmitamig, depatuxizumab, duligotuzumab, ficerafusp alfa, futuximab, imgatuzumab, izalontamab (SI-B-001), matuzumab, modotuximab, necitumumab (e.g., PORTRAZZA® (necitumumab), or a biosimilar thereof), nimotuzumab (e.g., BIOMAb EGFR® (nimotuzumab), or a biosimilar thereof), panitumumab (e.g., VECTIBIX® (panitumumab), or a biosimilar thereof), petosemtamab, tomuzotuximab, zalutumumab, EMD- 55900, EMD-82633, GC-1118, HLX-07, ICR-62, SCT-200, biosimilars thereof, or a combination thereof. In some embodiments, the EGFR inhibitor, or a pharmaceutically acceptable salt thereof, is cetuximab or panitumumab. In some embodiments, the EGFR inhibitor, or a pharmaceutically acceptable salt thereof, is panitumumab. In some embodiments, the EGFR inhibitor, or a pharmaceutically acceptable salt thereof, is cetuximab. Cetuximab (ERBITUX^®) is a recombinant, human/mouse chimeric monoclonal antibody against EGFR approved for use in squamous cell carcinoma of the head and neck (SCCHN) and KRas WT EGFR-expressing CRC. For CRC, cetuximab is approved in combination with FOLFIRI in the first-line setting. In the second-line setting, cetuximab is approved in combination with irinotecan in patients who are refractory, as a single agent in patients who have progressed on chemotherapy, and in BRAF V600E mutation-positive metastatic CRC in combination with encorafenib. Cetuximab is administered as an intravenous infusion on a weekly or biweekly schedule. For example, in CRC, when used as a single agent or in combination with irinotecan or FOLFIRI, cetuximab is given weekly at an initial dose of 400 mg/m² administered as a 120-minute IV infusion and subsequent 250 mg/m² weekly 60-minute infusions. It is given biweekly at 500 mg/m² as a 120-minute IV infusion (ERBITUX^® USPI). In some embodiments, the PARP inhibitor is iniparib, niraparib, olaparib (LYNPARZA®), pamiparib (BGB-290), rucaparib, talazoparib, veliparib, 2X-121, ABT-767, BMN 673, BSI-201, CEP 9722, E7016, IMP4297, INO-1001, JPI-289, KU-0059436 (AZD2281), NOV1401, PF-01367338, and RBN-2397. In some embodiments, the PARP inhibitor is fuzuloparib (fluzoparib), niraparib (e.g., niraparib tosylate monohydrate), olaparib, pamiparib, rucaparib (e.g., rucaparib camsylate), saruparib (AZD5305), senaparib, stenoparib, talazoparib (e.g., talazoparib tosylate), veliparib, CEP-9722, JPI-289, NMS-03305293, or a combination thereof. In some embodiments, the PARP inhibitor is a PARP1 inhibitor. In some embodiments, the PARP1 inhibitor is saruparib (AZD5305), NMS-03305293, or a combination thereof. Non-limiting examples of immunotherapy include immune checkpoint therapies. Non- limiting examples of immune checkpoint therapies include antibodies and/or inhibitors that target CTLA-4, PD-1, PD-L1, BTLA, LAG-3, ADORA2A, TIM-3, B7-H3, VISTA, IDO, and combinations thereof. In some embodiments, the anti-CTLA4 therapy is abatacept (e.g., ORENCIA® (abatacept), or a biosimilar thereof), botensilimab, cadonilimab, erfonrilimab, gotistobart, ipilimumab (e.g., YERVOY® (ipilimumab), or a biosimilar thereof), nurulimab, quavonlimab, tremelimumab (ticilimumab) (e.g., IMIUDO® (tremelimumab), or a biosimilar thereof), volrustomig, vudalimab, zalifrelimab, BMS-986218, PSB-205, biosimilars thereof, or a combination thereof. In some embodiments, the anti-CTLA4 therapy is ipilimumab or tremelimumab. In some embodiments, the anti-CTLA4 therapy is ipilimumab. In some embodiments, the anti-CTLA4 therapy is tremelimumab. In some embodiments, the anti- CTLA4 therapy is used in combination with anti-PD1 or anti-PD-L1 therapy. In some embodiments, the anti-PD-1 therapy, or a pharmaceutically acceptable salt thereof, is balstilimab, budigalimab, cadonilimab, camrelizumab, cemiplimab (e.g., cemiplimab-rwlc, or a biosimilar thereof), cetrelimab, danvilostomig, dostarlimab (e.g., dostarlimab-gxly, or a biosimilar thereof), enlonstobart (SG-001), ezabenlimab, geptanolimab, iparomlimab (QL-1604), ivonescimab, nivolumab (e.g., OPDIVO® (nivolumab), or a biosimilar thereof (e.g., ABP-206, BCD-263, or JPB-898)), nofazinlimab, pembrolizumab (e.g., KEYTRUDA® (pembrolizumab), or a biosimilar thereof (e.g., ABP-234, BAT-3306, BCD-201, FYB-206, GME-751, MB-12, RPH-075, or SB-27)), penpulimab, pidilizumab, pimivalimab, prolgolimab, pucotenlimab, retifanlimab (e.g., retifanlimab-dlwr, or a biosimilar thereof), rilvegostomig, rosnilimab, rulonilimab, sasanlimab, serplulimab, sintilimab (e.g., TYVYT® (sintilimab), or a biosimilar thereof), spartalizumab, tebotelimab, tislelizumab, toripalimab, treprilimab, volrustomig, vudalimab, zimberelimab, 609-A, BAT-1306, BAT- 1308, HX-009, IBI-363, INCB-086550, LZM-009, RC-148, RG-6139, SSGJ-707, ZG-005, biosimilars thereof, or a combination thereof. In some embodiments, the anti-PD1 therapy is a bispecific antibody or antigen-binding fragment thereof (e.g., cadonilimab, danvilostomig, ivonescimab, rilvegostomig, tebotelimab, volrustomig, vudalimab, AZD7709, HX-009, RC- 148, RG-6139, SSGJ-707, ZG-005, biosimilars thereof, or a combination thereof). In some embodiments, the anti-PD-1 therapy is an anti-PD-1 and anti-CD47 bispecific antibody or antigen-binding fragment thereof (e.g., HX-009, or a biosimilar thereof). In some embodiments, the anti-PD-1 therapy, or a pharmaceutically acceptable salt thereof, is cemiplimab, nivolumab, or pembrolizumab. In some embodiments, the anti-PD-1 therapy, or a pharmaceutically acceptable salt thereof, is cemiplimab. In some embodiments, the anti-PD-1 therapy, or a pharmaceutically acceptable salt thereof, is nivolumab. In some embodiments, the anti-PD-1 therapy, or a pharmaceutically acceptable salt thereof, is pembrolizumab. Pembrolizumab (KEYTRUDA^®) is a programmed death receptor-1 (PD-1)- blocking antibody indicated for the treatment of patients with NSCLC as a monotherapy and in combination depending on disease setting (KEYTRUDA^® USPI). Pembrolizumab is also approved across multiple other solid and hematologic malignancies. In NSCLC, pembrolizumab is administered as an intravenous infusion 200 mg every 3 weeks or 400 mg every 6 weeks (KEYTRUDA^® USPI). In some embodiments, the anti-PD-L1 therapy is adebrelimab, atezolizumab (e.g., TECENTRIQ® (atezolizumab), or a biosimilar thereof), avelumab (e.g., BAVENCIO® (avelumab), or a biosimilar thereof), benmelstobart (APL-502), bintrafusp alfa, cosibelimab, danburstotug, durvalumab (e.g., IMFINZI® (durvalumab), or a biosimilar thereof), envafolimab (e.g., ENWEIDA® (envafolimab), or a biosimilar thereof), erfonrilimab, lesabelimab, pacmilimab, socazolimab, sugemalimab (e.g., CEJEMLY® (sugemalimab), or a biosimilar thereof), tagitanlimab (A-167), AUPM-170, BNT-311, SHR-1701, biosimilars thereof, or a combination thereof. In some embodiments, the anti-PD-L1 therapy is atezolizumab or durvalumab. In some embodiments, the anti-PD-L1 therapy is atezolizumab. In some embodiments, the anti-PD-L1 therapy is durvalumab. In some embodiments, the anti- PD-L1 therapy is used in combination with anti-CTLA4 therapy. In some embodiments, the anti-PD-L1 therapy is an PD-L1 inhibitor. In some embodiments, the PD-L1 inhibitor is INCB-086550 or INCB-099280. In some embodiments, the anti-LAG3 therapy is eftilagimod alfa, favezelimab, fianlimab, ieramilimab, miptenalimab, negalstobart (IBI-110), relatlimab (e.g., relatlimab- rmbw, or a biosimilar thereof), tebotelimab, tobemstomig (RG-6139), tuparstobart (INCAGN- 02385), HLX-26, LBL-007, SHR-1802, biosimilars thereof, or a combination thereof. In some embodiments, the ADORA2A inhibitor is etrumadenant, inupadenant, istradefylline, mefloquine (e.g., mefloquine), taminadenant, CPI-444, PBF-999, or a combination thereof. In some embodiments, the ADORA2A inhibitor is etrumadenant, inupadenant, istradefylline, mefloquine (e.g., mefloquine), taminadenant, PBF-999, or a combination thereof. In some embodiments, the anti-TIM3 therapy is cobolimab, sabatolimab (MBG-453), surzebiclimab, AZD-7789, INCAGN-02390, TQB-2618, or a combination thereof. In some embodiments, the anti-B7-H3 therapy is omburtamab, enoblituzumab, or a combination thereof. In some embodiments, the anti-VISTA therapy is onvatilimab (JNJ-61610588), HMBD-002, K01401-020, KVA-12.1, SNS-101, or a combination thereof. In some embodiments, the IDO inhibitor (e.g., IDO1 and/or IDO2 inhibitor) is 3- deazaguanine, beta-lapachone, diindolylmethane, epacadostat, indole-3-carbinol, indoximod, linrodostat, sertaconazole (e.g., sertaconazole nitrate), or a combination thereof. See, for example, Marin-Acevedo, et al., J Hematol Oncol. 11: 39 (2018), doi: 10.1186/s13045-018-0582-8. In some embodiments, the additional therapy or therapeutic agent is a combination of atezolizumab and nab-paclitaxel. Accordingly, also provided herein is a method of treating cancer, comprising administering to a subject in need thereof (a) a compound provided herein, or a pharmaceutically acceptable salt thereof, (b) an additional therapeutic agent, and (c) optionally at least one pharmaceutically acceptable carrier for simultaneous, separate or sequential use for the treatment of cancer, wherein the amounts of the compound provided herein, or a pharmaceutically acceptable salt thereof, and the additional therapeutic agent are together effective in treating the cancer. In some embodiments, the additional therapeutic agent(s) includes any one of the above listed therapies or therapeutic agents which are standards of care in cancers wherein the cancer has a KRas dysregulation (e.g., a KRas mutation or amplification). In some embodiments, the additional therapeutic agent(s) includes any one of the above listed therapies or therapeutic agents which are standards of care in a KRas-associated cancer (e.g., a mutant KRas-associated cancer (e.g., a KRas G12D-associated cancer, a KRas G12R-associated cancer, or a KRas G12V-associated cancer (e.g., a KRas G12D-associated cancer or a KRas G12V-associated cancer))). These additional therapeutic agents may be administered with one or more doses of the compound provided herein, or a pharmaceutically acceptable salt thereof, or pharmaceutical composition thereof, as part of the same or separate dosage forms, via the same or different routes of administration, and/or on the same or different administration schedules according to standard pharmaceutical practice known to one skilled in the art. Also provided herein is (i) a pharmaceutical composition for treating a cancer in a subject in need thereof, which comprises (a) a compound provided herein, or a pharmaceutically acceptable salt thereof, (b) at least one additional therapeutic agent (e.g., any of the exemplary additional therapeutic agents described herein or known in the art), and (c) optionally at least one pharmaceutically acceptable carrier for simultaneous, separate or sequential use for the treatment of cancer, wherein the amounts of the compound provided herein, or a pharmaceutically acceptable salt thereof, and of the additional therapeutic agent are together effective in treating the cancer; (ii) the use of such a composition for the preparation of a medicament for the treatment of cancer; and (iii) a commercial package or product comprising such a composition for simultaneous, separate or sequential use. In some embodiments, the cancer is a KRas-associated cancer (e.g., a mutant KRas-associated cancer (e.g., a KRas G12D-associated cancer, a KRas G12R-associated cancer, or a KRas G12V- associated cancer (e.g., a KRas G12D-associated cancer or a KRas G12V-associated cancer))). Accordingly, also provided herein is a method of treating a cancer, comprising administering to a subject in need thereof (a) a compound provided herein, or a pharmaceutically acceptable salt thereof, and (b) an additional therapeutic agent, wherein the compound provided herein, or a pharmaceutically acceptable salt thereof, and the additional therapeutic agent are administered simultaneously, separately or sequentially, wherein the amounts of the compound provided herein, or a pharmaceutically acceptable salt thereof, and the additional therapeutic agent are together effective in treating the cancer. In some embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, and the additional therapeutic agent are administered simultaneously as separate dosages. In some embodiments, compound provided herein, or a pharmaceutically acceptable salt thereof, and the additional therapeutic agent are administered as separate dosages sequentially in any order, in jointly therapeutically effective amounts, e.g., in daily or intermittently dosages. In some embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof, and the additional therapeutic agent are administered simultaneously as a combined dosage. In some embodiments, the cancer is a KRas-associated cancer (e.g., a mutant KRas- associated cancer (e.g., a KRas G12D-associated cancer, a KRas G12R-associated cancer, or a KRas G12V-associated cancer (e.g., a KRas G12D-associated cancer or a KRas G12V- associated cancer))). The term “wild type” or “wild-type” describes a nucleic acid (e.g., a KRAS gene or a KRas mRNA) or protein (e.g., a KRas protein) sequence that is typically found in a subject that does not have a disease or disorder related to the reference nucleic acid or protein. Although a wild type nucleic acid or protein sequence is the sequence that is typically found in a subject that does not have a disease or disorder related to the reference nucleic acid or protein, it is not necessarily the case that a subject that has a disease or disorder related to the reference nucleic acid or protein lacks wild type sequence. For example, a subject with a gene duplication of the reference gene may have the wild type sequence but could still have a disease or disorder related to the reference nucleic acid or protein due to the duplication event. As another example, a subject with a disease or disorder related to the reference nucleic acid or protein may have one allele that encodes wild type protein, and another allele that encodes a mutant protein. The term “wild type KRas” or “wild-type KRas” describes a KRas nucleic acid (e.g., a KRAS gene or a KRas mRNA) or protein (e.g., a KRas protein) that is found in a subject that does not have a KRas-associated disease, e.g., a KRas-associated cancer (and optionally also does not have an increased risk of developing a KRas-associated disease and/or is not suspected of having a KRas-associated disease), or is found in a cell or tissue from a subject that does not have a KRas-associated disease, e.g., a KRas-associated cancer (and optionally also does not have an increased risk of developing a KRas-associated disease and/or is not suspected of having a KRas-associated disease). Although a wild type KRas nucleic acid or protein sequence is the sequence that is typically found in a subject that does not have a KRas-associated disease or disorder, it is not necessarily the case that a subject that has a KRas-associated disease or disorder lacks the wild type KRas sequence. For example, a subject with a KRas gene duplication may have the wild type sequence but could still have a KRas-associated disease or disorder due to the duplication event. As another example, a subject with a KRas-associated disease or disorder may have one allele that encodes wild type KRas protein, and another allele that encodes a mutant KRas protein. As used herein, terms “treat” or “treatment” refer to therapeutic or palliative measures. Beneficial or desired clinical results include, but are not limited to, alleviation, in whole or in part, of symptoms associated with a disease or disorder or condition, diminishment of the extent of disease, stabilized (i.e., not worsening) state of disease, delay or slowing of disease progression, amelioration or palliation of the disease state (e.g., one or more symptoms of the disease), and remission (whether partial or total), whether detectable or undetectable. “Treatment” can also mean prolonging survival as compared to expected survival if not receiving treatment. As used herein, treatment of a cancer can include treatment of a primary tumor (i.e., non-metastatic cancer) (e.g., as first, second, third, or later line of therapy, including, but not limited to, the relapsed/refractory setting), treatment of a metastatic (or secondary) tumor, neoadjuvant therapy (e.g., before treatment with an additional therapy or therapeutic agent, such as surgery, radiation, chemotherapy, or a line of therapy), adjuvant therapy (e.g., following treatment with an additional therapy or therapeutic agent, such as surgery, radiation, chemotherapy, or a line of therapy), or maintenance therapy (e.g., treatment following response to an additional therapy or therapeutic agent, such as surgery, radiation, chemotherapy, or a line of therapy). As used herein, the terms “subject,” “individual,” or “patient,” are used interchangeably, and refer to any animal, including mammals such as mice, rats, other rodents, rabbits, dogs, cats, swine, cattle, sheep, horses, primates, and humans. In some embodiments, the subject is a human. In some embodiments, the subject has experienced and/or exhibited at least one symptom of the disease or disorder to be treated and/or prevented. In some embodiments, the subject is a pediatric subject. The term “pediatric subject” as used herein refers to a subject under the age of 21 years at the time of diagnosis or treatment. The term “pediatric” can be further be divided into various subpopulations including: neonates (from birth through the first month of life); infants (1 month up to two years of age); children (two years of age up to 12 years of age); and adolescents (12 years of age through 21 years of age (up to, but not including, the twenty-second birthday)). Berhman RE, Kliegman R, Arvin AM, Nelson WE. Nelson Textbook of Pediatrics, 15th Ed. Philadelphia: W.B. Saunders Company, 1996; Rudolph AM, et al. Rudolph’s Pediatrics, 21st Ed. New York: McGraw-Hill, 2002; and Avery MD, First LR. Pediatric Medicine, 2nd Ed. Baltimore: Williams & Wilkins; 1994. In some embodiments, a pediatric subject is from birth through the first 28 days of life, from 29 days of age to less than two years of age, from two years of age to less than 12 years of age, or 12 years of age through 21 years of age (up to, but not including, the twenty-second birthday). In some embodiments, a pediatric subject is from birth through the first 28 days of life, from 29 days of age to less than 1 year of age, from one month of age to less than four months of age, from three months of age to less than seven months of age, from six months of age to less than 1 year of age, from 1 year of age to less than 2 years of age, from 2 years of age to less than 3 years of age, from 2 years of age to less than seven years of age, from 3 years of age to less than 5 years of age, from 5 years of age to less than 10 years of age, from 6 years of age to less than 13 years of age, from 10 years of age to less than 15 years of age, or from 15 years of age to less than 22 years of age. The term “activating mutation” in reference to KRas describes a mutation in a KRas gene that results in the expression of a KRas protein that has decreased GTPase activity and/or increased effector activation activity, e.g., as compared to a wild type KRas protein, e.g., when assayed under identical conditions. For example, an activating mutation can be a mutation in a KRAS gene that results in the expression of a KRas protein that has one or more (e.g., two, three, four, five, six, seven, eight, nine, or ten) amino acid substitutions (e.g., any combination of any of the amino acid substitutions described herein) that has decreased GTPase activity, e.g., as compared to a wild type KRas protein, e.g., when assayed under identical conditions. In another example, an activating mutation can be a mutation in a KRAS gene that results in the expression of a KRas protein that has one or more (e.g., two, three, four, five, six, seven, eight, nine, or ten) amino acids deleted, e.g., as compared to a wild type KRas protein, e.g., when assayed under identical conditions. In another example, an activating mutation can be a mutation in a KRAS gene that results in the expression of a KRas protein that has at least one (e.g., at least 2, at least 3, at least 4, at least 5, at least 6, at least 7, at least 8, at least 9, at least 10, at least 12, at least 14, at least 16, at least 18, or at least 20) amino acid inserted as compared to a wild type KRas protein, e.g., the exemplary wild type KRas protein described herein, e.g., when assayed under identical conditions. Additional examples of activating mutations are known in the art. The term “preventing” as used herein means to delay the onset, recurrence or spread, in whole or in part, of the disease or condition as described herein, or a symptom thereof. The term “regulatory agency” refers to a country's agency for the approval of the medical use of pharmaceutical agents with the country. For example, a non-limiting example of a regulatory agency is the U.S. Food and Drug Administration (FDA). The phrase “therapeutically effective amount” means an amount of compound that, when administered to a subject in need of such treatment, is sufficient to (i) treat a KRas- associated disease or disorder (e.g., a mutant KRas-associated disease or disorder (e.g., a KRas G12D-associated cancer, a KRas G12R-associated cancer, or a KRas G12V-associated cancer (e.g., a KRas G12D-associated cancer or a KRas G12V-associated cancer)), (ii) attenuate, ameliorate, or eliminate one or more symptoms of the particular disease, disorder, or condition, or (iii) delay the onset of one or more symptoms of the particular disease, disorder, or condition described herein. The amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, that will correspond to such an amount will vary depending upon factors such as the particular compound, disease condition and its severity, the identity (e.g., weight) of the subject in need of treatment. As used herein, an “effective amount” refers to an amount of the compound sufficient to effect a beneficial or desired result. For example, an “effective amount” as used herein can refer to an amount of the compound sufficient to modulate (e.g., increase or decrease) (1) activity or amount of a protein; (2) proliferation of a cell (e.g., a cancer cell); and/or (3) one or more cellular signaling pathways associated with a protein’s activity. Pharmaceutical Compositions and Administration General In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, is administered as a pharmaceutical composition that includes the compound, or a pharmaceutically acceptable salt thereof, and one or more pharmaceutically acceptable excipients, and optionally one or more additional therapeutic agents as described herein. In some embodiments, the compounds provided herein, or pharmaceutically acceptable salts thereof, can be administered in combination with one or more conventional pharmaceutical excipients. Pharmaceutically acceptable excipients include, but are not limited to, ion exchangers, alumina, aluminum stearate, lecithin, self-emulsifying drug delivery systems (SEDDS) such as d-α-tocopherol polyethylene glycol 1000 succinate, surfactants used in pharmaceutical dosage forms such as Tweens, poloxamers or other similar polymeric delivery matrices, serum proteins, such as human serum albumin, buffer substances such as phosphates, tris, glycine, sorbic acid, potassium sorbate, partial glyceride mixtures of saturated vegetable fatty acids, water, salts or electrolytes, such as protamine sulfate, disodium hydrogen phosphate, potassium hydrogen phosphate, sodium-chloride, zinc salts, colloidal silica, magnesium trisilicate, polyvinyl pyrrolidone, cellulose-based substances, polyethylene glycol, sodium carboxymethyl cellulose, polyacrylates, waxes, polyethylene-polyoxypropylene-block polymers, and wool fat. Cyclodextrins such as α-, -, and γ-cyclodextrin, or chemically modified derivatives such as hydroxyalkylcyclodextrins, including 2- and 3-hydroxypropyl-β- cyclodextrins, or other solubilized derivatives can also be used to enhance delivery of compounds described herein. Dosage forms or compositions containing a compound provided herein, or a pharmaceutically acceptable salt thereof, as described herein in the range of 0.005% to 100% with the balance made up from non-toxic excipient may be prepared. The contemplated compositions may contain 0.001%-100% of a compound provided herein, or a pharmaceutically acceptable salt thereof, provided herein, in one embodiment 0.1-95%, in another embodiment 75-85%, in a further embodiment 20-80%. Actual methods of preparing such dosage forms are known, or will be apparent, to those skilled in this art; for example, see Remington: The Science and Practice of Pharmacy, 22^nd Edition (Pharmaceutical Press, London, UK.2012). Routes of Administration and Composition Components In some embodiments, the compounds provided herein, or pharmaceutically acceptable salts thereof, or a pharmaceutical composition comprising a compound provided herein, or a pharmaceutically acceptable salt thereof , can be administered to a subject in need thereof by any accepted route of administration. Acceptable routes of administration include, but are not limited to, buccal, cutaneous, endocervical, endosinusial, endotracheal, enteral, epidural, interstitial, intra-abdominal, intra-arterial, intrabronchial, intrabursal, intracerebral, intracisternal, intracoronary, intradermal, intraductal, intraduodenal, intradural, intraepidermal, intraesophageal, intragastric, intragingival, intraileal, intralymphatic, intramedullary, intrameningeal, intramuscular, intraovarian, intraperitoneal, intraprostatic, intrapulmonary, intrasinal, intraspinal, intrasynovial, intratesticular, intrathecal, intratubular, intratumoral, intrauterine, intravascular, intravenous, nasal, nasogastric, oral, parenteral, percutaneous, peridural, rectal, respiratory (inhalation), subcutaneous, sublingual, submucosal, topical, transdermal, transmucosal, transtracheal, ureteral, urethral and vaginal. In certain embodiments, a preferred route of administration is parenteral (e.g., intratumoral). In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, as described herein, or a pharmaceutical composition thereof, can be administered orally to a subject in need thereof. Without being bound by any particular theory, it is believed that oral dosing (e.g., versus IV dosing) can be preferred by patients for convenience, perception of efficacy, and/or past experience. Compositions can be formulated for parenteral administration, e.g., formulated for injection via the intravenous, intramuscular, sub-cutaneous, or even intraperitoneal routes. Typically, such compositions can be prepared as injectables, either as liquid solutions or suspensions; solid forms suitable for use to prepare solutions or suspensions upon the addition of a liquid prior to injection can also be prepared; and the preparations can also be emulsified. The preparation of such formulations will be known to those of skill in the art in light of the present disclosure. The pharmaceutical forms suitable for injectable use include sterile aqueous solutions or dispersions; formulations including sesame oil, peanut oil, or aqueous propylene glycol; and sterile powders for the extemporaneous preparation of sterile injectable solutions or dispersions. In all cases the form must be sterile and must be fluid to the extent that it may be easily injected. It also should be stable under the conditions of manufacture and storage and must be preserved against the contaminating action of microorganisms, such as bacteria and fungi. The carrier also can be a solvent or dispersion medium containing, for example, water, ethanol, polyol (for example, glycerol, propylene glycol, and liquid polyethylene glycol, and the like), suitable mixtures thereof, and vegetable oils. The proper fluidity can be maintained, for example, by the use of a coating, such as lecithin, by the maintenance of the required particle size in the case of dispersion, and by the use of surfactants. The prevention of the action of microorganisms can be brought about by various antibacterial and antifungal agents, for example, parabens, chlorobutanol, phenol, sorbic acid, thimerosal, and the like. In many cases, it will be preferable to include isotonic agents, for example, sugars or sodium chloride. Prolonged absorption of the injectable compositions can be brought about by the use in the compositions of agents delaying absorption, for example, aluminum monostearate and gelatin. Sterile injectable solutions are prepared by incorporating the active compounds in the required amount in the appropriate solvent with various of the other ingredients enumerated above, as required, followed by filtered sterilization. Generally, dispersions are prepared by incorporating the various sterilized active ingredients into a sterile vehicle which contains the basic dispersion medium and the required other ingredients from those enumerated above. In the case of sterile powders for the preparation of sterile injectable solutions, the preferred methods of preparation are vacuum-drying and freeze-drying techniques, which yield a powder of the active ingredient, plus any additional desired ingredient from a previously sterile-filtered solution thereof. Intratumoral injections are discussed, e.g., in Lammers, et al., “Effect of Intratumoral Injection on the Biodistribution and the Therapeutic Potential of HPMA Copolymer-Based Drug Delivery Systems” Neoplasia.2006, 10, 788–795, doi: 10.1593/neo.06436. Pharmacologically acceptable excipients usable in the rectal composition as a gel, cream, enema, or rectal suppository, include, without limitation, any one or more of cocoa butter glycerides, synthetic polymers such as polyvinylpyrrolidone, PEG (like PEG ointments), glycerine, glycerinated gelatin, hydrogenated vegetable oils, poloxamers, mixtures of polyethylene glycols of various molecular weights and fatty acid esters of polyethylene glycol Vaseline, anhydrous lanolin, shark liver oil, sodium saccharinate, menthol, sweet almond oil, sorbitol, sodium benzoate, anoxid SBN, vanilla essential oil, aerosol, parabens in phenoxyethanol, sodium methyl p-oxybenzoate, sodium propyl p-oxybenzoate, diethylamine, carbomers, carbopol, methyloxybenzoate, macrogol cetostearyl ether, cocoyl caprylocaprate, isopropyl alcohol, propylene glycol, liquid paraffin, xanthan gum, carboxy-metabisulfite, sodium edetate, sodium benzoate, potassium metabisulfite, grapefruit seed extract, methyl sulfonyl methane (MSM) , lactic acid, glycine, vitamins, such as vitamin A and E and potassium acetate. In certain embodiments, suppositories can be prepared by mixing a compound provided herein, or a pharmaceutically acceptable salt thereof, with suitable non-irritating excipients or carriers such as cocoa butter, polyethylene glycol or a suppository wax which are solid at ambient temperature but liquid at body temperature and therefore melt in the rectum and release the active compound. In other embodiments, compositions for rectal administration are in the form of an enema. In other embodiments, the compounds described herein, or a pharmaceutical composition thereof, are suitable for local delivery to the digestive or GI tract by way of oral administration (e.g., solid or liquid dosage forms.). Solid dosage forms for oral administration include capsules, tablets, pills, powders, and granules. In such solid dosage forms, the compound provided herein, or a pharmaceutically acceptable salt thereof, is mixed with one or more pharmaceutically acceptable excipients, such as sodium citrate or dicalcium phosphate and/or: a) fillers or extenders such as starches, lactose, sucrose, glucose, mannitol, and silicic acid, b) binders such as, for example, carboxymethylcellulose, alginates, gelatin, polyvinylpyrrolidinone, sucrose, and acacia, c) humectants such as glycerol, d) disintegrating agents such as agar-agar, calcium carbonate, potato or tapioca starch, alginic acid, certain silicates, and sodium carbonate, e) solution retarding agents such as paraffin, f) absorption accelerators such as quaternary ammonium compounds, g) wetting agents such as, for example, cetyl alcohol and glycerol monostearate, h) absorbents such as kaolin and bentonite clay, and i) lubricants such as talc, calcium stearate, magnesium stearate, solid polyethylene glycols, sodium lauryl sulfate, and mixtures thereof. In the case of capsules, tablets and pills, the dosage form may also comprise buffering agents. Solid compositions of a similar type may also be employed as fillers in soft and hard-filled gelatin capsules using such excipients as lactose or milk sugar as well as high molecular weight polyethylene glycols and the like. In one embodiment, the compositions will take the form of a unit dosage form such as a pill or tablet and thus the composition may contain, along with a compound provided herein, or a pharmaceutically acceptable salt thereof, provided herein, a diluent such as lactose, sucrose, dicalcium phosphate, or the like; a lubricant such as magnesium stearate or the like; and a binder such as starch, gum acacia, polyvinylpyrrolidine, gelatin, cellulose, cellulose derivatives, or the like. In another solid dosage form, a powder, marume, solution or suspension (e.g., in propylene carbonate, vegetable oils, PEGs, poloxamer 124 or triglycerides) is encapsulated in a capsule (gelatin or cellulose base capsule). Unit dosage forms in which one or more compounds provided herein, or pharmaceutically acceptable salts thereof, provided herein or additional active agents are physically separated are also contemplated; e.g., capsules with granules (or tablets in a capsule) of each drug; two-layer tablets; two-compartment gel caps, etc. Enteric coated or delayed release oral dosage forms are also contemplated. Other physiologically acceptable compounds include wetting agents, emulsifying agents, dispersing agents or preservatives that are particularly useful for preventing the growth or action of microorganisms. Various preservatives are well known and include, for example, phenol and ascorbic acid. In certain embodiments the excipients are sterile and generally free of undesirable matter. These compositions can be sterilized by conventional, well-known sterilization techniques. For various oral dosage form excipients, such as tablets and capsules, sterility is not required. The USP/NF standard is usually sufficient. In certain embodiments, solid oral dosage forms can further include one or more components that chemically and/or structurally predispose the composition for delivery of the compound provided herein, or a pharmaceutically acceptable salt thereof, to the stomach or the lower GI; e.g., the ascending colon and/or transverse colon and/or distal colon and/or small bowel. Exemplary formulation techniques are described in, e.g., Filipski, K.J., et al., Current Topics in Medicinal Chemistry, 2013, 13, 776-802, doi: 10.2174/1568026611313070002. Examples include upper-GI targeting techniques, e.g., Accordion Pill (Intec Pharma), floating capsules, and materials capable of adhering to mucosal walls. Other examples include lower-GI targeting techniques. For targeting various regions in the intestinal tract, several enteric/pH-responsive coatings and excipients are available. These materials are typically polymers that are designed to dissolve or erode at specific pH ranges, selected based upon the GI region of desired drug release. These materials also function to protect acid labile drugs from gastric fluid or limit exposure in cases where the active ingredient may be irritating to the upper GI (e.g., hydroxypropyl methylcellulose phthalate series, Coateric (polyvinyl acetate phthalate), cellulose acetate phthalate, hydroxypropyl methylcellulose acetate succinate, Eudragit series (methacrylic acid–methyl methacrylate copolymers), and Marcoat). Other techniques include dosage forms that respond to local flora in the GI tract, Pressure-controlled colon delivery capsule, and Pulsincap. Ocular compositions can include, without limitation, one or more of any of the following: viscogens (e.g., Carboxymethylcellulose, Glycerin, Polyvinylpyrrolidone, Polyethylene glycol); Stabilizers (e.g., Pluronic (triblock copolymers), Cyclodextrins); Preservatives (e.g., Benzalkonium chloride, ETDA, SofZia (boric acid, propylene glycol, sorbitol, and zinc chloride; Alcon Laboratories, Inc.), Purite (stabilized oxychloro complex; Allergan, Inc.)). Topical compositions can include ointments and creams. Ointments are semisolid preparations that are typically based on petrolatum or other petroleum derivatives. Creams containing the selected active agent are typically viscous liquid or semisolid emulsions, often either oil-in-water or water-in-oil. Cream bases are typically water-washable, and contain an oil phase, an emulsifier, and an aqueous phase. The oil phase, also sometimes called the “internal” phase, is generally comprised of petrolatum and a fatty alcohol such as cetyl or stearyl alcohol; the aqueous phase usually, although not necessarily, exceeds the oil phase in volume, and generally contains a humectant. The emulsifier in a cream formulation is generally a nonionic, anionic, cationic, or amphoteric surfactant. As with other carriers or vehicles, an ointment base should be inert, stable, nonirritating, and non-sensitizing. In any of the foregoing embodiments, pharmaceutical compositions described herein can include one or more one or more of the following: lipids, interbilayer crosslinked multilamellar vesicles, biodegradable poly(D,L-lactic-co-glycolic acid) [PLGA]-based or poly anhydride-based nanoparticles or microparticles, and nanoporous particle-supported lipid bilayers. Dosages The dosages may be varied depending on the requirement of the patient, the severity of the condition being treated, and the particular compound being employed. Determination of the proper dosage for a particular situation can be determined by one skilled in the medical arts. The total daily dosage may be divided and administered in portions throughout the day or by means providing continuous delivery. In some embodiments, the compounds described herein are administered at a dosage of from about 0.001 mg/kg to about 500 mg/kg (e.g., from about 0.001 mg/kg to about 200 mg/kg; from about 0.01 mg/kg to about 200 mg/kg; from about 0.01 mg/kg to about 150 mg/kg; from about 0.01 mg/kg to about 100 mg/kg; from about 0.01 mg/kg to about 50 mg/kg; from about 0.01 mg/kg to about 10 mg/kg; from about 0.01 mg/kg to about 5 mg/kg; from about 0.01 mg/kg to about 1 mg/kg; from about 0.01 mg/kg to about 0.5 mg/kg; from about 0.01 mg/kg to about 0.1 mg/kg; from about 0.1 mg/kg to about 200 mg/kg; from about 0.1 mg/kg to about 150 mg/kg; from about 0.1 mg/kg to about 100 mg/kg; from about 0.1 mg/kg to about 50 mg/kg; from about 0.1 mg/kg to about 10 mg/kg; from about 0.1 mg/kg to about 5 mg/kg; from about 0.1 mg/kg to about 1 mg/kg; from about 0.1 mg/kg to about 0.5 mg/kg). Regimens The foregoing dosages can be administered on a daily basis (e.g., as a single dose or as two or more divided doses) or non-daily basis (e.g., every other day, every two days, every three days, once weekly, twice weeks, once every two weeks, once a month). In some embodiments, the period of administration of a compound described herein is for 1 day, 2 days, 3 days, 4 days, 5 days, 6 days, 7 days, 8 days, 9 days, 10 days, 11 days, 12 days, 13 days, 14 days, 3 weeks, 4 weeks, 5 weeks, 6 weeks, 7 weeks, 8 weeks, 9 weeks, 10 weeks, 11 weeks, 12 weeks, 4 months, 5 months, 6 months, 7 months, 8 months, 9 months, 10 months, 11 months, 12 months, or more. In a further embodiment, a period of during which administration is stopped is for 1 day, 2 days, 3 days, 4 days, 5 days, 6 days, 7 days, 8 days, 9 days, 10 days, 11 days, 12 days, 13 days, 14 days, 3 weeks, 4 weeks, 5 weeks, 6 weeks, 7 weeks, 8 weeks, 9 weeks, 10 weeks, 11 weeks, 12 weeks, 4 months, 5 months, 6 months, 7 months, 8 months, 9 months, 10 months, 11 months, 12 months, or more. In an embodiment, a therapeutic compound is administered to an individual for a period of time followed by a separate period of time. In another embodiment, a therapeutic compound is administered for a first period and a second period following the first period, with administration stopped during the second period, followed by a third period where administration of the therapeutic compound is started and then a fourth period following the third period where administration is stopped. In an aspect of this embodiment, the period of administration of a therapeutic compound followed by a period where administration is stopped is repeated for a determined or undetermined period of time. In a further embodiment, a period of administration is for 1 day, 2 days, 3 days, 4 days, 5 days, 6 days, 7 days, 8 days, 9 days, 10 days, 11 days, 12 days, 13 days, 14 days, 3 weeks, 4 weeks, 5 weeks, 6 weeks, 7 weeks, 8 weeks, 9 weeks, 10 weeks, 11 weeks, 12 weeks, 4 months, 5 months, 6 months, 7 months, 8 months, 9 months, 10 months, 11 months, 12 months, or more. In a further embodiment, a period of during which administration is stopped is for 1 day, 2 days, 3 days, 4 days, 5 days, 6 days, 7 days, 8 days, 9 days, 10 days, 11 days, 12 days, 13 days, 14 days, 3 weeks, 4 weeks, 5 weeks, 6 weeks, 7 weeks, 8 weeks, 9 weeks, 10 weeks, 11 weeks, 12 weeks, 4 months, 5 months, 6 months, 7 months, 8 months, 9 months, 10 months, 11 months, 12 months, or more. The term “acceptable” with respect to a formulation, composition, or ingredient, as used herein, means having no persistent detrimental effect on the general health of the subject being treated. “API” refers to an active pharmaceutical ingredient. The term “excipient” or “pharmaceutically acceptable excipient” means a pharmaceutically acceptable material, composition, or vehicle, such as a liquid or solid filler, diluent, carrier, solvent, or encapsulating material. In one embodiment, each component is “pharmaceutically acceptable” in the sense of being compatible with the other ingredients of a pharmaceutical formulation, and suitable for use in contact with the tissue or organ of humans and animals without excessive toxicity, irritation, allergic response, immunogenicity, or other problems or complications, commensurate with a reasonable benefit/risk ratio. See, e.g., Remington: The Science and Practice of Pharmacy, 21st ed.; Lippincott Williams & Wilkins: Philadelphia, PA, 2005; Handbook of Pharmaceutical Excipients, 6th ed.; Rowe et al., Eds.; The Pharmaceutical Press and the American Pharmaceutical Association: 2009; Handbook of Pharmaceutical Additives, 3rd ed.; Ash and Ash Eds.; Gower Publishing Company: 2007; Pharmaceutical Preformulation and Formulation, 2nd ed.; Gibson Ed.; CRC Press LLC: Boca Raton, FL, 2009. The term “pharmaceutically acceptable salt” refers to a formulation of a compound that does not cause significant irritation to an organism to which it is administered and does not abrogate the biological activity and properties of the compound. In certain instances, pharmaceutically acceptable salts are obtained by reacting a compound described herein, with acids such as hydrochloric acid, hydrobromic acid, sulfuric acid, nitric acid, phosphoric acid, methanesulfonic acid, ethanesulfonic acid, p-toluenesulfonic acid, salicylic acid, and the like. In some instances, pharmaceutically acceptable salts are obtained by reacting a compound having acidic group described herein with a base to form a salt such as an ammonium salt, an alkali metal salt, such as a sodium or a potassium salt, an alkaline earth metal salt, such as a calcium or a magnesium salt, a salt of organic bases such as dicyclohexylamine, N-methyl-D- glucamine, tris(hydroxymethyl)methylamine, and salts with amino acids such as arginine, lysine, and the like, or by other methods previously determined. The term “pharmacologically acceptable salts” is not specifically limited as far as it can be used in medicaments. Examples of a salt that the compounds described herein form with a base include the following: salts thereof with inorganic bases such as sodium, potassium, magnesium, calcium, and aluminum; salts thereof with organic bases such as methylamine, ethylamine, and ethanolamine; salts thereof with basic amino acids such as lysine and ornithine; and ammonium salt. The salts may be acid addition salts, which are specifically exemplified by acid addition salts with the following: mineral acids such as hydrochloric acid, hydrobromic acid, hydroiodic acid, sulfuric acid, nitric acid, and phosphoric acid:organic acids such as formic acid, acetic acid, propionic acid, oxalic acid, malonic acid, succinic acid, fumaric acid, maleic acid, lactic acid, malic acid, tartaric acid, citric acid, methanesulfonic acid, and ethanesulfonic acid; acidic amino acids such as aspartic acid and glutamic acid. In some embodiments, a pharmaceutically acceptable salt is an anion salt selected from the group consisting of: a mesylate salt, a besylate salt, an acetate salt, a benzenesulfonate salt, a benzoate salt, a bicarbonate salt, a bitartrate salt, a bromide salt, a calcium edetate salt, a camsylate salt, a carbonate salt, a chloride salt, a citrate salt, a dihydrochloride salt, an edetate salt, an edisylate salt, an estolate salt, an esylate salt, a fumarate salt, a gluceptate salt, a gluconate salt, a glucuronate salt, a glutamate salt, a glycollylarsanilate salt, a hexylresorcinol salt, a hydramine salt, a hydrobromide salt, a hydrochloride salt, a hydroxynaphthoate salt, an iodide salt, an isethionate salt, a lactate salt, a lactobionate salt, a malate salt, a maleate salt, a mandelate salt, a mesylate salt, a methylbromide salt, a methylnitrate salt, a methylsulfate salt, a mucate salt, a napsylate salt, a nitrate salt, a pamoate (embonate) salt, a pantothenate salt, a phosphate/diphosphate salt, a polygalacturonate salt, a salicylate salt, a stearate salt, a subacetate salt, a succinate salt, a sulfate salt, an oleate salt, a tannate salt, a tartrate salt, a teoclate salt, and a triethiodide salt. In some embodiments, a pharmaceutically acceptable salt is a cation salt selected from the group consisting of: a benzathine salt, a chloroprocaine salt, a choline salt, a tromethamine salt, a diethanolamine salt, an ethylenediamine salt, a meglumine salt, a procaine salt, an aluminum salt, a calcium salt, a lithium salt, a magnesium salt, a potassium salt, a sodium salt, and a zinc salt. Examples of pharmaceutically acceptable salts also include those disclosed in e.g., Berge, Stephen M., Lyle D. Bighley, and Donald C. Monkhouse. "Pharmaceutical salts." Journal of pharmaceutical sciences 66.1 (1977): 1-19 doi: 10.1002/jps.2600660104, Bharate, Sonali S. "Recent developments in pharmaceutical salts: FDA approvals from 2015 to 2019." Drug Discovery Today 26.2 (2021): 384-398 doi: 10.1016/j.drudis.2020.11.016, and Bharate, Sonali S. "Modulation of biopharmaceutical properties of drugs using sulfonate counterions: A critical analysis of FDA-approved pharmaceutical salts." Journal of Drug Delivery Science and Technology 66 (2021): 102913 doi: 10.1016/j.jddst.2021.102913. The term “pharmaceutical composition” refers to a mixture of a compound described herein with other chemical components (referred to collectively herein as “excipients”), such as carriers, stabilizers, diluents, dispersing agents, suspending agents, and/or thickening agents. The pharmaceutical composition facilitates administration of the compound to a subject. Multiple techniques of administering a compound exist in the art including, but not limited to: rectal, oral, intravenous, aerosol, parenteral, ophthalmic, pulmonary, and topical administration. Compound Preparation The compounds disclosed herein can be prepared in a variety of ways using commercially available starting materials, compounds known in the literature, or from readily prepared intermediates, by employing standard synthetic methods and procedures either known to those skilled in the art, or in light of the teachings herein. Standard synthetic methods and procedures for the preparation of organic molecules and functional group transformations and manipulations can be obtained from the relevant scientific literature or from standard textbooks in the field. Although not limited to any one or several sources, classic texts such as R. Larock, Comprehensive Organic Transformations, VCH Publishers (1989); L. Fieser and M. Fieser, Fieser and Fieser's Reagents for Organic Synthesis, John Wiley and Sons (1994); Smith, M. B., March, J., March' s Advanced Organic Chemistry: Reactions, Mechanisms, and Structure, 5th edition, John Wiley & Sons: New York, 2001 ; and Greene, T.W., Wuts, P.G. M., Protective Groups in Organic Synthesis, 3rd edition, John Wiley & Sons: New York, 1999, are useful and recognized reference textbooks of organic synthesis known to those in the art. The following descriptions of synthetic methods are designed to illustrate, but not to limit, general procedures for the preparation of compounds of the present disclosure. The synthetic processes disclosed herein can tolerate a wide variety of functional groups; therefore, various substituted starting materials can be used. The processes generally provide the desired final compound at or near the end of the overall process, although it may be desirable in certain instances to further convert the compound to a pharmaceutically acceptable salt thereof. Scheme 1 depicts exemplary methods for preparing compounds of Formula (I): Scheme 1 Compounds of Formula (SI), wherein Ring B, Y², and R³ are as defined for Formula (I), are reacted with compounds having the formula R¹-H, wherein R¹ is as defined for Formula (I), to provide compounds of Formula (I). In some embodiments, compounds of Formula (SI) are reacted with compounds having formula R¹-H under Condition (I). Condition (I): To a solution of a compound of Formula (SI) (1.0 equiv.) in an appropriate solvent such as N,N-dimethylformamide or ethanol (e.g., at 0.2 M) and an appropriate base such as N-ethyl-N-isopropylpropan-2-amine (e.g., at 3.0 equiv) is added R¹- H (e.g., at 1.5-3.0 equiv.). The reaction mixture is stirred at an elevated temperature (e.g., at 100 ^oC for 2 hours) and then quenched with ice to provide a compound of Formula (I) after appropriate workup and purification condition (e.g., quenching with ice followed by filtration and/or column chromatography). Compounds of Formula (SI) are synthesized using e.g., methods described in Example P. Scheme 2 depicts exemplary methods for preparing compounds of Formula (I-a1): Scheme 2 (4-Chloro-6-methyl-2-(methylthio)pyrimidin-5-yl)methanol is treated with a base (e.g., LDA (e.g., in THF at -78^oC)), followed by a compound of Formula (SV-a1) to provide an intermediate which is converted into a compound of Formula (SIV-a1) under appropriate conditions (e.g., H₃PO₄ in toluene under reflux; or TPP and DIAD in THF; or TsCl and nBuLi in THF), wherein X¹, X², X³, b1, and R¹⁰ are as defined for Formula (I-a1); and X is halo (e.g., -Br). A compound of Formula (SIV-a1) is then reacted with R¹-H, wherein R¹ is as defined for Formula (I-a1) (e.g., R¹ is attached to the pyrimidine ring via a nitrogen atom), to provide a compound of Formula (SIII-a1) under appropriate conditions (e.g., in the presence of a base (e.g., triethylamine or N,N-diisopropylethylamine) in an appropriate solvent (e.g., EtOH, 1,4- dioxane, or DMF)). A compound of Formula (SIII-a1) is then reacted with a compound having Formula R⁹-H, wherein R⁹ is as defined for Formula (I-a1), to provide a compound of Formula (SII-a1) under appropriate conditions (e.g., in the presence of a palladium catalyst and optionally a ligand and/or a base (e.g., Pd(OAc)₂, Xantphos, Cs₂CO₃, in 1,4-dioxane at 80 ^oC; or BrettPhos Pd G4, Cs₂CO₃, in 1,4-dioxane at 80 ^oC)). Subsequently, the thioether group in the compound of Formula (SII-a1) is oxidized (e.g., with Oxone or mCPBA). This is followed by coupling with R³-Y²-OH, wherein R³ and Y² are as defined for Formula (I-a1), to provide a compound of Formula (I-a1). Variations to the reaction sequence in Scheme 2 are also contemplated. For example, to provide certain compounds of Formula (I-a1) wherein R⁹ is halo, step d in Scheme 2 may be bypassed (i.e., compounds of Formula (SIII-a1) are reacted with R³-Y²-OH under steps e and f). For example, in the preparation of certain compounds of Formula (I-a1) wherein R⁹ is NH₂, the R⁹ group can be protected with one or two nitrogen protecting groups (e.g., the NH₂ can be protected as NBn₂ or NHBoc) during the reaction sequence e.g., in Formula (SII-a1) and/or R⁹-H of step d, followed by the appropriate deprotection steps (e.g., HCl in 1,4-dioxane for NHBoc group; or Pd(OAc)₂/H₂ for NBn₂). Representative examples of nitrogen protecting groups include: acetyl (Ac), benzoyl (Bz), benzyl (Bn), benzyloxycarbonyl (Cbz), formyl, phenylsulfonyl, pivaloyl, tert-butoxycarbonyl (Boc), tert-butyl acetyl, ethyloxycarbonyl, trifluoroacetyl, triphenylmethyl (trityl), and triisopropylsilane. See: T. W. Greene and P. G. M. Wuts in “Protective groups in organic chemistry” John Wiley and Sons, 4th Edition, 2006. A person of ordinary skill in the art would understand that the final product and/or intermediates in Scheme 2 can be subjected to standard functional group transformation(s) to provide additional examples of compounds of Formula (I-a1). For example, a compound of Formula (I-a1) as provided in Scheme 2 can be converted into a second compound of Formula (I-a1) having a different R⁹ group. For example, a compound of Formula (I-a1) wherein R⁹ is -NHC(O)O^tBu can be converted into a second compound of Formula (I-a1) wherein R⁹ is - NH₂ upon treatment with an acid (e.g., HCl in 1,4-dioxane). Scheme 3 depicts an exemplary method for synthesizing certain intermediates useful in the preparation of compounds of Formula (I) (e.g., Formula (I-a1)): Scheme 3 Compound G10 is reacted with compound G11 to provide compound G12 under appropriate conditions (e.g., in the presence of a palladium catalyst (e.g., Pd(OAc)₂, LiCl, LiOAc, tetrabutylammonium chloride), wherein R⁹, b1, and R¹⁰ are as defined for Formula (I) (e.g., Formula (I-a1)) (e.g., R⁹ is halo such as -Br); and X³ is CH₂, CHR^L, or C(R^L)₂ wherein R^L is as defined for Formula (I) (e.g., Formula (I-a1)) (e.g., X³ is CH₂ or CHR^L). The aldehyde group in compound G12 is subsequently oxidized (e.g., under Pinnick oxidation conditions (e.g., with NaClO2, NaH2PO4)). The oxidized product is then cyclized to provide compound G13 (e.g., with AlCl₃, oxalyl chloride, DMF). EXAMPLES In some of the examples disclosed herein, one or more compounds in a described chemical reaction sequence (e.g., starting materials, intermediates, or products) is structurally depicted with enhanced stereochemical notation(s) at one or more defined stereogenic center(s). Examples of such notations include or1, or2, &1, &2, and the like. In some such examples, in the chemical name of the same compound, each of such defined stereogenic center(s) is assigned a tentative configuration (e.g., (R)- or (S)-) shown by the wedge/hash representation of its structural formula. However, the defined stereogenic center(s) should be understood to have configurations consistent with the enhanced stereochemical notation(s), as described herein, based e.g., on the conventions explained below. For avoidance of doubt, the chemical names of these compounds, having one or more enhanced stereochemical notation(s), adopt the following conventions: When the chemical name of a compound having only one stereogenic center contains the prefix “rel,” the stereogenic center is resolved, but its absolute configuration is either (R) or (S), thereby corresponding to an or1 enhanced stereochemical notation at the corresponding stereogenic center in its structural formula. For example, the chemical name rel-(R)-(1- methylpyrrolidin-2-yl)methanol represents one stereoisomer selected from the group consisting of: and . When one stereogenic center is labelled with an asterisk (“*”) in the chemical name of a compound having more than one stereogenic centers (e.g., when a stereogenic center is denoted as (R*)), the stereogenic center labeled with the asterisk is resolved, but its absolute configuration is either (R) or (S), thereby corresponding to an or1 enhanced stereochemical notation at the corresponding stereogenic center in its structural formula. For example, the chemical name ((2R*,4R)-1,4-dimethylpyrrolidin-2-yl)methanol represents one stereoisomer selected from the group consisting of: and . When the chemical name of a compound contains two stereogenic centers labelled with asterisks, these two stereogenic centers may have (R) or (S) configurations, either concertedly or independently, in conformity with the orx (e.g., or1 or or2) notations in its structural formula in Table C1. When two stereogenic centers are labelled or1 and or1 in a compound structure, and they are labelled with asterisks in the chemical name, then the relative stereochemistry between the two stereogenic centers (e.g., syn or anti relationship) is as represented by the name, but the absolute configurations of the two stereogenic centers can vary concertedly (e.g., a compound designated (R*,R*) is one stereoisomer selected from (R,R) and (S,S); for avoidance of doubt, the compound designated (R*,R*) does not have (S,R) or (R,S) configurations across these stereogenic centers). For example, the chemical name of is ((2R*,3S,4R*)- 3-cyclopropyl-1,4-dimethylpyrrolidin-2-yl)methanol. This name, taken together with the structural formula, represents one stereoisomer selected from the group consisting of: and . When two stereogenic centers are labelled or1 and or2 in a compound structure, and they are labelled with asterisks in the chemical name, then the configuration of the two stereogenic centers can vary independently (e.g., a compound designated (R*,R*) is one stereoisomer selected from (R,R), (S,S), (R,S), and (S,R)). For example, the chemical name of is ((2R*,3S,4R*)-3-cyclopropyl-1,4-dimethylpyrrolidin-2-yl)methanol. This name, taken together with the structural formula, represents one stereoisomer selected from the group consisting of: , , ,and . When the chemical name of a compound having only one stereogenic center contains the prefix “rac,” a mixture of enantiomers (e.g., racemic mixture) is provided, thereby corresponding to an &1 enhanced stereochemical notation at the corresponding stereogenic center in its structural formula. For example, the chemical name rac-(R)-(1-methylpyrrolidin- 2-yl)methanol represents a mixture of: and . When one stereogenic center is designated “RS” or “SR” in the chemical name of a compound having more than one stereogenic centers, a mixture of stereoisomers differing at this stereogenic center is provided, thereby corresponding to an &1 enhanced stereochemical notation at the corresponding stereogenic center in its structural formula. For example, the chemical name ((2RS,4R)-1,4-dimethylpyrrolidin-2-yl)methanol (corresponding to ) represents a mixture of: and . When the chemical name of a compound contains two stereogenic centers designated “RS” and/or “SR,” a mixture of stereoisomers is provided wherein among the constituent stereoisomers these two stereogenic centers differ either concertedly or independently, in conformity with the &x (e.g., &1 or &2) notations in Table C1 for the corresponding compound. When two defined stereogenic centers are labelled &1 and &1 in a chemical structure, and they are designated “RS” and/or “SR” in the corresponding chemical name, then a mixture of two stereoisomers is provided, wherein each constituent stereoisomer has the relative stereochemistry between these two stereogenic centers (e.g., syn or anti relationship) as depicted by the structural formula and by the name. As an example, a chemical name designated (RS,SR) represents a mixture of (R,S) and (S,R) stereoisomers, and this mixture does not include (R,R) or (S,S) stereoisomers. As a second example, a chemical name designated (SR,SR) represents a mixture of (S,S) and (R,R) stereoisomers, and this mixture does not include (R,S) or (S,R) stereoisomers. For example, the chemical name of is ((2RS,3S,4RS)-3-cyclopropyl-1,4-dimethylpyrrolidin-2-yl)methanol. This name, taken together with the structural formula, represents a mixture of two stereoisomers: and . When two defined stereogenic centers are labelled &1 and &2 in a chemical structure, and they are designated “RS” and/or “SR” in the corresponding chemical name, then a mixture of four stereoisomers is provided each differing in configuration at one or both of these two stereogenic centers (e.g., a chemical name designated (RS,SR) represents a mixture of (R,S), (S,R), (R,R), and (S,S) stereoisomers). For example, the chemical name of is ((2RS,3S,4RS)-3-cyclopropyl-1,4-dimethylpyrrolidin-2-yl)methanol. This name, taken together with the structural formula, represents a mixture of four stereoisomers: , , , and . General Analytical Methods: Method A: VanGuard Pre-Column CSH C18, 1.7 μm, 2.1 × 5 mm, Pre-run: 1 mL/min for 0.7 minutes. Column: Acquity UPLC, CSH C18, 1.7 μm, 2.1 × 30 mm, Flow rate: 0.9 mL/min, 5 to 100% MeCN/ H₂O (+ 0.1% formic acid) for 3 minutes. Method B: VanGuard Pre-Column CSH C18, 1.7 μm, 2.1 × 5 mm, Pre-run: 1 mL/min for 0.7 minutes. Column: Acquity UPLC, CSH C18, 1.7 μm, 2.1 × 30 mm, Flow rate: 0.9 mL/min, 5 to 100% MeCN/ H₂O (+ 10 mM ammonium bicarbonate) for 3 minutes. Method C: Acquity UPLC, CSH C18, 1.7 μm, 2.1 × 30 mm, Mobile phase A: 0.1% formic acid in H₂O; Mobile phase B: 0.1% formic acid in MeCN (v/v); Gradient: 95% H₂O/5% MeCN linear to 5% H₂O/95% MeCN in 2.0 minutes, hold at 5% H₂O/95% MeCN to 2.50 minutes. Then 5% H₂O/95% MeCN linear to 95% H₂O/5% MeCN in 0.5 minutes. Flow rate: 0.6 mL/min. Method D: Acquity UPLC, CSH C18, 1.7 μm, 2.1 × 30 mm, Mobile phase A: 0.1% ammonium hydroxide in H₂O; Mobile phase B: 0.1% ammonium hydroxide in MeCN (v/v); Gradient: 95% H₂O/5% MeCN linear to 5% H₂O/95% MeCN in 2.0 minutes, hold at 5% H2O/95% MeCN to 2.50 minutes. Then 5% H2O/95% MeCN linear to 95% H2O/5% MeCN in 0.5 minutes. Flow rate: 0.6 mL/min. Method E: Acquity UPLC, CSH C18, 1.7 μm, 2.1 × 30 mm, Mobile phase A: 0.1% formic acid in H₂O; Mobile phase B: 0.1% formic acid in MeCN (v/v); Gradient: 95% H₂O/5% MeCN linear to 5% H₂O/95% MeCN in 4.0 minutes, hold at 5% H₂O/95% MeCN to 4.50 minutes. Then 5% H₂O/95% MeCN linear to 95% H₂O/5% MeCN in 0.5 minutes. Flow rate: 0.6 mL/min. Method F: Poroshell SB-C18, 4.6 × 150 mm, Mobile phase A: 0.1% TFA in H₂O (v/v), Mobile phase B: 0.1% TFA in MeCN (v/v), Gradient: 30-95% Mobile phase B over 15 minutes. Method G: Chiralpak IB-U (3.0 × 100 mm, 1.6 mM, P/N 81U83) Method H: Kinetex® EVO C182.1 × 30 mm 5 μm, Mobile phase A: 0.0375% TFA in H₂O (v/v), Mobile phase B: 0.01875% TFA in MeCN (v/v), Gradient: 95% H₂O/5% MeCN linear to 5% H₂O/95% MeCN in 0.6 minutes, hold at 5% H₂O/95% MeCN to 0.78 minutes. Flow rate: 2.0 mL/min. Then 5% H₂O/95% MeCN linear to 95% H₂O/5% MeCN in 0.02 minutes. Flow rate: 2.0 mL/min. Method I: VanGuard Pre-Column CSH C18, 1.7 μm, 3.0 × 50 mm, Pre-run: 0.65 mL/min for 2.5 minutes. Column: Acquity UPLC, CSH C18, 1.7 μm, 2.1 × 75 mm, Flow rate: 0.6 mL/min, 5 to 100% MeCN/ H₂O (+ 10 mM ammonium bicarbonate) for 7.5 minutes. Method J: Column: Chiralcel OD-3R (2.1 × 100 mm, 3 μm, P/N 14893); Mobile phase A = 0.1% v/v ammonium hydroxide in H₂O, 0.1% v/v ammonium hydroxide in MeCN; Gradient: 95% H₂O/5% MeCN linear to 5% H₂O/95% MeCN in 8.0 minutes, hold at 5% H₂O/95% MeCN to 9.00 minutes. Then 5% H₂O/95% MeCN linear to 95% H₂O/5% MeCN in 1.0 minute. Method K: Acquity UPLC, CSH C18, 1.7 μm, 2.1 x 30 mm, Mobile phase A: 0.1% TFA n H2O; Mobile phase B: 0.1% formic acid in MeCN (v/v); Gradient: 95% H2O/5% MeCN linear to 5% H2O/95% MeCN in 4.0 minutes, hold at 5% H2O/95% MeCN to 4.50 minutes. Then 5% H2O/95% MeCN linear to 95% H2O/5% MeCN in 0.5 minutes. Flow rate: 0.6 mL/min. Method L: Acquity UPLC, CSH C18, 1.7 μm, 2.1 × 30 mm, Mobile phase A: 0.1% TFA in H₂O; Mobile phase B: 0.1% TFA in MeCN (v/v); Gradient: 95% H₂O/5% MeCN linear to 5% H₂O/95% MeCN in 2.0 minutes, hold at 5% H₂O/95% MeCN to 2.50 minutes. Then 5% H₂O/95% MeCN linear to 95% H₂O/5% MeCN in 0.5 minutes. Flow rate: 0.6 mL/min. Method M: VanGuard Pre-Column CSH C18, 17 μm, 21 x 5 mm, Pre-run: 1mL/min for 07 min Column: Acquity UPLC, CSH C18, 17 μm, 21 x 30 mm, Flow rate: 09 mL/min, 5 to 100% MeCN/water (+ 10 mM ammonium bicarbonate) for 7 minutes. Table of Abbreviations: Example P. Preparation of Intermediates Intermediate 1: (4-Chloro-6-methyl-2-(methylthio)pyrimidin-5-yl)methanol To ethyl 4-chloro-6-methyl-2-(methylthio)pyrimidine-5-carboxylate (535 g, 2.17 mol) in toluene (1.5 L) and THF (1.5 L) at -14 °C was added DIBAL-H (4 L of 1.03 M in THF and 666 g of 25 wt% in toluene, 5.29 mol) over 66 minutes. The mixture was gradually warmed to 20 °C and held for 2 hours. This mixture was then added to potassium sodium tartrate tetrahydrate (4.5 kg, 15.9 mol) in water (9 L) at 2 °C over 15 minutes. Gas evolution and exotherm continued after the transfer was complete with a maximum internal temperature of 31 °C. Ethyl acetate (3.25 L) was added, and the layers were separated. The organic layer was washed with brine (4 L). The aqueous layers were extracted with ethyl acetate (3.25 L). The combined organic layers were dried over magnesium sulfate, filtered through a pad of Magnesol (380 g), and washed with ethyl acetate (1.5 L). The filtrate was concentrated to a solid, then triturated in ethyl acetate (800 mL) at 45-50 °C, diluted with n-heptane (2.4 L) over 20 minutes, and cooled to room temperature overnight. The slurry was filtered and washed with n-heptane, and the solids were dried under vacuum to afford (4-chloro-6-methyl-2- (methylthio)pyrimidin-5-yl)methanol (328 g, 1.60 mol) as a white solid. 1H NMR (400 MHz, CDCl₃) δ 4.80 (d, 2H), 2.64 (s, 3H), 2.59 (s, 3H), 1.90 (t, 1H). Intermediate 2: 7-Bromo-4'-chloro-2'-(methylthio)-3,4,5',8'-tetrahydro-2H- spiro[naphthalene-1,7'-pyrano[4,3-d]pyrimidine] Step 1: 7-Bromo-1-((6-chloro-5-(hydroxymethyl)-2-(methylthio)pyrimidin-4- yl)methyl)-1,2,3,4-tetrahydronaphthalen-1-ol To diisopropylamine (355 mL, 2.53 mol) in THF (3.5 L) at -28 °C was added nBuLi in hexanes (1 L, 2.5 M, 2.5 mol) over 24 minutes. The mixture was held at -16 to -26 °C for 10 minutes then cooled to -71 °C. (4-Chloro-6-methyl-2-(methylthio)pyrimidin-5-yl)methanol (255 g, 1.25 mol) in THF (1.4 L) was added over 45 minutes, rinsing with THF (100 mL) while maintaining the internal temperature below -66°C. The mixture was stirred for one hour at -70 °C, and then 7-bromo-3,4-dihydronaphthalen-1(2H)-one (280 g, 1.24 mol) in THF (1 L) was added over 37 minutes, maintaining the temperature below -70 °C. The mixture was allowed to warm to 2 °C over two hours and then quenched with ammonium chloride (500 g) in water (1.75 L). The layers were separated, and the organic layer was washed with brine (1.5 L). The aqueous layers were sequentially extracted with ethyl acetate (1 L). The combined organic layers were dried (MgSO₄) and then evaporated to a gummy residue. Dichloromethane (700 mL) was added, and the mixture was re-concentrated to a solid. The solid was triturated in dichloromethane (2 L) at 35°C for 20 minutes, cooled to 15 °C for 30 minutes, filtered, and washed with dichloromethane (400 mL). The solids were dried under vacuum at 35°C to afford 7-bromo-1-((6-chloro-5-(hydroxymethyl)-2-(methylthio)pyrimidin-4-yl)methyl)-1,2,3,4- tetrahydronaphthalen-1-ol (360 g, 0.84 mol) as a white solid. 1H NMR (400 MHz, CDCl₃) δ7.70 (s, 1H), 7.30 (d, 1H), 7.00 (d, 1H), 4.80-4.70 (m, 2H), 4.33 (s, 1H), 3.40-3.25 (m, 3H), 2.80 (t, 2H), 2.55 (s, 3H), 2.15-1.85 (m, 3H), 1.75-1.65 (m, 1H). Step 2: 7-Bromo-4'-chloro-2'-(methylthio)-3,4,5',8'-tetrahydro-2H- spiro[naphthalene-1,7'-pyrano[4,3-d]pyrimidine] 7-Bromo-1-((6-chloro-5-(hydroxymethyl)-2-(methylthio)pyrimidin-4-yl)methyl)- 1,2,3,4-tetrahydronaphthalen-1-ol (200 g, 465 mmol) was suspended in toluene (1 L, 5 vol). Phosphoric acid (86 wt%, 35 mL, 512 mmol) was added before heating the reaction to reflux for 27 hours. The solution was cooled to room temperature before adjusting the pH from 1 to 7 using 4 N NaOH (150 mL, 600 mmol). The reaction mixture was then diluted with ethyl acetate (500 mL, 2.5 vol) and water (500 mL, 2.5 vol). The phases were separated, and the organic phase washed further with brine (500 mL, 2.5 vol). The aqueous phases were sequentially back-extracted with ethyl acetate (500 mL, 2.5 vol). The organic phases were combined and dried over sodium sulfate and concentrated to a neat orange oil. The crude product was dissolved in EtOAc (140 mL, 1 vol) at 50 °C. Hexane (450 mL, 3 vol) was added to the solution over 5 minutes, and the resulting crystals were filtered and washed with EtOAc/hexane (1:4, 100 mL). This process was repeated three times to afford 7-bromo-4'- chloro-2'-(methylthio)-3,4,5',8'-tetrahydro-2H-spiro[naphthalene-1,7'-pyrano[4,3- d]pyrimidine] (113g, 274 mmol) as an off-white solid. 1H NMR (400 MHz, CDCl₃) δ7.55 (s, 1H), 7.35 (d, 1H), 7.05 (d, 1H), 4.80 (q, 2H), 3.15 (q, 2H), 2.90-2.78 (m, 2H), 2.60 (s, 3H), 2.07-1.92 (m, 3H), 1.85-1.70 (m, 1H). Intermediate 2a: (S)-7-Bromo-4'-chloro-2'-(methylthio)-3,4,5',8'-tetrahydro-2H- spiro[naphthalene-1,7'-pyrano[4,3-d]pyrimidine] The enantiomers of 7-bromo-4'-chloro-2'-(methylthio)-3,4,5',8'-tetrahydro-2H- spiro[naphthalene-1,7'-pyrano[4,3-d]pyrimidine] (5.0 g) were separated by chiral SFC (Chiralpak IB-N 21mm ID × 250 mm, 5μm (serial number IBS5MJ-BV001; MeOH, 40%, backpressure = 120 psi). The first eluting peak was isolated as Intermediate 2a (1.85 g). LCMS: m/z (ESI) [M+H]⁺ 413.0, t_R = 4.00 minutes (Method E ) Chiral HPLC: t_R = 4.78 minutes. (Method G; Gradient 5-40% MeOH over 10 minutes) 1H NMR (400 MHz, CDCl₃) δ 7.54 (d, 1H), 7.27 (dd, 1H), 6.93 (d, 1H), 4.70 (q, 2H), 3.17 – 2.85 (m, 2H), 2.82 – 2.61 (m, 2H), 2.50 (s, 3H), 1.99 – 1.79 (m, 3H), 1.78 – 1.62 (m, 1H). Intermediate 2b: (R)-7-Bromo-4'-chloro-2'-(methylthio)-3,4,5',8'-tetrahydro-2H- spiro[naphthalene-1,7'-pyrano[4,3-d]pyrimidine] The second eluting peak was isolated as Intermediate 2b (2.05 g). LCMS: m/z (ESI) [M+H]⁺ 413.0, t_R = 4.00 minutes (Method E) Chiral HPLC: t_R = 6.12 minutes. (Method G; Gradient 5-40% MeOH over 10 minutes) 1H NMR (400 MHz, CDCl₃) δ 7.61 (d, 1H), 7.34 (dd, 1H), 7.00 (d, 1H), 4.92 – 4.63 (m, 2H), 3.26 – 2.94 (m, 2H), 2.90 – 2.72 (m, 2H), 2.57 (s, 3H), 2.09 – 1.86 (m, 3H), 1.82 – 1.67 (m, 1H). Intermediate 3: tert-Butyl (2'-(((2R,7aS)-2-fluorotetrahydro-1H-pyrrolizin- 7a(5H)-yl)methoxy)-4'-oxo-3,3',4,4',5',8'-hexahydro-2H-spiro[naphthalene-1,7'- pyrano[4,3-d]pyrimidin]-7-yl)carbamate Step 1: 4'-(Benzyloxy)-7-bromo-2'-(methylthio)-3,4,5',8'-tetrahydro-2H- spiro[naphthalene-1,7'-pyrano[4,3-d]pyrimidine] Phenylmethanol (367 μL, 1.5 equiv., 3.53 mmol) was added to a suspension of sodium hydride (188 mg, 60% wt, 2 equiv., 4.71 mmol) in THF (6 mL). The mixture was stirred at room temperature for 5 minutes until gas evolution had ceased. A solution of 7-bromo-4'- chloro-2'-(methylthio)-3,4,5',8'-tetrahydro-2H-spiro[naphthalene-1,7'-pyrano[4,3- d]pyrimidine] (970 mg, 1 equiv., 2.36 mmol) in THF (6 mL) was added dropwise, and the reaction mixture was stirred for 1 hour. The mixture was cooled in an ice bath and quenched by the addition of saturated aqueous NH₄Cl (20 mL) and then extracted with EtOAc (2 × 50 mL). The combined organic phases were washed with brine (50 mL), dried over sodium sulfate, and concentrated to a solid which was triturated with ethanol (60 mL) (sonication was used to break up the material). The solid was separated by filtration, washed with ethanol (10 mL), and dried to yield 4'-(benzyloxy)-7-bromo-2'-(methylthio)-3,4,5',8'-tetrahydro-2H- spiro[naphthalene-1,7'-pyrano[4,3-d]pyrimidine] (1.05 g, 2.17 mmol). LCMS: m/z (ESI) [M+H]⁺ 485.1, t_R = 2.24 minutes (Method A) Step 2: tert-Butyl (4'-(benzyloxy)-2'-(methylthio)-3,4,5',8'-tetrahydro-2H- spiro[naphthalene-1,7'-pyrano[4,3-d]pyrimidin]-7-yl)carbamate A suspension of 4'-(benzyloxy)-7-bromo-2'-(methylthio)-3,4,5',8'-tetrahydro-2H- spiro[naphthalene-1,7'-pyrano[4,3-d]pyrimidine] (2.75 g, 1 equiv., 5.69 mmol), cesium carbonate (5.56 g, 3 equiv., 17.1 mmol), and tert-butyl carbamate (2.00 g, 3 equiv., 17.1 mmol) in 1,4-dioxane (80 mL) was degassed with nitrogen at room temperature for 5 minutes. BrettPhos Pd G4 (524 mg, 0.1 equiv., 0.57 mmol) was added, and nitrogen was bubbled through the mixture at room temperature for another 5 minutes. The reaction mixture was stirred for 5 hours, concentrated to a residue, and purified by flash chromatography (silica, 120 g silicycle cartridge, solid loading, gradient of EtOAc in DCM) to provide tert-butyl (4'- (benzyloxy)-2'-(methylthio)-3,4,5',8'-tetrahydro-2H-spiro[naphthalene-1,7'-pyrano[4,3- d]pyrimidin]-7-yl)carbamate (1.91 g) . LCMS: m/z (ESI) [M+H]+ 520.3, t_R = 2.14 minutes (Method A) Step 3: tert-Butyl (4'-(benzyloxy)-2'-(methylsulfonyl)-3,4,5',8'-tetrahydro-2H- spiro[naphthalene-1,7'-pyrano[4,3-d]pyrimidin]-7-yl)carbamate Tetrabutylammonium hydrogen sulfate (199 mg, 0.16 equiv., 0.59 mmol) and sodium tungstate dihydrate (121 mg, 0.1 equiv., 0.37 mmol) were added to a solution of tert-butyl (4'- (benzyloxy)-2'-(methylthio)-3,4,5',8'-tetrahydro-2H-spiro[naphthalene-1,7'-pyrano[4,3- d]pyrimidin]-7-yl)carbamate (1.90 g, 1 equiv., 3.66 mmol) in EtOAc (70 mL), and the temperature was raised to 40 °C. Hydrogen peroxide (2.61 mL, 30% wt, 7 equiv., 25.6 mmol) was added dropwise, and the reaction mixture was stirred for 100 minutes. The reaction mixture was diluted with EtOAc (100 mL), washed with water (100 mL) and brine (100 mL), dried over sodium sulfate, and concentrated. After the material was concentrated to dryness, DCM (20 mL) was added, and the resulting material was concentrated to dryness again to yield tert-butyl (4'-(benzyloxy)-2'-(methylsulfonyl)-3,4,5',8'-tetrahydro-2H-spiro[naphthalene-1,7'- pyrano[4,3-d]pyrimidin]-7-yl)carbamate (2.09 g). LCMS: m/z (ESI) [M+H]⁺ 552.2, t_R = 1.86 minutes (Method A) Step 4: tert-Butyl (4'-(benzyloxy)-2'-(((2R,7aS)-2-fluorotetrahydro-1H-pyrrolizin- 7a(5H)-yl)methoxy)-3,4,5',8'-tetrahydro-2H-spiro[naphthalene-1,7'-pyrano[4,3- d]pyrimidin]-7-yl)carbamate Sodium hydride (359 mg, 60% wt, 2.5 equiv., 8.97 mmol) was added to a solution of ((2R,7aS)-2-fluorotetrahydro-1H-pyrrolizin-7a(5H)-yl)methanol (1.43 g, 2.5 equiv., 8.97 mmol) in anhydrous THF (20 mL). This solution was stirred for 2 minutes until gas evolution had ceased, and then a solution of tert-butyl (4'-(benzyloxy)-2'-(methylsulfonyl)-3,4,5',8'- tetrahydro-2H-spiro[naphthalene-1,7'-pyrano[4,3-d]pyrimidin]-7-yl)carbamate (2.04 g, 1 equiv., 3.59 mmol) in anhydrous THF (20 mL) was added over 1 minute. The mixture was stirred for 2 hours at room temperature, and then water (20 mL) and brine (20 mL) were added. The mixture was extracted with DCM:MeOH 9:1 (3 ×100 mL). The combined organic phases were washed with brine (100 mL), dried over sodium sulfate, and concentrated to a residue which was purified by flash chromatography (silica, 120 g silicycle cartridge, gradient of DCM:MeOH:NH₄OH 85:13.5:1.5 in DCM) to yield tert-butyl (4'-(benzyloxy)-2'-(((2R,7aS)- 2-fluorotetrahydro-1H-pyrrolizin-7a(5H)-yl)methoxy)-3,4,5',8'-tetrahydro-2H- spiro[naphthalene-1,7'-pyrano[4,3-d]pyrimidin]-7-yl)carbamate (1.9 g). LCMS: m/z (ESI) [M+H]⁺ 631.5, t_R = 1.43 minutes (Method A) Step 5: tert-Butyl (2'-(((2R,7aS)-2-fluorotetrahydro-1H-pyrrolizin-7a(5H)- yl)methoxy)-4'-oxo-3,3',4,4',5',8'-hexahydro-2H-spiro[naphthalene-1,7'-pyrano[4,3- d]pyrimidin]-7-yl)carbamate tert-Butyl (4'-(benzyloxy)-2'-(((2R,7aS)-2-fluorotetrahydro-1H-pyrrolizin-7a(5H)- yl)methoxy)-3,4,5',8'-tetrahydro-2H-spiro[naphthalene-1,7'-pyrano[4,3-d]pyrimidin]-7- yl)carbamate (1.50 g, 1 equiv., 2.14 mmol) in methanol (60 mL) was added to Pd on carbon (114 mg, 10% wt, 0.05 equiv., 0.11 mmol). The mixture was degassed with nitrogen, and then hydrogen was bubbled through the mixture at room temperature for 5 minutes. The reaction mixture was stirred at room temperature for 2 hours and then purged with nitrogen, diluted with DCM (50 mL), and filtered through a syringe filter. The syringe filter was washed with DCM (3 × 10 mL). The combined liquid was concentrated to a residue which was purified by flash chromatography (silica, gradient of DCM:MeOH:NH₄OH 85:13.5:1.5 in DCM) to yield tert-butyl (2'-(((2R,7aS)-2-fluorotetrahydro-1H-pyrrolizin- 7a(5H)-yl)methoxy)-4'-oxo-3,3',4,4',5',8'-hexahydro-2H-spiro[naphthalene-1,7'-pyrano[4,3- d]pyrimidin]-7-yl)carbamate (1.13 g). LCMS: m/z (ESI) [M+H]⁺ 541.3, t_R = 1.04 minutes (Method A) 1H NMR (400 MHz, DMSO-d₆): δ 12.29 (s, 1H), 9.17 (s, 1H), 7.51 (s, 1H), 7.23 (d, 1 H), 6.97 (d, 1H), 5.26 (d, 1H), 4.37-4.24 (m, 2H), 4.03-3.92 (m, 2H), 3.12-2.95 (m, 3H), 2.82- 2.55 (m, 5H), 2.09-1.64 (m, 10H), 1.43 (s 9H). Intermediate 4: tert-Butyl ((S)-2'-(((2R,7aS)-2-fluorotetrahydro-1H-pyrrolizin- 7a(5H)-yl)methoxy)-4'-oxo-3,3',4,4',5',8'-hexahydro-2H-spiro[naphthalene-1,7'- pyrano[4,3-d]pyrimidin]-7-yl)carbamate Step 1: (S)-4'-(benzyloxy)-7-bromo-2'-(methylthio)-3,4,5',8'-tetrahydro-2H- spiro[naphthalene-1,7'-pyrano[4,3-d]pyrimidine] Phenylmethanol (1.05 mL, 1.5 equiv., 10.1 mmol) was added to a suspension of sodium hydride (540 mg, 60% wt dispersion in mineral oil, 2 equiv., 13.5 mmol) and stirred for 5 minutes at room temperature until gas evolution had ceased. A solution of (S)-7-bromo-4'- chloro-2'-(methylthio)-3,4,5',8'-tetrahydro-2H-spiro[naphthalene-1,7'-pyrano[4,3- d]pyrimidine] (2.78 g, 1 equiv., 6.75 mmol) in THF (12 mL) was added dropwise, resulting in the formation of a hazy solution. After 50 minutes, the mixture was cooled in an ice bath and quenched by addition of saturated aqueous NH₄Cl (40 mL), and the mixture was extracted with EtOAc (2 × 100 mL). The combined organic phases were washed with brine (50 mL), dried over anhydrous sodium sulfate, and concentrated to a residue which was purified by flash column chromatography [silica, 80 g silicycle cartridge, DCM in hexanes (0-100%)] yielding (S)-4'-(benzyloxy)-7-bromo-2'-(methylthio)-3,4,5',8'-tetrahydro-2H-spiro[naphthalene-1,7'- pyrano[4,3-d]pyrimidine] (3.13 g). LCMS: m/z (ESI) [M+H]⁺ 485.1, t_R = 2.25 minutes (Method A) 1H NMR (400 MHz, CDCl₃): δ7.62 (s, 1 H), 7.41-7.31 (m, 6 H), 6.98 (d, 1H), 5.51- 5.44 (m, 2 H), 4.78-4.65 (m, 2 H), 3.08-2.89 (m, 2 H), 2.78-2.75 (m, 2 H), 2.55 (s, 3 H), 1.97- 1.89 (m, 3 H), 1.76-1.73 (m, 1 H). Step 2: tert-Butyl (S)-(4'-(benzyloxy)-2'-(methylthio)-3,4,5',8'-tetrahydro-2H- spiro[naphthalene-1,7'-pyrano[4,3-d]pyrimidin]-7-yl)carbamate A suspension of (S)-4'-(benzyloxy)-7-bromo-2'-(methylthio)-3,4,5',8'-tetrahydro-2H- spiro[naphthalene-1,7'-pyrano[4,3-d]pyrimidine] (3.08 g, 1 equiv., 6.37 mmol), cesium carbonate (6.23 g, 3 equiv., 19.1 mmol), and tert-butyl carbamate (2.24 g, 3 equiv., 19.1 mmol) in 1,4-dioxane (90 mL) was degassed for 5 minutes. BrettPhos Pd G4 (587 mg, 0.1 equiv., 0.637 mmol) was added, and the mixture was degassed at room temperature for another 5 minutes and then stirred at 80 °C for 6 hours. The reaction mixture was concentrated to a residue which was purified by flash column chromatography [(silica, 120 g silicycle cartridge, gradient of EtOAc in DCM, (0-100%)] yielding tert-butyl (S)-(4'-(benzyloxy)-2'-(methylthio)- 3,4,5',8'-tetrahydro-2H-spiro[naphthalene-1,7'-pyrano[4,3-d]pyrimidin]-7-yl)carbamate (2.27 g). LCMS: m/z (ESI) [M+H]⁺ 520.3, t_R = 2.14 minutes (Method A) 1H NMR (400 MHz, CDCl₃): δ 7.44-7.30 (m, 7 H), 7.03 (d, 1 H), 6.37 (s, 1 H), 5.47 (s, 2 H), 4.74-4.64 (m, 2 H), 3.14-2.90 (m, 2 H), 2.79-2.76 (m, 2 H), 2.55 (s, 3 H), 1.97-1.91 (m, 3 H), 1.74-1.72 (m, 1 H), 1.49 (s, 9 H). Step 3: tert-Butyl (S)-(4'-(benzyloxy)-2'-(methylsulfonyl)-3,4,5',8'-tetrahydro-2H- spiro[naphthalene-1,7'-pyrano[4,3-d]pyrimidin]-7-yl)carbamate Tetrabutylammonium hydrogen sulfate (237 mg, 0.16 equiv., 0.70 mmol) and sodium tungstate dihydrate (144 mg, 0.1 equiv., 0.44 mmol) were added to a yellow solution of tert- butyl (S)-(4'-(benzyloxy)-2'-(methylthio)-3,4,5',8'-tetrahydro-2H-spiro[naphthalene-1,7'- pyrano[4,3-d]pyrimidin]-7-yl)carbamate (2.27 g, 1 equiv., 4.37 mmol) in EtOAc (90 mL), and the temperature was raised to 40 °C. Hydrogen peroxide (3.47 g, 3.12 mL, 30% wt, 7 equiv., 30.6 mmol) was added dropwise, and stirring was continued at 40 °C for 80 minutes. The crude reaction mixture was diluted with EtOAc (100 mL), washed with water (100 mL), brine (100 mL), dried over anhydrous sodium sulfate, and concentrated. DCM (20 mL) was added, and the material was concentrated to dryness twice to yield tert-butyl (S)-(4'-(benzyloxy)-2'- (methylsulfonyl)-3,4,5',8'-tetrahydro-2H-spiro[naphthalene-1,7'-pyrano[4,3-d]pyrimidin]-7- yl)carbamate (2.39 g), which was used without further purification. LCMS: m/z (ESI) [M-H]- 550.3, t_R = 1.86 minutes (Method A) 1H NMR (400 MHz, CDCl₃): δ 7.48-7.38 (m, 6 H), 7.19 (dd,1 H), 7.05 (d, 1H), 6.38 (s, 1H), 5.56 (s, 2H), 4.82-4.71 (m, 2H), 3.31-3.09 (m, 5H), 2.82-2.74 (m, 2H), 2.00-1.91 (m, 3H), 1.74-1.70 (m, 1H), 1.48 (s, 9H). Step 4: tert-Butyl ((S)-4'-(benzyloxy)-2'-(((2R,7aS)-2-fluorotetrahydro-1H- pyrrolizin-7a(5H)-yl)methoxy)-3,4,5',8'-tetrahydro-2H-spiro[naphthalene-1,7'- pyrano[4,3-d]pyrimidin]-7-yl)carbamate Sodium hydride (433 mg, 60% wt, dispersion in mineral oil, 2.5 equiv., 10.8 mmol) was added to a solution of ((2R,7aS)-2-fluorotetrahydro-1H-pyrrolizin-7a(5H)-yl)methanol (1.72 g, 2.5 equiv., 10.8 mmol) in anhydrous THF (24 mL) and stirred for 2 minutes at room temperature until gas evolution ceased. A solution of tert-butyl (S)-(4'-(benzyloxy)-2'- (methylsulfonyl)-3,4,5',8'-tetrahydro-2H-spiro[naphthalene-1,7'-pyrano[4,3-d]pyrimidin]-7- yl)carbamate (2.39 g, 1 equiv., 4.33 mmol) in anhydrous THF (24 mL) was added over 1 minute and stirred for 70 minutes. A mixture of water (20 mL) and brine (20 mL) was added, and the aqueous phase was extracted with DCM:MeOH 9:1 (3 × 100 mL). The combined organic phases were washed with brine (100 mL), dried over anhydrous sodium sulfate, filtered, and concentrated to a residue, which was purified using flash column chromatography (silica, 120 g silicycle cartridge, gradient of DCM:MeOH:NH₄OH 85:13.5:1.5/DCM (0-100%) to yield tert-butyl ((S)-4'-(benzyloxy)-2'-(((2R,7aS)-2-fluorotetrahydro-1H-pyrrolizin-7a(5H)- yl)methoxy)-3,4,5',8'-tetrahydro-2H-spiro[naphthalene-1,7'-pyrano[4,3-d]pyrimidin]-7- yl)carbamate (1.89 g). LCMS: m/z (ESI) [M+H]⁺ 631.5, t_R = 1.43 minutes (Method A) 1H NMR (400 MHz, CDCl₃): δ 7.36-7.22 (m, 7 H), 7.04 (d, 1H), 6.37 (s, 1H), 5.44 (s, 2H), 5.26 (d, 1H), 4.72-4.63 (m, 2 H), 4.16-4.02 (m, 2 H), 3.27-2.71 (m, 8 H), 2.27-2.12 (m, 3 H), 1.98-1.82 (m, 6 H), 1.74-1.70 (m, 1 H), 1.49 (s, 9 H). 1⁹F NMR (376 MHz, CDCl₃): δ -173.2. Step 5: tert-Butyl ((S)-2'-(((2R,7aS)-2-fluorotetrahydro-1H-pyrrolizin-7a(5H)- yl)methoxy)-4'-oxo-3,3',4,4',5',8'-hexahydro-2H-spiro[naphthalene-1,7'-pyrano[4,3- d]pyrimidin]-7-yl)carbamate Pd on carbon (159 mg, 10% wt, wet, 0.05 equiv., 0.15 mmol) was added to a degassed solution of tert-butyl ((S)-4'-(benzyloxy)-2'-(((2R,7aS)-2-fluorotetrahydro-1H-pyrrolizin- 7a(5H)-yl)methoxy)-3,4,5',8'-tetrahydro-2H-spiro[naphthalene-1,7'-pyrano[4,3-d]pyrimidin]- 7-yl)carbamate (1.89 g, 1 equiv., 3.00 mmol) in methanol (60 mL). The suspension was degassed for 5 minutes. Then hydrogen was bubbled through the mixture at room temperature for 5 minutes. The mixture was stirred at room temperature for 2 hours. The reaction mixture was purged with nitrogen, diluted with DCM (50 mL), and filtered. The solid was washed with DCM (3 × 10 mL), and the combined filtrates were concentrated under reduced pressure to yield tert-butyl ((S)-2'-(((2R,7aS)-2-fluorotetrahydro-1H-pyrrolizin-7a(5H)-yl)methoxy)-4'- oxo-3,3',4,4',5',8'-hexahydro-2H-spiro[naphthalene-1,7'-pyrano[4,3-d]pyrimidin]-7- yl)carbamate (1.62 g). LCMS: m/z (ESI) [M+H]⁺ 541.3, tR = 1.05 minutes (Method A) 1H NMR (400 MHz, DMSO-d₆): δ 12.29 (s, 1H), 9.17 (s, 1H), 7.51 (s, 1H), 7.23 (dd, 1H), 6.97 (d, 1H), 5.26 (d, 1H), 4.38-4.24 (m, 2H), 4.03-3.92 (m, 2H), 3.13-2.96 (m, 3H), 2.81-2.54 (m, 5H), 2.09-1.63 (m, 10H), 1.43 (s, 9 H). 1⁹F NMR (376 MHz, DMSO-d₆): δ -172.0. Intermediate 5: tert-Butyl ((S)-4'-((1H-benzo[d][1,2,3]triazol-1-yl)oxy)-2'- (((2R,7aS)-2-fluorotetrahydro-1H-pyrrolizin-7a(5H)-yl)methoxy)-3,4,5',8'-tetrahydro- 2H-spiro[naphthalene-1,7'-pyrano[4,3-d]pyrimidin]-7-yl)carbamate ((1H-benzo[d][1,2,3]triazol-1-yl)oxy)tris(dimethylamino)phosphonium hexafluorophosphate(V) (972 mg, 1.1 equiv., 2.20 mmol) was slowly added to a solution of tert-butyl ((S)-2'-(((2R,7aS)-2-fluorotetrahydro-1H-pyrrolizin-7a(5H)-yl)methoxy)-4'-oxo- 3,3',4,4',5',8'-hexahydro-2H-spiro[naphthalene-1,7'-pyrano[4,3-d]pyrimidin]-7-yl)carbamate (1.08 g, 1 equiv., 2.00 mmol) and N-ethyl-N-isopropylpropan-2-amine (516 mg, 2 equiv., 4.00 mmol) in DMF (20 mL). The resulting colorless solution was stirred at room temperature for 3 hours. The mixture was poured into water (20 mL) and stirred for 5 minutes. The resulting precipitate was removed by filtration, washed with water (3 × 10 mL) and dried under vacuum to yield tert-butyl ((S)-4'-((1H-benzo[d][1,2,3]triazol-1-yl)oxy)-2'-(((2R,7aS)-2- fluorotetrahydro-1H-pyrrolizin-7a(5H)-yl)methoxy)-3,4,5',8'-tetrahydro-2H- spiro[naphthalene-1,7'-pyrano[4,3-d]pyrimidin]-7-yl)carbamate (1.19 g). LCMS: m/z (ESI) [M+H]⁺ 658.4, t_R = 1.37 minutes (Method A). 1H NMR (400 MHz, DMSO-d₆): δ 9.23 (s, 1H), 8.18 (d, 1H), 7.86 (d, 1H), 7.62-7.67 (m, 2H), 7.53 (t, 1H), 7.23 (dd, 1H), 7.02 (d, 1H), 5.12 (s, 1H), 4.91 (t, 2H), 3.49-3.61 (m, 2H), 2.97-3.09 (m, 2H), 2.87 (d, 1H), 2.80-2.82 (m, 1H), 2.76-2.79 (m, 1H), 2.71-2.74 (m, 2H), 2.62-2.68 (m, 2H), 1.99 (s, 2H), 1.90 (br s, 1H), .85-1.68 (m, 3H), 1.64 (dd, 2H), 1.50- 1.58 (m, 1H), 1.40-1.43 (m, 9H). 1⁹F NMR (376 MHz, DMSO-d₆): F -172.46 to -171.99 (m). Intermediate 6: N,N-Dibenzyl-8-bromo-4'-chloro-2'-(methylthio)-3,4,5',8'- tetrahydro-2H-spiro[naphthalene-1,7'-pyrano[4,3-d]pyrimidin]-7-amine Step 1: 7-Amino-8-bromo-3,4-dihydronaphthalen-1(2H)-one A solution of 1-bromopyrrolidine-2,5-dione (2.86 g, 1 equiv., 16.1 mmol) in DMF (20 mL) was added dropwise to a solution of 7-amino-3,4-dihydronaphthalen-1(2H)-one (2.59 g, 1 equiv., 16.1 mmol) in DMF (20 mL) at 0 ^oC. The resulting mixture was stirred for 4 hours at room temperature and then poured into water. The mixture was extracted with DCM three times, and the combined extracts were washed with water. The combined organic phases were dried over sodium sulfate and passed through a Celite pad. The filtrate was concentrated to a residue which was purified by column chromatography (80 g, 0-20% hexane/EtOAc) to afford 7-amino-8-bromo-3,4-dihydronaphthalen-1(2H)-one (3.31 g). LCMS: m/z (ESI) [M+H]⁺ 239.9, t_R = 1.02 minutes (Method A). 1H NMR (400 MHz, CDCl₃): δ 7.01 (d, 1H), 6.88 (d, 1H), 4.30 (s, 2 H), 2.86 (t, 2 H), 2.66 (t, 2H), 2.03-2.09 (m, 2 H). Step 2: 8-Bromo-7-(dibenzylamino)-3,4-dihydronaphthalen-1(2H)-one Potassium carbonate (5.36 g, 3.5 equiv., 38.8 mmol) was added to 7-amino-8-bromo- 3,4-dihydronaphthalen-1(2H)-one (2.66 g, 1 equiv., 11.1 mmol) in anhydrous DMF (55.4 mL) followed by the dropwise addition of (bromomethyl)benzene (4.71 mL, 3.5 equiv., 38.8 mmol) at room temperature. The resulting mixture was stirred at 70 ^oC for 16 hours. Water was added, and the aqueous layer was extracted with EtOAc three times. The combined extracts were washed with brine, dried over sodium sulfate, filtered, and evaporated to a residue, which was purified by column chromatography (80 g silica, 0-5% hexane/EtOAc) to afford 8-bromo- 7-(dibenzylamino)-3,4-dihydronaphthalen-1(2H)-one (4.25 g). LCMS: m/z (ESI) [M+H]⁺ 422.2, t_R = 1.99 minutes (Method A). Step 3: 8-Bromo-1-((6-chloro-5-(hydroxymethyl)-2-(methylthio)pyrimidin-4- yl)methyl)-7-(dibenzylamino)-1,2,3,4-tetrahydronaphthalen-1-ol Lithium diisopropylamide (26.9 mL, 1 M, 2.5 equiv., 26.9 mmol) was added to a solution of (4-chloro-6-methyl-2-(methylthio)pyrimidin-5-yl)methanol (2.20 g, 1 equiv., 10.8 mmol) in THF (108 mL) at -78 °C over 15 minutes. The mixture was stirred at that temperature for 1 hour, and then a solution of 8-bromo-7-(dibenzylamino)-3,4-dihydronaphthalen-1(2H)- one (4.970 g, 1.1 equiv., 11.8 mmol) in THF (50 mL) was added over 15 minutes. The reaction mixture was stirred at that temperature for 1 hour and then quenched with aqueous NH₄Cl at - 78 °C. The reaction mixture was warmed slowly to room temperature, extracted with EtOAc, and washed with brine. The combined organic layers were dried over sodium sulfate, filtered, and concentrated to a residue which was purified by flash column (120 g silica, 0-20% hexane/EtOAc) to give 8-bromo-1-((6-chloro-5-(hydroxymethyl)-2-(methylthio)pyrimidin-4- yl)methyl)-7-(dibenzylamino)-1,2,3,4-tetrahydronaphthalen-1-ol (4 g). LCMS: m/z (ESI) [M+H]⁺ 626.1, t_R = 2.07 minutes (Method B). Step 4: N,N-Dibenzyl-8-bromo-4'-chloro-2'-(methylthio)-3,4,5',8'-tetrahydro-2H- spiro[naphthalene-1,7'-pyrano[4,3-d]pyrimidin]-7-amine Butyllithium (5.70 mL, 1.6 M, 2.5 equiv., 9.12 mmol) was added dropwise to a solution of 8-bromo-1-((6-chloro-5-(hydroxymethyl)-2-(methylthio)pyrimidin-4-yl)methyl)-7- (dibenzylamino)-1,2,3,4-tetrahydronaphthalen-1-ol (2.28 g, 1 equiv., 3.65 mmol) in THF (25.6 mL) at -65 ^oC. The reaction mixture was left to stir for 30 minutes. A solution of 4- methylbenzenesulfonyl chloride (1.04 g, 1.5 equiv., 5.47 mmol) in THF (20 mL) was added dropwise at -65 ^oC, and the resulting mixture was warmed to room temperature and stirred for 2 hours. Saturated aqueous ammonium chloride solution was added, and the mixture was extracted with EtOAc three times. The organic phase was washed with brine, dried over sodium sulfate, filtered, and concentrated under reduced pressure. The residue was combined with a second batch run according to this procedure (2.45 mmol scale) for purification by flash chromatography (80 g, 0-10% hexane/EtOAc) to give N,N-dibenzyl-8-bromo-4'-chloro-2'- (methylthio)-3,4,5',8'-tetrahydro-2H-spiro[naphthalene-1,7'-pyrano[4,3-d]pyrimidin]-7- amine (1.7 g). LCMS: m/z (ESI) [M+H]⁺ 608.0, t_R = 2.31 minutes (84%, Method B). Intermediate 7: 7-Bromo-4-methyl-3,4-dihydronaphthalen-1(2H)-one Aluminum chloride (20.8 g, 2.5 eq., 156 mmol) was stirred rapidly as 4-methyl-3,4- dihydronaphthalen-1(2H)-one (10.0 g, 1 eq., 62.4 mmol) was added dropwise by syringe over 20 minutes. The resulting dark-red mass was heated at 85 °C until it melted, at which point Br₂ (12.0 g, 3.86 mL, 1.2 eq., 74.9 mmol) was added dropwise by syringe over 40 minutes and stirred for 1 hour at 85 °C. The reaction mixture was allowed to cool to room temperature and then added to ice-water (500 mL) and concentrated HCl (100 mL). The resulting mixture was extracted with ethyl acetate (4 × 300 mL), and the combined organic layers were filtered through Celite. The filtrate was washed with saturated aqueous sodium bicarbonate solution (250 mL), water (250 mL), and brine (250 mL), dried over sodium sulfate, filtered, and concentrated to give a residue which was purified by reverse-phase HPLC (0.1% formic acid condition) to give 7-bromo-4-methyl-3,4-dihydronaphthalen-1(2H)-one (10.5 g). LCMS: m/z (ESI) [M+H]⁺ 240.9, t_R = 0.462 minutes (Method H). The enantiomers of 7-bromo-4-methyl-3,4-dihydronaphthalen-1(2H)-one (5 g, 20.9 mmol) were separated by chiral SFC (Column: Chiralpak AD-350 × 4.6 mm I.D., 3 μm Mobile phase: Phase A for CO₂, and Phase B for MeOH (0.05% DEA), Gradient elution: B in A from 5% to 40% Flow rate: 3 mL/min, Detector: PDA, Column Temp: 35 ^oC, Back Pressure: 100 bar) to afford Intermediate 7A and Intermediate 7B. Intermediate 7A: First eluting peak, t_R = 1.027 minutes (1780 mg) ¹H NMR (400 MHz, CD₃OD) δ 8.03 (d, 1H), 7.69 (dd, 1H), 7.36 (d, 1H), 3.15 - 3.04 (m, 1H), 2.84 - 2.74 (m, 1H), 2.66 - 2.55 (m, 1H), 2.31 - 2.20 (m, 1H), 1.96 - 1.84 (m, 1H), 1.40 (d, 3H). Intermediate 7B: Second eluting peak, t_R = 1.167 minutes (1549 mg) 1H NMR (400 MHz, CD₃OD) δ 8.03 (d, 1H), 7.69 (dd, 1H), 7.36 (d, 1H), 3.17 - 3.01 (m, 1H), 2.85 - 2.73 (m, 1H), 2.69 - 2.53 (m, 1H), 2.31 - 2.20 (m, 1H), 1.96 - 1.82 (m, 1H), 1.40 (d, 3H). Intermediate 9: 6-Bromo-4'-chloro-2'-(methylthio)-5',8'- dihydrospiro[isochromane-4,7'-pyrano[4,3-d]pyrimidine] Step 1: 6-bromo-4-((6-chloro-5-(hydroxymethyl)-2-(methylthio)pyrimidin-4- yl)methyl)isochroman-4-ol To a dry flask was combined (4-chloro-6-methyl-2-(methylthio)pyrimidin-5- yl)methanol (2.00 g, 1 equiv., 9.77 mmol) and THF (40.0 mL). The mixture was cooled to -78 °C. Lithium diisopropylamide solution (2.62 g, 24.4 mL, 1.0 M, 2.5 equiv., 24.4 mmol) was added dropwise at -78 °C, maintaining an internal temperature below -60 °C. After 1 hour, a degassed solution of 6-bromoisochroman-4-one (2.22 g, 1 equiv., 9.77 mmol) in THF (30.0 mL) was added dropwise, and the resulting mixture was allowed to stir at -78 °C for 10 minutes. The reaction mixture, while still cold, was then quickly quenched by being poured into a round- bottom flask containing room temperature saturated aqueous ammonium chloride (80 mL). The organic contents were then extracted with ethyl acetate (80 mL × 2) followed by dichloromethane (80 mL × 2). The combined organic layers were dried over sodium sulfate, filtered, and concentrated under reduced pressure to give a residue which was purified by column chromatography (220 g SiO₂ cartridge, 0-40% ethyl acetate in heptane) to give 6- bromo-4-((6-chloro-5-(hydroxymethyl)-2-(methylthio)pyrimidin-4-yl)methyl)isochroman-4- ol (1.84 g). 1H NMR (400 MHz, CDCl₃) δ 7.85 (m, 1H), 7.41 (m, 1H), 6.90 (m, 1H), 5.52 (s, 1H), 4.93 – 4.68 (m, 5H), 3.64 – 3.49 (m, 3H), 3.26 (m, 1H), 3.05 (m, 1H). Step 2: 6-Bromo-4'-chloro-2'-(methylthio)-5',8'-dihydrospiro[isochromane-4,7'- pyrano[4,3-d]pyrimidine] To a vial of 6-bromo-4-((6-chloro-5-(hydroxymethyl)-2-(methylthio)pyrimidin-4- yl)methyl)isochroman-4-ol (736 mg, 1 equiv., 1.70 mmol) was added triphenylphosphine (2.13 g, 2.0 equiv., 3.41 mmol) (polymer supported, ~1.6 mmol/g loading). The vial was degassed and filled with N₂ before dry THF (20.0 mL) and dry DCM (20.0 mL) were added. To this mixture was added dropwise diisopropyl (E)-diazene-1,2-dicarboxylate (345 mg, 1 equiv., 1.70 mmol) at ambient temperature. The reaction mixture was stirred for 4 hours. The reaction mixture was diluted with ethyl acetate (100 mL) and then dichloromethane (100 mL). The mixture was then filtered over celite and sodium sulfate and concentrated to a residue which was purified by column chromatography (50 g SiO₂ cartridge, 0-40% ethyl acetate in heptane) to give 6-bromo-4'-chloro-2'-(methylthio)-5',8'-dihydrospiro[isochromane-4,7'-pyrano[4,3- d]pyrimidine] (383 mg). 1H NMR (400 MHz, DMSO-d6) δ 7.69 (d, 1H), 7.51 (dd, 1H), 7.11 (d, 1H), 4.82 (m, 1H), 4.74 – 4.65 (m, 3H), 3.93 (m, 1H), 3.78 (m, 1H), 3.25 (m, 1H), 2.99 (m, 1H), 2.53 (s, 3H). Intermediate 10: (S)-7-amino-2'-(((2R,7aS)-2-fluorotetrahydro-1H-pyrrolizin- 7a(5H)-yl)methoxy)-4'-hydroxy-3,4,5',8'-tetrahydro-2H-spiro[naphthalene-1,7'- pyrano[4,3-d]pyrimidine]-8-carbonitrile Step 1: (S)-N,N-dibenzyl-8-bromo-4'-((4-methoxybenzyl)oxy)-2'-(methylthio)- 3,4,5',8'-tetrahydro-2H-spiro[naphthalene-1,7'-pyrano[4,3-d]pyrimidin]-7-amine sodium 2-methylbutan-2-olate (9.3 g, 60 mL, 1.4 M, 1.7 equiv., 84 mmol) was added dropwise to a stirred solution of N,N-dibenzyl-8-bromo-4'-chloro-2'-(methylthio)-3,4,5',8'- tetrahydro-2H-spiro[naphthalene-1,7'-pyrano[4,3-d]pyrimidin]-7-amine (30 g, 1 equiv., 49 mmol) and 4-methoxybenzyl alcohol (7.5 g, 6.7 mL, 54 mmol) in THF (100 mL) over 25 minutes. The resulting dark brown mixture was stirred at room temperature for 2 hours. The reaction mixture was quenched by the addition of a saturated aqueous sodium bicarbonate (150 mL) and diluted with EtOAc (150 mL). The two phases were separated. The aqueous layer was extracted with EtOAc (2 x 100 mL). The combined organic extracts were dried over sodium sulfate, filtered, and concentrated to give the crude product, which was dissolved in EtOAc (50 mL), and sonicated. To this mixture, Et₂O was added to initiate further precipitation and the mixture was filtered to afford N,N-dibenzyl-8-bromo-4'-((4-methoxybenzyl)oxy)-2'- (methylthio)-3,4,5',8'-tetrahydro-2H-spiro[naphthalene-1,7'-pyrano[4,3-d]pyrimidin]-7-amine was isolated. 1H NMR (400 MHz, CDCl₃) δ 7.42 – 7.15 (m, 12H), 7.02 – 6.72 (m, 4H), 5.42 (s, 2H), 4.85 (d, J = 16.2 Hz, 1H), 4.65 (d, J = 16.2 Hz, 1H), 4.21 – 3.92 (m, 5H), 3.85 – 3.79 (m, 3H), 2.79 (m, 3H), 2.58 (d, J = 1.5 Hz, 3H), 2.11 (d, J = 12.6 Hz, 1H), 1.94 – 1.63 (m, 3H). The diastereomers of N,N-dibenzyl-8-bromo-4'-((4-methoxybenzyl)oxy)-2'- (methylthio)-3,4,5',8'-tetrahydro-2H-spiro[naphthalene-1,7'-pyrano[4,3-d]pyrimidin]-7-amine (14.2 g) were separated by chiral SFC (ChiralPak IC-H 21 x 250 mm, 5μm; EtOH, 35%, flow rate = 80 mL/min) to afford (S)-N,N-dibenzyl-8-bromo-4'-((4-methoxybenzyl)oxy)-2'- (methylthio)-3,4,5',8'-tetrahydro-2H-spiro[naphthalene-1,7'-pyrano[4,3-d]pyrimidin]-7-amine (5.82g). Analytical Chiral SFC: t_R = 2.61 minutes ChiralPak IC-H 21 x 250 mm, 5μm; EtOH, 35%, flow rate = 2.5 mL/min). 1H NMR (400 MHz, CDCl₃) δ 7.43 – 7.15 (m, 12H), 6.96 – 6.86 (m, 3H), 6.80 (d, J = 8.2 Hz, 1H), 5.42 (s, 2H), 4.85 (d, J = 16.2 Hz, 1H), 4.65 (d, J = 16.4 Hz, 1H), 4.25 – 3.91 (m, 5H), 3.83 (s, 3H), 2.91 – 2.67 (m, 3H), 2.58 (s, 3H), 2.15 – 2.07 (m, 1H), 1.88 (m, 2H), 1.68 (m, 1H). Step 2: (S)-7-(dibenzylamino)-4'-hydroxy-2'-(methylthio)-3,4,5',8'-tetrahydro- 2H-spiro[naphthalene-1,7'-pyrano[4,3-d]pyrimidine]-8-carbonitrile Copper(I) cyanide (1.25 g, 428 μL, 10 equiv., 13.9 mmol) was added in one portion to a stirred solution of (S)-N,N-dibenzyl-8-bromo-4'-((4-methoxybenzyl)oxy)-2'-(methylthio)- 3,4,5',8'-tetrahydro-2H-spiro[naphthalene-1,7'-pyrano[4,3-d]pyrimidin]-7-amine (1.05 g, 94% wt, 1 equiv., 1.39 mmol) in DMF (27.9 mL). The resulting mixture was heated to 120 °C for approximately 8 hours. The reaction mixture was cooled to room temperature and concentrated under reduced pressure. The resulting residue was diluted with water, DCM and a 1:1 mixture of NH₄OH and methanol (200 mL). This mixture was stirred at room temperature for approximately 15 minutes until two clear layers were observed. The two layers were separated. The aqueous layer was extracted with DCM (x 3). The combined organic extracts were dried over sodium sulfate, filtered, and concentrated to give the crude product which was dissolved in EtOAc and washed with 10% LiCl aqueous solution (x 3). The organic layer was dried over sodium sulfate, filtered, and concentrated to give the crude product. The crude product was purified via silica gel chromatography (0:100-A:B to 30:70-A:B where A is a premixed solution of 2.5% NH₄OH and 20% MeOH in DCM and B is DCM) to give (S)-7- (dibenzylamino)-4'-hydroxy-2'-(methylthio)-3,4,5',8'-tetrahydro-2H-spiro[naphthalene-1,7'- pyrano[4,3-d]pyrimidine]-8-carbonitrile (430 mg) as an orange solid. LCMS: m/z (ESI) [M+H]⁺ 535.3, t_R = 2.17 minutes (Method C) Step 3: (S)-7-(dibenzylamino)-4'-hydroxy-2'-(methylsulfonyl)-3,4,5',8'- tetrahydro-2H-spiro[naphthalene-1,7'-pyrano[4,3-d]pyrimidine]-8-carbonitrile To a light orange suspension of (S)-7-(dibenzylamino)-4'-hydroxy-2'-(methylthio)- 3,4,5',8'-tetrahydro-2H-spiro[naphthalene-1,7'-pyrano[4,3-d]pyrimidine]-8-carbonitrile (430 mg, 1.00 equiv., 804 μmol) in MeCN (10.7 mL) and water (5.36 mL) at room temperature was added potassium phosphate tribasic (427 mg, 2.50 equiv., 2.01 mmol). The resulting mixture was stirred at 40 °C for 30 minutes. The reaction mixture was cooled to room temperature, and the orange organic layers was syringed out and filtered. The organic solution (pH = 11) was cooled to 3 °C. To this mixture, hydrogen peroxide (195 mg, 173 μL, 35% wt, 2.50 equiv., 2.01 mmol) was added dropwise using a glass pipette. The resulting solution was stirred at 0 °C for 45 minutes followed by gradual warming to 10 °C. The reaction mixture was quenched by the addition of a saturated aqueous ammonium chloride solution and diluted with EtOAc. The two layers were separated, and the aqueous layer was extracted with EtOAc (3 x 40 mL). The combined organic layers were dried over magnesium sulfate, filtered, and concentrated to give the crude product (S)-7-(dibenzylamino)-4'-hydroxy-2'-(methylsulfonyl)-3,4,5',8'-tetrahydro- 2H-spiro[naphthalene-1,7'-pyrano[4,3-d]pyrimidine]-8-carbonitrile (334 mg) as a light yellow solid which was used in the next step without further purification. LCMS: m/z (ESI) [M+H]⁺ 567.2, t_R = 2.14 minutes (Method C) Step 4: (S)-7-(dibenzylamino)-2'-(((2R,7aS)-2-fluorotetrahydro-1H-pyrrolizin- 7a(5H)-yl)methoxy)-4'-hydroxy-3,4,5',8'-tetrahydro-2H-spiro[naphthalene-1,7'- pyrano[4,3-d]pyrimidine]-8-carbonitrile To a flask charged with (S)-7-(dibenzylamino)-4'-hydroxy-2'-(methylsulfonyl)- 3,4,5',8'-tetrahydro-2H-spiro[naphthalene-1,7'-pyrano[4,3-d]pyrimidine]-8-carbonitrile (334.2 mg, 1 equiv., 589.8 μmol) was added ((2R,7aS)-2-fluorotetrahydro-1H-pyrrolizin-7a(5H)- yl)methanol (225.3 mg, 2.4 equiv., 1.415 mmol). The reaction mixture was then cooled to 0 °C, and sodium 2-methylbutan-2-olate (155.9 mg, 2.4 equiv., 1.415 mmol) was added in one portion. The reaction mixture was stirred at 0 °C for 30 minutes then stirred at room temperature for 20 minutes. The reaction mixture was quenched by the addition of a 1:1 mixture of a saturated aqueous ammonium chloride solution and water and diluted with EtOAc (10 mL). The two layers were separated. The aqueous phase was extracted with EtOAc (3 x 10 mL). The combined organic layers were dried over magnesium sulfate, filtered, and concentrated to give the crude product which was purified by silica gel chromatography (0:100- A:B to 50:50-A:B where A is a premixed solution of 2.5% NH₄OH and 22.5% MeOH in DCM and B is DCM). The isolated product was repurified by silica gel chromatography (0:100-A:B to 30:70-A:B where A is a premixed solution of 2.5% NH₄OH and 22.5% MeOH in DCM and B is DCM) to give (S)-7-(dibenzylamino)-2'-(((2R,7aS)-2-fluorotetrahydro-1H-pyrrolizin- 7a(5H)-yl)methoxy)-4'-hydroxy-3,4,5',8'-tetrahydro-2H-spiro[naphthalene-1,7'-pyrano[4,3- d]pyrimidine]-8-carbonitrile (225 mg). LCMS: m/z (ESI) [M+H]⁺ 646.3, t_R = 1.57 minutes (Method C) Step 5: (S)-7-amino-2'-(((2R,7aS)-2-fluorotetrahydro-1H-pyrrolizin-7a(5H)- yl)methoxy)-4'-hydroxy-3,4,5',8'-tetrahydro-2H-spiro[naphthalene-1,7'-pyrano[4,3- d]pyrimidine]-8-carbonitrile Pd(OH)₂ on carbon (613.2 mg, 20% wt, 2.5 equiv., 873.4 μmol) was added to a solution of (S)-7-(dibenzylamino)-2'-(((2R,7aS)-2-fluorotetrahydro-1H-pyrrolizin-7a(5H)- yl)methoxy)-4'-hydroxy-3,4,5',8'-tetrahydro-2H-spiro[naphthalene-1,7'-pyrano[4,3- d]pyrimidine]-8-carbonitrile (225.6 mg, 1 equiv., 349.3 μmol) in methanol (7 mL). The resulting mixture was sparged with hydrogen for 5 minutes. The mixture was stirred under a hydrogen atmosphere for 2.5 hours. The reaction mixture was filtered, and the filtrate was concentrated to give (S)-7-amino-2'-(((2R,7aS)-2-fluorotetrahydro-1H-pyrrolizin-7a(5H)- yl)methoxy)-4'-hydroxy-3,4,5',8'-tetrahydro-2H-spiro[naphthalene-1,7'-pyrano[4,3- d]pyrimidine]-8-carbonitrile (82.6 mg) as an off-white solid. LCMS: m/z (ESI) [M+H]⁺ 466.2, tR = 1.16 minutes (Method C) ¹H NMR (400 MHz, DMSO-d₆) δ 7.03 (d, 1H), 6.72 (d, 1H), 5.75 (s, 2H), 5.27 (d, 1H), 4.53 – 4.36 (m, 2H), 4.11 – 3.91 (m, 2H), 3.14 – 2.94 (m, 4H), 2.86 – 2.76 (m, 1H), 2.65 – 2.54 (m, 3H), 2.08 – 1.89 (m, 4H), 1.86 – 1.72 (m, 4H), 1.69 – 1.58 (m, 2H). Intermediate 11a: (R)-7-bromo-4-methyl-3,4-dihydronaphthalen-1(2H)-one Aluminum chloride (20.8 g, 2.5 equiv., 156 mmol) was stirred rapidly as 4-methyl-3,4- dihydronaphthalen-1(2H)-one (10.0 g, 1 equiv., 62.4 mmol) was added dropwise by syringe over 20 minutes. The resulting dark-red mass was heated at 85 °C until it melted, at which point Br2 (12.0 g, 3.86 mL, 1.2 equiv., 74.9 mmol) was added dropwise by syringe over 40 minutes. The mixture was stirred for 1 hour at 85 °C. The reaction mixture was cooled to room temperature, added to ice-water (500 mL) and concentrated HCl (100 mL). The resulting mixture was extracted with ethyl acetate (4 × 300 mL), and the combined organic layers were filtered through Celite. The filtrate was washed with saturated aqueous sodium bicarbonate solution (250 mL), water (250 mL) and brine (250 mL), dried over sodium sulfate, filtered, and concentrated to give a residue. The residue was purified by reverse-phase HPLC (0.1% formic acid condition) to give 7-bromo-4-methyl-3,4-dihydronaphthalen-1(2H)-one (10.5 g). LCMS: m/z (ESI) [M+H]⁺ 240.9, t_R = 0.462 minutes (Method H). The enantiomers of 7-bromo-4-methyl-3,4-dihydronaphthalen-1(2H)-one (5 g, 20.9 mmol) were separated by chiral SFC (Column: Chiralpak AD-350 × 4.6 mm I.D., 3 μm Mobile phase: Phase A for CO₂, and Phase B for MeOH (0.05% DEA), Gradient elution: B in A from 5% to 40% Flow rate: 3 mL/min, Detector: PDA, Column Temp: 35 °C, Back Pressure: 100 bar) to afford (R)-7-bromo-4-methyl-3,4-dihydronaphthalen-1(2H)-one (Intermediate 11a) and (S)-7-bromo-4-methyl-3,4-dihydronaphthalen-1(2H)-one (Intermediate 11b). Intermediate 11a: First eluting peak, tR = 1.027 minutes (1780 mg) 1H NMR (400 MHz, CD₃OD) δ 8.03 (d, 1H), 7.69 (dd, 1H), 7.36 (d, 1H), 3.15 - 3.04 (m, 1H), 2.84 - 2.74 (m, 1H), 2.66 - 2.55 (m, 1H), 2.31 - 2.20 (m, 1H), 1.96 - 1.84 (m, 1H), 1.40 (d, 3H). Intermediate 11b: (S)-7-bromo-4-methyl-3,4-dihydronaphthalen-1(2H)-one Intermediate 11b: Second eluting peak, t_R = 1.167 minutes (1549 mg) 1H NMR (400 MHz, CD₃OD) δ 8.03 (d, 1H), 7.69 (dd, 1H), 7.36 (d, 1H), 3.17 - 3.01 (m, 1H), 2.85 - 2.73 (m, 1H), 2.69 - 2.53 (m, 1H), 2.31 - 2.20 (m, 1H), 1.96 - 1.82 (m, 1H), 1.40 (d, 3H). Intermediate 12: (S)-8-bromo-7-(dibenzylamino)-4-methyl-3,4- dihydronaphthalen-1(2H)-one Step 1: (S)-7-amino-4-methyl-3,4-dihydronaphthalen-1(2H)-one NMP (27.9 mL) and ammonium hydroxide (29.3 g, 32.4 mL, 20 equiv, 836 mmol) were delivered to a pressure vessel charged with (S)-7-bromo-4-methyl-3,4-dihydronaphthalen- 1(2H)-one (Intermediate 11b) (10.0 g, 1.00 equiv, 41.8 mmol) and copper(I) oxide (598 mg, 0.10 equiv, 4.18 mmol) under nitrogen. The pressure vessel was sealed, and the reaction mixture was stirred at 80 °C for 17 hours. The reaction mixture was cooled to ambient temperature and poured in a separatory funnel charged with water (100 mL) and EtOAc (200 mL). The layers were separated, and the aqueous phase was extracted with EtOAc (3 x 150 mL). The combined organic extracts were dried over sodium sulfate, filtered, and concentrated to a residue. The crude residue was purified by silica gel chromatography (2 to 45% heptane/EtOAc) to afford (S)-7-amino-4-methyl-3,4-dihydronaphthalen-1(2H)-one (6.79 g, 38.8 mmol). 1H NMR (400 MHz, CDCl₃) δ 7.34 (d, 1H), 7.16 (d, 1H), 6.94 – 6.86 (m, 1H), 3.68 (bs, 2H), 3.07 – 2.95 (m, 1H), 2.88 – 2.72 (m, 1H), 2.64 – 2.52 (m, 1H), 2.28 – 2.16 (m, 1H), 1.93 – 1.80 (m, 1H), 1.37 (d, 3H). LCMS: m/z (ESI) [M+H]⁺ 176.2, t_R = 1.51 minutes (Method E) Step 2: (S)-7-amino-8-bromo-4-methyl-3,4-dihydronaphthalen-1(2H)-one A solution of N-bromosuccinimide (6.90 g, 1.0 equiv, 38.8 mmol) in DMF (25.9 mL) was delivered dropwise to a flask containing (S)-7-amino-4-methyl-3,4-dihydronaphthalen- 1(2H)-one (6.79 g, 1.00 equiv, 38.79 mmol) in DMF (51.7 mL) at 0 °C, under nitrogen. The resulting mixture was stirred at 0 °C for 5 minutes. The mixture was then warmed to room temperature and stirred for 2 hours. The reaction mixture was quenched by the addition of water (150 mL) and EtOAc (200 mL). The layers were separated, and the aqueous phase was extracted with EtOAc (3 x 150 mL). The combined organic extracts were dried over sodium sulfate, filtered, and concentrated to give a residue, which was purified by silica gel chromatography (0 to 30% heptane/EtOAc) to afford (S)-7-amino-8-bromo-4-methyl-3,4- dihydronaphthalen-1(2H)-one (7.96 g, 31.3 mmol). 1H NMR (400 MHz, CDCl₃) δ 7.07 (d, 1H), 6.92 (d, 1H), 4.15 (bs, 2H), 3.05 – 2.91 (m, 1H), 2.86 – 2.74 (m, 1H), 2.68 – 2.56 (m, 1H), 2.25 – 2.12 (m, 1H), 1.90 – 1.77 (m, 1H), 1.31 (d, 3H). LCMS: m/z (ESI) [M+H]⁺ 254.1, t_R = 2.47 minutes (Method E) Step 3. (S)-8-bromo-7-(dibenzylamino)-4-methyl-3,4-dihydronaphthalen-1(2H)- one Benzyl bromide (16.1 g, 11.2 mL, 3 equiv, 94.0 mmol) and potassium carbonate (15.2 g, 3.5 equiv, 110 mmol) were sequentially delivered to a solution of (S)-7-amino-8-bromo-4- methyl-3,4-dihydronaphthalen-1(2H)-one (7.96 g, 1.0 equiv, 31.3 mmol) in MeCN (313 mL) at room temperature. The resulting mixture was stirred vigorously at reflux for 18 hours at which point the reaction mixture was cooled to room temperature. The solids were filtered and rinsed with EtOAc. The filtrate was concentrated, and the remaining crude residue was purified by silica gel chromatography (1 to 35% heptane/EtOAc) to afford (S)-8-bromo-7- (dibenzylamino)-4-methyl-3,4-dihydronaphthalen-1(2H)-one (12.5 g, 28.7 mmol). 1H NMR (400 MHz, CDCl₃) δ 7.36 – 7.19 (m, 10H), 7.09 – 6.97 (m, 2H), 4.24 – 4.10 (m, 4H), 3.03 – 2.90 (m, 1H), 2.89 – 2.76 (m, 1H), 2.73 – 2.61 (m, 1H), 2.24 – 2.12 (m, 1H), 1.90 – 1.77 (m, 1H), 1.30 (d, 3H). LCMS: m/z (ESI) [M+H]⁺ 434.3, t_R = 3.78 minutes (Method E) Intermediate 13: (1S,4S)-N,N-dibenzyl-8-bromo-4'-chloro-4-methyl-2'- (methylthio)-3,4,5',8'-tetrahydro-2H-spiro[naphthalene-1,7'-pyrano[4,3-d]pyrimidin]-7- amine

Step 1: (4S)-8-bromo-1-((6-chloro-5-(hydroxymethyl)-2-(methylthio)pyrimidin-4- yl)methyl)-7-(dibenzylamino)-4-methyl-1,2,3,4-tetrahydronaphthalen-1-ol Lithium diisopropylamide (1.0 M in THF/hexanes) (9.25 g, 86.3 mL, 1.0 M, 3.01 equiv, 86.3 mmol) was delivered dropwise to a solution of (4-chloro-6-methyl-2- (methylthio)pyrimidin-5-yl)methanol (8.83 g, 1.51 equiv, 43.1 mmol) in THF (191 mL) at -78 °C. The resulting mixture was stirred at -78 °C for 1.25 hours, followed by the dropwise addition of a solution of (S)-8-bromo-7-(dibenzylamino)-4-methyl-3,4-dihydronaphthalen- 1(2H)-one (Intermediate 12) (12.5 g, 1.0 equiv, 28.7 mmol) in THF (96 mL) keeping the internal temperature below -65 °C. The resulting solution was stirred for 1 hour at -78 °C. The reaction was quenched by the dropwise addition of HCl (2.0 M in Et₂O) (3.34 g, 45.9 mL, 3.2 equiv, 91.7 mmol) at -78 °C, followed by water (200 mL). The mixture was warmed to room temperature, transferred to a separatory funnel, and the resulting layers were separated. The aqueous phase was extracted with EtOAc (1 x 200 mL) and DCM (2 x 200 mL). The combined organic extracts were dried over sodium sulfate, filtered, and concentrated to a residue which _{was purified by silica gel chromatography (2 → 50% CH CL /EtOAc, (product elutes around} 15% EtOAc)) to afford (4S)-8-bromo-1-((6-chloro-5-(hydroxymethyl)-2- (methylthio)pyrimidin-4-yl)methyl)-7-(dibenzylamino)-4-methyl-1,2,3,4- tetrahydronaphthalen-1-ol (16.05 g, 24 mmol). LCMS: m/z (ESI) [M+H]⁺ 640.2, t_R = 4.39 minutes (Method E) Step 2: (1S,4S)-N,N-dibenzyl-8-bromo-4'-chloro-4-methyl-2'-(methylthio)- 3,4,5',8'-tetrahydro-2H-spiro[naphthalene-1,7'-pyrano[4,3-d]pyrimidin]-7-amine n-Butyllithium (2.5 M in hexanes) (3.35 g, 20.9 mL, 2.2 equiv, 52.3 mmol) was added dropwise to a solution of (4S)-8-bromo-1-((6-chloro-5-(hydroxymethyl)-2- (methylthio)pyrimidin-4-yl)methyl)-7-(dibenzylamino)-4-methyl-1,2,3,4- tetrahydronaphthalen-1-ol (16.0 g, 95wt%, 1.0 equiv, 23.8 mmol) in THF (198 mL) at -78 °C. The resulting solution was stirred at -78 °C for 35 minutes, followed by the dropwise addition of a solution of p-toluenesulfonyl chloride (6.80 g, 1.5 equiv, 35.7 mmol) in THF (99 mL). The resulting mixture was stirred at -78 °C for 10 minutes, and the acetone/dry ice bath was removed. The resulting reaction mixture was stirred for another 45 minutes after reaching ambient temperature. The mixture was quenched by the addition of a 1:1 mixture of saturated aqueous ammonium chloride solution and water (250 mL). The reaction mixture was transferred to a separatory funnel. EtOAc (100 mL) was added, and the layers were separated. The aqueous phase was extracted with EtOAc (3 x 300 mL). The combined organic extracts were dried over sodium sulfate, filtered, and concentrated. The crude material was purified by silica gel chromatography (0 → 10% heptane/EtOAc). Material isolated from column chromatography was stirred in MeCN (200 mL) at 40 °C overnight. The mixture was filtered, and the solid rinsed with MeCN to afford a white solid. The filtrate was concentrated to a brown oil which was purified by silica gel chromatography (0 → 10% heptane/EtOAc) to give (1S,4S)-N,N-dibenzyl-8-bromo-4'-chloro-4-methyl-2'-(methylthio)-3,4,5',8'-tetrahydro-2H- spiro[naphthalene-1,7'-pyrano[4,3-d]pyrimidin]-7-amine (1.64 g, 2.63 mmol) LCMS: m/z (ESI) [M+H]⁺ 620.0, tR = 4.63 minutes (Method E) Intermediate 14: (1S,4S)-7-amino-2'-(((2R,7aS)-2-fluorotetrahydro-1H- pyrrolizin-7a(5H)-yl)methoxy)-4'-hydroxy-4-methyl-3,4,5',8'-tetrahydro-2H- spiro[naphthalene-1,7'-pyrano[4,3-d]pyrimidine]-8-carbonitrile Step 1: (1S,4S)-N,N-dibenzyl-4'-(benzyloxy)-8-bromo-4-methyl-2'-(methylthio)- 3,4,5',8'-tetrahydro-2H-spiro[naphthalene-1,7'-pyrano[4,3-d]pyrimidin]-7-amine To a solution of benzyl alcohol (666 mg, 640 μL, 1.01 equiv., 6.15 mmol) in THF (10 mL) was added sodium hydride as a dispersion in mineral oil (392 mg, 60% wt, 1.61 equiv., 9.80 mmol) in an ice bath. To this mixture, (1S,4S)-N,N-dibenzyl-8-bromo-4'-chloro-4-methyl- 2'-(methylthio)-3,4,5',8'-tetrahydro-2H-spiro[naphthalene-1,7'-pyrano[4,3-d]pyrimidin]-7- amine (3.77 g, 1 equiv., 6.07 mmol) in THF (10 mL) was added, and the ice bath was removed. The resulting mixture was stirred for 55 minutes at room temperature and then cooled back down in an ice bath. The reaction mixture was quenched with saturated aqueous ammonium chloride solution (10 mL). Ethyl acetate was added (20 mL), and the layers that formed were separated. The aqueous layer was extracted with ethyl acetate (2 x 20 mL). The combined organic layers were washed with brine, dried over magnesium sulfate, filtered, and concentrated. The resulting residue was azeotroped with toluene (3 x 20 mL) at 50 °C to afford (1S,4S)-N,N-dibenzyl-4'-(benzyloxy)-8-bromo-4-methyl-2'-(methylthio)-3,4,5',8'-tetrahydro- 2H-spiro[naphthalene-1,7'-pyrano[4,3-d]pyrimidin]-7-amine (4.26 g, 6.15 mmol) which was used without further purification. LCMS: m/z (ESI) [M+H]⁺ 692.6, t_R = 4.45 minutes (Method K) Step 2: (1S,4S)-4'-(benzyloxy)-7-(dibenzylamino)-4-methyl-2'-(methylthio)- 3,4,5',8'-tetrahydro-2H-spiro[naphthalene-1,7'-pyrano[4,3-d]pyrimidine]-8-carbonitrile Copper(I) cyanide (1.09 g, 2 equiv., 12.1 mmol) was added to a solution of (1S,4S)- N,N-dibenzyl-4'-(benzyloxy)-8-bromo-4-methyl-2'-(methylthio)-3,4,5',8'-tetrahydro-2H- spiro[naphthalene-1,7'-pyrano[4,3-d]pyrimidin]-7-amine (4.20 g, 1 equiv., 6.06 mmol) in DMF (30 mL) under a nitrogen atmosphere room temperature. The reaction mixture was stirred for 1.25 hours at 120 °C. The reaction mixture was allowed to cool to room temperature. To this mixture, DCM (50 mL) was added, and the resulting precipitate was filtered. Water (50 mL) and NH₄OH (20 mL) were added to the filtrate. The biphasic mixture was transferred to a separatory funnel, and the layers that formed were separated. The aqueous layer was extracted with DCM (50 mL). The combined organic layers were washed with 10% saturated LiCl solution (2 x 50 mL) and then concentrated. The residue obtained was re- dissolved in ether (40 mL) and washed with water (2 x 20 mL). The combined aqueous layers were extracted with ether (20 mL). The combined organic layers were dried over magnesium sulfate, filtered, and concentrated to yield (1S,4S)-4'-(benzyloxy)-7-(dibenzylamino)-4- methyl-2'-(methylthio)-3,4,5',8'-tetrahydro-2H-spiro[naphthalene-1,7'-pyrano[4,3- d]pyrimidine]-8-carbonitrile (3.68 g, 5.76 mmol) which was used without further purification. LCMS: m/z (ESI) [M+H]⁺ 639.9, t_R = 4.26 minutes (Method K) Step 3: (1S,4S)-4'-(benzyloxy)-7-(dibenzylamino)-4-methyl-2'-(methylsulfinyl)- 3,4,5',8'-tetrahydro-2H-spiro[naphthalene-1,7'-pyrano[4,3-d]pyrimidine]-8-carbonitrile and (1S,4S)-4'-(benzyloxy)-7-(dibenzylamino)-4-methyl-2'-(methylsulfonyl)-3,4,5',8'- tetrahydro-2H-spiro[naphthalene-1,7'-pyrano[4,3-d]pyrimidine]-8-carbonitrile Oxone (7.08 g, 2 equiv., 11.5 mmol) was added to a solution of (1S,4S)-4'-(benzyloxy)- 7-(dibenzylamino)-4-methyl-2'-(methylthio)-3,4,5',8'-tetrahydro-2H-spiro[naphthalene-1,7'- pyrano[4,3-d]pyrimidine]-8-carbonitrile (3.68 g, 1 equiv., 5.76 mmol) in THF (100 mL) and water (50 mL). The cloudy reaction mixture was stirred for 2 hours at room temperature. The reaction mixture was quenched with a 10% aqueous solution of sodium ascorbate (100 mL) and stirred for 5 minutes. The quenched mixture was transferred to a separatory funnel, and the aqueous layer was extracted with EtOAc (2 x 100 mL). The combined organic layers were washed with 1:1 brine:water (100 mL), dried over magnesium sulfate, filtered, and concentrated to provide a mixture of (1S,4S)-4'-(benzyloxy)-7- (dibenzylamino)-4-methyl-2'-(methylsulfinyl)-3,4,5',8'-tetrahydro-2H-spiro[naphthalene-1,7'- pyrano[4,3-d]pyrimidine]-8-carbonitrile and (1S,4S)-4'-(benzyloxy)-7-(dibenzylamino)-4- methyl-2'-(methylsulfonyl)-3,4,5',8'-tetrahydro-2H-spiro[naphthalene-1,7'-pyrano[4,3- d]pyrimidine]-8-carbonitrile (4.07 g, 6.22 mmol), which was used without further purification. (1S,4S)-4'-(benzyloxy)-7-(dibenzylamino)-4-methyl-2'-(methylsulfinyl)-3,4,5',8'- tetrahydro-2H-spiro[naphthalene-1,7'-pyrano[4,3-d]pyrimidine]-8-carbonitrile LCMS: m/z (ESI) [M+H]⁺ 655.3, t_R = 2.29 minutes (Method L) (1S,4S)-4'-(benzyloxy)-7-(dibenzylamino)-4-methyl-2'-(methylsulfonyl)-3,4,5',8'- tetrahydro-2H-spiro[naphthalene-1,7'-pyrano[4,3-d]pyrimidine]-8-carbonitrile LCMS: m/z (ESI) [M+H]⁺ 671.3, t_R = 2.32 minutes (Method L) Step 4: (1S,4S)-4'-(benzyloxy)-7-(dibenzylamino)-2'-(((2R,7aS)-2- fluorotetrahydro-1H-pyrrolizin-7a(5H)-yl)methoxy)-4-methyl-3,4,5',8'-tetrahydro-2H- spiro[naphthalene-1,7'-pyrano[4,3-d]pyrimidine]-8-carbonitrile The mixture of (1S,4S)-4'-(benzyloxy)-7-(dibenzylamino)-4-methyl-2'- (methylsulfinyl)-3,4,5',8'-tetrahydro-2H-spiro[naphthalene-1,7'-pyrano[4,3-d]pyrimidine]-8- carbonitrile and (1S,4S)-4'-(benzyloxy)-7-(dibenzylamino)-4-methyl-2'-(methylsulfonyl)- 3,4,5',8'-tetrahydro-2H-spiro[naphthalene-1,7'-pyrano[4,3-d]pyrimidine]-8-carbonitrile (994 mg, 1 equiv., 1.52 mmol) and ((2R,7aS)-2-fluorotetrahydro-1H-pyrrolizin-7a(5H)-yl)methanol (252 mg, 1.04 equiv., 1.58 mmol) in toluene (16 mL) was cooled in a -30 °C bath. To this mixture, sodium 2-methylbutan-2-olate (201 mg, 1.20 equiv., 1.83 mmol) was added in one portion. The resulting reaction mixture was stirred for 15 minutes at -30 °C, warmed to -20 °C, and stirred for 5 minutes. The product mixture was quenched with a 4 M solution of HCl in dioxanes (0.5 mL) followed by a saturated aqueous sodium bicarbonate solution (10 mL). The aqueous layer was extracted with EtOAc (3 x 15 mL). The combined organic layers were washed with brine (30 mL), dried over magnesium sulfate, filtered, and concentrated to yield (1S,4S)-4'-(benzyloxy)-7-(dibenzylamino)-2'-(((2R,7aS)-2-fluorotetrahydro-1H-pyrrolizin- 7a(5H)-yl)methoxy)-4-methyl-3,4,5',8'-tetrahydro-2H-spiro[naphthalene-1,7'-pyrano[4,3- d]pyrimidine]-8-carbonitrile (980 mg, 1.31 mmol) which was used without further purification. LCMS: m/z (ESI) [M+H]⁺ 750.4, t_R = 1.97 minutes (Method C) Step 5: (1S,4S)-7-amino-2'-(((2R,7aS)-2-fluorotetrahydro-1H-pyrrolizin-7a(5H)- yl)methoxy)-4'-hydroxy-4-methyl-3,4,5',8'-tetrahydro-2H-spiro[naphthalene-1,7'- pyrano[4,3-d]pyrimidine]-8-carbonitrile Pd(OH)₂ on carbon (1.08 g, 20% wt, 1.2 equiv., 1.54 mmol) was added to a solution of (1S,4S)-4'-(benzyloxy)-7-(dibenzylamino)-2'-(((2R,7aS)-2-fluorotetrahydro-1H-pyrrolizin- 7a(5H)-yl)methoxy)-4-methyl-3,4,5',8'-tetrahydro-2H-spiro[naphthalene-1,7'-pyrano[4,3- d]pyrimidine]-8-carbonitrile (958 mg, 1 equiv., 1.28 mmol) in methanol (33 mL) and DCM (6.2 mL) under a N2 atmosphere. The mixture was then sparged with H2. The resulting reaction mixture was stirred under a hydrogen atmosphere for 25 hours. The reaction mixture was filtered over celite and concentrated in vacuo. The residue was purified by column chromatography (SiO₂, eluting with 5% MeOH/DCM +1% NH₄OH) to afford (1S,4S)-7- amino-2'-(((2R,7aS)-2-fluorotetrahydro-1H-pyrrolizin-7a(5H)-yl)methoxy)-4'-hydroxy-4- methyl-3,4,5',8'-tetrahydro-2H-spiro[naphthalene-1,7'-pyrano[4,3-d]pyrimidine]-8- carbonitrile (321 mg, 669 μmol) as a white solid. LCMS: m/z (ESI) [M+H]⁺ 480.3, t_R = 1.21 minutes (Method C) 1H NMR (400 MHz, MeOD) δ 7.12 (d, 1H), 6.77 (d, 1H), 5.32 (d, 1H), 4.82 – 4.49 (m, 2H), 4.30 – 4.18 (m, 2H), 3.49 – 3.33 (m, 2H), 3.16 – 3.03 (m, 2H), 2.91 – 2.83 (m, 1H), 2.75 – 2.67 (m, 1H), 2.38 – 2.23 (m, 2H), 2.13 – 1.85 (m, 8H), 1.72 – 1.64 (m, 1H), 1.24 (d, 3H). Example 1: (S)-7-amino-4'-(dimethylamino)-2'-(((2R,7aS)-2-fluorotetrahydro- 1H-pyrrolizin-7a(5H)-yl)methoxy)-3,4,5',8'-tetrahydro-2H-spiro[naphthalene-1,7'- pyrano[4,3-d]pyrimidine]-8-carbonitrile (Compound 111a) To a 2 dram vial equipped with a magnetic stir bar was added dimethylamine, HCl (11 mg, 3 equiv., 0.13 mmol), PyBOP (29 mg, 1.3 equiv., 56 μmol), and (S)-7-Amino-2'- (((2R,7aS)-2-fluorotetrahydro-1H-pyrrolizin-7a(5H)-yl)methoxy)-4'-hydroxy-3,4,5',8'- tetrahydro-2H-spiro[naphthalene-1,7'-pyrano[4,3-d]pyrimidine]-8-carbonitrile (20 mg, 0.86 mL, 0.05 M, 1 equiv., 43 μmol) via solution in DMF (0.86 mL). To this solution was added DIPEA (44 mg, 60 μL, 8 equiv., 0.34 mmol). The resulting reaction mixture was stirred at 60 °C for 2 hours. The reaction mixture was then treated with 0.5 mL of H₂O, 0.5 mL of aqueous LiCl (5% solution in water) and 1.0 mL of EtOAc. The organic layers were then further extracted with EtOAc (1.0 mL, x3) combined, dried over sodium sulfate, filtered via disposable filter funnel, and concentrated under reduced pressure to yield a crude residue which was purified via normal phase chromatography (DCM/MeOH, 0 to 20%) to afford (S)-7-amino-4'- (dimethylamino)-2'-(((2R,7aS)-2-fluorotetrahydro-1H-pyrrolizin-7a(5H)-yl)methoxy)- 3,4,5',8'-tetrahydro-2H-spiro[naphthalene-1,7'-pyrano[4,3-d]pyrimidine]-8-carbonitrile (4 mg). 1H NMR (400 MHz, CDCl₃) δ 7.04 (d, 1H), 6.64 (d, 1H), 5.44 – 5.18 (m, 1H), 5.01 – 4.90 (m, 2H), 4.42 (s, 2H), 4.18 (d, 1H), 4.07 (d, 1H), 3.48 – 3.36 (m, 1H), 3.34 – 3.20 (m, 2H), 3.08 – 2.97 (m, 7H), 2.93 (d, 1H), 2.71 – 2.62 (m, 2H), 2.40 – 2.30 (m, 1H), 2.27 – 2.15 (m, 3H), 1.99 – 1.86 (m, 5H), 1.80 – 1.71 (m, 2H). LCMS: m/z (ESI) [M+H]⁺ 493.5, t_R = 1.56 minutes (Method C) Example 2: (1S,4S)-7-Amino-4'-(dimethylamino)-2'-(((2R,7aS)-2- fluorotetrahydro-1H-pyrrolizin-7a(5H)-yl)methoxy)-4-methyl-3,4,5',8'-tetrahydro-2H- spiro[naphthalene-1,7'-pyrano[4,3-d]pyrimidine]-8-carbonitrile (Compound 109a) DBU (676 mg, 669 μL, 4 equiv., 4.44 mmol) was added to a stirred solution of (1S,4S)- 7-amino-2'-(((2R,7aS)-2-fluorotetrahydro-1H-pyrrolizin-7a(5H)-yl)methoxy)-4'-hydroxy-4- methyl-3,4,5',8'-tetrahydro-2H-spiro[naphthalene-1,7'-pyrano[4,3-d]pyrimidine]-8- carbonitrile (560 mg, 1 equiv., 1.11 mmol), benzotriazol-1- yloxy)tris(dimethylamino)phosphonium hexafluorophosphate (638 mg, 1.3 equiv., 1.44 mmol), and dimethylamine (60.0 mg, 666 μL, 2.0 M, 1.2 equiv., 1.33 mmol) in acetonitrile (11.1 mL). The resulting mixture was stirred at room temperature for 50 minutes and then diluted with water and EtOAc. The two phases were separated. The aqueous layer was extracted with EtOAc (× 3). The combined organic layers were washed with brine (× 2), 10% LiCl aqueous solution (× 3), dried over sodium sulfate, filtered, and concentrated to a yellow solid, which was purified twice by column chromatography (RediSep Rf Gold silica gel cartridge; liquid load in DCM with gradient elution 0:100-A:B to 20:80-A:B where A is a premixed solution of 2.5% NH₄OH and 20% MeOH in DCM; and B is DCM) to afford (1S,4S)- 7-amino-4'-(dimethylamino)-2'-(((2R,7aS)-2-fluorotetrahydro-1H-pyrrolizin-7a(5H)- yl)methoxy)-4-methyl-3,4,5',8'-tetrahydro-2H-spiro[naphthalene-1,7'-pyrano[4,3- d]pyrimidine]-8-carbonitrile (100 mg). LCMS: m/z (ESI) [M+H]⁺ 507.3, t_R = 1.18 minutes (Method C) 1H NMR (400 MHz, CDCl₃) δ 7.07 (d, 1H), 6.66 (d, 1H), 5.35 – 5.14 (m, 1H), 5.00 (d, 2H), 4.43 (s, 2H), 4.11 (d, 1H), 3.95 (d, 1H), 3.31 – 3.09 (m, 4H), 3.07 (s, 6H), 2.99 – 2.80 (m, 3H), 2.37 – 2.06 (m, 3H), 1.98 (d, 3H), 1.94 – 1.75 (m, 2H), 1.69 – 1.61 (m, 1H), 1.23 (d, 3H). Example 3: (S)-N4'-((R*)-1-(2-aminopyridin-3-yl)ethyl)-2'-(((2R,7aS)-2- fluorotetrahydro-1H-pyrrolizin-7a(5H)-yl)methoxy)-N4'-methyl-3,4,5',8'-tetrahydro- 2H-spiro[naphthalene-1,7'-pyrano[4,3-d]pyrimidine]-4',7-diamine (Compound 101b) Step 1: 1-(2-(Bis(4-methoxybenzyl)amino)pyridin-3-yl)ethan-1-one To a solution of 1-(2-chloropyridin-3-yl)ethan-1-one (2.00 g, 1 equiv., 12.9 mmol), N- (4-methoxybenzyl)-1-(4-methoxyphenyl)methanamine (6.62 g, 2 equiv., 25.7 mmol), and potassium fluoride (1.12 g, 1.5 equiv., 19.3 mmol) in DMSO (20 mL) was added DIPEA (4.98 g, 6.72 mL, 3 equiv., 38.6 mmol). The mixture was heated at 120 °C for 24 hours. The reaction mixture was cooled to room temperature and diluted with water, brine, and EtOAc. The two layers were separated. The aqueous layer was extracted with EtOAc (x 3). The combined organic extracts were dried over sodium sulfate, filtered, and concentrated to give the crude oil which was purified using a RediSep Rf Gold 120 g silica gel cartridge (DCM with gradient elution from 0:100-EtOAc:DCM to 10:90-EtOAc:DCM) to give 1-(2-(bis(4- methoxybenzyl)amino)pyridin-3-yl)ethan-1-one (4.52g, 11 mmol). ¹H NMR (400 MHz, CDCl₃) δ 8.31 (dd, 1H), 7.76 (dd, 1H), 7.05 – 6.95 (m, 4H), 6.83 – 6.77 (m, 5H), 4.41 (s, 4H), 3.78 (s, 6H), 2.48 (s, 3H). Step 2: rel-(R)-N,N-Bis(4-methoxybenzyl)-3-(1-(methylamino)ethyl)pyridin-2- amine To a stirred solution of 1-(2-(bis(4-methoxybenzyl)amino)pyridin-3-yl)ethan-1-one (310 mg, 1 equiv., 824 μmol) in methanol (3.30 mL) were added methylamine (51.2 mg, 824 μL, 2.0 M, 2 equiv., 1.65 mmol) and titanium(IV) isopropoxide (585 mg, 624 μL, 2.5 equiv., 2.06 mmol). The resulting mixture was heated to 80 °C for 15 hours, then cooled to 0 °C. NaBH₄ (62.3 mg, 2 equiv., 1.65 mmol) was added in one portion and the ice bath was removed. The reaction mixture was stirred at room temperature for 2 hours then quenched by the addition of a saturated aqueous solution of ammonium chloride. The mixture was filtered through a fritted funnel to remove emulsions and white solids. The resulting two layers present in the filtrate were separated. The aqueous layer was extracted with EtOAc (x 3) and the combined organic extracts were dried over sodium sulfate, filtered, and concentrated under reduced pressure to give a residue, which was purified by column chromatography (RediSep Rf Gold 24 g silica gel cartridge;liquid load in DCM with gradient elution from 0:100-premixed solution made up of 2.5% NH₄OH in 20% MeOH/DCM:DCM to 30:70-premixed solution made up of 2.5% NH₄OH in 20% MeOH/DCM:DCM) to give N,N-bis(4-methoxybenzyl)-3- (1-(methylamino)ethyl)pyridin-2-amine (250 mg; 0.59 mmol). 1H NMR (400 MHz, CDCl₃) δ 8.31 (dd, 1H), 7.66 (dd, 1H), 7.21 – 7.08 (m, 4H), 7.03 (dd, 1H), 6.85 – 6.72 (m, 4H), 4.30 (q, 1H), 4.17 (d, 2H), 4.08 (d, 2H), 3.77 (s, 6H), 2.10 (s, 3H), 1.18 (d, 3H). The enantiomers of N,N-bis(4-methoxybenzyl)-3-(1-(methylamino)ethyl)pyridin-2- amine (250 mg, 0.59 mmol) were separated by chiral SFC (Column: Chiralpak IG 21 × 250 mm I.D., 5 μm; Mobile phase: Phase A for CO₂, and Phase B for MeOH (0.05% DEA), Gradient elution: B in A at 20% Flow rate: 50 mL/min, Detector: PDA, Column Temp: 40 °C, Back Pressure: 120 bar) to afford rel-(R)-N,N-bis(4-methoxybenzyl)-3-(1- (methylamino)ethyl)pyridin-2-amine (Peak 1) and rel-(S)-N,N-bis(4-methoxybenzyl)-3-(1- (methylamino)ethyl)pyridine-2-amine (Peak 2). Peak 1: 48.9 mg LCMS: m/z (ESI) [M+H]⁺ 392.4; t_R = 3.67 minutes (Column: Chiralpak IG 4.6 × 100 mm I.D., 5 μm; Mobile phase: Phase A for CO₂, and Phase B for MeOH (0.05% DEA), Isocratic elution: B in A at 20% Flow rate: 0.8 mL/min, Detector: PDA, Column Temp: 40 °C, Runtime = 5 min) Peak 2: 24.2 mg LCMS: m/z (ESI) [M+H]⁺ 392.4; t_R = 4.33 minutes (Column: Chiralpak IG 4.6 × 100 mm I.D., 5 μm; Mobile phase: Phase A for CO₂, and Phase B for MeOH (0.05% DEA), Isocratic elution: B in A at 20% Flow rate: 0.8 mL/min, Detector: PDA, Column Temp: 40 °C, Runtime = 5 min) Step 3: tert-butyl ((S)-4'-(((R*)-1-(2-(bis(4-methoxybenzyl)amino)pyridin-3- yl)ethyl)(methyl)amino)-2'-(((2R,7aS)-2-fluorotetrahydro-1H-pyrrolizin-7a(5H)- yl)methoxy)-3,4,5',8'-tetrahydro-2H-spiro[naphthalene-1,7'-pyrano[4,3-d]pyrimidin]-7- yl)carbamate A solution of tert-butyl ((S)-4'-((1H-benzo[d][1,2,3]triazol-1-yl)oxy)-2'-(((2R,7aS)-2- fluorotetrahydro-1H-pyrrolizin-7a(5H)-yl)methoxy)-3,4,5',8'-tetrahydro-2H- spiro[naphthalene-1,7'-pyrano[4,3-d]pyrimidin]-7-yl)carbamate (50 mg, 1.0 equiv., 74 μmol) and rel-(R)-N,N-bis(4-methoxybenzyl)-3-(1-(methylamino)ethyl)pyridin-2-amine (first eluting peak; 58 mg, 2.0 equiv., 150 μmol) in DMF (0.5 mL) was treated with DIPEA (24 mg, 32 μL, 2.5 equiv., 180 μmol). The reaction mixture was heated at 100 °C for 24 hours. The mixture was purified via reverse phase chromatography (C-18 Biotage column by reverse prep using 10 mM ammonium bicarbonate solution and acetonitrile) to obtain tert-butyl ((S)-4'- (((R*)-1-(2-(bis(4-methoxybenzyl)amino)pyridin-3-yl)ethyl)(methyl)amino)-2'-(((2R,7aS)-2- fluorotetrahydro-1H-pyrrolizin-7a(5H)-yl)methoxy)-3,4,5',8'-tetrahydro-2H- spiro[naphthalene-1,7'-pyrano[4,3-d]pyrimidin]-7-yl)carbamate as a white solid (35 mg). LCMS: m/z (ESI) [M+H]⁺ 914.6, t_R = 2.18 minutes (Method B). 1H NMR (400 MHz, CDCl₃) δ 8.40 (dd, 1 H), 7.66 (dd, 1 H), 7.13-7.16 (m, 1 H), 7.05- 7.09 (m, 1 H), 6.99-7.01 (m, 4 H), 6.88-6.93 (m, 1 H), 6.76-6.81 (m, 4 H), 5.13-5.28 (m, 1 H), 4.72-4.76 (m, 1 H), 3.94-4.32 (m, 6 H), 3.76-3.77 (m, 6 H), 3.11-3.28 (m, 1 H), 2.92-3.00 (m, 2 H), 2.70-2.74 (m, 1 H), 2.59 (s, 3 H), 2.02-2.29 (m, 3 H), 1.71-1.96 (m, 3 H), 1.51 (s, 5H). Step 2: (S)-N4'-((R*)-1-(2-aminopyridin-3-yl)ethyl)-2'-(((2R,7aS)-2- fluorotetrahydro-1H-pyrrolizin-7a(5H)-yl)methoxy)-N4'-methyl-3,4,5',8'-tetrahydro- 2H-spiro[naphthalene-1,7'-pyrano[4,3-d]pyrimidine]-4',7-diamine tert-Butyl ((S)-4'-(((R*)-1-(2-(bis(4-methoxybenzyl)amino)pyridin-3- yl)ethyl)(methyl)amino)-2'-(((2R,7aS)-2-fluorotetrahydro-1H-pyrrolizin-7a(5H)-yl)methoxy)- 3,4,5',8'-tetrahydro-2H-spiro[naphthalene-1,7'-pyrano[4,3-d]pyrimidin]-7-yl)carbamate (40 mg, 1.0 equiv., 44 μmol) in DCM (1.0 mL) was treated with trifluoroacetic acid (25 mg, 17μL, 5.0 equiv., 220 μmol). The reaction mixture was stirred at room temperature for 30 minutes, then heated at 60 ℃ for 27 hours. The solvent was removed in vacuo and the crude residue was subjected to reverse phase purification (Pre-column: VanGuard Pre-Column CSH C18, 1.7 μm, 2.1 x 5 mm, Pre-run: 1mL/min for 0.7 min. Column: Acquity UPLC, CSH C18, 1.7 μm, 2.1 x 30 mm, Flow rate: 0.9 mL/min, 5 to 100% MeCN/water (+ 10 mM ammonium bicarbonate) for 3 min) to obtain (S)-N4'-((R*)-1-(2-aminopyridin-3-yl)ethyl)-2'-(((2R,7aS)-2- fluorotetrahydro-1H-pyrrolizin-7a(5H)-yl)methoxy)-N4'-methyl-3,4,5',8'-tetrahydro-2H- spiro[naphthalene-1,7'-pyrano[4,3-d]pyrimidine]-4',7-diamine as a white solid (2 mg). LCMS: m/z (ESI) [M+H]⁺ 574.4, t_R = 1.55 minutes (Method B). 1H NMR (400 MHz, DMSO-d6) δ 7.91 (dd, 1 H), 7.52 (dd, 1 H), 6.75 (d, 1 H), 6.58- 6.62 (m, 2 H), 6.43 (dd, 1 H), 5.73-5.73 (m, 2 H), 5.63 (d, 1 H), 5.18-5.33 (m, 1 H), 4.76-4.80 (m, 3 H), 4.55 (d, 1 H), 3.93 (dd, 2 H), 2.75-3.09 (m, 6 H), 2.54-2.61 (m, 3 H), 1.63-2.10 (m, 8 H), 1.48-1.50 (m, 3 H), 1.20-1.25 (m, 2 H). Example 4: (SR)-7-amino-2'-(((2R,7aS)-2-fluorotetrahydro-1H-pyrrolizin- 7a(5H)-yl)methoxy)-3,4,5',8'-tetrahydro-2H-spiro[naphthalene-1,7'-pyrano[4,3- d]pyrimidine]-8-carbonitrile (Compound 110a) Step 1: (rac)-N,N-dibenzyl-8-bromo-4'-hydrazineyl-2'-(methylthio)-3,4,5',8'- tetrahydro-2H-spiro[naphthalene-1,7'-pyrano[4,3-d]pyrimidin]-7-amine To a slurry of (rac)-N,N-dibenzyl-8-bromo-4'-chloro-2'-(methylthio)-3,4,5',8'- tetrahydro-2H-spiro[naphthalene-1,7'-pyrano[4,3-d]pyrimidin]-7-amine (2000 mg, 1 equiv., 3.295 mmol) in EtOH (32.95 mL) was added hydrazine, hydrate (1.320 g, 1.293 mL, 8 equiv., 26.36 mmol). The reaction mixture was heated to 80 °C for 16 hours. The mixture was cooled to room temperature, concentrated under reduced pressure and diluted in MeCN (15 mL). The solids were filtered to afford (rac)-N,N-dibenzyl-8-bromo-4'-hydrazineyl-2'-(methylthio)- 3,4,5',8'-tetrahydro-2H-spiro[naphthalene-1,7'-pyrano[4,3-d]pyrimidin]-7-amine (720 mg). The filtrate was concentrated and dry loaded onto silica using DCM/MeOH and purified on a 40 g silica column (100% DCM to 10% MeOH/DCM) to afford a second batch of (rac)-N,N- dibenzyl-8-bromo-4'-hydrazineyl-2'-(methylthio)-3,4,5',8'-tetrahydro-2H-spiro[naphthalene- 1,7'-pyrano[4,3-d]pyrimidin]-7-amine (1.185 g) as a white foamy solid. LCMS: m/z (ESI) [M+H]⁺ = 602, 604 , t_R = 3.06 minutes, (Method E). 1H NMR (400 MHz, CDCl₃) δ 7.35 – 7.30 (m, 4H), 7.29 – 7.27 (m, 1H), 7.25 – 7.24 (m, 1H), 7.23 – 7.17 (m, 2H), 6.90 (d, 1H), 6.80 (d, 1H), 5.63 (s, 1H), 5.30 (s, 1H), 4.68 – 4.52 (m, 2H), 4.19 – 4.02 (m, 6H), 3.96 (d, 1H), 2.86 – 2.72 (m, 3H), 2.56 (s, 2H), 2.52 (s, 1H), 2.17 – 2.09 (m, 1H), 1.91 – 1.81 (m, 2H), 1.77 – 1.67 (m, 1H). Step 2: (rac)-N,N-dibenzyl-8-bromo-2'-(methylthio)-3,4,5',8'-tetrahydro-2H- spiro[naphthalene-1,7'-pyrano[4,3-d]pyrimidin]-7-amine To a solution of (rac)-N,N-dibenzyl-8-bromo-4'-hydrazineyl-2'-(methylthio)-3,4,5',8'- tetrahydro-2H-spiro[naphthalene-1,7'-pyrano[4,3-d]pyrimidin]-7-amine (1.15 g, 1 equiv., 1.91 mmol) in chloroform (19.1 mL) was added manganese dioxide (1.66 g, 10 equiv., 19.1 mmol) in one portion at room temperature. The reaction was stirred at room temperature for 3 hours. The mixture was filtered through a pad of celite and washed with 100 mL of DCM. The dark mixture was concentrated under reduced pressure and the resulting residue was purified by silica column, (100% Heptanes to 45% EtOAc/Heptanes) to afford (rac)-N,N-dibenzyl-8- bromo-2'-(methylthio)-3,4,5',8'-tetrahydro-2H-spiro[naphthalene-1,7'-pyrano[4,3- d]pyrimidin]-7-amine (280 mg) as an off-white solid. LCMS: m/z (ESI) [M+H]⁺ = 572, 574 , t_R = 4.24 minutes, (Method E). 1H NMR (400 MHz, CDCl₃) δ 8.29 (s, 1H), 7.36 – 7.26 (m, 7H), 7.25 – 7.17 (m, 3H), 6.92 (d, 1H), 6.82 (d, 1H), 4.97 – 4.84 (m, 2H), 4.18 – 4.03 (m, 5H), 2.91 (d, 1H), 2.86 – 2.74 (m, 2H), 2.58 (s, 3H), 2.13 – 2.05 (m, 1H), 1.92 (q, 2H), 1.74 (q, 1H). Step 3: (rac)-7-(dibenzylamino)-2'-(methylthio)-3,4,5',8'-tetrahydro-2H- spiro[naphthalene-1,7'-pyrano[4,3-d]pyrimidine]-8-carbonitrile To a stirred solution of (rac)-N,N-dibenzyl-8-bromo-2'-(methylthio)-3,4,5',8'- tetrahydro-2H-spiro[naphthalene-1,7'-pyrano[4,3-d]pyrimidin]-7-amine (280 mg, 1 equiv., 489 μmol) in DMF (4.89 mL) was added copper(I)cyanide (263 mg, 6 equiv., 2.93 mmol). The reaction mixture was stirred for 6 hours at 80 °C. The reaction mixture was quenched with 20 mL of aqueous ammonium hydroxide and water (10 mL). The resulting suspension was allowed to stand at room temperature for 16 hours. The resulting light colored slurry and a blue supernatant was filtered and washed with water/dilute ammonia to afford (rac)-7- (dibenzylamino)-2'-(methylthio)-3,4,5',8'-tetrahydro-2H-spiro[naphthalene-1,7'-pyrano[4,3- d]pyrimidine]-8-carbonitrile (234 mg). LCMS: m/z (ESI) [M+H]⁺ = 519 , t_R = 3.84 minutes, (Method E) 1H NMR (400 MHz, DMSO) δ 8.49 (s, 1H), 7.39 – 7.11 (m, 14H), 4.95 – 4.79 (m, 2H), 4.29 – 4.17 (m, 4H), 3.38 (d, 1H), 3.31 (s, 3H), 3.03 (d, 1H), 2.04 – 1.95 (m, 1H), 1.85 – 1.65 (m, 3H). Step 4: (SR)-7-(dibenzylamino)-2'-(((2R,7aS)-2-fluorotetrahydro-1H-pyrrolizin- 7a(5H)-yl)methoxy)-3,4,5',8'-tetrahydro-2H-spiro[naphthalene-1,7'-pyrano[4,3- d]pyrimidine]-8-carbonitrile To a stirred solution of (rac)-7-(dibenzylamino)-2'-(methylthio)-3,4,5',8'-tetrahydro- 2H-spiro[naphthalene-1,7'-pyrano[4,3-d]pyrimidine]-8-carbonitrile (70 mg, 1 equiv., 0.13 mmol) in THF (0.67 mL), water (0.34 mL) and methanol (0.34 mL) was added Oxone (0.37 g, 45% wt, 2 equiv., 0.27 mmol) at room temperature. The mixture was stirred at room temperature for 90 minutes, followed by the addition of 200 mg more Oxone. The resulting mixture was stirred at room temperature for 3 hours. The reaction mixture was then quenched by the addition of water, sodium thiosulfate, and extracted with DCM (30 mL). The combined organic extracts were dried over magnesium sulfate, filtered, and concentrated to afford (rac)- 7-(dibenzylamino)-2'-(methylsulfonyl)-3,4,5',8'-tetrahydro-2H-spiro[naphthalene-1,7'- pyrano[4,3-d]pyrimidine]-8-carbonitrile, which was taken without further purification into the next step. LCMS: m/z (ESI) [M+H]⁺ = 551.2, t^ = 3.4 min, (Method E) To a stirred solution of crude (rac)-7-(dibenzylamino)-2'-(methylsulfonyl)-3,4,5',8'- tetrahydro-2H-spiro[naphthalene-1,7'-pyrano[4,3-d]pyrimidine]-8-carbonitrile (60 mg, 1 equiv., 0.11 mmol) in THF (1.1 mL) was added ((2R,7aS)-2-fluorotetrahydro-1H-pyrrolizin- 7a(5H)-yl)methanol (69 mg, 4 equiv., 0.44 mmol) and the orange mixture was cooled on ice. Then, a 1 M THF solution of LiHMDS (27 mg, 0.16 mL, 1 M, 1.5 equiv., 0.16 mmol) was added dropwise and the resulting mixture was stirred at room temperature for 90 minutes. The reaction mixture was quenched by the addition of water and EtOAc, basified with aqueous sodium bicarbonate. The layers were separated and the aqueous phase was extracted with EtOAc (30 mL). The combined organic extracts were dried over magnesium sulfate, filtered, concentrated, and purified by column chromatography (100% DCM to 10% MeOH/DCM with 1.5% NH₄OH) to afford (SR)-7-(dibenzylamino)-2'-(((2R,7aS)-2-fluorotetrahydro-1H- pyrrolizin-7a(5H)-yl)methoxy)-3,4,5',8'-tetrahydro-2H-spiro[naphthalene-1,7'-pyrano[4,3- d]pyrimidine]-8-carbonitrile (20 mg). LCMS: m/z (ESI) [M+H]⁺ = 630.4, t_R = 2.48 minutes, (Method E) Step 5: (SR)-7-amino-2'-(((2R,7aS)-2-fluorotetrahydro-1H-pyrrolizin-7a(5H)- yl)methoxy)-3,4,5',8'-tetrahydro-2H-spiro[naphthalene-1,7'-pyrano[4,3-d]pyrimidine]- 8-carbonitrile To a solution of (SR)-7-(dibenzylamino)-2'-(((2R,7aS)-2-fluorotetrahydro-1H- pyrrolizin-7a(5H)-yl)methoxy)-3,4,5',8'-tetrahydro-2H-spiro[naphthalene-1,7'-pyrano[4,3- d]pyrimidine]-8-carbonitrile (35 mg, 1 equiv., 56 μmol), EtOH (1.0 mL), and acetic acid (0.10 mL) was added Pd(OH)₂ on carbon (39 mg, 20% wt, 1 equiv., 56 μmol) under an atmosphere of nitrogen. A balloon with hydrogen was attached and the mixture was backfilled with hydrogen (3x). The resulting reaction was stirred at room temperature for 4 hours. The mixture was filtered through a pad of celite and washed with DCM. The filtrate was concentrated and the crude material was purified by reverse phase chromatography (DMF/MeCN (2.0 mL); column: XSelect® CSH™ Prep C185 μm OBD™ 19×150 mm; mobile phase: water 0.1% FA / MeCN 0.1% FA; flow: 18.9 mL/min; gradient: 5 → 100% over 22 minutes) to afford (SR)-7- amino-2'-(((2R,7aS)-2-fluorotetrahydro-1H-pyrrolizin-7a(5H)-yl)methoxy)-3,4,5',8'- tetrahydro-2H-spiro[naphthalene-1,7'-pyrano[4,3-d]pyrimidine]-8-carbonitrile (2.3 mg). LCMS: m/z (ESI) [M+H]⁺ 450.0, t_R = 1.55 minutes, (Method E) Example 45: (1S,4S)-7-Amino-2'-(((2R,7aS)-2-fluorotetrahydro-1H-pyrrolizin- 7a(5H)-yl)methoxy)-4'-((2-hydroxyethyl)(methyl)amino)-4-methyl-3,4,5',8'-tetrahydro- 2H-spiro[naphthalene-1,7'-pyrano[4,3-d]pyrimidine]-8-carbonitrile (Compound 150a) ((1H-Benzo[d][1,2,3]triazol-1-yl)oxy)tris(dimethylamino)phosphonium hexafluorophosphate(V) (33 mg, 0.075 mmol) was added to a solution of (1S,4S)-7-amino-2'- (((2R,7aS)-2-fluorotetrahydro-1H-pyrrolizin-7a(5H)-yl)methoxy)-4'-hydroxy-4-methyl- 3,4,5',8'-tetrahydro-2H-spiro[naphthalene-1,7'-pyrano[4,3-d]pyrimidine]-8-carbonitrile (30 mg, 0.063 mmol) and DIPEA (0.11 mL, 0.63 mmol) in DMF (0.5 mL). The reaction mixture was stirred at room temperature for 1 hour followed by the addition of 2-(methylamino)ethanol (25 L, 0.31 mmol). The resulting mixture was stirred at room temperature for 80 minutes then purified directly by reverse phase chromatography (C18 silica, 20g Santai C18 cartridge using 10mM ammonium bicarbonate in acetonitrile) to afford (1S,4S)-7-amino-2'-(((2R,7aS)-2- fluorotetrahydro-1H-pyrrolizin-7a(5H)-yl)methoxy)-4'-((2-hydroxyethyl)(methyl)amino)-4- methyl-3,4,5',8'-tetrahydro-2H-spiro[naphthalene-1,7'-pyrano[4,3-d]pyrimidine]-8- carbonitrile (14 mg, 0.026 mmol). LCMS: m/z (ESI) [M+H]⁺ 537.4, t_R = 1.38 minutes (Method B) 1H NMR (400 MHz, CD₃OD) δ 7.12 (d, 1H), 6.76 (d, 1H), 5.23 (d, 1H), 5.08 (d, 1H), 4.95 (d, 1H), 4.14 (d, 1H), 4.04 (d, 1H), 3.90 – 3.77 (m, 2H), 3.77 – 3.66 (m, 1H), 3.59 (dt, 1H), 3.22 (s, 5H), 3.20 – 3.10 (m, 3H), 2.98 (td, 1H), 2.95 – 2.78 (m, 2H), 2.36 – 2.14 (m, 2H), 2.14 – 2.04 (m, 3H), 2.04 – 1.91 (m, 3H), 1.91 – 1.59 (m, 1H), 1.24 (d, 3H). Example 46: (1S,4S)-7-Amino-2'-(((2R,7aS)-2-fluorotetrahydro-1H-pyrrolizin- 7a(5H)-yl)methoxy)-4'-((1-hydroxy-2-methylpropan-2-yl)amino)-4-methyl-3,4,5',8'- tetrahydro-2H-spiro[naphthalene-1,7'-pyrano[4,3-d]pyrimidine]-8-carbonitrile (Compound 159a) DIPEA (0.11 mL, 0.63 mmol) was added to a solution of (1S,4S)-7-amino-2'- (((2R,7aS)-2-fluorotetrahydro-1H-pyrrolizin-7a(5H)-yl)methoxy)-4'-hydroxy-4-methyl- 3,4,5',8'-tetrahydro-2H-spiro[naphthalene-1,7'-pyrano[4,3-d]pyrimidine]-8-carbonitrile (30 mg, 0.063 mmol), 2-amino-2-methylpropan-1-ol (54 mg, 0.61 mmol), and ((1H- benzo[d][1,2,3]triazol-1-yl)oxy)tris(dimethylamino)phosphonium hexafluorophosphate(V) (55 mg, 0.13 mmol) in acetonitrile (0.5 mL). The mixture was stirred at 90ºC for 2 days, then cooled and concentrated. The residue was partitioned between ethyl acetate (3 mL) and water (3 mL). The aqueous layer was extracted with ethyl acetate (3x3 mL). The combined organic layers were washed with saturated sodium bicarbonate (5 mL), dried over sodium sulfate, and concentrated to a residue which was purified by column chromatography twice (12g silica eluting with 0-20% MeOH in DCM) to afford (1S,4S)-7-amino-2'-(((2R,7aS)-2- fluorotetrahydro-1H-pyrrolizin-7a(5H)-yl)methoxy)-4'-((1-hydroxy-2-methylpropan-2- yl)amino)-4-methyl-3,4,5',8'-tetrahydro-2H-spiro[naphthalene-1,7'-pyrano[4,3-d]pyrimidine]- 8-carbonitrile (10.4 mg, 0.019 mmol). LCMS: m/z (ESI) [M+H]⁺ 551.3, tR = 1.26 minutes (Method L) 1H NMR (400 MHz, CDCl₃) δ 7.08 (d, 1H), 6.67 (d, 1H), 5.27 (d, 1H), 4.69 (d, 1H), 4.57 (d, 1H), 4.46 (s, 2H), 4.21 (s, 1H), 4.13 – 3.96 (m, 2H), 3.68 (s, 2H), 3.34 – 3.11 (m, 4H), 3.00 – 2.92 (m, 1H), 2.91 – 2.74 (m, 2H), 2.38 – 2.03 (m, 3H), 2.00 – 1.78 (m, 6H), 1.69 – 1.52 (m, 1H), 1.41 (d, 6H), 1.34 – 1.13 (m, 4H). The following examples were synthesized using methods similar to those described in the examples above: Example B1. Surface Plasmon Resonance Methods herein pertain to Cytiva (formerly Biacore) instrumentation and consumables and are applicable to other SPR-based systems. A Series S Streptavidin or Neutravidin chip is docked into a Biacore 8K. The instrument is then primed into an appropriate running buffer (for example, 20 mM HEPES, pH 7.4, 150 mM NaCl, 5 mM MgCl₂, 1 mM TCEP, 0.005% Tween-20, and 2% DMSO) supplemented with either 5 μM GDP or GMPPNP to match the nucleotide state of the KRas state being tested (GDP for KRas in the GDP-bound state; and GMPPNP for KRas in the GTP-bound state). Biotinylated-KRas loaded with the appropriate nucleotide state (e.g., GDP or GMPPNP) is then captured to between 500-2000 RU to provide adequate signal for small molecules of interest, typically in a range of 300-600 Da, as well as to accommodate a range of potencies, when appropriate. The remaining biotin binding sites can be blocked with Biocytin. Compounds are injected over both a reference surface (Streptavidin or Neutravidin alone) as well as the active surface (KRas captured to Neutravidin or Streptavidin), and all curves are double-referenced before analysis (specifically, a signal subtraction of the reference flow cell from the active flow cell as well as a buffer subtraction). Where appropriate, a solvent correction is applied to all curves to account for differential bulk effects from DMSO on the reference and active surfaces. Data is then analyzed using the Biacore software fitting kinetics if resolvable, or fitting via a Langmuir isotherm model if no kinetics are resolvable, to report a binding affinity as a dissociation constant, K_D. Example B2. SOS1-Catalyzed Nucleotide Exchange Assay KRas G12R and WT: Compounds are pre-dispensed using acoustic transfer technology into a black, low volume 384-well assay plate. A 10-point dose response of each compound is performed with a 30 μM top dose. Biotinylated KRas WT(1-169) or KRas G12R (1-169) loaded with GDP nucleotide is mixed with Streptavidin-Tb cryptate (Cisbio) in assay buffer (20 mM HEPES pH 7.4, 150 mM NaCl, 2 mM MgCl₂, and 0.005% CA680) to produce a 1.5x solution. 10 μL of the 1.5x KRas-cryptate solution is added to wells of a black, low- volume 384-well assay plate. The KRas/cryptate-compound mixture is incubated for 1 hour at room temperature. A 3x solution of SOS1 (564-1049) and EDA-GTP-DY-647P1 (Jena Bioscience) is prepared in assay buffer.5 μL of the SOS1-labeled GTP solution is added to the wells to initiate the nucleotide exchange reaction. The final concentration of KRas G12R and SOS1 are 10 nM and 200 nM, respectively. The final concentration of KRas WT and SOS1 are 20 nM and 10 nM, respectively. The plate is allowed to incubate for 1 hr, then time resolved fluorescence is read on a PHERAstar plate reader equipped with a filter module with excitation = 337 nm and emission 1 = 620 nm, emission 2 = 665 nm. The TR-FRET signal is calculated as the ratio of fluorescence intensity [emission 665 nm]/[emission 620 nm]. IC₅₀ values are calculated using a four-parameter, variable response sigmoidal dose response curve fit in PerkinElmer Signals VitroVivo. KRas G12V: Compounds were pre-dispensed via Echo liquid handling (acoustic, touch-free) to generate assay ready plates (ARP). More precisely, a 10-point concentration response curve for each compound was prepared with appropriate top concentration (1 μM, 10 μM, 100 μM). Biotinylated KRas G12V (aa 1-169) loaded with GDP nucleotide and Streptavidin-Europium (SA-EU, Columbia Biosciences) were preincubated in assay buffer (20 mM HEPES pH 7.4, 150 mM NaCl, 5 mM MgCl₂, 1 mM DTT, 0.01% Brij-35, 0.3 mg/mL BSA) on ice for 30 min. Separately SOS1 (aa 546-1049) and EDA-GTP-DY647P1 (Jena Bioscience) were preincubated in assay buffer on ice for 30 min. After 30 minutes of incubation for the assay components, 5 μL buffer and 5 μL of KRas G12V-SA-Eu were added to each well of the ARP. After a further 30 min, 5 μL of SOS1-EDA-GTP-D467P1 was added to start the nucleotide exchange reaction. Final concentration in the assay were 5 nM KRas G12V, 50 nM SOS1 (aa 564-1049). The reaction was allowed to proceed for 60-90 minutes after which the plate was read on a plate reader. After normalization of the raw data, the data was fit to a four-parameter logistic curve. The geometric mean IC₅₀ value is presented in Table B1 below with two significant figures. Table B1. Example B3. KRas-cRAF Protein-Protein Interaction (PPI) Assay Compounds are pre-dispensed using acoustic transfer technology into a black, low volume 384-well assay plate. A 10-point dose response of each compound is performed with a 30μM top dose. Biotinylated KRas protein (e.g., KRas G12R(1-169)) is loaded with GppNHp (i.e., GMPPNP) nucleotide and GST-cRAF(1-149) are diluted to 90 nM and 30 nM, respectively, in assay buffer (20 mM HEPES pH 7.4, 150 mM NaCl, 5 mM MgCl₂, and 0.005% CA680).5 μL of KRas protein is added to wells of a black, low-volume 384-well assay plate. The KRas-compound mixture is incubated for 30 minutes at room temperature.5 μL of GST- cRAF protein is added to the KRas-compound mixture and incubated for 30 minutes at room temperature. 100x stocks of Tb cryptate-labeled anti-GST antibody (Anti-GST-Tb) (Cisbio) and Streptavidin-XL655 (Cisbio) are used to make a 3x detection mixture in a total volume of 5 μL of assay buffer. The detection mixture is added to the assay wells and incubated an additional 1 hour at room temperature. Time resolved fluorescence is read on a PHERAstar plate reader equipped with a filter module with excitation = 337 nm and emission 1 = 620 nm, emission 2 = 665 nm. The TR-FRET signal is calculated as the ratio of fluorescence intensity [emission 665 nm]/[excitation 337 nm]. IC₅₀ values are calculated using a four-parameter, variable response sigmoidal dose response curve fit in PerkinElmer Signals VitroVivo. Example B4. KRas-cRAF Protein-Protein Interaction (PPI) Assay Version 1: Compounds are pre-dispensed via Echo liquid handling (acoustic, touch- free) to generate assay ready plates (ARP). A 10-point dose response of each compound is performed with a 30 μM top dose. Biotinylated KRas G12V (aa 1-169) loaded with GMPPNP nucleotide and Streptavidin-Europium (SA-EU, Columbia Biosciences) are preincubated in assay buffer (20 mM HEPES pH 7.4, 150 mM NaCl, 5 mM MgCl₂, 1 mM DTT, 0.01% Brij- 35, 0.3 mg/ml BSA) on ice for 30 min. Separately GST-tagged cRAF(1-149) and anti-GST- APC antibody (Columbia Biosciences) are preincubated in assay buffer on ice for 30 min. After incubation, 5 μL buffer and 5 μL of KRas G12V-SA-Eu are added to each well of the ARP. After a 30-minute equilibration phase at room temperature, 5 uL of GST-cRAF-anti-GST-APC is added to each well. The final concentrations in the assay are 10 nM KRas G12V, 10 nM cRAF. The reaction is allowed to proceed for 60-90 minutes after which the plate is read on a PHERAstar FSX plate reader (exc: 337 nm, em 1: 665 nm, em 2: 620 nm). After normalization of the raw data (ratio of Signal_665nm/Signal_620nm) the data is fit to a four-parameter logistic curve in GraphPad Prism (v9.4.1). Version 2: Compounds are pre-dispensed via Echo liquid handling (acoustic, touch- free) to generate assay ready plates (ARP). More precisely, a 10-point concentration response curve for each compound is prepared with appropriate top concentration (e.g., 1 μM or 30 μM). Biotinylated KRas G12V (aa 1-169) loaded with GMPPNP nucleotide and Streptavidin- Europium (SA-EU, Columbia Biosciences) are preincubated in assay buffer (20 mM HEPES pH 7.4, 150 mM NaCl, 5 mM MgCl₂, 1 mM DTT, 0.01% Brij-35, 0.3 mg/ml BSA) on ice for 30 min. Separately, GST-tagged cRAF(1-149) and anti-GST-APC antibody (Columbia Biosciences) are preincubated in assay buffer on ice for 30 min. After incubation, 5 μL of KRas G12V-SA-Eu is added to each well of the ARP. After a 30 min equilibration phase at room temperature, 5 μL of GST-cRAF-anti-GST-APC is added to each well. Final concentrations in the assay are 5 nM KRas G12V, 5 nM cRAF. The reaction is allowed to proceed for 60-90 minutes after which the plate is read on a PHERAstar FSX plate reader (exc: 337 nm, em 1: 665 nm, em 2: 620 nm). After normalization of the raw data (ratio of Signal_665nm/Signal_620nm) the data is fit to a four-parameter logistic curve. Version 3: Compounds are pre-dispensed via Echo liquid handling (acoustic, touch- free) to generate assay ready plates (ARP). More precisely, a 10-point concentration response curve for each compound is prepared with appropriate top concentration (e.g., 1 μM or 30 μM). Biotinylated KRas G12D (aa 1-169) loaded with GMPPNP nucleotide and Streptavidin- Europium (SA-EU, Columbia Biosciences) are preincubated in assay buffer (20 mM HEPES pH 7.4, 150 mM NaCl, 5 mM MgCl2, 1 mM DTT, 0.01% Brij-35, 0.3 mg/ml BSA) on ice for 30 min. Separately, GST-tagged cRAF(1-149) and anti-GST-APC antibody (Columbia Biosciences) are preincubated in assay buffer on ice for 30 min. After incubation, 5 μL of KRas G12D-SA-Eu is added to each well of the ARP. After a 30 min equilibration phase at room temperature, 5 μL of GST-cRAF-anti-GST-APC is added to each well. Final concentrations in the assay are 4 nM KRas G12D, 4 nM cRAF. The reaction is allowed to proceed for 60-90 minutes after which the plate is read on a PHERAstar FSX plate reader (exc: 337 nm, em 1: 665 nm, em 2: 620 nm). After normalization of the raw data (ratio of Signal_665nm/Signal_620nm) the data is fit to a four-parameter logistic curve. Example B5. Surface Plasmon Resonance (SPR) Biacore 8K buffer line was placed into 1 L of Immobilization buffer (20 mM HEPES pH 7.5 / 150 mM NaCl / 5 mM MgCl₂ / 0.5 mM TCEP / 0.005% P20 / 500 nM GDP) and Change Solutions was performed. A Biacore Series S SA chip (Cytiva 29104992) was inserted and Change Solutions was performed 3 times. The chip surface was conditioned by injecting conditioning solution (40 mM NaOH / 1 mM NaCl) in four pulses of 30 seconds at 30 μL/min. These pulses were followed by pulses of running buffer injected for 30 seconds at 30 μL/min. Normalization was run using the BiaNormalize solution (Cytiva 29207950). 300 nM Biotinylated KRas G12V 1-169 was injected over all active flow cells at a flow rate of 5 μL/min until reaching a response of 1000 RUs. The buffer line was switched into Running Buffer (20 mM HEPES pH 7.5 / 150 mM NaCl / 5 mM MgCl₂ / 0.5mM TCEP / 0.005% P20 / 500 nM GDP / 2% DMSO) and Change Solutions was performed. Compounds were plated into a Greiner v-bottom 384-well Microplate (Greiner 781280) in 8-point dose-response with a log- fold dilution with a final volume of 2 μL in DMSO. 98 μL of non-DMSO containing buffer was backfilled into all compound wells (final volume of 100 uL with 2% DMSO). Solvent corrections of 1%, 1.5%, 2%, 2.5%, and 3% DMSO were plated into a Greiner U-bottom 96- well microplate (Greiner 650201). The SPR method was run with both flow cell and sample compartment at 20 °C or 37 °C with 5 startup cycles of 30 second association, and 30 second dissociation at a flow rate of 70 μL/min. An eight-point single cycle kinetics (SCK) analysis was run with 30 second association time, 1600 second dissociation time, 70 μL/min flow rate, 1600 sec stability period, and a 50% DMSO wash after injection. Solvent corrections were run at the end of the method. Results were analyzed with the Biacore Insights Evaluation Software using the Single Cycle Kinetics analysis method. Sensorgrams were fit using a 1:1 binding model. KD values, as an average of multiple runs, if applicable, are presented in Table B2 with two significant figures. Table B2. Example B6 – Measurement of cellular phospho- and total ERK1/2 In a white, opaque-bottom Revvity CulturPlate-384, SW620 [SW-620] (ATCC CCL- 227™) cells were seeded at previously determined seeding densities such that the well would be approximately 80% confluent at the end of the assay, and incubated overnight in a standard 37 °C, 5% CO₂ humidified incubator. The day after seeding, compounds were dispensed into the treatment plates using a Tecan D300e compound printer in 9-point DRC format, 10- micromolar top concentration, in triplicate. Treatment plates were then returned to a 37 °C, 5% CO2 humidified incubator for 2 hours unless otherwise stated. Following compound treatment, phosphoERK and total ERK were measured using the Alpha SureFire Ultra Multiplex Phospho/Total ERK1/2 Assay Kit (Revvity). All media was removed from the treatment plate(s) and the cells subsequently lysed using 1X Lysis Buffer in accordance with manufacturer protocol. Next, the Acceptor Mix (prepared in accordance with manufacturers protocol) was added to each well of the assay plate and incubated on an orbital shaker at room temperature for 2 hours. Following Acceptor incubation, the Donor Mix (prepared in accordance with manufacturer protocol) was added to each well of the assay plate, covered to protect from light and incubated on an orbital shaker at room temperature overnight. Assay plates were read the following day on a BMG Labtech PHERAstar FSX microplate reader. Data were then analyzed by calculating the ratio of ERK1/2-phosphorylation relative to Total ERK1/2 for each individual well. 1/2 The replicate ratios for each concentration were averaged and normalized to DMSO control or other corresponding co-treatment before performing a variable slope (4-parameter), non-linear regression curve fit for each compound of interest. IC₅₀ values, as a geometric mean of multiple runs, if applicable, are presented in Table B3 with two significant figures. Table B3. Example B7 - Measurement of cellular proliferation In a black, clear-bottom 384-well tissue culture treated plates, SW620 [SW-620] (ATCC CCL-227™) cells were seeded at previously determined seeding densities such that the well would be approximately 80% confluent at the end of the assay. Immediately after seeding, compounds were dispensed into the treatment plates using a Tecan D300e compound printer in 9-point DRC format, 10- micromolar top concentration, in triplicate. Treatment plates were then transferred to a 37 °C, 5% CO₂ humidified incubator for 72 hours unless otherwise stated. After the completion of treatment, CELLTITER-GLO® 2.0 reagent (Promega) was added directly to each well. The plates were covered to protect from light and incubated on an orbital shaker at room temperature for 30 minutes. Immediately before reading the assay plates, an opaque seal was attached to the bottom of each clear-bottom plate; assay plates were then read on a BMG Labtech PHERAstar FSX microplate reader. Data were analyzed by calculating the ratio of signal from treated wells relative to negative control-treated wells. The replicates were averaged and a variable slope (4-parameter), non-linear regression curve was fitted for each compound of interest. IC₅₀ values, as a geometric mean of multiple runs, if applicable, are presented in Table B4 with two significant figures. Compounds of the disclosure also showed activity in similar CTG assays using AGS (KRas G12D; ATCC AGS (ATCC CRL-1739™)) and MIAPaCa-2 (KRas G12C; (Sigma cb_85062806)) cells with a similar potency range to SW620. Table B4. Example B8 – Protein Production A KRas construct of amino acid residues 1-169, harboring the G12V mutation, a C- terminal Avi tag, and an N-terminal 6x Histidine tag followed by a tobacco etch virus (TEV) protease site was expressed in E. coli BL21(DE3). A single colony was inoculated in 100 mL LB with 100 μg/mL ampicillin and incubated at 37 °C overnight on an orbital shaker at 225 rpm. The overnight strain was inoculated into 2L TB with 100 μg/mL ampicillin at a ratio of 1:100. The culture was grown at 37 °C on an orbital shaker until the OD₆₀₀ reached 0.8. The culture was cooled to 18 °C, induced with IPTG at a final concentration of 0.2 mM and grown 16 hours at 18 °C on an orbital shaker at 180 rpm. Cells were harvested at 13,600 x g for 5 minutes at 4 °C. The KRas G12V protein was purified by affinity chromatography using NiNTA resin. The cell pellet resuspended in 20 mM Tris pH 8.0, 500 mM NaCl, 2 mM beta-mercaptoethanol supplemented with EDTA-free protease inhibitor (Roche). Cells were sonicated at a power of 350 W with 3 s on and 3 s off pulses for a total of 300 cycles. The lysate was centrifuged at 13,600 x g at 4 °C for 30 min. The supernatant was collected and centrifuged a second time with the same parameters. 5 mL NiNTA resin was pre-equilibrated with 20 mM Tris pH 8.0, 500 mM NaCl, 2 mM beta-mercaptoethanol, added to the cleared lysate, and incubated for 2 h at 4 °C on a rotator. The resin was washed in succession with 20 mM Tris pH 8.0, 500 mM NaCl, 10 mM imidazole, 2 mM beta-mercaptoethanol, and then 20 mM Tris pH 8.0, 500 mM NaCl, 20 mM imidazole, 2 mM beta-mercaptoethanol. Finally, the protein was eluted from the resin using 20 mM Tris pH 8.0, 500 mM NaCl, 250 mM imidazole, 2 mM beta- mercaptoethanol. The 6x Histidine tag was removed from the KRas G12V protein by overnight incubation with TEV protease at 4 °C while dialyzing against 20 mM HEPES pH 7.5, 150 mM NaCl. The Avi tag on the C terminus was specifically labeled with biotin using recombinant BirA enzyme during the tag cleavage process. 16 mg of recombinant BirA enzyme, 1 mM biotin, 7 mM ATP, and 7.5 mM MgCl₂ was added to the 4 °C overnight reaction. KRas G12V protein was subsequently mixed with NiNTA resin pre-equilibrated with 20 mM HEPES pH 7.5, 150 mM NaCl – the cleaved and biotinylated protein was collected in the flow-through. KRas G12V protein was subsequently loaded with nucleotide by adding 10 mM EDTA and 2 mM GDP. The mixture was incubated on a rotator overnight at 4 °C.20 mM MgCl₂ was added to quench loading and stabilize the protein. KRas G12V was further purified and excess GDP nucleotide was removed by size exclusion chromatography. The protein was loaded on a Superdex 75 pg 16/600 column equilibrated with 20 mM HEPES pH 7.5, 150 mM NaCl and eluted with an isocratic flow. Biotin incorporation and GDP loading was confirmed by mass spectrometry on an Agilent 1290 Infinity II UPLC connected to an Agilent 6545XT qTOF. EXEMPLARY EMBODIMENTS: P01 Embodiments Embodiment 1. A compound of Formula (I): Formula (I) or a pharmaceutically acceptable salt thereof, wherein: R¹ is selected from the group consisting of: a) -H; b) -N(R²)₂, wherein each R² is independently selected from the group consisting of: H and C_1-6 alkyl optionally substituted with 1-3 R^c; c) -O-C_1-3 alkyl optionally substituted with 1-3 R^c; d) C1-6 alkyl optionally substituted with 1-3 R^c; and e) -Z⁰–(Z¹)m1-Z², wherein: Z⁰ is -N(R^f)- or -O-; m1 is 0 or 1; Z¹ is C_1-4 alkylene optionally substituted with 1-3 R^c; Z² is selected from the group consisting of: C_3-10 cycloalkyl, 4-10 membered heterocyclyl, and 5-10 membered heteroaryl, each of which is optionally substituted with 1-3 R⁷, wherein: each R⁷ is independently selected from the group consisting of R^a and R^b; Ring B is wherein: the * marks the ring carbon atom common to both Ring B and ; X¹ is selected from the group consisting of a bond, S(O)_0-2, CH₂, CHR^L, C(R^L)₂, and O; X² and X³ are independently selected from the group consisting of: CH₂, CHR^L, C(R^L)₂, O, and S(O)_0-2, provided that no more than one of X¹, X², and X³ is selected from the group consisting of: O and S(O)_0-2; b1 is 0, 1, 2, or 3; R⁹ is selected from the group consisting of: H, OH, NR^dR^e, and halo; each R¹⁰ is independently selected from the group consisting of R^a and R^b; each R^L is independently selected from the group consisting of C_1-3 alkoxy, -F, CN, and C_1-3 alkyl optionally substituted with 1-3 R^c; a pair of R^L on the same or different ring carbon atom(s) taken together with the ring atom(s) connecting them form a C_3-6 cycloalkyl ring; Y² is a bond or straight-chain C_1-6 alkylene optionally substituted with 1-6 R^Y; each R^Y is independently selected from the group consisting of: halo, cyano, -OH, oxo, C_1-6 alkoxy, C_1-6 haloalkoxy, C_1-6 alkyl, and C_1-6 haloalkyl, or a pair of R^Y on the same or different carbon atom(s) taken together with the atom(s) connecting them forms a C_3-6 cycloalkyl ring or 4-6 membered heterocyclyl ring, each of which is optionally substituted with 1-3 independently selected C_1-3 alkyl; R³ is selected from the group consisting of: (a) 4-15 membered heterocyclyl optionally substituted with 1-6 substituents independently selected from the group consisting of: R^a and R^b; and (b) -NR^dR^e; each R^a is independently selected from the group consisting of: (a) halo; (b) cyano; (c) -OH; (d) oxo; (e) -C_1-6 alkoxy; (f) -C1-6 haloalkoxy; (g) -NR^dR^e; (h) C(=O)C_1-6 alkyl; (i) C(=O)C_1-6 haloalkyl; (j) C(=O)OH; (k) C(=O)OC_1-6 alkyl; (l) C(=O)OC_1-6 haloalkyl; (m) C(=O)N(R^f)₂; (n) S(O)_0-2(C_1-6 alkyl); (o) S(O)_0-2(C_1-6 haloalkyl); (p) S(O)_1-2N(R^f)₂; and (q) C_1-6 alkyl, C_2-6 alkenyl, or C_2-6 alkynyl, each optionally substituted with 1-6 R^c; each R^b is independently selected from the group consisting of: -(L^b)b-R^b1 and -R^b1, wherein: b is 1, 2, or 3; each -L^b is independently selected from the group consisting of: -O-, -N(H)-, -N(C1-3 alkyl)-, -S(O)_0-2-, C(=O), and C_1-3 alkylene; and each R^b1 is independently selected from the group consisting of: C_3-10 cycloalkyl, 4-10 membered heterocyclyl, C_6-10 aryl, and 5-10 membered heteroaryl, each of which is optionally substituted with 1-3 R^g; each R^c is independently selected from the group consisting of: halo, cyano, -OH, -C_1- ₆ alkoxy, -C_1-6 haloalkoxy, -NR^dR^e, C(=O)C_1-6 alkyl, C(=O)C_1-6 haloalkyl, C(=O)OC_1-6 alkyl, C(=O)OC_1-6 haloalkyl, C(=O)OH, C(=O)N(R^f)₂, S(O)_0-2(C_1-6 alkyl), S(O)_0-2(C_1-6 haloalkyl), and S(O)_1-2N(R^f)₂; each R^d and R^e is independently selected from the group consisting of: H, C(=O)C_1-6 alkyl, C(=O)C_1-6 haloalkyl, C(=O)OC_1-6 alkyl, C(=O)OC_1-6 haloalkyl, C(=O)N(R^f)₂, S(O)_1- ₂(C_1-6 alkyl), S(O)_1-2(C_1-6 haloalkyl), S(O)_1-2N(R^f)₂, and C_1-6 alkyl optionally substituted with 1-3 R^h; each R^f is independently selected from the group consisting of: H and C_1-6 alkyl optionally substituted with 1-3 R^h; each R^g is independently selected from the group consisting of: R^h, C_1-3 alkyl, and C_1- 3 haloalkyl; and each R^h is independently selected from the group consisting of: halo, cyano, -OH, -C_1- ₆ alkoxy, -C_1-6 haloalkoxy, -NH₂, -N(H)(C_1-3 alkyl), and -N(C_1-3 alkyl)₂-. Embodiment 2. The compound of Embodiment 1, wherein R¹ is -Z⁰–(Z¹)m1-Z² (.e.g., -N(R^f)–(Z¹)_m1-Z²). Embodiment 3. The compound of Embodiment 1 or 2, wherein Z⁰ is -N(C_1-3 alkyl)-, wherein the C_1-3 alkyl portion of -N(C_1-3 alkyl)- is optionally substituted with 1-3 R^h. Embodiment 4. The compound of any one of Embodiments 1-3, wherein Z⁰ is - N(C_1-3 alkyl)- (e.g., -NMe-). Embodiment 5. The compound of Embodiment 1 or 2, wherein Z⁰ is -NH-. Embodiment 6. The compound of any one of Embodiments 1-5, wherein m1 is 0; and Z² is C_3-10 cycloalkyl optionally substituted with 1-3 R⁷. Embodiment 7. The compound of Embodiment 6, wherein Z² is C_3-6 cycloalkyl optionally substituted with 1-3 R⁷, wherein each R⁷ is independently selected from the group consisting of: -F, -OH, -CN, and C_1-3 alkyl optionally substituted with 1-3 F. Embodiment 8. The compound of Embodiment 6 or 7, wherein Z² is cyclopropyl or cyclobutyl, each optionally substituted with 1-3 R⁷, wherein each R⁷ is independently selected from the group consisting of: -F, -OH, -CN, and C_1-3 alkyl optionally substituted with 1-3 F. Embodiment 9. The compound of any one of Embodiments 6-8, wherein Z² is (e.g., ) or . Embodiment 10. The compound of any one of Embodiments 6-9, wherein Z² is (e.g., ). Embodiment 11. The compound of any one of Embodiments 6-8, wherein Z² is , , or . Embodiment 12. The compound of Embodiment 1 or 2, wherein Z⁰ is -N(C1-3 alkyl)- (e.g., -NMe-) or -NH-; and Z² is C_3-6 cycloalkyl optionally substituted with 1-3 R⁷, wherein each R⁷ is independently selected from the group consisting of: -F, -OH, -CN, and C_1- ₃ alkyl optionally substituted with 1-3 F. Embodiment 13. The compound of Embodiment 12, wherein m1 is 0; and Z² is cyclopropyl or cyclobutyl, each optionally substituted with 1-3 R⁷, wherein each R⁷ is independently selected from the group consisting of: -F, -OH, -CN, and C_1-3 alkyl optionally substituted with 1-3 F. Embodiment 14. The compound of any one of Embodiments 11-13, wherein each R⁷ is -F. Embodiment 15. The compound of Embodiments 1 or 2, wherein m1 is 1; Z¹ is C_1-3 alkylene optionally substituted with 1-2 R^c; and Z² is selected from the group consisting of: 4-10 membered heterocyclyl and 5-10 membered heteroaryl, each of which is optionally substituted with 1-3 R⁷. Embodiment 16. The compound of Embodiment 15, wherein Z¹ is C_1-3 alkylene; and Z² is selected from the group consisting of: 4-6 membered heterocyclyl and 5-membered heteroaryl, each of which is optionally substituted with 1-2 R⁷. Embodiment 17. The compound of Embodiment 16, wherein Z² is selected from the group consisting of: tetrahydrofuranyl, piperidinyl, isoxazolyl, oxazolyl, and pyrazolyl, each of which is optionally substituted with 1-2 R⁷, wherein each R⁷ is independently selected from the group consisting of: -F, -OH, oxo, -CN, and C_1-3 alkyl optionally substituted with 1- 3 F. Embodiment 18. The compound of Embodiment 16 or 17, wherein Z² is selected from the group consisting of: tetrahydrofuranyl, isoxazolyl, and oxazolyl. Embodiment 19. The compound of any one of Embodiments 1-2 or 15, wherein Z¹ is C_1-3 alkylene (e.g., C_2-3 alkylene); and Z² is 6-membered heteroaryl, which is substituted with one NH₂ and further optionally substituted with 1-2 R⁷. Embodiment 20. The compound of Embodiment 19, wherein Z¹ is ; and Z² is pyridyl (e.g., 3-pyridyl), which is substituted with one NH₂ and further optionally substituted with 1-2 R⁷. Embodiment 21. The compound of Embodiment 19 or 20, wherein Z² is . Embodiment 22. The compound of Embodiment 1, wherein R¹ is -N(R²)₂. Embodiment 23. The compound of Embodiment 22, wherein each R² is an independently selected C_1-3 alkyl optionally substituted with 1-3 R^c. Embodiment 24. The compound of Embodiment 22 or 23, wherein each R² is independently methyl or ethyl, each optionally substituted with 1-3 R^c, wherein each R^c present on R² is independently selected from the group consisting of: -F, cyano, -OH, -C_1-6 alkoxy, and -C_1-6 haloalkoxy. Embodiment 25. The compound of any one of Embodiments 22-24, wherein R¹ is -N(Me)2, -N(Et)2, or -N(Me)Et. Embodiment 26. The compound of Embodiment 1, wherein R¹ is -H. Embodiment 27. The compound of any one of Embodiments 1-26, wherein X¹ is selected from the group consisting of: CH₂, CHR^L, and C(R^L)₂. Embodiment 28. The compound of any one of Embodiments 1-27, wherein X¹ is CH₂. Embodiment 29. The compound of any one of Embodiments 1-26, wherein X¹ is a bond. Embodiment 30. The compound of any one of Embodiments 1-29, wherein X² and X³ are independently selected from the group consisting of: CH₂, CHR^L, and C(R^L)₂. Embodiment 31. The compound of Embodiment 30, wherein X² and X³ are both CH₂. Embodiment 32. The compound of Embodiment 30, wherein X² is CH₂; and X³ is selected from the group consisting of: CHR^L and C(R^L)₂. Embodiment 33. The compound of Embodiment 30 or 32, wherein X² is CH2; and X³ is CHR^L. Embodiment 34. The compound of any one of Embodiments 30 or 32-33, wherein X² is CH₂; and X³ is CHMe. Embodiment 35. The compound of any one of Embodiments 1-29, wherein one of X² and X³ is -O-; and the other of X² and X³ is selected from the group consisting of: CH₂, CHR^L, and C(R^L)₂. Embodiment 36. The compound of any one of Embodiments 1-29 or 35, wherein X² is -O-; and X³ is CH₂ or CHMe. Embodiment 37. The compound of any one of Embodiments 1-36, wherein R⁹ is para to -X³-. Embodiment 38. The compound of any one of Embodiments 1-37, wherein R⁹ is -OH or -NH₂. Embodiment 39. The compound of any one of Embodiments 1-38, wherein R⁹ is -NH₂. Embodiment 40. The compound of any one of Embodiments 1-39, wherein b1 is 0, 1, or 2. Embodiment 41. The compound of any one of Embodiments 1-40, wherein b1 is 1 or 2. Embodiment 42. The compound of any one of Embodiments 1-41, wherein b1 is 1 or 2; and each R¹⁰ is independently selected from the group consisting of: -Cl, -F, -CN, and C_1-3 alkyl optionally substituted with 1-3 R^c. Embodiment 43. The compound of any one of Embodiments 1-42, wherein b1 is 1; and R¹⁰ is -CN. Embodiment 44. The compound of any one of Embodiments 1-43, wherein b1 is 1; R¹⁰ is ortho to R⁹; and R¹⁰ is -CN. Embodiment 45. The compound of any one of Embodiments 1-41, wherein b1 is 1 or 2; and each R¹⁰ is independently -Cl or -F. Embodiment 46. The compound of any one of Embodiments 1-41 or 45, wherein b1 is 1 or 2; 1-2 occurrence(s) of R¹⁰ is ortho to R⁹; and each R¹⁰ is independently -Cl or -F. Embodiment 47. The compound of any one of Embodiments 1-26, wherein Ring B is selected from the group consisting of: , , and , wherein: X² is -O- or -CH₂-; X³ is -CH₂- or -CHR^L-, wherein R^L is C_1-3 alkyl (e.g., methyl); and each R¹⁰ is independently selected from the group consisting of: -Cl, -F, -CN, and C_1-3 alkyl optionally substituted with 1-3 R^c. Embodiment 48. The compound of any one of Embodiments 1-26 or 47, wherein Ring B is selected from the group consisting of: and , wherein: X² is -O- or -CH₂-; X³ is -CH₂- or -CHR^L-, wherein R^L is C_1-3 alkyl (e.g., methyl); and each R¹⁰ is independently selected from the group consisting of: -Cl, -F, -CN, and C_1-3 alkyl optionally substituted with 1-3 R^c. Embodiment 49. The compound of any one of Embodiments 1-26 or 48, wherein Ring B is selected from the group consisting of: , , , , , , , and . Embodiment 50. The compound of any one of Embodiments 1-49, wherein Y² is -CH₂-. Embodiment 51. The compound of any one of Embodiments 1-50, wherein R³ is a 4-10 membered heterocyclyl optionally substituted with 1-6 substituents independently selected from the group consisting of: R^a and R^b. Embodiment 52. The compound of any one of Embodiments 1-51, wherein R³ is a 4-10 membered heterocyclyl having one ring nitrogen atom and 0-1 additional ring heteroatom selected from the group consisting of oxygen and nitrogen, wherein the heterocyclyl is optionally substituted with 1-6 R^a. Embodiment 53. The compound of any one of Embodiments 1-52, wherein R³ is a bicyclic 7-10 membered heterocyclyl optionally substituted with 1-6 R^a. Embodiment 54. The compound of any one of Embodiments 1-53, wherein R³ is optionally substituted with 1-3 R^a . Embodiment 55. The compound of any one of Embodiments 1-54, wherein R³ is optionally substituted with 1-2 -F. Embodiment 56. The compound of any one of Embodiments 1-54, wherein R³ is (e.g., ). Embodiment 57. The compound of any one of Embodiments 1-56, wherein the ring carbon atom labelled with * in Formula (I) has (S)-stereochemistry. Embodiment 58. The compound of Embodiment 1, wherein the compound is a compound of Formula (II): Formula (II) or a pharmaceutically acceptable salt thereof, wherein: X¹ is selected from the group consisting of a bond, S(O)_0-2, CH₂, CHR^L, C(R^L)₂, and O; X² and X³ are independently selected from the group consisting of: CH₂, CHR^L, C(R^L)₂, O, and S(O)_0-2, provided that no more than one of X¹, X², and X³ is selected from the group consisting of: O and S(O)_0-2; b1 is 1 or 2; each R¹⁰ is independently selected from the group consisting of R^a and R^b; and each R^L is independently selected from the group consisting of C_1-3 alkoxy, -F, CN, and C_1-3 alkyl optionally substituted with 1-3 R^c; or one pair of R^L on the same or different ring carbon atom(s) taken together with the ring atom(s) connecting them form a C_3-6 cycloalkyl ring. Embodiment 59. The compound of Embodiment 58, wherein the compound is a compound of Formula (II-a): Formula (II-a) or a pharmaceutically acceptable salt thereof, wherein: b4 is 0 or 1; and each R¹⁰ is independently selected from the group consisting of: -Cl, -F, -CN, and C_1-3 alkyl optionally substituted with 1-3 R^c. Embodiment 60. The compound of Embodiment 59, wherein b4 is 0. Embodiment 61. The compound of Embodiment 1, wherein the compound is a compound of Formula (III): Formula (III) or a pharmaceutically acceptable salt thereof, wherein: X¹ is selected from the group consisting of a bond, S(O)_0-2, CH₂, CHR^L, C(R^L)₂, and O; X² and X³ are independently selected from the group consisting of: CH₂, CHR^L, C(R^L)₂, O, and S(O)_0-2, provided that no more than one of X¹, X², and X³ is selected from the group consisting of: O and S(O)_0-2; R⁹ is selected from the group consisting of: H, NR^dR^e, -OH, and halo; b4 is 0 or 1; each R¹⁰ is independently selected from the group consisting of R^a and R^b; and each R^L is independently selected from the group consisting of C_1-3 alkoxy, -F, CN, and C_1-3 alkyl optionally substituted with 1-3 R^c; or one pair of R^L on the same or different ring carbon atom(s) taken together with the ring atom(s) connecting them form a C_3-6 cycloalkyl ring. Embodiment 62. The compound of Embodiment 61, wherein R⁹ is -NH₂; and each R¹⁰ is independently selected from the group consisting of: -Cl, -F, -CN, and C1-3 alkyl optionally substituted with 1-3 R^c. Embodiment 63. The compound of any one of Embodiments 58-62, wherein X¹ is CH₂ or CHR^L (e.g., CH₂). Embodiment 64. The compound of any one of Embodiments 58-63, wherein X² and X³ are independently selected from the group consisting of: CH₂, CHR^L, and C(R^L)₂. Embodiment 65. The compound of any one of Embodiments 58-64, wherein X¹ is CH₂; and X² and X³ are both CH₂. Embodiment 66. The compound of any one of Embodiments 58-64, wherein at least one (e.g., one) of X¹, X², and X³ is selected from the group consisting of: CHR^L and C(R^L)₂. Embodiment 67. The compound of any one of Embodiments 58-64 or 66, wherein one of X¹, X², and X³ is CHR^L; and each remaining of X¹, X², and X³ is CH₂. Embodiment 68. The compound of any one of Embodiments 58-64 or 66, wherein X¹ is CH2; and X² and X³ are independently selected from the group consisting of: CH2, CHR^L, and C(R^L)_2, provided that 1-2 of X² and X³ is independently CHR^L or C(R^L)₂. Embodiment 69. The compound of any one of Embodiments 58-64 or 66-68, wherein X¹ is CH₂; X² is CH₂; and X³ is CHR^L. Embodiment 70. The compound of any one of Embodiments 58-69, wherein each R^L is independently selected from the group consisting of: CH₃, CF₃, CHF₂, and CH₂F. Embodiment 71. The compound of any one of Embodiments 58-70, wherein each R^L is CH₃. Embodiment 72. The compound of any one of Embodiments 58-62, wherein X¹ is CH₂; X² is CH₂; and X³ is CHMe or CH₂ (e.g., CHMe). Embodiment 73. The compound of Embodiment 1, wherein the compound is a compound of Formula (IV): Formula (IV) or a pharmaceutically acceptable salt thereof, wherein: X¹ is selected from the group consisting of a bond, S(O)0-2, CH2, CHR^L, C(R^L)2, and O; X² and X³ are independently selected from the group consisting of: CH₂, CHR^L, C(R^L)₂, O, and S(O)_0-2, provided that at least one of X¹, X², and X³ is CHR^L or C(R^L)₂; further provided that no more than one of X¹, X², and X³ is selected from the group consisting of: O and S(O)_0-2; b1 is 0, 1 or 2; R⁹ is selected from the group consisting of: H, OH, NR^dR^e, and halo; each R¹⁰ is independently selected from the group consisting of R^a and R^b; and each R^L is independently selected from the group consisting of C_1-3 alkoxy, -F, CN, and C_1-3 alkyl optionally substituted with 1-3 R^c. Embodiment 74. The compound of Embodiment 73, wherein the compound is a compound of Formula (IV-a): Formula (IV-a) or a pharmaceutically acceptable salt thereof, wherein: each R¹⁰ is independently selected from the group consisting of: -Cl, -F, -CN, and C_1-3 alkyl optionally substituted with 1-3 R^c. Embodiment 75. The compound of Embodiment 74, wherein b1 is 1; and R¹⁰ is - CN. Embodiment 76. The compound of Embodiment 73, wherein the compound is a compound of Formula (IV-b): Formula (IV-b) or a pharmaceutically acceptable salt thereof, wherein: b4 is 0 or 1; and each R¹⁰ is independently selected from the group consisting of: -Cl, -F, -CN, and C_1-3 alkyl optionally substituted with 1-3 R^c. Embodiment 77. The compound of Embodiment 76, wherein b4 is 0. Embodiment 78. The compound of Embodiment 76 or 77, wherein R⁹ is NH₂. Embodiment 79. The compound of any one of Embodiments 73-78, wherein X¹ is CH₂. Embodiment 80. The compound of any one of Embodiments 73-79, wherein X² is CH2; and X³ is CHR^L. Embodiment 81. The compound of any one of Embodiments 73-79, wherein X² is -O-; and X³ is selected from the group consisting of: CHR^L and C(R^L)₂. Embodiment 82. The compound of any one of Embodiments 73-81, wherein each R^L is independently selected from the group consisting of: CH₃, CF₃, CHF₂, and CH₂F. Embodiment 83. The compound of any one of Embodiments 73-82, wherein each R^L is CH₃. Embodiment 84. The compound of Embodiment 73, wherein the compound is a compound of Formula (IV-c): Formula (IV-c) or a pharmaceutically acceptable salt thereof, wherein: b4 is 0 or 1; and each R¹⁰ is independently selected from the group consisting of: -Cl, -F, -CN, and C_1-3 alkyl optionally substituted with 1-3 R^c. Embodiment 85. The compound of Embodiment 84, wherein R^L is CH₃. Embodiment 86. The compound of Embodiment 84 or 85, wherein b4 is 0. Embodiment 87. The compound of any one of Embodiments 58-86, wherein Z⁰ is -N(C_1-3 alkyl)- (e.g., -NMe-) or -NH-; and Z² is C_3-6 cycloalkyl optionally substituted with 1-3 R⁷, wherein each R⁷ is independently selected from the group consisting of: -F, -OH, -CN, and C_1-3 alkyl optionally substituted with 1-3 F. Embodiment 88. The compound of Embodiment 87, wherein m1 is 0; and Z² is cyclopropyl or cyclobutyl, each optionally substituted with 1-3 R⁷, wherein each R⁷ is independently selected from the group consisting of: -F, -OH, -CN, and C_1-3 alkyl optionally substituted with 1-3 F. Embodiment 89. The compound of Embodiment 87 or 88, wherein each R⁷ is -F. Embodiment 90. The compound of any one of Embodiments 58-86, wherein R¹ is -N(R²)₂. Embodiment 91. The compound of any one of Embodiments 58-86 or 90, wherein each R² is independently methyl or ethyl, each of which is optionally substituted with 1-3 R^c, wherein each R^c present on R² is independently selected from the group consisting of: -F, cyano, -OH, -C_1-6 alkoxy, and -C_1-6 haloalkoxy. Embodiment 92. The compound of any one of Embodiments 58-86 or 90-91, wherein R¹ is -N(Me)2, -N(Et)2, or -N(Me)Et. Embodiment 93. The compound of any one of Embodiments 58-92, wherein Y² is -CH₂-; and R³ is a 4-10 membered heterocyclyl having one ring nitrogen atom and 0-1 additional ring heteroatom selected from the group consisting of oxygen and nitrogen, wherein the heterocyclyl is optionally substituted with 1-6 R^a. Embodiment 94. The compound of any one of Embodiments 58-93, wherein Y² is -CH₂-; and R³ is optionally substituted with 1-2 -F. Embodiment 95. The compound of Embodiment 94, wherein R³ is (e.g., ). Embodiment 96. The compound of any one of Embodiments 58-95, wherein the moiety is . Embodiment 97. The compound of Embodiment 58, wherein the compound is a compound of Formula (II-1): Formula (II-1) or a pharmaceutically acceptable salt thereof, wherein: b1 is 1 or 2; each R¹⁰ is independently selected from the group consisting of: -Cl, -F, -CN, and C_1-3 alkyl optionally substituted with 1-3 R^c; X¹ is CH₂; and X² and X³ are independently selected from the group consisting of: O, CH₂, CHR^L, and C(R^L)₂. Embodiment 98. The compound of Embodiment 97, wherein b1 is 1. Embodiment 99. The compound of Embodiment 58 or 59, wherein the compound is a compound of Formula (II-a1): Formula (II-a1) or a pharmaceutically acceptable salt thereof, wherein: b4 is 0 or 1; each R¹⁰ is independently selected from the group consisting of: -Cl, -F, -CN, and C_1-3 alkyl optionally substituted with 1-3 R^c; X¹ is CH₂; and X² and X³ are independently selected from the group consisting of: O, CH₂, CHR^L, and C(R^L)₂. Embodiment 100. The compound of Embodiment 99, wherein b4 is 0. Embodiment 101. The compound of Embodiment 61, wherein the compound is a compound of Formula (III-1): Formula (III-1) or a pharmaceutically acceptable salt thereof, wherein: b4 is 0 or 1; each R¹⁰ is independently selected from the group consisting of: -Cl, -F, -CN, and C_1-3 alkyl optionally substituted with 1-3 R^c; X¹ is CH₂; and X² and X³ are independently selected from the group consisting of: O, CH₂, CHR^L, and C(R^L)₂. Embodiment 102. The compound of Embodiment 101, wherein b4 is 0. Embodiment 103. The compound of Embodiment 101 or 102, wherein R⁹ is - NR^dR^e (e.g., -NH₂). Embodiment 104. The compound of Embodiment 73, wherein the compound is a compound of Formula (IV-a1) or (IV-b1): Formula (IV-a1) Formula (IV-b1) or a pharmaceutically acceptable salt thereof, wherein: b1 is 0, 1, or 2; b4 is 0 or 1; each R¹⁰ is independently selected from the group consisting of: -Cl, -F, -CN, and C_1-3 alkyl optionally substituted with 1-3 R^c; X¹ is CH₂; one of X² and X³ is independently selected from the group consisting of: CHR^L and C(R^L)2; and the other of X² and X³ is CH₂ or O. Embodiment 105. The compound of Embodiment 104, wherein the compound is a compound of Formula (IV-a1), or a pharmaceutically acceptable salt thereof, wherein b1 is 1; and the moiety is (e.g., ). Embodiment 106. The compound of Embodiment 104, wherein the compound is a compound of Formula (IV-b1), or a pharmaceutically acceptable salt thereof, wherein b4 is 0. Embodiment 107. The compound of any one of Embodiments 97-106, wherein X² is CH₂; and X³ is CHR^L (e.g., CH(CH₃)). Embodiment 108. The compound of any one of Embodiments 97-103, wherein X² is CH₂; and X³ is CH₂. Embodiment 109. The compound of any one of Embodiments 97-107, wherein each R² is independently methyl or ethyl, each optionally substituted with 1-3 R^c, wherein each R^c present on R² is independently selected from the group consisting of: -F, cyano, -OH, -C_1-6 alkoxy, and -C_1-6 haloalkoxy. Embodiment 110. The compound of any one of Embodiments 97-108, wherein each R² is independently methyl or ethyl. Embodiment 111. The compound of any one of Embodiments 97-110, wherein Y² is -CH₂-; and R³ is a 4-10 membered heterocyclyl having one ring nitrogen atom and 0-1 additional ring heteroatom selected from the group consisting of oxygen and nitrogen, wherein the heterocyclyl is optionally substituted with 1-6 R^a. Embodiment 112. The compound of any one of Embodiments 97-111, wherein Y² is -CH₂-; and R³ is optionally substituted with 1-2 -F. Embodiment 113. The compound of Embodiment 111 or 112, wherein R³ is (e.g., ). Embodiment 114. The compound of any one of Embodiments 97-113, wherein the moiety is . Embodiment 115. The compound of Embodiment 1, wherein the compound of Formula (I) is selected from the group consisting of compounds in Table C1, or a pharmaceutically acceptable salt thereof. Embodiment 116. A pharmaceutical composition comprising a compound of any one of Embodiments 1-115, or a pharmaceutically acceptable salt thereof, and a pharmaceutically acceptable excipient. Embodiment 117. A dysregulated KRas protein non-covalently bound with a compound of any one of Embodiments 1-115, or a pharmaceutically acceptable salt thereof. Embodiment 118. A method for treating a KRas-associated cancer in a subject in need thereof, the method comprising administering to the subject a therapeutically effective amount of a compound of any one of Embodiments 1-115, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition according to Embodiment 116. Embodiment 119. A method for treating a KRas-associated cancer in a subject in need thereof, the method comprising (a) determining that the cancer in the subject has a KRas dysregulation; and (b) administering to the subject a therapeutically effective amount of a compound of any one of Embodiments 1-115, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition according to Embodiment 116. Embodiment 120. A method of treating a KRas-associated cancer in a subject, the method administering to a subject identified or diagnosed as having a cancer having a KRas dysregulation a therapeutically effective amount of a compound of any one of Embodiments 1-115 or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition according to Embodiment 116. Embodiment 121. A method of treating a KRas-associated cancer in a subject, the method comprising: (a) determining that the cancer in the subject has a KRas dysregulation; and (b) administering to the subject a therapeutically effective amount of a compound of any one of Embodiments 1-115 or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition according to Embodiment 116. Embodiment 122. The method of any one of Embodiments 118-121, wherein the KRas-associated cancer is a mutant KRas-associated cancer. Embodiment 123. The method of Embodiment 122, wherein the mutant KRas- associated cancer is a KRas G12A-associated cancer, a KRas G12C-associated cancer, a KRas G12D-associated cancer, a KRas G12R-associated cancer, a KRas G12S-associated cancer, or a KRas G12V-associated cancer. Embodiment 124. The method of Embodiment 123, wherein the mutant KRas- associated cancer is a KRas G12D-associated cancer or a KRas G12V-associated cancer. Embodiment 125. The method of Embodiment 123, wherein the mutant KRas- associated cancer is a KRas G12D-associated cancer. Embodiment 126. The method of Embodiment 123, wherein the mutant KRas- associated cancer is a KRas G12R-associated cancer. Embodiment 127. The method of Embodiment 118, wherein the mutant KRas- associated cancer is a KRas G12V-associated cancer. Embodiment 128. The method of any one of Embodiments 119 or 121, wherein the step of determining that the cancer in the subject has a KRas dysregulation includes performing an assay to detect the KRas dysregulation (e.g., a KRas mutation) in a tumor sample from the subject. Embodiment 129. The method of Embodiment 128, wherein detecting the KRas dysregulation includes detecting a KRAS gene having a mutation corresponding to a substitution of glycine 12 in a KRas protein and/or a KRas protein having a substitution of glycine 12. Embodiment 130. The method of Embodiment 129, wherein the substitution of glycine 12 is a substitution to alanine, cysteine, aspartic acid, arginine, serine, or valine. Embodiment 131. The method of Embodiment 130, wherein the substitution of glycine 12 is a substitution to aspartic acid. Embodiment 132. The method of Embodiment 130, wherein the substitution of glycine 12 is a substitution to arginine. Embodiment 133. The method of Embodiment 130, wherein the substitution of glycine 12 is a substitution to valine. Embodiment 134. The method of any one of Embodiments 128-133, comprising obtaining a tumor sample from the subject. Embodiment 135. The method of Embodiment 134, wherein the tumor sample is a biopsy sample. Embodiment 136. The method of any one of Embodiments 128-135, wherein the assay is selected from the group consisting of sequencing, immunohistochemistry, and enzyme-linked immunosorbent assay, and fluorescence in situ hybridization (FISH). Embodiment 137. The method of Embodiment 136, wherein the sequencing is pyrosequencing or next generation sequencing. Embodiment 138. The method of any one of Embodiments 118-137, wherein the KRas-associated cancer is selected from the group consisting of: a hematological cancer, a soft tissue cancer, bile duct cancer, bladder cancer, brain cancer, breast cancer, cervical cancer, colon cancer, endometrial cancer, esophageal cancer, kidney cancer, liver cancer, lung cancer, mucinous carcinoma, ovarian cancer, pancreatic cancer, prostate cancer, rectal cancer, skin cancer, stomach cancer, testicular cancer, thymus cancer, thyroid cancer, urothelial cancer, uterine cancer, and a combination thereof. Embodiment 139. The method of Embodiment 138, wherein the KRas-associated cancer is pancreatic cancer. Embodiment 140. The method of Embodiment 138, wherein the KRas-associated cancer is selected from the group consisting of: a hematological cancer, brain cancer, cervical cancer, colon cancer, endometrial cancer, esophageal cancer, kidney cancer, liver cancer, lung cancer, mucinous carcinoma, pancreatic cancer, prostate cancer, rectal cancer, skin cancer, stomach cancer, thymus cancer, urothelial cancer, and uterine cancer. Embodiment 141. The method of Embodiment 138, wherein the KRas-associated cancer is selected from the group consisting of: a hematological cancer, bladder cancer, bile duct cancer, brain cancer, breast cancer, cervical cancer, colon cancer, endometrial cancer, esophageal cancer, kidney cancer, liver cancer, lung cancer, mucinous carcinoma, ovarian cancer, pancreatic cancer, rectal cancer, skin cancer, stomach cancer, testicular cancer (e.g., seminoma), thymus cancer, and uterine cancer. Embodiment 142. The method of Embodiment 138, wherein the KRas-associated cancer is selected from the group consisting of: bladder cancer, breast cancer, cervical cancer, colorectal cancer, endometrial cancer, esophageal or stomach cancer, leukemia, lung cancer (e.g., NSCLC), pancreatic cancer, and kidney cancer. Embodiment 143. The method of any one of Embodiments 118-142, comprising administering an additional therapy or therapeutic agent to the subject. Embodiment 144. The method of Embodiment 143, wherein the additional therapy or therapeutic agent is selected from the group consisting of Ras pathway targeted therapeutic agents, kinase-targeted therapeutics, mTORC1 inhibitors or degraders, YAP inhibitors or degraders, proteasome inhibitors or degraders, HSP90 inhibitors or degraders, farnesyl transferase inhibitors or degraders, PTEN inhibitors or degraders, signal transduction pathway inhibitors or degraders, checkpoint inhibitors, modulators of the apoptosis pathway, chemotherapeutics, angiogenesis-targeted therapies, immune-targeted agents, radiotherapy, and combinations thereof. Embodiment 145. A method for a method for modulating KRas protein activity in a mammalian cell, the method comprising contacting the mammalian cell with an effective amount of a compound of any one of Embodiments 1-115, or a pharmaceutically acceptable salt thereof. Embodiment 146. The method of Embodiment 145, wherein the contacting occurs in vivo. Embodiment 147. The method of Embodiment 145, wherein the contacting occurs in vitro. Embodiment 148. The method of Embodiment 145, wherein the contacting occurs ex vivo. Embodiment 149. The method of any one of Embodiments 145-148, wherein the mammalian cell is a mammalian cancer cell. Embodiment 150. The method of any one of Embodiments 145-149, wherein the KRas protein is a mutant KRas protein. Embodiment 151. The method of Embodiment 150 wherein the mutant KRas protein is a mutant KRas protein selected from the group consisting of: a KRas G12A mutant protein, a KRas G12C mutant protein, a KRas G12D mutant protein, a KRas G12R mutant protein, a KRas G12S mutant protein, and a KRas G12V mutant protein. P02 Embodiments Embodiment 1. A compound of Formula (A): Formula (A) or a pharmaceutically acceptable salt thereof, wherein: E¹ is N or CH; R¹ is selected from the group consisting of: (a) -H; (b) -N(R²)₂; (c) –N(R²)C(=O)R²; (d) -O-C_1-3 alkyl optionally substituted with 1-3 R^c; (e) C_1-6 alkyl optionally substituted with 1-3 R^c; and (f) -Z⁰–(Z¹)m1-Z²; each R² is independently selected from the group consisting of: -H and C_1-6 alkyl optionally substituted with 1-3 R^c; Z⁰ is -N(R^f)- or -O-; m1 is 0 or 1; Z¹ is C_1-4 alkylene optionally substituted with 1-3 R^c; Z² is selected from the group consisting of: C_3-10 cycloalkyl, 4-10 membered heterocyclyl, and 5-10 membered heteroaryl, each of which is optionally substituted with 1-3 R⁷, wherein: each R⁷ is independently selected from the group consisting of R^a and R^b; Ring B is wherein: the * marks the ring carbon atom common to both Ring B and ; X¹ is selected from the group consisting of a bond, S(O)_0-2, CH₂, CHR^L, C(R^L)₂, and O; X² and X³ are independently selected from the group consisting of: CH₂, CHR^L, C(R^L)₂, O, and S(O)_0-2, provided that no more than one of X¹, X², and X³ is selected from the group consisting of: O and S(O)_0-2; b1 is 0, 1, 2, or 3; R⁹ is selected from the group consisting of: -H, -OH, -NR^dR^e, and halo; each R¹⁰ is independently selected from the group consisting of R^a and R^b; each R^L is independently selected from the group consisting of C_1-3 alkoxy, -F, -CN, and C_1-3 alkyl optionally substituted with 1-3 R^c; or a pair of R^L on the same or different ring carbon atom(s) taken together with the ring atom(s) connecting them form a C_3-6 cycloalkyl ring; Y² is a bond or straight-chain C_1-6 alkylene optionally substituted with 1-6 R^Y; each R^Y is independently selected from the group consisting of: halo, cyano, -OH, oxo, C_1-6 alkoxy, C_1-6 haloalkoxy, C_1-6 alkyl, and C_1-6 haloalkyl, or a pair of R^Y on the same or different carbon atom(s) taken together with the atom(s) connecting them forms a C_3-6 cycloalkyl ring or 4-6 membered heterocyclyl ring, each of which is optionally substituted with 1-3 independently C_1-3 alkyl; R³ is selected from the group consisting of: (a) 4-15 membered heterocyclyl optionally substituted with 1-6 substituents independently selected from the group consisting of: R^a and R^b; and (b) -NR^dR^e; each R^a is independently selected from the group consisting of: (a) halo; (b) cyano; (c) -OH; (d) oxo; (e) -C1-6 alkoxy; (f) -C_1-6 haloalkoxy; (g) -NR^dR^e; (h) C(=O)C_1-6 alkyl; (i) C(=O)C_1-6 haloalkyl; (j) C(=O)OH; (k) C(=O)OC_1-6 alkyl; (l) C(=O)OC_1-6 haloalkyl; (m) C(=O)N(R^f)₂; (n) S(O)_0-2(C_1-6 alkyl); (o) S(O)_0-2(C_1-6 haloalkyl); (p) S(O)_1-2N(R^f)₂; and (q) C_1-6 alkyl, C_2-6 alkenyl, or C_2-6 alkynyl, each optionally substituted with 1-6 R^c; each R^b is independently selected from the group consisting of: -(L^b)_b-R^b1 and -R^b1, wherein: b is 1, 2, or 3; each -L^b is independently selected from the group consisting of: -O-, -N(H)-, -N(C1-3 alkyl)-, -S(O)_0-2-, C(=O), and C_1-3 alkylene; and each R^b1 is independently selected from the group consisting of: C_3-10 cycloalkyl, 4-10 membered heterocyclyl, C_6-10 aryl, and 5-10 membered heteroaryl, each of which is optionally substituted with 1-3 R^g; each R^c is independently selected from the group consisting of: halo, cyano, -OH, -C_1- ₆ alkoxy, -C_1-6 haloalkoxy, -NR^dR^e, C(=O)C_1-6 alkyl, C(=O)C_1-6 haloalkyl, C(=O)OC_1-6 alkyl, C(=O)OC_1-6 haloalkyl, C(=O)OH, C(=O)N(R^f)₂, S(O)_0-2(C_1-6 alkyl), S(O)_0-2(C_1-6 haloalkyl), and S(O)_1-2N(R^f)₂; each R^d and R^e is independently selected from the group consisting of: H, C(=O)C_1-6 alkyl, C(=O)C_1-6 haloalkyl, C(=O)OC_1-6 alkyl, C(=O)OC_1-6 haloalkyl, C(=O)N(R^f)₂, S(O)_1- ₂(C_1-6 alkyl), S(O)_1-2(C_1-6 haloalkyl), S(O)_1-2N(R^f)₂, and C_1-6 alkyl optionally substituted with 1-3 R^h; each R^f is independently selected from the group consisting of: H and C1-6 alkyl optionally substituted with 1-3 R^h; each R^g is independently selected from the group consisting of: R^h, C1-3 alkyl, and C1- ₃ haloalkyl; and each R^h is independently selected from the group consisting of: halo, cyano, -OH, -C_1- ₆ alkoxy, -C_1-6 haloalkoxy, -NH₂, -N(H)(C_1-3 alkyl), and -N(C_1-3 alkyl)₂-. Embodiment 2. The compound of Embodiment 1, wherein the compound is a compound of Formula (I): Formula (I) or a pharmaceutically acceptable salt thereof, wherein: R¹ is selected from the group consisting of: a) -H; b) -N(R²)₂, wherein each R² is independently selected from the group consisting of: H and C_1-6 alkyl optionally substituted with 1-3 R^c; c) -O-C_1-3 alkyl optionally substituted with 1-3 R^c; d) C_1-6 alkyl optionally substituted with 1-3 R^c; and e) -Z⁰–(Z¹)_m1-Z², wherein: Z⁰ is -N(R^f)- or -O-; m1 is 0 or 1; Z¹ is C_1-4 alkylene optionally substituted with 1-3 R^c; Z² is selected from the group consisting of: C_3-10 cycloalkyl, 4-10 membered heterocyclyl, and 5-10 membered heteroaryl, each of which is optionally substituted with 1-3 R⁷, wherein: each R⁷ is independently selected from the group consisting of R^a and R^b; Ring B is wherein: the * marks the ring carbon atom common to both Ring B and ; X¹ is selected from the group consisting of a bond, S(O)_0-2, CH₂, CHR^L, C(R^L)₂, and O; X² and X³ are independently selected from the group consisting of: CH₂, CHR^L, C(R^L)₂, O, and S(O)_0-2, provided that no more than one of X¹, X², and X³ is selected from the group consisting of: O and S(O)_0-2; b1 is 0, 1, 2, or 3; R⁹ is selected from the group consisting of: H, OH, NR^dR^e, and halo; each R¹⁰ is independently selected from the group consisting of R^a and R^b; each R^L is independently selected from the group consisting of C_1-3 alkoxy, -F, CN, and C_1-3 alkyl optionally substituted with 1-3 R^c; a pair of R^L on the same or different ring carbon atom(s) taken together with the ring atom(s) connecting them form a C_3-6 cycloalkyl ring; Y² is a bond or straight-chain C_1-6 alkylene optionally substituted with 1-6 R^Y; each R^Y is independently selected from the group consisting of: halo, cyano, -OH, oxo, C_1-6 alkoxy, C_1-6 haloalkoxy, C_1-6 alkyl, and C_1-6 haloalkyl, or a pair of R^Y on the same or different carbon atom(s) taken together with the atom(s) connecting them forms a C_3-6 cycloalkyl ring or 4-6 membered heterocyclyl ring, each of which is optionally substituted with 1-3 independently selected C_1-3 alkyl; R³ is selected from the group consisting of: (a) 4-15 membered heterocyclyl optionally substituted with 1-6 substituents independently selected from the group consisting of: R^a and R^b; and (b) -NR^dR^e; each R^a is independently selected from the group consisting of: (a) halo; (b) cyano; (c) -OH; (d) oxo; (e) -C1-6 alkoxy; (f) -C_1-6 haloalkoxy; (g) -NR^dR^e; (h) C(=O)C_1-6 alkyl; (i) C(=O)C_1-6 haloalkyl; (j) C(=O)OH; (k) C(=O)OC_1-6 alkyl; (l) C(=O)OC_1-6 haloalkyl; (m) C(=O)N(R^f)₂; (n) S(O)_0-2(C_1-6 alkyl); (o) S(O)_0-2(C_1-6 haloalkyl); (p) S(O)_1-2N(R^f)₂; and (q) C_1-6 alkyl, C_2-6 alkenyl, or C_2-6 alkynyl, each optionally substituted with 1-6 R^c; each R^b is independently selected from the group consisting of: -(L^b)_b-R^b1 and -R^b1, wherein: b is 1, 2, or 3; each -L^b is independently selected from the group consisting of: -O-, -N(H)-, -N(C1-3 alkyl)-, -S(O)_0-2-, C(=O), and C_1-3 alkylene; and each R^b1 is independently selected from the group consisting of: C_3-10 cycloalkyl, 4-10 membered heterocyclyl, C_6-10 aryl, and 5-10 membered heteroaryl, each of which is optionally substituted with 1-3 R^g; each R^c is independently selected from the group consisting of: halo, cyano, -OH, -C_1- ₆ alkoxy, -C_1-6 haloalkoxy, -NR^dR^e, C(=O)C_1-6 alkyl, C(=O)C_1-6 haloalkyl, C(=O)OC_1-6 alkyl, C(=O)OC_1-6 haloalkyl, C(=O)OH, C(=O)N(R^f)₂, S(O)_0-2(C_1-6 alkyl), S(O)_0-2(C_1-6 haloalkyl), and S(O)_1-2N(R^f)₂; each R^d and R^e is independently selected from the group consisting of: H, C(=O)C_1-6 alkyl, C(=O)C_1-6 haloalkyl, C(=O)OC_1-6 alkyl, C(=O)OC_1-6 haloalkyl, C(=O)N(R^f)₂, S(O)_1- ₂(C_1-6 alkyl), S(O)_1-2(C_1-6 haloalkyl), S(O)_1-2N(R^f)₂, and C_1-6 alkyl optionally substituted with 1-3 R^h; each R^f is independently selected from the group consisting of: H and C1-6 alkyl optionally substituted with 1-3 R^h; each R^g is independently selected from the group consisting of: R^h, C1-3 alkyl, and C1- ₃ haloalkyl; and each R^h is independently selected from the group consisting of: halo, cyano, -OH, -C_1- ₆ alkoxy, -C_1-6 haloalkoxy, -NH₂, -N(H)(C_1-3 alkyl), and -N(C_1-3 alkyl)₂-. Embodiment 3. The compound of Embodiment 1 or 2, wherein R¹ is -Z⁰–(Z¹)m1- Z² (e.g., -N(R^f)–(Z¹)_m1-Z²). Embodiment 4. The compound of any one of Embodiments 1-3, wherein Z⁰ is - N(C_1-3 alkyl)-, wherein the C_1-3 alkyl portion of -N(C_1-3 alkyl)- is optionally substituted with 1-3 R^h. Embodiment 5. The compound of any one of Embodiments 1-4, wherein Z⁰ is - N(C_1-3 alkyl)- (e.g., -NMe-). Embodiment 6. The compound of Embodiment any one of Embodiments 1-3, wherein Z⁰ is -NH-. Embodiment 7. The compound of any one of Embodiments 1-6, wherein m1 is 0; and Z² is a C_3-10 cycloalkyl optionally substituted with 1-3 R⁷. Embodiment 8. The compound of Embodiment 7, wherein Z² is a C_3-6 cycloalkyl optionally substituted with 1-3 R⁷, wherein each R⁷ is independently selected from the group consisting of: -F, -OH, -CN, and C_1-3 alkyl optionally substituted with 1-3 F. Embodiment 9. The compound of Embodiment 7 or 8, wherein Z² is cyclopropyl or cyclobutyl, each optionally substituted with 1-3 R⁷, wherein each R⁷ is independently selected from the group consisting of: -F, -OH, -CN, and C_1-3 alkyl optionally substituted with 1-3 F. Embodiment 10. The compound of any one of Embodiments 7-9, wherein Z² is (e.g., ) or . Embodiment 11. The compound of any one of Embodiments 7-10, wherein Z² is (e.g., ). Embodiment 12. The compound of any one of Embodiments 7-9, wherein Z² is , , or . Embodiment 13. The compound of any one of Embodiments 1-3, wherein Z⁰ is - N(C_1-3 alkyl)- (e.g., -NMe-) or -NH-; and Z² is C_3-6 cycloalkyl optionally substituted with 1-3 R⁷, wherein each R⁷ is independently selected from the group consisting of: -F, -OH, -CN, and C_1-3 alkyl optionally substituted with 1-3 F. Embodiment 14. The compound of Embodiment 13, wherein m1 is 0; and Z² is cyclopropyl or cyclobutyl, each optionally substituted with 1-3 R⁷, wherein each R⁷ is independently selected from the group consisting of: -F, -OH, -CN, and C_1-3 alkyl optionally substituted with 1-3 F. Embodiment 15. The compound of any one of Embodiments 1-14, wherein each R⁷ is -F. Embodiment 16. The compound of any one of Embodiments 1-14, wherein one R⁷ is -OH; and each remaining R⁷ if present is independently selected from the group consisting of: -F, -OH, -CN, and C_1-3 alkyl optionally substituted with 1-3 F. Embodiment 17. The compound of any one of Embodiments 1-3, wherein R¹ is - N(H)-Z² or -N(C_1-3 alkyl)-Z², wherein Z² is a C_3-6 cycloalkyl optionally substituted with 1-3 R⁷, wherein: one R⁷ is -OH; and each remaining R⁷ if present is independently selected from the group consisting of: - F, -OH, -CN, and C_1-3 alkyl optionally substituted with 1-3 F. Embodiment 18. The compound of Embodiment 17, wherein Z² is C_3-6 cycloalkyl substituted with one -OH (e.g., Z² is or ). Embodiment 19. The compound of Embodiment 1, wherein R¹ is -N(R²)₂. Embodiment 20. The compound of Embodiment 19, wherein each R² is an independently selected C_1-3 alkyl optionally substituted with 1-3 R^c. Embodiment 21. The compound of Embodiment 19 or 20, wherein each R² is independently methyl or ethyl, each optionally substituted with 1-3 R^c, wherein each R^c present on R² is independently selected from the group consisting of: -F, cyano, -OH, -C_1-6 alkoxy, and -C_1-6 haloalkoxy. Embodiment 22. The compound of any one of Embodiments 19-21, wherein R¹ is -N(Me)₂, -N(Et)₂, or -N(Me)Et. Embodiment 23. The compound of Embodiment 19, wherein one R² is a C_2-6 alkyl substituted with -OH. Embodiment 24. The compound of Embodiment 19 or 23, wherein one R² is or . Embodiment 25. The compound of Embodiment 23 or 24, wherein the other R² is -H or C_1-3 alkyl (e.g., -H or methyl). Embodiment 26. The compound of Embodiment 1, wherein R¹ is -H. Embodiment 27. The compound of any one of Embodiments 1-26, wherein X¹ is selected from the group consisting of: CH₂, CHR^L, and C(R^L)₂. Embodiment 28. The compound of any one of Embodiments 1-27, wherein X¹ is CH₂. Embodiment 29. The compound of any one of Embodiments 1-26, wherein X¹ is a bond. Embodiment 30. The compound of any one of Embodiments 1-29, wherein X² and X³ are independently selected from the group consisting of: CH₂, CHR^L, and C(R^L)₂. Embodiment 31. The compound of Embodiment 30, wherein X² and X³ are both CH₂. Embodiment 32. The compound of Embodiment 30, wherein X² is CH₂; and X³ is selected from the group consisting of: CHR^L and C(R^L)₂. Embodiment 33. The compound of Embodiment 30 or 32, wherein X² is CH₂; and X³ is CHR^L. Embodiment 34. The compound of any one of Embodiments 30 or 32-33, wherein X² is CH₂; and X³ is CHMe. Embodiment 35. The compound of any one of Embodiments 1-29, wherein one of X² and X³ is -O-; and the other of X² and X³ is selected from the group consisting of: CH₂, CHR^L, and C(R^L)2. Embodiment 36. The compound of any one of Embodiments 1-29 or 35, wherein X² is -O-; and X³ is CH2 or CHMe. Embodiment 37. The compound of any one of Embodiments 1-36, wherein R⁹ is para to -X³-. Embodiment 38. The compound of any one of Embodiments 1-37, wherein R⁹ is -OH or -NH₂. Embodiment 39. The compound of any one of Embodiments 1-38, wherein R⁹ is -NH₂. Embodiment 40. The compound of any one of Embodiments 1-39, wherein b1 is 0, 1, or 2. Embodiment 41. The compound of any one of Embodiments 1-40, wherein b1 is 1 or 2. Embodiment 42. The compound of any one of Embodiments 1-41, wherein b1 is 1 or 2; and each R¹⁰ is independently selected from the group consisting of: -Cl, -F, -CN, and C_1-3 alkyl optionally substituted with 1-3 R^c. Embodiment 43. The compound of any one of Embodiments 1-42, wherein b1 is 1; and R¹⁰ is -CN. Embodiment 44. The compound of any one of Embodiments 1-43, wherein b1 is 1; R¹⁰ is ortho to R⁹; and R¹⁰ is -CN. Embodiment 45. The compound of any one of Embodiments 1-41, wherein b1 is 1 or 2; and each R¹⁰ is independently -Cl or -F. Embodiment 46. The compound of any one of Embodiments 1-41 or 45, wherein b1 is 1 or 2; 1-2 occurrence(s) of R¹⁰ is ortho to R⁹; and each R¹⁰ is independently -Cl or -F. Embodiment 47. The compound of any one of Embodiments 1-26, wherein Ring B is selected from the group consisting of: , , and , wherein: X² is -O- or -CH₂-; X³ is -CH₂- or -CHR^L-, wherein R^L is C_1-3 alkyl (e.g., methyl); and each R¹⁰ is independently selected from the group consisting of: -Cl, -F, -CN, and C_1-3 alkyl optionally substituted with 1-3 R^c. Embodiment 48. The compound of any one of Embodiments 1-26 or 47, wherein Ring B is selected from the group consisting of: and , wherein: X² is -O- or -CH₂-; X³ is -CH₂- or -CHR^L-, wherein R^L is C_1-3 alkyl (e.g., methyl); and each R¹⁰ is independently selected from the group consisting of: -Cl, -F, -CN, and C_1-3 alkyl optionally substituted with 1-3 R^c.

Embodiment 49. The compound of any one of Embodiments 1-26 or 48, wherein Ring B is selected from the group consisting of: , , , , , , , and . Embodiment 50. The compound of any one of Embodiments 1-49, wherein Y² is -CH₂-. Embodiment 51. The compound of any one of Embodiments 1-50, wherein R³ is a 4-10 membered heterocyclyl optionally substituted with 1-6 substituents independently selected from the group consisting of: R^a and R^b. Embodiment 52. The compound of any one of Embodiments 1-51, wherein R³ is a 4-10 membered heterocyclyl having one ring nitrogen atom and 0-1 additional ring heteroatom selected from the group consisting of oxygen and nitrogen, wherein the heterocyclyl is optionally substituted with 1-6 R^a. Embodiment 53. The compound of any one of Embodiments 1-52, wherein R³ is a bicyclic 7-10 membered heterocyclyl optionally substituted with 1-6 R^a. Embodiment 54. The compound of any one of Embodiments 1-53, wherein R³ is optionally substituted with 1-3 R^a . Embodiment 55. The compound of any one of Embodiments 1-54, wherein R³ is optionally substituted with 1-2 -F. Embodiment 56. The compound of any one of Embodiments 1-54, wherein R³ is (e.g., ). Embodiment 57. The compound of any one of Embodiments 1-56, wherein the ring carbon atom labelled with * in Formula (I) has (S)-stereochemistry. Embodiment 58. The compound of Embodiment 1, wherein the compound is a compound of Formula (II): Formula (II) or a pharmaceutically acceptable salt thereof, wherein: X¹ is selected from the group consisting of a bond, S(O)_0-2, CH₂, CHR^L, C(R^L)₂, and O; X² and X³ are independently selected from the group consisting of: CH₂, CHR^L, C(R^L)₂, O, and S(O)_0-2, provided that no more than one of X¹, X², and X³ is selected from the group consisting of: O and S(O)_0-2; b1 is 1 or 2; each R¹⁰ is independently selected from the group consisting of R^a and R^b; and each R^L is independently selected from the group consisting of C1-3 alkoxy, -F, CN, and C_1-3 alkyl optionally substituted with 1-3 R^c; or one pair of R^L on the same or different ring carbon atom(s) taken together with the ring atom(s) connecting them form a C_3-6 cycloalkyl ring. Embodiment 59. The compound of Embodiment 58, wherein the compound is a compound of Formula (II-a): Formula (II-a) or a pharmaceutically acceptable salt thereof, wherein: b4 is 0 or 1; and each R¹⁰ is independently selected from the group consisting of: -Cl, -F, -CN, and C_1-3 alkyl optionally substituted with 1-3 R^c. Embodiment 60. The compound of Embodiment 59, wherein b4 is 0. Embodiment 61. The compound of Embodiment 1, wherein the compound is a compound of Formula (III): Formula (III) or a pharmaceutically acceptable salt thereof, wherein: X¹ is selected from the group consisting of a bond, S(O)_0-2, CH₂, CHR^L, C(R^L)₂, and O; X² and X³ are independently selected from the group consisting of: CH₂, CHR^L, C(R^L)₂, O, and S(O)_0-2, provided that no more than one of X¹, X², and X³ is selected from the group consisting of: O and S(O)_0-2; R⁹ is selected from the group consisting of: H, NR^dR^e, -OH, and halo; b4 is 0 or 1; each R¹⁰ is independently selected from the group consisting of R^a and R^b; and each R^L is independently selected from the group consisting of C_1-3 alkoxy, -F, CN, and C_1-3 alkyl optionally substituted with 1-3 R^c; or one pair of R^L on the same or different ring carbon atom(s) taken together with the ring atom(s) connecting them form a C_3-6 cycloalkyl ring. Embodiment 62. The compound of Embodiment 61, wherein R⁹ is -NH₂; and each R¹⁰ is independently selected from the group consisting of: -Cl, -F, -CN, and C_1-3 alkyl optionally substituted with 1-3 R^c. Embodiment 63. The compound of any one of Embodiments 58-62, wherein X¹ is CH₂ or CHR^L (e.g., CH₂). Embodiment 64. The compound of any one of Embodiments 58-63, wherein X² and X³ are independently selected from the group consisting of: CH₂, CHR^L, and C(R^L)₂. Embodiment 65. The compound of any one of Embodiments 58-64, wherein X¹ is CH2; and X² and X³ are both CH2. Embodiment 66. The compound of any one of Embodiments 58-64, wherein at least one (e.g., one) of X¹, X², and X³ is selected from the group consisting of: CHR^L and C(R^L)₂. Embodiment 67. The compound of any one of Embodiments 58-64 or 66, wherein one of X¹, X², and X³ is CHR^L; and each remaining of X¹, X², and X³ is CH₂. Embodiment 68. The compound of any one of Embodiments 58-64 or 66, wherein X¹ is CH₂; and X² and X³ are independently selected from the group consisting of: CH₂, CHR^L, and C(R^L)_2, provided that 1-2 of X² and X³ is independently CHR^L or C(R^L)₂. Embodiment 69. The compound of any one of Embodiments 58-64 or 66-68, wherein X¹ is CH₂; X² is CH₂; and X³ is CHR^L. Embodiment 70. The compound of any one of Embodiments 58-69, wherein each R^L is independently selected from the group consisting of: CH₃, CF₃, CHF₂, and CH₂F. Embodiment 71. The compound of any one of Embodiments 58-70, wherein each R^L is CH3. Embodiment 72. The compound of any one of Embodiments 58-71, wherein X¹ is CH₂; X² is CH₂; and X³ is CHMe or CH₂ (e.g., CHMe). Embodiment 73. The compound of Embodiment 1, wherein the compound is a compound of Formula (IV): Formula (IV) or a pharmaceutically acceptable salt thereof, wherein: X¹ is selected from the group consisting of a bond, S(O)0-2, CH2, CHR^L, C(R^L)2, and O; X² and X³ are independently selected from the group consisting of: CH2, CHR^L, C(R^L)₂, O, and S(O)_0-2, provided that at least one of X¹, X², and X³ is CHR^L or C(R^L)₂; further provided that no more than one of X¹, X², and X³ is selected from the group consisting of: O and S(O)_0-2; b1 is 0, 1 or 2; R⁹ is selected from the group consisting of: H, OH, NR^dR^e, and halo; each R¹⁰ is independently selected from the group consisting of R^a and R^b; and each R^L is independently selected from the group consisting of C_1-3 alkoxy, -F, CN, and C_1-3 alkyl optionally substituted with 1-3 R^c. Embodiment 74. The compound of Embodiment 73, wherein the compound is a compound of Formula (IV-a): Formula (IV-a) or a pharmaceutically acceptable salt thereof, wherein: each R¹⁰ is independently selected from the group consisting of: -Cl, -F, -CN, and C_1-3 alkyl optionally substituted with 1-3 R^c. Embodiment 75. The compound of Embodiment 74, wherein b1 is 1; and R¹⁰ is - CN. Embodiment 76. The compound of Embodiment 73, wherein the compound is a compound of Formula (IV-b): Formula (IV-b) or a pharmaceutically acceptable salt thereof, wherein: b4 is 0 or 1; and each R¹⁰ is independently selected from the group consisting of: -Cl, -F, -CN, and C_1-3 alkyl optionally substituted with 1-3 R^c. Embodiment 77. The compound of Embodiment 76, wherein b4 is 0. Embodiment 78. The compound of Embodiment 76 or 77, wherein R⁹ is NH₂. Embodiment 79. The compound of any one of Embodiments 73-78, wherein X¹ is CH₂. Embodiment 80. The compound of any one of Embodiments 73-79, wherein X² is CH₂; and X³ is CHR^L. Embodiment 81. The compound of any one of Embodiments 73-79, wherein X² is -O-; and X³ is selected from the group consisting of: CHR^L and C(R^L)₂. Embodiment 82. The compound of any one of Embodiments 73-81, wherein each R^L is independently selected from the group consisting of: CH3, CF3, CHF2, and CH2F. Embodiment 83. The compound of any one of Embodiments 73-82, wherein each R^L is CH₃. Embodiment 84. The compound of Embodiment 73, wherein the compound is a compound of Formula (IV-c): Formula (IV-c) or a pharmaceutically acceptable salt thereof, wherein: b4 is 0 or 1; and each R¹⁰ is independently selected from the group consisting of: -Cl, -F, -CN, and C_1-3 alkyl optionally substituted with 1-3 R^c. Embodiment 85. The compound of Embodiment 74, wherein R^L is CH₃. Embodiment 86. The compound of Embodiment 74 or 75, wherein b4 is 0. Embodiment 87. The compound of any one of Embodiments 58-86, wherein R¹ is -Z⁰–(Z¹)_m1-Z²; Z⁰ is -N(C_1-3 alkyl)- (e.g., -NMe-) or -NH-; and Z² is C_3-6 cycloalkyl optionally substituted with 1-3 R⁷, wherein each R⁷ is independently selected from the group consisting of: -F, -OH, -CN, and C_1-3 alkyl optionally substituted with 1-3 F. Embodiment 88. The compound of Embodiment 87, wherein m1 is 0; and Z² is cyclopropyl or cyclobutyl, each optionally substituted with 1-3 R⁷, wherein each R⁷ is independently selected from the group consisting of: -F, -OH, -CN, and C_1-3 alkyl optionally substituted with 1-3 F. Embodiment 89. The compound of Embodiment 87 or 88, wherein each R⁷ is -F. Embodiment 90. The compound of any one of Embodiments 58-87, wherein R¹ is -N(H)-Z² or -N(C1-3 alkyl)-Z², wherein Z² is C3-6 cycloalkyl optionally substituted with 1-3 R⁷, wherein: one R⁷ is -OH; and each remaining R⁷, if present, is independently selected from the group consisting of: - F, -OH, -CN, and C_1-3 alkyl optionally substituted with 1-3 F. Embodiment 91. The compound of Embodiment 90, wherein Z² is C_3-6 cycloalkyl substituted with one -OH (e.g., Z² is or ). Embodiment 92. The compound of any one of Embodiments 58-86, wherein R¹ is -N(R²)₂. Embodiment 93. The compound of any one of Embodiments 58-86 or 92, wherein each R² is independently methyl or ethyl, each of which is optionally substituted with 1-3 R^c, wherein each R^c present on R² is independently selected from the group consisting of: -F, cyano, -OH, -C_1-6 alkoxy, and -C_1-6 haloalkoxy. Embodiment 94. The compound of any one of Embodiments 58-86 or 92-93, wherein R¹ is -N(Me)₂, -N(Et)₂, or -N(Me)Et. Embodiment 95. The compound of any one of Embodiments 58-86 or 92, wherein R¹ is -N(R²)₂; one R² is a C_2-6 alkyl substituted with -OH; and the other R² is -H or C_1-3 alkyl (e.g., -H or methyl). Embodiment 96. The compound of Embodiment 95, wherein one R² is or ; and the other R² is -H or methyl. Embodiment 97. The compound of any one of Embodiments 58-96, wherein Y² is -CH2-; and R³ is a 4-10 membered heterocyclyl having one ring nitrogen atom and 0-1 additional ring heteroatom selected from the group consisting of oxygen and nitrogen, wherein the heterocyclyl is optionally substituted with 1-6 R^a. Embodiment 98. The compound of any one of Embodiments 58-97, wherein Y² is -CH₂-; and R³ is optionally substituted with 1-2 substituents each independently selected from the group consisting of: -F, -C_1-6 alkoxy, and -C_1-6 haloalkoxy. Embodiment 99. The compound of any one of Embodiments 58-98, wherein Y² is -CH₂-; and R³ is optionally substituted with 1-2 -F. Embodiment 100. The compound of Embodiment 99, wherein R³ is (e.g., ). Embodiment 101. The compound of any one of Embodiments 58-100, wherein the moiety is . Embodiment 102. The compound of Embodiment 58, wherein the compound is a compound of Formula (II-1): Formula (II-1) or a pharmaceutically acceptable salt thereof, wherein: b1 is 1 or 2; each R¹⁰ is independently selected from the group consisting of: -Cl, -F, -CN, and C_1-3 alkyl optionally substituted with 1-3 R^c; X¹ is CH₂; and X² and X³ are independently selected from the group consisting of: O, CH₂, CHR^L, and C(R^L)₂. Embodiment 103. The compound of Embodiment 102, wherein b1 is 1. Embodiment 104. The compound of any one of Embodiments 58-59 or 102, wherein the compound is a compound of Formula (II-a1): Formula (II-a1) or a pharmaceutically acceptable salt thereof, wherein: b4 is 0 or 1; each R¹⁰ is independently selected from the group consisting of: -Cl, -F, -CN, and C_1-3 alkyl optionally substituted with 1-3 R^c; X¹ is CH₂; and X² and X³ are independently selected from the group consisting of: O, CH2, CHR^L, and C(R^L)₂. Embodiment 105. The compound of Embodiment 104, wherein b4 is 0. Embodiment 106. The compound of Embodiment 61, wherein the compound is a compound of Formula (III-1): Formula (III-1) or a pharmaceutically acceptable salt thereof, wherein: b4 is 0 or 1; each R¹⁰ is independently selected from the group consisting of: -Cl, -F, -CN, and C_1-3 alkyl optionally substituted with 1-3 R^c; X¹ is CH₂; and X² and X³ are independently selected from the group consisting of: O, CH₂, CHR^L, and C(R^L)₂. Embodiment 107. The compound of Embodiment 106, wherein b4 is 0. Embodiment 108. The compound of Embodiment 106 or 107, wherein R⁹ is - NR^dR^e (e.g., -NH₂). Embodiment 109. The compound of Embodiment 73, wherein the compound is a compound of Formula (IV-a1) or (IV-b1): Formula (IV-a1) Formula (IV-b1) or a pharmaceutically acceptable salt thereof, wherein: b1 is 0, 1, or 2; b4 is 0 or 1; each R¹⁰ is independently selected from the group consisting of: -Cl, -F, -CN, and C_1-3 alkyl optionally substituted with 1-3 R^c; X¹ is CH₂; one of X² and X³ is independently selected from the group consisting of: CHR^L and C(R^L)₂; and the other of X² and X³ is CH₂ or O. Embodiment 110. The compound of Embodiment 109, wherein the compound is a compound of Formula (IV-a1), or a pharmaceutically acceptable salt thereof, wherein b1 is 1; and the moiety is (e.g., ). Embodiment 111. The compound of Embodiment 109, wherein the compound is a compound of Formula (IV-b1), or a pharmaceutically acceptable salt thereof, wherein b4 is 0. Embodiment 112. The compound of any one of Embodiments 102-111, wherein X² is CH₂; and X³ is CHR^L (e.g., CH(CH₃)). Embodiment 113. The compound of any one of Embodiments 102-111, wherein X² is CH₂; and X³ is CH₂. Embodiment 114. The compound of any one of Embodiments 102-113, wherein each R² is independently methyl or ethyl, each optionally substituted with 1-3 R^c, wherein each R^c present on R² is independently selected from the group consisting of: -F, cyano, -OH, -C_1-6 alkoxy, and -C_1-6 haloalkoxy. Embodiment 115. The compound of any one of Embodiments 102-114, wherein each R² is independently methyl or ethyl. Embodiment 116. The compound of any one of Embodiments 102-113, wherein one R² is a C_2-6 alkyl substituted with -OH; and the other R² is -H or C_1-3 alkyl. Embodiment 117. The compound of any one of Embodiments 102-116, wherein Y² is -CH₂-; and R³ is a 4-10 membered heterocyclyl having one ring nitrogen atom and 0-1 additional ring heteroatom selected from the group consisting of oxygen and nitrogen, wherein the heterocyclyl is optionally substituted with 1-6 R^a. Embodiment 118. The compound of any one of Embodiments 102-117, wherein Y² is -CH2-; and R³ is optionally substituted with 1-2 -F. Embodiment 119. The compound of Embodiment 117 or 118, wherein R³ is (e.g., ). Embodiment 120. The compound of any one of Embodiments 102-119, wherein the moiety is . Embodiment 121. The compound of Embodiment 58 or 59, wherein the compound is a compound of Formula (II-a2): Formula (II-a2) or a pharmaceutically acceptable salt thereof, wherein: X³ is CH₂ or CHR^L, wherein R^L is C_1-3 alkyl optionally substituted with 1-3 -F; one R² is a C_2-6 alkyl substituted with -OH; the other R² is -H or C_1-3 alkyl; Y² is -CH₂-; and R³ is optionally substituted with 1-2 substituents each independently selected from the group consisting of: -F, -C_1-6 alkoxy, and -C_1-6 haloalkoxy. Embodiment 122. The compound of Embodiment 121, wherein one R² is a C_2-6 alkyl substituted with -OH (e.g., or ); and the other R² is -H or methyl. Embodiment 123. The compound of Embodiment 58 or 59, wherein the compound is a compound of Formula (II-a3): Formula (II-a3) or a pharmaceutically acceptable salt thereof, wherein: X³ is CH₂ or CHR^L, wherein R^L is C_1-3 alkyl optionally substituted with 1-3 -F; R^f is -H or C_1-3 alkyl; Z² is a C_3-6 cycloalkyl optionally substituted with 1-3 R⁷, wherein: one R⁷ is -OH; each remaining R⁷ if present is independently selected from the group consisting of: - F, -OH, -CN, and C_1-3 alkyl optionally substituted with 1-3 F; Y² is -CH₂-; and R³ is optionally substituted with 1-2 substituents each independently selected from the group consisting of: -F, -C_1-6 alkoxy, and -C_1-6 haloalkoxy. Embodiment 124. The compound of Embodiment 123, wherein R^f is -H or methyl; and Z² is C_3-6 cycloalkyl substituted with one -OH (e.g., Z² is or ). Embodiment 125. The compound of any one of Embodiments 121-124, wherein X³ is CH(Me). Embodiment 126. The compound of any one of Embodiments 121-125, wherein R³ is (e.g., ). Embodiment 127. The compound of any one of Embodiments 121-126, wherein the moiety is . Embodiment 128. The compound of Embodiment 1, wherein the compound of Formula (A) is selected from the group consisting of compounds in Table C1, or a pharmaceutically acceptable salt thereof. Embodiment 129. A pharmaceutical composition comprising a compound of any one of Embodiments 1-128, or a pharmaceutically acceptable salt thereof, and a pharmaceutically acceptable excipient. Embodiment 130. A dysregulated KRas protein non-covalently bound with a compound of any one of Embodiments 1-128, or a pharmaceutically acceptable salt thereof. Embodiment 131. A method for treating a KRas-associated cancer in a subject in need thereof, the method comprising administering to the subject a therapeutically effective amount of a compound of any one of Embodiments 1-128, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition according to Embodiment 129. Embodiment 132. A method for treating a KRas-associated cancer in a subject in need thereof, the method comprising (a) determining that the cancer in the subject has a KRas dysregulation; and (b) administering to the subject a therapeutically effective amount of a compound of any one of Embodiments 1-128, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition according to Embodiment 129. Embodiment 133. A method of treating a KRas-associated cancer in a subject, the method administering to a subject identified or diagnosed as having a cancer having a KRas dysregulation a therapeutically effective amount of a compound of any one of Embodiments 1-128 or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition according to Embodiment 129. Embodiment 134. A method of treating a KRas-associated cancer in a subject, the method comprising: (a) determining that the cancer in the subject has a KRas dysregulation; and (b) administering to the subject a therapeutically effective amount of a compound of any one of Embodiments 1-128 or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition according to Embodiment 129. Embodiment 135. The method of any one of Embodiments 131-134, wherein the KRas-associated cancer is a mutant KRas-associated cancer. Embodiment 136. The method of Embodiment 135, wherein the mutant KRas- associated cancer is a KRas G12A-associated cancer, a KRas G12C-associated cancer, a KRas G12D-associated cancer, a KRas G12R-associated cancer, a KRas G12S-associated cancer, or a KRas G12V-associated cancer. Embodiment 137. The method of Embodiment 136, wherein the mutant KRas- associated cancer is a KRas G12D-associated cancer or a KRas G12V-associated cancer. Embodiment 138. The method of Embodiment 136, wherein the mutant KRas- associated cancer is a KRas G12D-associated cancer. Embodiment 139. The method of Embodiment 136, wherein the mutant KRas- associated cancer is a KRas G12R-associated cancer. Embodiment 140. The method of Embodiment 131, wherein the mutant KRas- associated cancer is a KRas G12V-associated cancer. Embodiment 141. The method of any one of Embodiments 132 or 134, wherein the step of determining that the cancer in the subject has a KRas dysregulation includes performing an assay to detect the KRas dysregulation (e.g., a KRas mutation) in a tumor sample from the subject. Embodiment 142. The method of Embodiment 141, wherein detecting the KRas dysregulation includes detecting a KRAS gene having a mutation corresponding to a substitution of glycine 12 in a KRas protein and/or a KRas protein having a substitution of glycine 12. Embodiment 143. The method of Embodiment 142, wherein the substitution of glycine 12 is a substitution to alanine, cysteine, aspartic acid, arginine, serine, or valine. Embodiment 144. The method of Embodiment 143, wherein the substitution of glycine 12 is a substitution to aspartic acid. Embodiment 145. The method of Embodiment 143, wherein the substitution of glycine 12 is a substitution to arginine. Embodiment 146. The method of Embodiment 143, wherein the substitution of glycine 12 is a substitution to valine. Embodiment 147. The method of any one of Embodiments 141-146, comprising obtaining a tumor sample from the subject. Embodiment 148. The method of Embodiment 147, wherein the tumor sample is a biopsy sample. Embodiment 149. The method of any one of Embodiments 141-148, wherein the assay is selected from the group consisting of sequencing, immunohistochemistry, and enzyme-linked immunosorbent assay, and fluorescence in situ hybridization (FISH). Embodiment 150. The method of Embodiment 149, wherein the sequencing is pyrosequencing or next generation sequencing. Embodiment 151. The method of any one of Embodiments 141-150, wherein the KRas-associated cancer is selected from the group consisting of: a hematological cancer, a soft tissue cancer, bile duct cancer, bladder cancer, brain cancer, breast cancer, cervical cancer, colon cancer, endometrial cancer, esophageal cancer, kidney cancer, liver cancer, lung cancer, mucinous carcinoma, ovarian cancer, pancreatic cancer, prostate cancer, rectal cancer, skin cancer, stomach cancer, testicular cancer, thymus cancer, thyroid cancer, urothelial cancer, uterine cancer, and a combination thereof. Embodiment 152. The method of Embodiment 151, wherein the KRas-associated cancer is pancreatic cancer. Embodiment 153. The method of Embodiment 151, wherein the KRas-associated cancer is selected from the group consisting of: a hematological cancer, brain cancer, cervical cancer, colon cancer, endometrial cancer, esophageal cancer, kidney cancer, liver cancer, lung cancer, mucinous carcinoma, pancreatic cancer, prostate cancer, rectal cancer, skin cancer, stomach cancer, thymus cancer, urothelial cancer, and uterine cancer. Embodiment 154. The method of Embodiment 151, wherein the KRas-associated cancer is selected from the group consisting of: a hematological cancer, bladder cancer, bile duct cancer, brain cancer, breast cancer, cervical cancer, colon cancer, endometrial cancer, esophageal cancer, kidney cancer, liver cancer, lung cancer, mucinous carcinoma, ovarian cancer, pancreatic cancer, rectal cancer, skin cancer, stomach cancer, testicular cancer (e.g., seminoma), thymus cancer, and uterine cancer. Embodiment 155. The method of Embodiment 151, wherein the KRas-associated cancer is selected from the group consisting of: bladder cancer, breast cancer, cervical cancer, colorectal cancer, endometrial cancer, esophageal or stomach cancer, leukemia, lung cancer (e.g., NSCLC), pancreatic cancer, and kidney cancer. Embodiment 156. The method of any one of Embodiments 131-155, comprising administering an additional therapy or therapeutic agent to the subject. Embodiment 157. The method of Embodiment 156, wherein the additional therapy or therapeutic agent is selected from the group consisting of Ras pathway targeted therapeutic agents, kinase-targeted therapeutics, mTORC1 inhibitors or degraders, YAP inhibitors or degraders, proteasome inhibitors or degraders, HSP90 inhibitors or degraders, farnesyl transferase inhibitors or degraders, PTEN inhibitors or degraders, signal transduction pathway inhibitors or degraders, checkpoint inhibitors, modulators of the apoptosis pathway, chemotherapeutics, angiogenesis-targeted therapies, immune-targeted agents, radiotherapy, and combinations thereof. Embodiment 158. A method for a method for modulating KRas protein activity in a mammalian cell, the method comprising contacting the mammalian cell with an effective amount of a compound of any one of Embodiments 1-128, or a pharmaceutically acceptable salt thereof. Embodiment 159. The method of Embodiment 158, wherein the contacting occurs in vivo. Embodiment 160. The method of Embodiment 158, wherein the contacting occurs in vitro. Embodiment 161. The method of Embodiment 158, wherein the contacting occurs ex vivo. Embodiment 162. The method of any one of Embodiments 158-161, wherein the mammalian cell is a mammalian cancer cell. Embodiment 163. The method of any one of Embodiments 158-162, wherein the KRas protein is a mutant KRas protein. Embodiment 164. The method of Embodiment 163, wherein the mutant KRas protein is a mutant KRas protein selected from the group consisting of: a KRas G12A mutant protein, a KRas G12C mutant protein, a KRas G12D mutant protein, a KRas G12R mutant protein, a KRas G12S mutant protein, and a KRas G12V mutant protein. Formula (II-a) Exemplary Embodiments Embodiment 1. A compound of Formula (II-a): Formula (II-a) or a pharmaceutically acceptable salt thereof, wherein: R¹ is selected from the group consisting of: (a) -H; (b) -N(R²)₂; (c) –N(R²)C(=O)R²; (d) -O-C_1-3 alkyl optionally substituted with 1-3 R^c; (e) C_1-6 alkyl optionally substituted with 1-3 R^c; and (f) -Z⁰–(Z¹)_m1-Z²; each R² is independently selected from the group consisting of: -H and C_1-6 alkyl optionally substituted with 1-3 R^c; Z⁰ is -N(R^f)- or -O-; m1 is 0 or 1; Z¹ is C_1-4 alkylene optionally substituted with 1-3 R^c; Z² is selected from the group consisting of: C3-10 cycloalkyl, 4-10 membered heterocyclyl, and 5-10 membered heteroaryl, each of which is optionally substituted with 1-3 R⁷, wherein each R⁷ is independently selected from the group consisting of R^a and R^b; b4 is 0 or 1; each R¹⁰ is independently selected from the group consisting of: -Cl, -F, -CN, and C_1-3 alkyl optionally substituted with 1-3 R^c; X¹ is selected from the group consisting of a bond, S(O)_0-2, CH₂, CHR^L, C(R^L)₂, and O; X² and X³ are independently selected from the group consisting of: CH₂, CHR^L, C(R^L)₂, O, and S(O)_0-2, provided that no more than one of X¹, X², and X³ is selected from the group consisting of: O and S(O)_0-2; each R^L is independently selected from the group consisting of C_1-3 alkoxy, -F, -CN, and C_1-3 alkyl optionally substituted with 1-3 R^c; or a pair of R^L on the same or different ring carbon atom(s) taken together with the ring atom(s) connecting them form a C_3-6 cycloalkyl ring; Y² is a bond or straight-chain C_1-6 alkylene optionally substituted with 1-6 R^Y; each R^Y is independently selected from the group consisting of: halo, cyano, -OH, oxo, C_1-6 alkoxy, C_1-6 haloalkoxy, C_1-6 alkyl, and C_1-6 haloalkyl, or a pair of R^Y on the same or different carbon atom(s) taken together with the atom(s) connecting them forms a C_3-6 cycloalkyl ring or 4-6 membered heterocyclyl ring, each of which is optionally substituted with 1-3 independently C_1-3 alkyl; R³ is selected from the group consisting of: (a) 4-15 membered heterocyclyl optionally substituted with 1-6 substituents independently selected from the group consisting of: R^a and R^b; and (b) -NR^dR^e; R^4a and R^4b are independently selected from the group consisting of: -H and C_1-3 alkyl optionally substituted with 1-3 R^c; each R^a is independently selected from the group consisting of: (a) halo; (b) cyano; (c) -OH; (d) oxo; (e) -C_1-6 alkoxy; (f) -C_1-6 haloalkoxy; (g) -NR^dR^e; (h) C(=O)C_1-6 alkyl; (i) C(=O)C_1-6 haloalkyl; (j) C(=O)OH; (k) C(=O)OC_1-6 alkyl; (l) C(=O)OC_1-6 haloalkyl; (m) C(=O)N(R^f)₂; (n) S(O)_0-2(C_1-6 alkyl); (o) S(O)0-2(C1-6 haloalkyl); (p) S(O)_1-2N(R^f)₂; and (q) C1-6 alkyl, C2-6 alkenyl, or C2-6 alkynyl, each optionally substituted with 1-6 R^c; each R^b is independently selected from the group consisting of: -(L^b)_b-R^b1 and -R^b1, wherein: b is 1, 2, or 3; each -L^b is independently selected from the group consisting of: -O-, -N(H)-, -N(C_1-3 alkyl)-, -S(O)_0-2-, C(=O), and C_1-3 alkylene; and each R^b1 is independently selected from the group consisting of: C_3-10 cycloalkyl, 4-10 membered heterocyclyl, C_6-10 aryl, and 5-10 membered heteroaryl, each of which is optionally substituted with 1-3 R^g; each R^c is independently selected from the group consisting of: halo, cyano, -OH, -C_1- ₆ alkoxy, -C_1-6 haloalkoxy, -NR^dR^e, C(=O)C_1-6 alkyl, C(=O)C_1-6 haloalkyl, C(=O)OC_1-6 alkyl, C(=O)OC_1-6 haloalkyl, C(=O)OH, C(=O)N(R^f)₂, S(O)_0-2(C_1-6 alkyl), S(O)_0-2(C_1-6 haloalkyl), and S(O)_1-2N(R^f)₂; each R^d and R^e is independently selected from the group consisting of: H, C(=O)C_1-6 alkyl, C(=O)C_1-6 haloalkyl, C(=O)OC_1-6 alkyl, C(=O)OC_1-6 haloalkyl, C(=O)N(R^f)₂, S(O)_1- 2(C1-6 alkyl), S(O)1-2(C1-6 haloalkyl), S(O)1-2N(R^f)2, and C1-6 alkyl optionally substituted with 1-3 R^h; each R^f is independently selected from the group consisting of: H and C_1-6 alkyl optionally substituted with 1-3 R^h; each R^g is independently selected from the group consisting of: R^h, C_1-3 alkyl, and C_1- ₃ haloalkyl; and each R^h is independently selected from the group consisting of: halo, cyano, -OH, -C_1- ₆ alkoxy, -C_1-6 haloalkoxy, -NH₂, -N(H)(C_1-3 alkyl), and -N(C_1-3 alkyl)₂-. Embodiment 2. The compound of Embodiment 1, wherein b4 is 0. Embodiment 3. The compound of Embodiment 1 or 2, wherein X¹ is CH₂; and X² and X³ are both CH₂. Embodiment 4. The compound of Embodiment 1 or 2, wherein X¹ is CH₂; X² is CH2; and X³ is CHR^L, optionally where R^L is CH3. Embodiment 5. The compound of any one of Embodiments 1-4, wherein R¹ is - Z⁰–(Z¹)_m1-Z²; Z⁰ is -N(C_1-3 alkyl)- (e.g., -NMe-) or -NH-; and Z² is C_3-6 cycloalkyl optionally substituted with 1-3 R⁷, wherein each R⁷ is independently selected from the group consisting of: -F, -OH, -CN, and C_1-3 alkyl optionally substituted with 1-3 F; or wherein R¹ is -N(H)-Z² or -N(C_1-3 alkyl)-Z², wherein Z² is C_3-6 cycloalkyl optionally substituted with 1-3 R⁷, wherein: one R⁷ is -OH; and each remaining R⁷, if present, is independently selected from the group consisting of: -F, -OH, -CN, and C_1-3 alkyl optionally substituted with 1-3 F; or wherein Z² is C_3-6 cycloalkyl substituted with one -OH (e.g., Z² is or ). Embodiment 6. The compound of any one of Embodiments 1-4, wherein R¹ is - N(R²)₂, Embodiment 7. The compound of Embodiment 6, wherein each R² is independently methyl or ethyl, each of which is optionally substituted with 1-3 R^c, wherein each R^c present on R² is independently selected from the group consisting of: -F, cyano, -OH, -C_1-6 alkoxy, and -C_1-6 haloalkoxy. Embodiment 8. The compound of any one of Embodiments 1-4 or 6, wherein R¹ is -N(Me)₂, -N(Et)₂, or -N(Me)Et; or wherein R¹ is -N(R²)₂; one R² is a C_2-6 alkyl substituted with -OH; and the other R² is -H or C_1-3 alkyl (e.g., -H or methyl). Embodiment 9. The compound of any one of Embodiments 1-4, wherein R¹ is - O-C_1-3 alkyl optionally substituted with 1-3 R^c, optionally wherein each R^c present on R¹ is independently selected from the group consisting of: -F, cyano, -OH, -C_1-6 alkoxy, and -C_1-6 haloalkoxy (e.g., -OH, -C_1-6 alkoxy, and -C_1-6 haloalkoxy). Embodiment 10. The compound of any one of Embodiments 1-10, wherein Y² is -CH₂-; and R³ is optionally substituted with 1-2 substituents independently selected from the group consisting of: -F, -C1-6 alkoxy, and -C1-6 haloalkoxy; or wherein Y² is -CH2-; and R³ is optionally substituted with 1-2 -F; or wherein R³ is (e.g., ). Embodiment 11. The compound of any one of Embodiments 1-10, wherein the moiety is . Embodiment 12. The compound of Embodiment 1, wherein the compound is selected from the group consisting of compound nos.103, 103a, 103b, 104, 104a, 104b, 107, 107a, 107b, 108, 108a, 108b, 109, 109a, 110, 110a, 111, 111a, 112, 112a, 113, 113a, 114, 114a, 115, 115a, 116, 116a, 117, 117a, 118, 118a, 119, 119a, 120, 120a, 121, 121a, 122, 122a, 122b, 123, 123a, 123b, 124, 124a, 124b, 125, 125a, 126, 126a, 127, 127a, 128, 128a, 129, 129a, 129b, 130, 130a, 130b, 131, 131a, 132, 132a, 133, 133a, 134, 134a, 134b, 135, 135a, 138, 138a, 138b, 139, 139a, 139b, 139c, 140, 140a, 141, 141a, 142, 142a, 143, 143a, 144, 144a, 145, 145a, 146, 146a, 147, 147a, 148, 148a, 149, 149a, 150, 150a, 151, 151a, 152, 152a, 153, 153a, 154, 154a, 154b, 155, 155a, 156, 156a, 157, 157a, 157b, 158, 158a, 159, 159a, 161, 161a, 162, 162a, and 162b, as depicted in Table C1, or a pharmaceutically acceptable salt thereof. Embodiment 13. A pharmaceutical composition comprising a compound of any one of Embodiments 1-12, or a pharmaceutically acceptable salt thereof, and a pharmaceutically acceptable excipient. Embodiment 14. A compound of any one of Embodiments 1-13, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition of Embodiment 13, for use in the treatment of a KRas-associated cancer. Embodiment 15. The compound or pharmaceutical composition of Embodiment 14, wherein the KRas-associated cancer is a mutant KRas-associated cancer; optionally wherein the mutant KRas-associated cancer is a KRas G12A-associated cancer, a KRas G12C-associated cancer, a KRas G12D-associated cancer, a KRas G12R-associated cancer, a KRas G12S-associated cancer, or a KRas G12V-associated cancer; optionally wherein the mutant KRas-associated cancer is a KRas G12D-associated cancer or a KRas G12V-associated cancer; optionally wherein the mutant KRas-associated cancer is a KRas G12D-associated cancer; optionally wherein the mutant KRas-associated cancer is a KRas G12R-associated cancer; or optionally wherein the mutant KRas-associated cancer is a KRas G12V-associated cancer.

Claims

WHAT IS CLAIMED IS: 1. A compound of Formula (AA): Formula (AA) or a pharmaceutically acceptable salt thereof, wherein: E¹ is N or CH; R¹ is selected from the group consisting of: (a) -H; (b) -N(R²)₂; (c) –N(R²)C(=O)R²; (d) -O-C_1-3 alkyl optionally substituted with 1-3 R^c; (e) C_1-6 alkyl optionally substituted with 1-3 R^c; and (f) -Z⁰–(Z¹)_m1-Z²; each R² is independently selected from the group consisting of: -H and C_1-6 alkyl optionally substituted with 1-3 R^c; Z⁰ is -N(R^f)- or -O-; m1 is 0 or 1; Z¹ is C_1-4 alkylene optionally substituted with 1-3 R^c; Z² is selected from the group consisting of: C_3-10 cycloalkyl, 4-10 membered heterocyclyl, and 5-10 membered heteroaryl, each of which is optionally substituted with 1-3 R⁷, wherein: each R⁷ is independently selected from the group consisting of R^a and R^b; Ring B is wherein: the * marks the ring carbon atom common to both Ring B and ; X¹ is selected from the group consisting of a bond, S(O)0-2, CH2, CHR^L, C(R^L)2, and O; X² and X³ are independently selected from the group consisting of: CH₂, CHR^L, C(R^L)₂, O, and S(O)_0-2, provided that no more than one of X¹, X², and X³ is selected from the group consisting of: O and S(O)_0-2; b1 is 0, 1, 2, or 3; R⁹ is selected from the group consisting of: -H, -OH, -NR^dR^e, and halo; each R¹⁰ is independently selected from the group consisting of R^a and R^b; each R^L is independently selected from the group consisting of C_1-3 alkoxy, -F, -CN, and C_1-3 alkyl optionally substituted with 1-3 R^c; or a pair of R^L on the same or different ring carbon atom(s) taken together with the ring atom(s) connecting them form a C_3-6 cycloalkyl ring; Y² is a bond or straight-chain C_1-6 alkylene optionally substituted with 1-6 R^Y; each R^Y is independently selected from the group consisting of: halo, cyano, -OH, oxo, C_1-6 alkoxy, C_1-6 haloalkoxy, C_1-6 alkyl, and C_1-6 haloalkyl, or a pair of R^Y on the same or different carbon atom(s) taken together with the atom(s) connecting them forms a C3-6 cycloalkyl ring or 4-6 membered heterocyclyl ring, each of which is optionally substituted with 1-3 independently C_1-3 alkyl; R³ is selected from the group consisting of: (a) 4-15 membered heterocyclyl optionally substituted with 1-6 substituents independently selected from the group consisting of: R^a and R^b; and (b) -NR^dR^e; R^4a and R^4b are independently selected from the group consisting of: -H and C_1-3 alkyl optionally substituted with 1-3 R^c; each R^a is independently selected from the group consisting of: (a) halo; (b) cyano; (c) -OH; (d) oxo; (e) -C_1-6 alkoxy; (f) -C_1-6 haloalkoxy; (g) -NR^dR^e; (h) C(=O)C_1-6 alkyl; (i) C(=O)C_1-6 haloalkyl; (j) C(=O)OH; (k) C(=O)OC_1-6 alkyl; (l) C(=O)OC_1-6 haloalkyl; (m) C(=O)N(R^f)₂; (n) S(O)0-2(C1-6 alkyl); (o) S(O)_0-2(C_1-6 haloalkyl); (p) S(O)1-2N(R^f)2; and (q) C_1-6 alkyl, C_2-6 alkenyl, or C_2-6 alkynyl, each optionally substituted with 1-6 R^c; each R^b is independently selected from the group consisting of: -(L^b)b-R^b1 and -R^b1, wherein: b is 1, 2, or 3; each -L^b is independently selected from the group consisting of: -O-, -N(H)-, -N(C_1-3 alkyl)-, -S(O)_0-2-, C(=O), and C_1-3 alkylene; and each R^b1 is independently selected from the group consisting of: C_3-10 cycloalkyl, 4-10 membered heterocyclyl, C_6-10 aryl, and 5-10 membered heteroaryl, each of which is optionally substituted with 1-3 R^g; each R^c is independently selected from the group consisting of: halo, cyano, -OH, -C_1- ₆ alkoxy, -C_1-6 haloalkoxy, -NR^dR^e, C(=O)C_1-6 alkyl, C(=O)C_1-6 haloalkyl, C(=O)OC_1-6 alkyl, C(=O)OC_1-6 haloalkyl, C(=O)OH, C(=O)N(R^f)₂, S(O)_0-2(C_1-6 alkyl), S(O)_0-2(C_1-6 haloalkyl), and S(O)_1-2N(R^f)₂; each R^d and R^e is independently selected from the group consisting of: H, C(=O)C_1-6 alkyl, C(=O)C1-6 haloalkyl, C(=O)OC1-6 alkyl, C(=O)OC1-6 haloalkyl, C(=O)N(R^f)2, S(O)1- ₂(C_1-6 alkyl), S(O)_1-2(C_1-6 haloalkyl), S(O)_1-2N(R^f)₂, and C_1-6 alkyl optionally substituted with 1-3 R^h; each R^f is independently selected from the group consisting of: H and C_1-6 alkyl optionally substituted with 1-3 R^h; each R^g is independently selected from the group consisting of: R^h, C_1-3 alkyl, and C_1- ₃ haloalkyl; and each R^h is independently selected from the group consisting of: halo, cyano, -OH, -C_1- ₆ alkoxy, -C_1-6 haloalkoxy, -NH₂, -N(H)(C_1-3 alkyl), and -N(C_1-3 alkyl)₂-.

2. The compound of claim 1, wherein R^4a is selected from the group consisting of: -H and C_1-3 alkyl optionally substituted with -OH or C_1-3 alkoxy; and R^4b is -H.

3. The compound of claim 1 or 2, wherein the compound is a compound of Formula (A): Formula (A) or a pharmaceutically acceptable salt thereof, wherein: E¹ is N or CH; R¹ is selected from the group consisting of: (a) -H; (b) -N(R²)₂; (c) –N(R²)C(=O)R²; (d) -O-C_1-3 alkyl optionally substituted with 1-3 R^c; (e) C_1-6 alkyl optionally substituted with 1-3 R^c; and (f) -Z⁰–(Z¹)m1-Z²; each R² is independently selected from the group consisting of: -H and C_1-6 alkyl optionally substituted with 1-3 R^c; Z⁰ is -N(R^f)- or -O-; m1 is 0 or 1; Z¹ is C_1-4 alkylene optionally substituted with 1-3 R^c; Z² is selected from the group consisting of: C_3-10 cycloalkyl, 4-10 membered heterocyclyl, and 5-10 membered heteroaryl, each of which is optionally substituted with 1-3 R⁷, wherein: each R⁷ is independently selected from the group consisting of R^a and R^b; Ring B is wherein: the * marks the ring carbon atom common to both Ring B and ; X¹ is selected from the group consisting of a bond, S(O)_0-2, CH₂, CHR^L, C(R^L)₂, and O; X² and X³ are independently selected from the group consisting of: CH₂, CHR^L, C(R^L)₂, O, and S(O)_0-2, provided that no more than one of X¹, X², and X³ is selected from the group consisting of: O and S(O)_0-2; b1 is 0, 1, 2, or 3; R⁹ is selected from the group consisting of: -H, -OH, -NR^dR^e, and halo; each R¹⁰ is independently selected from the group consisting of R^a and R^b; each R^L is independently selected from the group consisting of C_1-3 alkoxy, -F, -CN, and C_1-3 alkyl optionally substituted with 1-3 R^c; or a pair of R^L on the same or different ring carbon atom(s) taken together with the ring atom(s) connecting them form a C3-6 cycloalkyl ring; Y² is a bond or straight-chain C1-6 alkylene optionally substituted with 1-6 R^Y; each R^Y is independently selected from the group consisting of: halo, cyano, -OH, oxo, C_1-6 alkoxy, C_1-6 haloalkoxy, C_1-6 alkyl, and C_1-6 haloalkyl, or a pair of R^Y on the same or different carbon atom(s) taken together with the atom(s) connecting them forms a C_3-6 cycloalkyl ring or 4-6 membered heterocyclyl ring, each of which is optionally substituted with 1-3 independently C_1-3 alkyl; R³ is selected from the group consisting of: (a) 4-15 membered heterocyclyl optionally substituted with 1-6 substituents independently selected from the group consisting of: R^a and R^b; and (b) -NR^dR^e; each R^a is independently selected from the group consisting of: (a) halo; (b) cyano; (c) -OH; (d) oxo; (e) -C_1-6 alkoxy; (f) -C_1-6 haloalkoxy; (g) -NR^dR^e; (h) C(=O)C_1-6 alkyl; (i) C(=O)C1-6 haloalkyl; (j) C(=O)OH; (k) C(=O)OC_1-6 alkyl; (l) C(=O)OC_1-6 haloalkyl; (m) C(=O)N(R^f)₂; (n) S(O)_0-2(C_1-6 alkyl); (o) S(O)_0-2(C_1-6 haloalkyl); (p) S(O)_1-2N(R^f)₂; and (q) C_1-6 alkyl, C_2-6 alkenyl, or C_2-6 alkynyl, each optionally substituted with 1-6 R^c; each R^b is independently selected from the group consisting of: -(L^b)_b-R^b1 and -R^b1, wherein: b is 1, 2, or 3; each -L^b is independently selected from the group consisting of: -O-, -N(H)-, -N(C_1-3 alkyl)-, -S(O)_0-2-, C(=O), and C_1-3 alkylene; and each R^b1 is independently selected from the group consisting of: C_3-10 cycloalkyl, 4-10 membered heterocyclyl, C_6-10 aryl, and 5-10 membered heteroaryl, each of which is optionally substituted with 1-3 R^g; each R^c is independently selected from the group consisting of: halo, cyano, -OH, -C_1- ₆ alkoxy, -C_1-6 haloalkoxy, -NR^dR^e, C(=O)C_1-6 alkyl, C(=O)C_1-6 haloalkyl, C(=O)OC_1-6 alkyl, C(=O)OC_1-6 haloalkyl, C(=O)OH, C(=O)N(R^f)₂, S(O)_0-2(C_1-6 alkyl), S(O)_0-2(C_1-6 haloalkyl), and S(O)_1-2N(R^f)₂; each R^d and R^e is independently selected from the group consisting of: H, C(=O)C_1-6 alkyl, C(=O)C_1-6 haloalkyl, C(=O)OC_1-6 alkyl, C(=O)OC_1-6 haloalkyl, C(=O)N(R^f)₂, S(O)_1- ₂(C_1-6 alkyl), S(O)_1-2(C_1-6 haloalkyl), S(O)_1-2N(R^f)₂, and C_1-6 alkyl optionally substituted with 1-3 R^h; each R^f is independently selected from the group consisting of: H and C_1-6 alkyl optionally substituted with 1-3 R^h; each R^g is independently selected from the group consisting of: R^h, C_1-3 alkyl, and C_1- ₃ haloalkyl; and each R^h is independently selected from the group consisting of: halo, cyano, -OH, -C1- ₆ alkoxy, -C_1-6 haloalkoxy, -NH₂, -N(H)(C_1-3 alkyl), and -N(C_1-3 alkyl)₂-. 4. The compound of any one of claims 1-3, wherein the compound is a compound of Formula (I): Formula (I) or a pharmaceutically acceptable salt thereof, wherein: R¹ is selected from the group consisting of: a) -H; b) -N(R²)₂, wherein each R² is independently selected from the group consisting of: H and C1-6 alkyl optionally substituted with 1-3 R^c; c) -O-C_1-3 alkyl optionally substituted with 1-3 R^c; d) C1-6 alkyl optionally substituted with 1-3 R^c; and e) -Z⁰–(Z¹)m1-Z², wherein: Z⁰ is -N(R^f)- or -O-; m1 is 0 or 1; Z¹ is C_1-4 alkylene optionally substituted with 1-3 R^c; Z² is selected from the group consisting of: C_3-10 cycloalkyl, 4-10 membered heterocyclyl, and 5-10 membered heteroaryl, each of which is optionally substituted with 1-3 R⁷, wherein: each R⁷ is independently selected from the group consisting of R^a and R^b; Ring B is wherein: the * marks the ring carbon atom common to both Ring B and ; X¹ is selected from the group consisting of a bond, S(O)_0-2, CH₂, CHR^L, C(R^L)₂, and O; X² and X³ are independently selected from the group consisting of: CH₂, CHR^L, C(R^L)₂, O, and S(O)_0-2, provided that no more than one of X¹, X², and X³ is selected from the group consisting of: O and S(O)_0-2; b1 is 0, 1, 2, or 3; R⁹ is selected from the group consisting of: H, OH, NR^dR^e, and halo; each R¹⁰ is independently selected from the group consisting of R^a and R^b; each R^L is independently selected from the group consisting of C_1-3 alkoxy, -F, CN, and C_1-3 alkyl optionally substituted with 1-3 R^c; a pair of R^L on the same or different ring carbon atom(s) taken together with the ring atom(s) connecting them form a C_3-6 cycloalkyl ring; Y² is a bond or straight-chain C_1-6 alkylene optionally substituted with 1-6 R^Y; each R^Y is independently selected from the group consisting of: halo, cyano, -OH, oxo, C_1-6 alkoxy, C_1-6 haloalkoxy, C_1-6 alkyl, and C_1-6 haloalkyl, or a pair of R^Y on the same or different carbon atom(s) taken together with the atom(s) connecting them forms a C3-6 cycloalkyl ring or 4-6 membered heterocyclyl ring, each of which is optionally substituted with 1-3 independently selected C_1-3 alkyl; R³ is selected from the group consisting of: (a) 4-15 membered heterocyclyl optionally substituted with 1-6 substituents independently selected from the group consisting of: R^a and R^b; and (b) -NR^dR^e; each R^a is independently selected from the group consisting of: (a) halo; (b) cyano; (c) -OH; (d) oxo; (e) -C_1-6 alkoxy; (f) -C_1-6 haloalkoxy; (g) -NR^dR^e; (h) C(=O)C_1-6 alkyl; (i) C(=O)C1-6 haloalkyl; (j) C(=O)OH; (k) C(=O)OC_1-6 alkyl; (l) C(=O)OC_1-6 haloalkyl; (m) C(=O)N(R^f)₂; (n) S(O)_0-2(C_1-6 alkyl); (o) S(O)_0-2(C_1-6 haloalkyl); (p) S(O)_1-2N(R^f)₂; and (q) C_1-6 alkyl, C_2-6 alkenyl, or C_2-6 alkynyl, each optionally substituted with 1-6 R^c; each R^b is independently selected from the group consisting of: -(L^b)_b-R^b1 and -R^b1, wherein: b is 1, 2, or 3; each -L^b is independently selected from the group consisting of: -O-, -N(H)-, -N(C_1-3 alkyl)-, -S(O)_0-2-, C(=O), and C_1-3 alkylene; and each R^b1 is independently selected from the group consisting of: C_3-10 cycloalkyl,

4-10 membered heterocyclyl, C_6-10 aryl, and 5-10 membered heteroaryl, each of which is optionally substituted with 1-3 R^g; each R^c is independently selected from the group consisting of: halo, cyano, -OH, -C_1- ₆ alkoxy, -C_1-6 haloalkoxy, -NR^dR^e, C(=O)C_1-6 alkyl, C(=O)C_1-6 haloalkyl, C(=O)OC_1-6 alkyl, C(=O)OC_1-6 haloalkyl, C(=O)OH, C(=O)N(R^f)₂, S(O)_0-2(C_1-6 alkyl), S(O)_0-2(C_1-6 haloalkyl), and S(O)_1-2N(R^f)₂; each R^d and R^e is independently selected from the group consisting of: H, C(=O)C_1-6 alkyl, C(=O)C_1-6 haloalkyl, C(=O)OC_1-6 alkyl, C(=O)OC_1-6 haloalkyl, C(=O)N(R^f)₂, S(O)_1- ₂(C_1-6 alkyl), S(O)_1-2(C_1-6 haloalkyl), S(O)_1-2N(R^f)₂, and C_1-6 alkyl optionally substituted with 1-3 R^h; each R^f is independently selected from the group consisting of: H and C_1-6 alkyl optionally substituted with 1-3 R^h; each R^g is independently selected from the group consisting of: R^h, C_1-3 alkyl, and C_1- ₃ haloalkyl; and each R^h is independently selected from the group consisting of: halo, cyano, -OH, -C1- ₆ alkoxy, -C_1-6 haloalkoxy, -NH₂, -N(H)(C_1-3 alkyl), and -N(C_1-3 alkyl)₂-.

5. The compound of any one of claims 1-4, wherein R¹ is -Z⁰–(Z¹)m1-Z² (e.g., - N(R^f)–(Z¹)_m1-Z²).

6. The compound of any one of claims 1-5, wherein Z⁰ is -N(C_1-3 alkyl)-, wherein the C_1-3 alkyl portion of -N(C_1-3 alkyl)- is optionally substituted with 1-3 R^h.

7. The compound of any one of claims 1-6, wherein Z⁰ is -N(C_1-3 alkyl)- (e.g., - NMe-).

8. The compound of claim any one of claims 1-5, wherein Z⁰ is -NH-.

9. The compound of any one of claims 1-8, wherein m1 is 0; and Z² is a C_3-10 cycloalkyl optionally substituted with 1-3 R⁷.

10. The compound of claim 9, wherein Z² is a C_3-6 cycloalkyl optionally substituted with 1-3 R⁷, wherein each R⁷ is independently selected from the group consisting of: -F, -OH, -CN, and C1-3 alkyl optionally substituted with 1-3 F.

11. The compound of claim 9 or 10, wherein Z² is cyclopropyl or cyclobutyl, each optionally substituted with 1-3 R⁷, wherein each R⁷ is independently selected from the group consisting of: -F, -OH, -CN, and C_1-3 alkyl optionally substituted with 1-3 F.

12. The compound of any one of claims 9-11, wherein Z² is (e.g., ) or .

13. The compound of any one of claims 9-12, wherein Z² is (e.g., ).

14. The compound of any one of claims 9-11, wherein Z² is , , or .

15. The compound of any one of claims 1-5, wherein Z⁰ is -N(C_1-3 alkyl)- (e.g., - NMe-) or -NH-; and Z² is C_3-6 cycloalkyl optionally substituted with 1-3 R⁷, wherein each R⁷ is independently selected from the group consisting of: -F, -OH, -CN, and C_1-3 alkyl optionally substituted with 1-3 F.

16. The compound of claim 15, wherein m1 is 0; and Z² is cyclopropyl or cyclobutyl, each optionally substituted with 1-3 R⁷, wherein each R⁷ is independently selected from the group consisting of: -F, -OH, -CN, and C_1-3 alkyl optionally substituted with 1-3 F.

17. The compound of any one of claims 1-16, wherein each R⁷ is -F.

18. The compound of any one of claims 1-16, wherein one R⁷ is -OH; and each remaining R⁷ if present is independently selected from the group consisting of: -F, -OH, -CN, and C_1-3 alkyl optionally substituted with 1-3 F.

19. The compound of any one of claims 1-5, wherein R¹ is -N(H)-Z² or -N(C_1-3 alkyl)-Z², wherein Z² is a C_3-6 cycloalkyl optionally substituted with 1-3 R⁷, wherein: one R⁷ is -OH; and each remaining R⁷ if present is independently selected from the group consisting of: - F, -OH, -CN, and C_1-3 alkyl optionally substituted with 1-3 F.

20. The compound of claim 19, wherein Z² is C_3-6 cycloalkyl substituted with one -OH (e.g., Z² is or ).

21. The compound of any one of claims 1-3, wherein R¹ is -N(R²)₂.

22. The compound of claim 21, wherein each R² is an independently selected C_1-3 alkyl optionally substituted with 1-3 R^c.

23. The compound of claim 21 or 22, wherein each R² is independently methyl or ethyl, each optionally substituted with 1-3 R^c, wherein each R^c present on R² is independently selected from the group consisting of: -F, cyano, -OH, -C_1-6 alkoxy, and -C_1-6 haloalkoxy.

24. The compound of any one of claims 21-23, wherein R¹ is -N(Me)₂, -N(Et)₂, or -N(Me)Et.

25. The compound of claim 21, wherein one R² is a C_2-6 alkyl substituted with -OH.

26. The compound of claim 21 or 25, wherein one R² is or .

27. The compound of claim 25 or 26, wherein the other R² is -H or C_1-3 alkyl (e.g., -H or methyl).

28. The compound of any one of claims 1-3, wherein R¹ is -H.

29. The compound of any one of claims 1-28, wherein X¹ is selected from the group consisting of: CH₂, CHR^L, and C(R^L)₂.

30. The compound of any one of claims 1-29, wherein X¹ is CH₂.

31. The compound of any one of claims 1-28, wherein X¹ is a bond.

32. The compound of any one of claims 1-31, wherein X² and X³ are independently selected from the group consisting of: CH₂, CHR^L, and C(R^L)₂.

33. The compound of claim 32, wherein X² and X³ are both CH₂.

34. The compound of claim 32, wherein X² is CH₂; and X³ is selected from the group consisting of: CHR^L and C(R^L)₂.

35. The compound of claim 32 or 34, wherein X² is CH₂; and X³ is CHR^L.

36. The compound of any one of claims 32 or 34-35, wherein X² is CH2; and X³ is CHMe.

37. The compound of any one of claims 1-31, wherein one of X² and X³ is -O-; and the other of X² and X³ is selected from the group consisting of: CH₂, CHR^L, and C(R^L)₂.

38. The compound of any one of claims 1-31 or 37, wherein X² is -O-; and X³ is CH₂ or CHMe.

39. The compound of any one of claims 1-38, wherein R⁹ is para to -X³-.

40. The compound of any one of claims 1-39, wherein R⁹ is -OH or -NH₂.

41. The compound of any one of claims 1-40, wherein R⁹ is -NH₂.

42. The compound of any one of claims 1-41, wherein b1 is 0, 1, or 2.

43. The compound of any one of claims 1-42, wherein b1 is 1 or 2.

44. The compound of any one of claims 1-43, wherein b1 is 1 or 2; and each R¹⁰ is independently selected from the group consisting of: -Cl, -F, -CN, and C1-3 alkyl optionally substituted with 1-3 R^c.

45. The compound of any one of claims 1-44, wherein b1 is 1; and R¹⁰ is -CN.

46. The compound of any one of claims 1-45, wherein b1 is 1; R¹⁰ is ortho to R⁹; and R¹⁰ is -CN.

47. The compound of any one of claims 1-43, wherein b1 is 1 or 2; and each R¹⁰ is independently -Cl or -F.

48. The compound of any one of claims 1-43 or 47, wherein b1 is 1 or 2; 1-2 occurrence(s) of R¹⁰ is ortho to R⁹; and each R¹⁰ is independently -Cl or -F.

49. The compound of any one of claims 1-28, wherein Ring B is selected from the _{group consisting of: , , and , wherein:} X² is -O- or -CH₂-; X³ is -CH₂- or -CHR^L-, wherein R^L is C_1-3 alkyl (e.g., methyl); and each R¹⁰ is independently selected from the group consisting of: -Cl, -F, -CN, and C_1-3 alkyl optionally substituted with 1-3 R^c.

50. The compound of any one of claims 1-28 or 49, wherein Ring B is selected from the group consisting of: and , wherein: X² is -O- or -CH₂-; X³ is -CH₂- or -CHR^L-, wherein R^L is C_1-3 alkyl (e.g., methyl); and each R¹⁰ is independently selected from the group consisting of: -Cl, -F, -CN, and C_1-3 alkyl optionally substituted with 1-3 R^c.

51. The compound of any one of claims 1-28 or 50, wherein Ring B is selected from the group consisting of: , , , , , , , and .

52. The compound of any one of claims 1-28, wherein Ring B is , wherein X³ is -CH₂- or -CHR^L-; and R^L is C_1-3 alkyl optionally substituted with 1-3 -F.

53. The compound of claim 52, wherein X³ is -CHR^L-.

54. The compound of claim 52 or 53, wherein R^L is methyl.

55. The compound of any one of claims 1-54, wherein Y² is -CH₂-.

56. The compound of any one of claims 1-55, wherein R³ is a 4-10 membered heterocyclyl optionally substituted with 1-6 substituents independently selected from the group consisting of: R^a and R^b.

57. The compound of any one of claims 1-56, wherein R³ is a 4-10 membered heterocyclyl having one ring nitrogen atom and 0-1 additional ring heteroatom selected from the group consisting of oxygen and nitrogen, wherein the heterocyclyl is optionally substituted with 1-6 R^a.

58. The compound of any one of claims 1-57, wherein R³ is a bicyclic 7-10 membered heterocyclyl optionally substituted with 1-6 R^a.

59. The compound of any one of claims 1-58, wherein R³ is optionally substituted with 1-3 R^a .

60. The compound of any one of claims 1-59, wherein R³ is optionally substituted with 1-3 substituents independently selected from the group consisting of: -F, -C_1- ₃ alkoxy, -C_1-3 haloalkoxy, and -OH.

61. The compound of any one of claims 1-60, wherein R³ is optionally substituted with 1-2 -F.

62. The compound of any one of claims 1-61, wherein R³ is (e.g., ).

63. The compound of any one of claims 1-62, wherein the ring carbon atom labelled with * in Formula (I) has (S)-stereochemistry.

64. The compound of claim 1, wherein the compound is a compound of Formula (II): Formula (II) or a pharmaceutically acceptable salt thereof, wherein: X¹ is selected from the group consisting of a bond, S(O)_0-2, CH₂, CHR^L, C(R^L)₂, and O; X² and X³ are independently selected from the group consisting of: CH₂, CHR^L, C(R^L)₂, O, and S(O)_0-2, provided that no more than one of X¹, X², and X³ is selected from the group consisting of: O and S(O)_0-2; b1 is 1 or 2; each R¹⁰ is independently selected from the group consisting of R^a and R^b; and each R^L is independently selected from the group consisting of C_1-3 alkoxy, -F, CN, and C_1-3 alkyl optionally substituted with 1-3 R^c; or one pair of R^L on the same or different ring carbon atom(s) taken together with the ring atom(s) connecting them form a C_3-6 cycloalkyl ring.

65. The compound of claim 64, wherein the compound is a compound of Formula (II-a): Formula (II-a) or a pharmaceutically acceptable salt thereof, wherein: b4 is 0 or 1; and each R¹⁰ is independently selected from the group consisting of: -Cl, -F, -CN, and C_1-3 alkyl optionally substituted with 1-3 R^c.

66. The compound of claim 65, wherein b4 is 0.

67. The compound of claim 1, wherein the compound is a compound of Formula (III): Formula (III) or a pharmaceutically acceptable salt thereof, wherein: X¹ is selected from the group consisting of a bond, S(O)_0-2, CH₂, CHR^L, C(R^L)₂, and O; X² and X³ are independently selected from the group consisting of: CH₂, CHR^L, C(R^L)₂, O, and S(O)_0-2, provided that no more than one of X¹, X², and X³ is selected from the group consisting of: O and S(O)_0-2; R⁹ is selected from the group consisting of: H, NR^dR^e, -OH, and halo; b4 is 0 or 1; each R¹⁰ is independently selected from the group consisting of R^a and R^b; and each R^L is independently selected from the group consisting of C_1-3 alkoxy, -F, CN, and C_1-3 alkyl optionally substituted with 1-3 R^c; or one pair of R^L on the same or different ring carbon atom(s) taken together with the ring atom(s) connecting them form a C_3-6 cycloalkyl ring.

68. The compound of claim 67, wherein R⁹ is -NH₂; and each R¹⁰ is independently selected from the group consisting of: -Cl, -F, -CN, and C_1-3 alkyl optionally substituted with 1-3 R^c.

69. The compound of any one of claims 64-68, wherein X¹ is CH₂ or CHR^L (e.g., CH₂).

70. The compound of any one of claims 64-69, wherein X² and X³ are independently selected from the group consisting of: CH₂, CHR^L, and C(R^L)₂.

71. The compound of any one of claims 64-70, wherein X¹ is CH₂; and X² and X³ are both CH₂.

72. The compound of any one of claims 64-70, wherein at least one (e.g., one) of X¹, X², and X³ is selected from the group consisting of: CHR^L and C(R^L)₂.

73. The compound of any one of claims 64-70 or 72, wherein one of X¹, X², and X³ is CHR^L; and each remaining of X¹, X², and X³ is CH₂.

74. The compound of any one of claims 64-70 or 72, wherein X¹ is CH₂; and X² and X³ are independently selected from the group consisting of: CH₂, CHR^L, and C(R^L)_2, provided that 1-2 of X² and X³ is independently CHR^L or C(R^L)₂.

75. The compound of any one of claims 64-70 or 72-74, wherein X¹ is CH₂; X² is CH₂; and X³ is CHR^L.

76. The compound of any one of claims 64-75, wherein each R^L is independently selected from the group consisting of: CH₃, CF₃, CHF₂, and CH₂F.

77. The compound of any one of claims 64-76, wherein each R^L is CH₃.

78. The compound of any one of claims 64-77, wherein X¹ is CH₂; X² is CH₂; and X³ is CHMe or CH2 (e.g., CHMe).

79. The compound of claim 1, wherein the compound is a compound of Formula (IV): Formula (IV) or a pharmaceutically acceptable salt thereof, wherein: X¹ is selected from the group consisting of a bond, S(O)_0-2, CH₂, CHR^L, C(R^L)₂, and O; X² and X³ are independently selected from the group consisting of: CH₂, CHR^L, C(R^L)₂, O, and S(O)_0-2, provided that at least one of X¹, X², and X³ is CHR^L or C(R^L)₂; further provided that no more than one of X¹, X², and X³ is selected from the group consisting of: O and S(O)_0-2; b1 is 0, 1 or 2; R⁹ is selected from the group consisting of: H, OH, NR^dR^e, and halo; each R¹⁰ is independently selected from the group consisting of R^a and R^b; and each R^L is independently selected from the group consisting of C1-3 alkoxy, -F, CN, and C_1-3 alkyl optionally substituted with 1-3 R^c.

80. The compound of claim 79, wherein the compound is a compound of Formula (IV-a): Formula (IV-a) or a pharmaceutically acceptable salt thereof, wherein: each R¹⁰ is independently selected from the group consisting of: -Cl, -F, -CN, and C_1-3 alkyl optionally substituted with 1-3 R^c.

81. The compound of claim 80, wherein b1 is 1; and R¹⁰ is -CN.

82. The compound of claim 79, wherein the compound is a compound of Formula (IV-b): Formula (IV-b) or a pharmaceutically acceptable salt thereof, wherein: b4 is 0 or 1; and each R¹⁰ is independently selected from the group consisting of: -Cl, -F, -CN, and C_1-3 alkyl optionally substituted with 1-3 R^c.

83. The compound of claim 82, wherein b4 is 0.

84. The compound of claim 82 or 83, wherein R⁹ is NH₂.

85. The compound of any one of claims 79-84, wherein X¹ is CH₂.

86. The compound of any one of claims 79-85, wherein X² is CH₂; and X³ is CHR^L.

87. The compound of any one of claims 79-85, wherein X² is -O-; and X³ is selected from the group consisting of: CHR^L and C(R^L)₂.

88. The compound of any one of claims 79-87, wherein each R^L is independently selected from the group consisting of: CH₃, CF₃, CHF₂, and CH₂F.

89. The compound of any one of claims 79-88, wherein each R^L is CH₃.

90. The compound of claim 79, wherein the compound is a compound of Formula (IV-c): Formula (IV-c) or a pharmaceutically acceptable salt thereof, wherein: b4 is 0 or 1; and each R¹⁰ is independently selected from the group consisting of: -Cl, -F, -CN, and C_1-3 alkyl optionally substituted with 1-3 R^c.

91. The compound of claim 90, wherein R^L is CH₃.

92. The compound of claim 90 or 91, wherein b4 is 0.

93. The compound of any one of claims 64-92, wherein R¹ is -Z⁰–(Z¹)_m1-Z²; Z⁰ is -N(C_1-3 alkyl)- (e.g., -NMe-) or -NH-; and Z² is C_3-6 cycloalkyl optionally substituted with 1-3 R⁷, wherein each R⁷ is independently selected from the group consisting of: -F, -OH, -CN, and C_1-3 alkyl optionally substituted with 1-3 F.

94. The compound of claim 93, wherein m1 is 0; and Z² is cyclopropyl or cyclobutyl, each optionally substituted with 1-3 R⁷, wherein each R⁷ is independently selected from the group consisting of: -F, -OH, -CN, and C_1-3 alkyl optionally substituted with 1-3 F.

95. The compound of claim 93 or 94, wherein each R⁷ is -F.

96. The compound of any one of claims 64-93, wherein R¹ is -N(H)-Z² or -N(C_1-3 alkyl)-Z², wherein Z² is C_3-6 cycloalkyl optionally substituted with 1-3 R⁷, wherein: one R⁷ is -OH; and each remaining R⁷, if present, is independently selected from the group consisting of: - F, -OH, -CN, and C_1-3 alkyl optionally substituted with 1-3 F.

97. The compound of claim 96, wherein Z² is C_3-6 cycloalkyl substituted with one -OH (e.g., Z² is or ).

98. The compound of any one of claims 64-92, wherein R¹ is -N(R²)₂.

99. The compound of any one of claims 64-92 or 98, wherein each R² is independently methyl or ethyl, each of which is optionally substituted with 1-3 R^c, wherein each R^c present on R² is independently selected from the group consisting of: -F, cyano, -OH, -C_1-6 alkoxy, and -C_1-6 haloalkoxy.

100. The compound of any one of claims 64-92 or 98-99, wherein R¹ is -N(Me)₂, - N(Et)₂, or -N(Me)Et.

101. The compound of any one of claims 64-92 or 98, wherein R¹ is -N(R²)₂; one R² is a C_2-6 alkyl substituted with -OH; and the other R² is -H or C_1-3 alkyl (e.g., -H or methyl); optionally wherein one R² is or ; and the other R² is -H or methyl.

102. The compound of any one of claims 64-92, wherein R¹ is -O-C_1-3 alkyl optionally substituted with 1-3 R^c, optionally wherein each R^c present on R¹ is independently selected from the group consisting of: -F, cyano, -OH, -C_1-6 alkoxy, and -C_1-6 haloalkoxy (e.g., -OH, -C_1-6 alkoxy, and -C_1-6 haloalkoxy).

103. The compound of any one of claims 64-102, wherein Y² is -CH₂-; and R³ is a 4-10 membered heterocyclyl having one ring nitrogen atom and 0-1 additional ring heteroatom selected from the group consisting of oxygen and nitrogen, wherein the heterocyclyl is optionally substituted with 1-6 R^a.

104. The compound of any one of claims 64-103, wherein Y² is -CH₂-; and R³ is optionally substituted with 1-2 substituents independently selected from the group consisting of: -F, -C_1-6 alkoxy, and -C_1-6 haloalkoxy.

105. The compound of any one of claims 64-104, wherein Y² is -CH₂-; and R³ is optionally substituted with 1-2 -F.

106. The compound of claim 105, wherein R³ is (e.g., ).

107. The compound of any one of claims 64-106, wherein the moiety is .

108. The compound of claim 64, wherein the compound is a compound of Formula (II-1): Formula (II-1) or a pharmaceutically acceptable salt thereof, wherein: b1 is 1 or 2; each R¹⁰ is independently selected from the group consisting of: -Cl, -F, -CN, and C_1-3 alkyl optionally substituted with 1-3 R^c; X¹ is CH₂; and X² and X³ are independently selected from the group consisting of: O, CH2, CHR^L, and C(R^L)₂.

109. The compound of claim 108, wherein b1 is 1.

110. The compound of any one of claims 64-65 or 108, wherein the compound is a compound of Formula (II-a1): Formula (II-a1) or a pharmaceutically acceptable salt thereof, wherein: b4 is 0 or 1; each R¹⁰ is independently selected from the group consisting of: -Cl, -F, -CN, and C_1-3 alkyl optionally substituted with 1-3 R^c; X¹ is CH₂; and X² and X³ are independently selected from the group consisting of: O, CH₂, CHR^L, and C(R^L)2.

111. The compound of claim 110, wherein b4 is 0.

112. The compound of claim 67, wherein the compound is a compound of Formula (III-1): Formula (III-1) or a pharmaceutically acceptable salt thereof, wherein: b4 is 0 or 1; each R¹⁰ is independently selected from the group consisting of: -Cl, -F, -CN, and C_1-3 alkyl optionally substituted with 1-3 R^c; X¹ is CH₂; and X² and X³ are independently selected from the group consisting of: O, CH₂, CHR^L, and C(R^L)₂.

113. The compound of claim 112, wherein b4 is 0.

114. The compound of claim 112 or 113, wherein R⁹ is -NR^dR^e (e.g., -NH₂).

115. The compound of claim 79, wherein the compound is a compound of Formula (IV-a1) or (IV-b1): Formula (IV-a1) Formula (IV-b1) or a pharmaceutically acceptable salt thereof, wherein: b1 is 0, 1, or 2; b4 is 0 or 1; each R¹⁰ is independently selected from the group consisting of: -Cl, -F, -CN, and C_1-3 alkyl optionally substituted with 1-3 R^c; X¹ is CH₂; one of X² and X³ is independently selected from the group consisting of: CHR^L and C(R^L)₂; and the other of X² and X³ is CH₂ or O.

116. The compound of claim 115, wherein the compound is a compound of Formula (IV-a1), or a pharmaceutically acceptable salt thereof, wherein b1 is 1; and the moiety is (e.g., ).

117. The compound of claim 115, wherein the compound is a compound of Formula (IV-b1), or a pharmaceutically acceptable salt thereof, wherein b4 is 0.

118. The compound of any one of claims 108-117, wherein X² is CH₂; and X³ is CHR^L (e.g., CH(CH3)).

119. The compound of any one of claims 108-117, wherein X² is CH₂; and X³ is CH₂.

120. The compound of any one of claims 108-119, wherein each R² is independently methyl or ethyl, each optionally substituted with 1-3 R^c, wherein each R^c present on R² is independently selected from the group consisting of: -F, cyano, -OH, -C_1-6 alkoxy, and -C_1-6 haloalkoxy.

121. The compound of any one of claims 108-120, wherein each R² is independently methyl or ethyl.

122. The compound of any one of claims 108-120, wherein one R² is a C_2-6 alkyl substituted with -OH; and the other R² is -H or C_1-3 alkyl.

123. The compound of any one of claims 108-122, wherein Y² is -CH₂-; and R³ is a 4-10 membered heterocyclyl having one ring nitrogen atom and 0-1 additional ring heteroatom selected from the group consisting of oxygen and nitrogen, wherein the heterocyclyl is optionally substituted with 1-6 R^a.

124. The compound of any one of claims 108-123, wherein R³ is optionally substituted with 1-3 substituents independently selected from the group consisting of: -F, -C_1- ₃ alkoxy, -C_1-3 haloalkoxy, and -OH.

125. The compound of any one of claims 108-124, wherein Y² is -CH₂-; and R³ is optionally substituted with 1-2 -F.

126. The compound of claim 124 or 125, wherein R³ is (e.g., ).

127. The compound of any one of claims 108-126, wherein the moiety is .

128. The compound of claim 64 or 65, wherein the compound is a compound of Formula (II-a2): Formula (II-a2) or a pharmaceutically acceptable salt thereof, wherein: X³ is CH₂ or CHR^L, wherein R^L is C_1-3 alkyl optionally substituted with 1-3 -F; one R² is a C_2-6 alkyl substituted with -OH; the other R² is -H or C1-3 alkyl; Y² is -CH2-; and R³ is optionally substituted with 1-2 substituents independently selected from the group consisting of: -F, -C_1-6 alkoxy, and -C_1-6 haloalkoxy.

129. The compound of claim 128, wherein one R² is a C_2-6 alkyl substituted with - OH (e.g., or ); and the other R² is -H or methyl.

130. The compound of claim 64 or 65, wherein the compound is a compound of Formula (II-a3): Formula (II-a3) or a pharmaceutically acceptable salt thereof, wherein: X³ is CH₂ or CHR^L, wherein R^L is C_1-3 alkyl optionally substituted with 1-3 -F; R^f is -H or C_1-3 alkyl; Z² is a C_3-6 cycloalkyl optionally substituted with 1-3 R⁷, wherein: one R⁷ is -OH; each remaining R⁷ if present is independently selected from the group consisting of: - F, -OH, -CN, and C_1-3 alkyl optionally substituted with 1-3 F; Y² is -CH₂-; and R³ is optionally substituted with 1-2 substituents independently selected from the group consisting of: -F, -C_1-6 alkoxy, and -C_1-6 haloalkoxy.

131. The compound of claim 130, wherein R^f is -H or methyl; and Z² is C_3-6 cycloalkyl substituted with one -OH (e.g., Z² is or ).

132. The compound of any one of claims 128-131, wherein X³ is CH(Me).

133. The compound of any one of claims 128-132, wherein R³ is (e.g., ).

134. The compound of any one of claims 128-133, wherein the moiety is .

135. The compound of any one of claims 1-3, wherein the compound is selected from the group consisting of compounds in Table C1, or a pharmaceutically acceptable salt thereof.

136. A pharmaceutical composition comprising a compound of any one of claims 1- 135, or a pharmaceutically acceptable salt thereof, and a pharmaceutically acceptable excipient.

137. A method of treating cancer in a subject, the method comprising administering to a subject identified or diagnosed as having a cancer having a KRas dysregulation a therapeutically effective amount of a compound of any one of claims 1-135 or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition according to claim 136.

138. A method of treating cancer in a subject, the method comprising: (a) determining that the cancer in the subject has a KRas dysregulation; and (b) administering to the subject a therapeutically effective amount of a compound of any one of claims 1-135 or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition according to claim 136.

139. The method of any one of claims 138-141, wherein the KRas dysregulation is a KRas mutation.

140. The method of claim 149, wherein the KRas mutation is a KRas G12A mutation, a KRas G12C mutation, a KRas G12D mutation, a KRas G12R mutation, a KRas G12S mutation, or a KRas G12V mutation.

141. The method of claim 140, wherein the KRas mutation is a KRas G12C mutation, a KRas G12D mutation or a KRas G12V mutation.

142. The method of claim 138, wherein the step of determining that the cancer in the subject has a KRas dysregulation includes performing an assay to detect the KRas dysregulation (e.g., a KRas mutation) in a tumor sample from the subject.

143. The method of claim 142, wherein detecting the KRas dysregulation includes detecting a KRAS gene having a mutation corresponding to a substitution of glycine 12 in a KRas protein and/or a KRas protein having a substitution of glycine 12.

144. The method of claim 143, wherein the substitution of glycine 12 is a substitution to alanine, cysteine, aspartic acid, arginine, serine, or valine.

145. The method of any one of claims 137-144, wherein the cancer is selected from the group consisting of: a hematological cancer, a soft tissue cancer, bile duct cancer, bladder cancer, brain cancer, breast cancer, cervical cancer, colorectal cancer, endometrial cancer, esophageal cancer, kidney cancer, liver cancer, lung cancer, mucinous carcinoma, ovarian cancer, pancreatic cancer, prostate cancer, skin cancer, stomach cancer, testicular cancer, thymus cancer, thyroid cancer, urothelial cancer, uterine cancer, and a combination thereof.

146. The method of claim 145, wherein the cancer is selected from the group consisting of: colorectal cancer, endometrial cancer, lung cancer (e.g., NSCLC), ovarian cancer, and pancreatic cancer.

147. The method of any one of claims 137-146, comprising administering an additional therapy or therapeutic agent to the subject.

148. The method of claim 147, wherein the additional therapy or therapeutic agent is selected from the group consisting of Ras pathway targeted therapeutic agents, kinase-targeted therapeutics, Bcl-X_L inhibitors or degraders, mTORC1 inhibitors or degraders, YAP inhibitors or degraders, TEAD inhibitors or degraders, proteasome inhibitors or degraders, HSP90 inhibitors or degraders, farnesyl transferase inhibitors or degraders, PTEN inhibitors or degraders, signal transduction pathway inhibitors or degraders, checkpoint inhibitors, modulators of the apoptosis pathway, chemotherapeutics, angiogenesis-targeted therapies, immune-targeted agents, radiotherapy, and combinations thereof.