Compositions and methods for treating or preventing squamous cell carcinoma

Abstract

The present disclosure relates to pharmaceutical compositions, including topical formulations thereof, comprising a serine / arginine-rich splicing factor 3 (SRSF3) inhibitor and uses thereof in methods of treating or preventing squamous cell carcinoma and other cutaneous diseases and disorders.

Description

[0001]Attorney Docket No.047162-7528WO1(02689) COMPOSITIONS AND METHODS FOR TREATING OR PREVENTING SQUAMOUS CELL CARCINOMA CROSS-REFERENCE TO RELATED APPLICATIONS This application claims priority under 35 U.S.C. § 119(e) to U.S. Provisional Patent Application No.63 / 695,055, filed September 16, 2024, and to U.S. Provisional Patent Application No.63 / 762,936, filed February 25, 2025, each which applications is hereby incorporated herein by reference in its entirety. BACKGROUND OF THE INVENTION An estimated 1.8 million cases of squamous cell carcinoma (SCC) are diagnosed in the U.S. each year and more than 5,400 people worldwide die of nonmelanoma skin cancer each month. For late-stage SCC, which accounts for less than 5% of cases, medical treatments include cytotoxic chemotherapy, EGFR inhibitors (e.g., cetuximab), and PD1 inhibitors (e.g., cemiplimab and pembrolizumab). Although early-stage SCC accounts for greater than 95% of SCC cases, there is currently no approved medical treatment and the existing standard of care is surgical excision. Excision therapy has several drawbacks including high morbidity and cost for the patient and high cost to the healthcare system. For example, at least two appointments are needed and there can be long wait times to schedule the appointments. Additionally, excision can lead to scarring, bleeding, and infection. Further, many SCC patients present with multiple SCC lesions at the same time, but simultaneous excision surgery is not feasible. As such, a medical treatment for early-stage SCC is needed which would be safer and less costly than excision therapy. The present invention addresses this unmet need. SUMMARY OF THE INVENTION In some aspects, the invention provides a method of treating or preventing squamous cell carcinoma (SCC) in a subject in need thereof, the method comprising administering to the subject a pharmaceutical composition comprising an effective amount of a serine / arginine-rich splicing factor 3 (SRSF3) inhibitor. In some embodiments, the pharmaceutical composition is a topical formulation that is administered to the skin of the subject. In some embodiments, the SRSF3 inhibitor is a small molecule having molecular mass less than about 600 g / mol. Attorney Docket No.047162-7528WO1(02689) In some embodiments, the SRSF3 inhibitor is characterized by an effective level of skin permeability and / or is formulated in a topical formulation to exhibit an effective level of skin permeability. In some embodiments, the SRSF3 inhibitor reduces SRSF3 amount or activity in SCC cells by at least about 10%, at least about 15%, at least about 20%, at least about 25%, at least about 30%, at least about 35%, at least about 40%, at least about 45%, at least about 50%, at least about 55%, at least about 60%, at least about 65%, at least about 70%, at least about 75%, at least about 80%, at least about 85%, at least about 90%, at least about 95%, or at least about 100% compared to SRSF3 amount or activity in SCC cells in the absence of the SRSF3 inhibitor. In some embodiments, the SRSF3 inhibitor induces terminal differentiation of SCC cells. In some embodiments, the SRSF3 inhibitor is a compound of Formula (I), or a salt, stereoisomer, or isotopologue thereof: , wherein: ; AA B the group consisting of H, CN, NO2, OR , N(R )(R ), SRA, C(=O)RA, C(=O)ORA, C(=O)N(RA)(RB), S(=O)RA, S(=O)2RA, S(=O)N(RA)(RB), S(=O)2N(RA)(RB), P(=O)(ORA)(ORB), halogen, optionally substituted C1-C6alkyl, optionally substituted C3-C8cycloalkyl, optionally substituted C2-C8 heterocycloalkyl, optionally substituted C6-C10 aryl, and optionally substituted C2-C8heteroaryl; R4is selected from the group consisting of H and optionally substituted C1-C6 alkyl; R5is selected from the group consisting of H and optionally substituted C1-C6 alkyl; Attorney Docket No.047162-7528WO1(02689) R6is selected from the group consisting of H, optionally substituted C1-C6 alkyl, optionally substituted C3-C8cycloalkyl, optionally substituted C2-C8heterocycloalkyl, optionally substituted C6-C10 aryl, and optionally substituted C2-C8 heteroaryl; R7a, R7b, and R7c, if present, are each independently selected from the group consisting of H, CN, NO2, ORA, N(RA)(RB), C(=O)RA, C(=O)ORA, C(=O)N(RA)(RB), S(=O)RA, S(=O)2RA, S(=O)N(RA)(RB), S(=O)2N(RA)(RB), P(=O)(ORA)(ORB), halogen, optionally substituted C2-C8 heteroaryl, wherein R7aand R7bcan combine with the atoms to which they are bound to form an optionally substituted C6-C10 aryl or optionally substituted C2-C8heteroaryl; X1selected from the group consisting of N and CR7c; Z1is CR8aor N, Z2is CR8bor N, Z3is CR8cor N, Z4is CR8dor N, and Z5is CR8eor N, wherein no more than two of Z1, Z2, Z3, Z4, and Z5are N; R8a, R8b, R8c, R8d, and R8e, if present, are each independently selected from the group consisting of H, CN, NO2, ORA, N(RA)(RB), SRA, halogen, optionally substituted C1-C6 alkyl, optionally substituted C3-C8 cycloalkyl, optionally substituted C2-C8heterocycloalkyl, optionally substituted C6-C10aryl, and optionally substituted C2-C8 heteroaryl; each occurrence of RAand RB, if present, is independently selected from the group consisting of H, optionally substituted C1-C6 alkyl, optionally substituted C3-C8 cycloalkyl, optionally substituted C2-C8heterocycloalkyl, optionally substituted C6- C10 aryl, optionally substituted C2-C8 heteroaryl, C(=O)RC, C(=O)ORC, C(=O)N(RC)(RD), S(=O)RC, S(=O)2RC, S(=O)N(RC)(RD), S(=O)2N(RC)(RD), and P(=O)(ORC)(ORD); each occurrence of RCand RD, if present, is independently selected from the group consisting of H, optionally substituted C1-C6 alkyl, optionally substituted C3-C8 cycloalkyl, optionally substituted C2-C8 heterocycloalkyl, optionally substituted C6- C10aryl, and optionally substituted C2-C8heteroaryl. In some embodiments, the SRSF3 inhibitor is a compound of Formula (I), wherein at least one of the following applies: Attorney Docket No.047162-7528WO1(02689) (a) R7a, R7b, and R7c, if present, are each independently selected from the group consisting of H, CN, NO2, ORA, N(RA)(RB), C(=O)RA, C(=O)ORA, C(=O)N(RA)(RB), S(=O)RA, S(=O)2RA, S(=O)N(RA)(RB), S(=O)2N(RA)(RB), P(=O)(ORA) substituted C3- optionally substituted C6-C10aryl, and optionally substituted C2-C8heteroaryl; (b) R7aand R7bcan combine with the atoms to which they are bound to form a substituted C6-C10aryl or optionally substituted C2-C8heteroaryl; (c) R7aand R7bcan combine with the atoms to which they are bound to form unsubstituted phenyl, and R8c, if present, is selected from the group consisting of H, CN, NO2, SRA, NH(substituted C1-C6alkyl), NH(optionally substituted C2-C6 alkyl), halogen, optionally substituted C1-C6 alkyl, substituted C1-C6 alkoxy, optionally substituted C2-C6alkoxy, optionally substituted C3-C8cycloalkyl, optionally substituted C2-C8 heterocycloalkyl, optionally substituted C6-C10aryl, and optionally substituted C2-C8heteroaryl; (d) R7aand R7bcan combine with the atoms to which they are bound to form unsubstituted phenyl, R8cis N(RA)(RB), and RAis C(=O)RC; and (e) R8cis N(RA)(RB), and RAis C(=O)RC. In some embodiments, R6is H. In some embodiments, one of the following applies: (a) R7aand R7bare each independently selected from the group consisting of H and CH3; or (b) R7aand R7bcombine with the atoms to which they are bound to . In some embodiments, X1is selected from the group consisting of N and CH. , (a) Z1is CR8a, Z2is N, Z3is CR8c, Z4is CR8d, and Z5is CR8e; or Attorney Docket No.047162-7528WO1(02689) (b) Z1is CR8a, Z2is CR8b, Z3is CR8c, Z4is CR8d, and Z5is CR8e. In some embodiments, R8a, R8b, R8d, and R8eare each independently H. In some embodiments, R8cis selected from the group consisting of O(C1-C6 alkyl), O(C1-C6haloalkyl), S(C1-C6alkyl), NH(C1-C6alkyl), and N(C1-C6alkyl)C(=O)(C1-C6haloalkyl), optionally wherein R8cis selected from the group consisting of OCH3, OCF3, SCH3, NHCH3,and N(CH3)C(=O)CF3. In some embodiments, R2is selected from the group , . some In some embodiments, wherein R4is H. In some embodiments, R5is CH3. In some embodiments, the compound of formula (I) is selected from the group consisting of: (E)-2-(2-(1-(1H-benzo[d]imidazol-2-yl)ethylidene)hydrazineyl)-4-(4- methoxyphenyl)thiazole; (E)-4-(2-(2-(1-(1H-benzo[d]imidazol-2-yl)ethylidene)hydrazineyl)thiazol-4- yl)-N-methylaniline; (E)-2-(2-(1-(1H-pyrrol-2-yl)ethylidene)hydrazineyl)-4-(4- methoxyphenyl)thiazole; (E)-2-(2-(1-(1H-imidazol-2-yl)ethylidene)hydrazineyl)-4-(4- methoxyphenyl)thiazole; (E)-2-(2-(1-(1H-pyrrol-2-yl)ethylidene)hydrazineyl)-4-(6-methoxypyridin-3- yl)thiazole; (E)-2-(2-(1-(4,5-dimethyl-1H-imidazol-2-yl)ethylidene)hydrazineyl)-4-(6- methoxypyridin-3-yl)thiazole; (E)-2-(2-(1-(1H-imidazol-2-yl)ethylidene)hydrazineyl)-4-(6-methoxypyridin- 3-yl)thiazole; (E)-2-(2-(1-(1H-benzo[d]imidazol-2-yl)ethylidene)hydrazineyl)-4-(4- (trifluoromethoxy)phenyl)thiazole; Attorney Docket No.047162-7528WO1(02689) (E)-2-(2-(1-(1H-imidazol-2-yl)ethylidene)hydrazineyl)-4-(4- (trifluoromethoxy)phenyl)thiazole; (E)-2-(2-(1-(1H-benzo[d]imidazol-2-yl)ethylidene)hydrazineyl)-4-(4- (methylthio)phenyl)thiazole; (E)-2-(2-(1-(1H-imidazol-2-yl)ethylidene)hydrazineyl)-4-(4- (methylthio)phenyl)thiazole; (E)-4-(2-(2-(1-(1H-imidazol-2-yl)ethylidene)hydrazineyl)thiazol-4-yl)-N- methylaniline; (E)-N-(4-(2-(2-(1-(1H-benzo[d]imidazol-2-yl)ethylidene)hydrazineyl)thiazol- 4-yl)phenyl)-2,2,2-trifluoro-N-methylacetamide; and (E)-N-(4-(2-(2-(1-(1H-imidazol-2-yl)ethylidene)hydrazineyl)thiazol-4- yl)phenyl)-2,2,2-trifluoro-N-methylacetamide. In some embodiments, the SRSF3 inhibitor is selected from the group consisting of: (a) SFI003, or a salt, solvate, stereoisomer, isotopologue, or tautomer thereof; (b) (E)-N-(4-(2-(2-(1-(1H-benzo[d]imidazol-2-yl)ethylidene)hydrazineyl)thiazol- 4-yl)phenyl)-2,2,2-trifluoro-N-methylacetamide), or a salt, solvate, stereoisomer, isotopologue, or tautomer thereof; (c) (E)-4-(2-(2-(1-(1H-benzo[d]imidazole-2-yl)ethylidene)hydrazineyl)thiazol-4- yl)-N-methylaniline), or a salt, solvate, stereoisomer, isotopologue, or tautomer thereof; and (d) (E)-2-(2-(1-(1H-benzo[d]imidazol-2-yl)ethylidene)hydrazineyl)-4-(4- (trifluoromethoxy)phenyl)thiazole), or a salt, solvate, stereoisomer, isotopologue, or tautomer thereof. In some embodiments, the SRSF3 inhibitor is the only anticancer agent administered to the subject. In some embodiments, the method further comprises administering to the subject at least one additional agent or therapy useful for treating or preventing the SCC, optionally wherein the additional agent or therapy comprises surgical resection of at least one SCC lesion. In some embodiments, the topical formulation comprises a gel or an ointment. In some embodiments, the SCC is early-stage cutaneous SCC. In some embodiments, the subject has multiple simultaneous SCC lesions. In some embodiments, the subject is a mammal. Attorney Docket No.047162-7528WO1(02689) In some embodiments, the subject is a human. In some aspects, the invention provides a pharmaceutical composition comprising a serine / arginine-rich splicing factor 3 (SRSF3) inhibitor, for use in any one of the methods disclosed herein. In some aspects, the invention provides a pharmaceutical composition comprising a serine / arginine-rich splicing factor 3 (SRSF3) inhibitor. In some embodiments, the pharmaceutical composition is a topical formulation for administration to skin. In some embodiments, the SRSF3 inhibitor is a small molecule having molecular mass less than about 600 g / mol. In some embodiments, the SRSF3 inhibitor is characterized by an effective level of skin permeability and / or is formulated in a topical formulation to exhibit an effective level of skin permeability. In some embodiments, the SRSF3 inhibitor reduces SRSF3 amount or activity in squamous cell carcinoma (SCC) cells by at least about 10%, at least about 15%, at least about 20%, at least about 25%, at least about 30%, at least about 35%, at least about 40%, at least about 45%, at least about 50%, at least about 55%, at least about 60%, at least about 65%, at least about 70%, at least about 75%, at least about 80%, at least about 85%, at least about 90%, at least about 95%, or at least about 100% compared to SRSF3 amount or activity in SCC cells in the absence of the SRSF3 inhibitor. In some embodiments, the SRSF3 inhibitor induces terminal differentiation of SCC cells. In some embodiments, the topical formulation comprises a gel or an ointment. In some embodiments, the SRSF3 inhibitor is a compound of Formula (I), or a salt, stereoisomer, or isotopologue thereof: , wherein: ; Attorney Docket No.047162-7528WO1(02689) R2; the group consisting of H, CN, NO2, ORA, N(RA)(RB), SRA, C(=O)N(RA)(RB), S(=O)RA, S(=O)2RA, S(=O)N(RA)(RB), S(=O)2N(RA)(RB), P(=O)(ORA)(ORB), halogen, optionally substituted C1-C6 alkyl, optionally substituted C3-C8 cycloalkyl, optionally substituted C2-C8heterocycloalkyl, optionally substituted C6-C10aryl, and optionally substituted C2-C8 heteroaryl; R4is selected from the group consisting of H and optionally substituted C1-C6alkyl; R5is selected from the group consisting of H and optionally substituted C1-C6alkyl; R6is selected from the group consisting of H, optionally substituted C1-C6alkyl, optionally substituted C3-C8 cycloalkyl, optionally substituted C2-C8 heterocycloalkyl, optionally substituted C6-C10 aryl, and optionally substituted C2-C8 heteroaryl; R7a, R7b, and R7c, if present, are each independently selected from the group NO2, ORA, N(RA)(RB), C(=O)RA, C(=O)ORA, C(=O)N(RA)(RB), S(=O)RA, S(=O)2RA, S(=O)N(RA)(RB), S(=O)2N(RA)(RB), P(=O)(ORA)(ORB), halogen, optionally substituted C1-C6alkyl, optionally substituted C3-C8cycloalkyl, optionally substituted C2-C8 heterocycloalkyl, optionally substituted C6-C10 aryl, and optionally substituted C2-C8heteroaryl, wherein R7aand R7bcan combine with the atoms to which they are bound to form an optionally substituted C6-C10aryl or optionally substituted C2-C8 heteroaryl; X1selected from the group consisting of N and CR7c; Z1is CR8aor N, Z2is CR8bor N, Z3is CR8cor N, Z4is CR8dor N, and Z5is CR8eor N, wherein no more than two of Z1, Z2, Z3, Z4, and Z5are N; R8a, R8b, R8c, R8d, and R8e, if present, are each independently selected from the group consisting of H, CN, NO2, ORA, N(RA)(RB), SRA, halogen, optionally substituted C1-C6alkyl, optionally substituted C3-C8cycloalkyl, optionally substituted C2-C8 heterocycloalkyl, optionally substituted C6-C10 aryl, and optionally substituted C2-C8 heteroaryl; Attorney Docket No.047162-7528WO1(02689) each occurrence of RAand RB, if present, is independently selected from the group consisting of H, optionally substituted C1-C6alkyl, optionally substituted C3-C8cycloalkyl, optionally substituted C2-C8 heterocycloalkyl, optionally substituted C6- C10aryl, optionally substituted C2-C8heteroaryl, C(=O)RC, C(=O)ORC, C(=O)N(RC)(RD), S(=O)RC, S(=O)2RC, S(=O)N(RC)(RD), S(=O)2N(RC)(RD), and P(=O)(ORC)(ORD); each occurrence of RCand RD, if present, is independently selected from the group consisting of H, optionally substituted C1-C6alkyl, optionally substituted C3-C8cycloalkyl, optionally substituted C2-C8 heterocycloalkyl, optionally substituted C6- C10 aryl, and optionally substituted C2-C8 heteroaryl. In some embodiments, the SRSF3 inhibitor is a compound of Formula (I), wherein at least one of the following applies: (a) R7a, R7b, and R7c, if present, are each independently selected from the group consisting of H, CN, NO2, ORA, N(RA)(RB), C(=O)RA, C(=O)ORA, C(=O)N(RA) , P(=O)(ORA) substituted C3-C8 cycloalkyl, optionally substituted C2-C8 heterocycloalkyl, optionally substituted C6-C10aryl, and optionally substituted C2-C8heteroaryl; (b) R7aand R7bcan combine with the atoms to which they are bound to form a substituted C6-C10aryl or optionally substituted C2-C8heteroaryl; (c) R7aand R7bcan combine with the atoms to which they are bound to form unsubstituted phenyl, and R8c, if present, is selected from the group consisting of H, CN, NO2, SRA, NH(substituted C1-C6 alkyl), NH(optionally substituted C2-C6alkyl), halogen, optionally substituted C1-C6alkyl, substituted C1-C6alkoxy, optionally substituted C2-C6 alkoxy, optionally substituted C3-C8 cycloalkyl, optionally substituted C2-C8heterocycloalkyl, optionally substituted C6-C10 aryl, and optionally substituted C2-C8 heteroaryl; (d) R7aand R7bcan combine with the atoms to which they are bound to form unsubstituted phenyl, R8cis N(RA)(RB), and RAis C(=O)RC; and (e) R8cis N(RA)(RB), and RAis C(=O)RC. In some embodiments, the SRSF3 inhibitor is the compound of Formula (I), wherein R6is H. Attorney Docket No.047162-7528WO1(02689) In some embodiments, the SRSF3 inhibitor is the compound of Formula (I), wherein one of the following applies: (a) R7aand R7bare each independently selected from the group consisting of H and CH3; or (b) R7aand R7bcombine with the atoms to which they are bound to form . In some embodiments, the SRSF3 inhibitor is the compound of Formula , X1is selected from the group consisting of N and CH. In some embodiments, the SRSF3 inhibitor is the compound of Formula (I), wherein H N . one (a) Z1is CR8a, Z2is N, Z3is CR8c, Z4is CR8d, and Z5is CR8e; or (b) Z1is CR8a, Z2is CR8b, Z3is CR8c, Z4is CR8d, and Z5is CR8e. In some embodiments, the SRSF3 inhibitor is the compound of Formula (I), wherein R8a, R8b, R8d, and R8eare each independently H. is the compound of Formula (I), wherein R8cis selected from the group consisting of O(C1-C6alkyl), O(C1-C6haloalkyl), S(C1-C6alkyl), NH(C1-C6 alkyl), and N(C1-C6 alkyl)C(=O)(C1-C6 haloalkyl), optionally wherein R8cis selected from the group consisting of OCH3, OCF3, SCH3, NHCH3,and N(CH3)C(=O)CF3. In some embodiments, the SRSF3 inhibitor is the compound of Formula (I), wherein , In some embodiments, the SRSF3 inhibitor is the compound of Formula (I), wherein R3is H. In some embodiments, the SRSF3 inhibitor is the compound of Formula (I), wherein R4is H. Attorney Docket No.047162-7528WO1(02689) In some embodiments, the SRSF3 inhibitor is the compound of Formula (I), wherein R5is CH3. In some embodiments, the SRSF3 inhibitor is the compound of Formula (I), wherein the compound of formula (I) is selected from the group consisting of: (E)-2-(2-(1-(1H-benzo[d]imidazol-2-yl)ethylidene)hydrazineyl)-4-(4- methoxyphenyl)thiazole; (E)-4-(2-(2-(1-(1H-benzo[d]imidazol-2-yl)ethylidene)hydrazineyl)thiazol-4- yl)-N-methylaniline; (E)-2-(2-(1-(1H-pyrrol-2-yl)ethylidene)hydrazineyl)-4-(4- methoxyphenyl)thiazole; (E)-2-(2-(1-(1H-imidazol-2-yl)ethylidene)hydrazineyl)-4-(4- methoxyphenyl)thiazole; (E)-2-(2-(1-(1H-pyrrol-2-yl)ethylidene)hydrazineyl)-4-(6-methoxypyridin-3- yl)thiazole; (E)-2-(2-(1-(4,5-dimethyl-1H-imidazol-2-yl)ethylidene)hydrazineyl)-4-(6- methoxypyridin-3-yl)thiazole; (E)-2-(2-(1-(1H-imidazol-2-yl)ethylidene)hydrazineyl)-4-(6-methoxypyridin- 3-yl)thiazole; (E)-2-(2-(1-(1H-benzo[d]imidazol-2-yl)ethylidene)hydrazineyl)-4-(4- (trifluoromethoxy)phenyl)thiazole; (E)-2-(2-(1-(1H-imidazol-2-yl)ethylidene)hydrazineyl)-4-(4- (trifluoromethoxy)phenyl)thiazole; (E)-2-(2-(1-(1H-benzo[d]imidazol-2-yl)ethylidene)hydrazineyl)-4-(4- (methylthio)phenyl)thiazole; (E)-2-(2-(1-(1H-imidazol-2-yl)ethylidene)hydrazineyl)-4-(4- (methylthio)phenyl)thiazole; (E)-4-(2-(2-(1-(1H-imidazol-2-yl)ethylidene)hydrazineyl)thiazol-4-yl)-N- methylaniline; (E)-N-(4-(2-(2-(1-(1H-benzo[d]imidazol-2-yl)ethylidene)hydrazineyl)thiazol- 4-yl)phenyl)-2,2,2-trifluoro-N-methylacetamide; and (E)-N-(4-(2-(2-(1-(1H-imidazol-2-yl)ethylidene)hydrazineyl)thiazol-4- yl)phenyl)-2,2,2-trifluoro-N-methylacetamide. In some embodiments, the SRSF3 inhibitor is selected from the group consisting of: Attorney Docket No.047162-7528WO1(02689) (a) SFI003, or a salt, solvate, stereoisomer, isotopologue, or tautomer thereof; (b) (E)-N-(4-(2-(2-(1-(1H-benzo[d]imidazol-2-yl)ethylidene)hydrazineyl)thiazol- 4-yl)phenyl)-2,2,2-trifluoro-N-methylacetamide), or a salt, solvate, stereoisomer, isotopologue, or tautomer thereof; (c) (E)-4-(2-(2-(1-(1H-benzo[d]imidazole-2-yl)ethylidene)hydrazineyl)thiazol-4- yl)-N-methylaniline), or a salt, solvate, stereoisomer, isotopologue, or tautomer thereof; and (d) (E)-2-(2-(1-(1H-benzo[d]imidazol-2-yl)ethylidene)hydrazineyl)-4-(4- (trifluoromethoxy)phenyl)thiazole), or a salt, solvate, stereoisomer, isotopologue, or tautomer thereof. In some aspects, the invention provides a compound of Formula (II), or a salt, stereoisomer, or isotopologue thereof: , wherein: ; AA B the group consisting of H, CN, NO2, OR , N(R )(R ), SRA, C(=O)RA, C(=O)ORA, C(=O)N(RA)(RB), S(=O)RA, S(=O)2RA, , halogen, optionally optionally substituted C2-C8heterocycloalkyl, optionally substituted C6-C10aryl, and optionally substituted C2-C8 heteroaryl; R4is selected from the group consisting of H and optionally substituted C1-C6alkyl; R5is selected from the group consisting of H and optionally substituted C1-C6alkyl; R6is selected from the group consisting of H, optionally substituted C1-C6alkyl, optionally substituted C3-C8 cycloalkyl, optionally substituted C2-C8 Attorney Docket No.047162-7528WO1(02689) heterocycloalkyl, optionally substituted C6-C10 aryl, and optionally substituted C2-C8 heteroaryl; R7a, R7b, and R7c, if present, are each independently selected from the group consisting of H, CN, NO2, ORA, N(RA)(RB), C(=O)RA, C(=O)ORA, C(=O)N(RA)(RB), optionally substituted C2-C8heteroaryl, wherein R7aand R7bcan combine with the atoms to which they are bound to form an optionally substituted C6-C10 aryl or optionally substituted C2-C8heteroaryl; X1selected from the group consisting of N and CR7c; Z1is CR8aor N, Z2is CR8bor N, Z3is CR8cor N, Z4is CR8dor N, and Z5is CR8eor N, wherein no more than two of Z1, Z2, Z3, Z4, and Z5are N; R8a, R8b, R8c, R8d, and R8e, if present, are each independently selected from the group consisting of H, CN, NO2, ORA, N(RA)(RB), SRA, halogen, optionally substituted C1-C6 alkyl, optionally substituted C3-C8 cycloalkyl, optionally substituted C2-C8heterocycloalkyl, optionally substituted C6-C10aryl, and optionally substituted C2-C8 heteroaryl; each occurrence of RAand RB, if present, is independently selected from the group consisting of H, optionally substituted C1-C6 alkyl, optionally substituted C3-C8 cycloalkyl, optionally substituted C2-C8heterocycloalkyl, optionally substituted C6- C10 aryl, optionally substituted C2-C8 heteroaryl, C(=O)RC, C(=O)ORC, C(=O)N(RC)(RD), S(=O)RC, S(=O)2RC, S(=O)N(RC)(RD), S(=O)2N(RC)(RD), and P(=O)(ORC)(ORD); each occurrence of RCand RD, if present, is independently selected from the group consisting of H, optionally substituted C1-C6 alkyl, optionally substituted C3-C8 cycloalkyl, optionally substituted C2-C8 heterocycloalkyl, optionally substituted C6- C10 aryl, and optionally substituted C2-C8 heteroaryl; wherein the compound of formula (II) is not a compound selected from the group consisting of: (E)-4-(2-(2-(1-(1H-benzo[d]imidazol-2-yl)ethylidene)hydrazineyl)thiazol-4- yl)-N-methylaniline; and Attorney Docket No.047162-7528WO1(02689) (E)-2-(2-(1-(1H-benzo[d]imidazol-2-yl)ethylidene)hydrazineyl)-4-(4- methoxyphenyl)thiazole. In some embodiments, at least one of the following applies: (a) R7a, R7b, and R7c, if present, are each independently selected from the group consisting of H, CN, NO2, ORA, N(RA)(RB), C(=O)RA, C(=O)ORA, C(=O)N(RA)(RB), S(=O)RA, S(=O)2RA, S(=O)N(RA)(RB), S(=O)2N(RA)(RB), P(=O)(ORA) substituted C3- optionally substituted C6-C10 aryl, and optionally substituted C2-C8 heteroaryl; (b) R7aand R7bcan combine with the atoms to which they are bound to form a substituted C6-C10 aryl or optionally substituted C2-C8 heteroaryl; (c) R7aand R7bcan combine with the atoms to which they are bound to form unsubstituted phenyl, and R8c, if present, is selected from the group consisting of H, CN, NO2, SRA, NH(substituted C1-C6alkyl), NH(optionally substituted C2-C6 alkyl), halogen, optionally substituted C1-C6 alkyl, substituted C1-C6 alkoxy, optionally substituted C2-C6alkoxy, optionally substituted C3-C8cycloalkyl, optionally substituted C2-C8 heterocycloalkyl, optionally substituted C6-C10aryl, and optionally substituted C2-C8heteroaryl; (d) R7aand R7bcan combine with the atoms to which they are bound to form unsubstituted phenyl, R8cis N(RA)(RB), and RAis C(=O)RC; and (e) R8cis N(RA)(RB), and RAis C(=O)RC. In some embodiments, R6is H. In some embodiments, one of the following applies: (a) R7aand R7bare each independently selected from the group consisting of H and CH3; or (b) R7aand R7bcombine with the atoms to which they are bound to . In some embodiments, X1is selected from the group consisting of N and CH. Attorney Docket No.047162-7528WO1(02689) In some embodiments, R1is selected from the group consisting , H N . one of the following applies: (a) Z1is CR8a, Z2is N, Z3is CR8c, Z4is CR8d, and Z5is CR8e; or (b) Z1is CR8a, Z2is CR8b, Z3is CR8c, Z4is CR8d, and Z5is CR8e. In some embodiments, R8a, R8b, R8d, and R8eare each independently H. In some embodiments, R8cis selected from the group consisting of O(C1-C6 alkyl), O(C1-C6haloalkyl), S(C1-C6alkyl), NH(C1-C6alkyl), and N(C1-C6alkyl)C(=O)(C1-C6haloalkyl), optionally wherein R8cis selected from the group consisting of OCH3, OCF3, SCH3, NHCH3, and N(CH3)C(=O)CF3. In some embodiments, R2is selected from the group consisting , . In some embodiments, R3is H. In some embodiments, R4is H. In some embodiments, R5is CH3. In some embodiments, the compound of formula (II) is selected from the group consisting of: (E)-2-(2-(1-(1H-pyrrol-2-yl)ethylidene)hydrazineyl)-4-(4- methoxyphenyl)thiazole; (E)-2-(2-(1-(1H-imidazol-2-yl)ethylidene)hydrazineyl)-4-(4- methoxyphenyl)thiazole; (E)-2-(2-(1-(1H-pyrrol-2-yl)ethylidene)hydrazineyl)-4-(6-methoxypyridin-3- yl)thiazole; (E)-2-(2-(1-(4,5-dimethyl-1H-imidazol-2-yl)ethylidene)hydrazineyl)-4-(6- methoxypyridin-3-yl)thiazole; Attorney Docket No.047162-7528WO1(02689) (E)-2-(2-(1-(1H-imidazol-2-yl)ethylidene)hydrazineyl)-4-(6-methoxypyridin- 3-yl)thiazole; (E)-2-(2-(1-(1H-benzo[d]imidazol-2-yl)ethylidene)hydrazineyl)-4-(4- (trifluoromethoxy)phenyl)thiazole; (E)-2-(2-(1-(1H-imidazol-2-yl)ethylidene)hydrazineyl)-4-(4- (trifluoromethoxy)phenyl)thiazole; (E)-2-(2-(1-(1H-benzo[d]imidazol-2-yl)ethylidene)hydrazineyl)-4-(4- (methylthio)phenyl)thiazole; (E)-2-(2-(1-(1H-imidazol-2-yl)ethylidene)hydrazineyl)-4-(4- (methylthio)phenyl)thiazole; (E)-4-(2-(2-(1-(1H-imidazol-2-yl)ethylidene)hydrazineyl)thiazol-4-yl)-N- methylaniline; (E)-N-(4-(2-(2-(1-(1H-benzo[d]imidazol-2-yl)ethylidene)hydrazineyl)thiazol- 4-yl)phenyl)-2,2,2-trifluoro-N-methylacetamide; and (E)-N-(4-(2-(2-(1-(1H-imidazol-2-yl)ethylidene)hydrazineyl)thiazol-4- yl)phenyl)-2,2,2-trifluoro-N-methylacetamide. In some embodiments, the compound of Formula (II) is an SRSF3 inhibitor selected from the group consisting of: (a) (E)-N-(4-(2-(2-(1-(1H-benzo[d]imidazol-2-yl)ethylidene)hydrazineyl)thiazol- 4-yl)phenyl)-2,2,2-trifluoro-N-methylacetamide), or a salt, solvate, stereoisomer, isotopologue, or tautomer thereof; (b) (E)-4-(2-(2-(1-(1H-benzo[d]imidazole-2-yl)ethylidene)hydrazineyl)thiazol-4- yl)-N-methylaniline), or a salt, solvate, stereoisomer, isotopologue, or tautomer thereof; and (c) (E)-2-(2-(1-(1H-benzo[d]imidazol-2-yl)ethylidene)hydrazineyl)-4-(4- (trifluoromethoxy)phenyl)thiazole), or a salt, solvate, stereoisomer, isotopologue, or tautomer thereof. BRIEF DESCRIPTION OF THE DRAWINGS The foregoing and other features and advantages of the present invention will be more fully understood from the following detailed description of illustrative embodiments taken in conjunction with the accompanying drawings. FIG.1 provides information on SCC and the cons of surgical resection for early-stage SCC. Attorney Docket No.047162-7528WO1(02689) FIG.2 shows images of SCC lesions and scarring in patients. FIG.3 is a schematic summary of the complex interactions of MDM2 which negatively regulates p53 (as published in Nag, et al., J Biomed Res, 2013;27:254). FIG.4 is a schematic of a mutated p53 gene which leads to cancer and the p53 beta isoform (p53β) that leads to cancer regression (as published in Camus, et al, Cell Cycle, 2012;11:1646; Fujita, et al., Nat Cell Biol, 2009;11:1135). FIG.5 is a schematic and a chart showing that knockdown of serine / arginine-rich splicing factor 3 (SRSF3) in human fibroblasts leads to increased p53β that promotes cellular senescence (as published in Tang, et al., Oncogene, 2013, 32(22): 2792–2798). FIG.6 provides Western blot data showing that inhibition of SRSF3 with a small molecule SRSF3 inhibitor (SFI003) promotes differentiation of colorectal cancer cells (as published in Zhang, et al., Cell Death Discov., 2022, 8, Article Number 238). FIG.7 is a chart showing the incidence of SCC in patients with a history of atrial fibrillation or heart failure. Shown is the SCC incidence in patients treated with the SRSF3 inhibitor, digoxin, vs. the SCC incidence in patients who never received digoxin but received beta-blockers. The data show that, with systemic SRSF3 inhibition, more individuals are free of SCC. FIG.8 shows photographs of keratoacanthoma (a subtype of squamous cell cancer that grows rapidly but then self-regresses) and microscopy images of biopsy tissues taken therefrom, at two different time points one month apart. The microscopy reveals that keratoacanthoma self-regresses via terminal differentiation. FIGs.9A – 9D are stained microscopy images showing that p53β expression is increased in regressing tumors and terminally differentiating keratinocytes (as published in Ko, et al, J Clin Pathol, 2018;71:1120). FIG.9A shows increased expression (dark pigment, arrows) in differentiating keratinocytes of the granular layer in the epidermis and hair follicle epithelium. FIG.9B shows that the less differentiated follicular bulb and stem does not express p53β, but the granular layer of the epidermis does express p53β (arrow). FIG.9C shows p53β expression (dark pigment) in the cytoplasm of a regressing keratoacanthoma. FIG.9D shows the keratoacanthoma in panel C at higher magnification. p53β expression (dark pigment) is present in the cytoplasm. FIG.10 shows stained microscopy images of SCC tissues showing high SRSF3 expression (dark pigment in the nuclei) and low p53β (virtually no dark staining). FIG.11 is a chart showing that SRSF3 levels are approximately 25% lower in keratoacanthoma cells compared to SRSF3 levels SCC cells. Attorney Docket No.047162-7528WO1(02689) FIG.12 is a fluorescence microscopy image of keratinocytes treated with a small molecule SRSF3 inhibitor (SFI003); six differentiation genes are upregulated in two- dimensional and three-dimensional keratinocyte (skin cell) models. FIG.13 shows the simulated binding mode of the small molecule inhibitor SFI003 to SRSF3 (as published in Zhang, et al., Cell Death Discov., 2022, 8, Article Number 238). FIGs.14A – 14C show SRSF3 inhibition assay data for SFI003. FIG.14A is a graph of the toxicity assay data for cells treated with SFI003 for 24h, 48h, and 72h. FIG.14B is a chart of the Cyclin D1 level versus SFI003 concentration for cells treated with SFI003 for 48h. FIG.14C is a chart of the cell cycle analysis versus SFI003 concentration for cells treated with SFI003 for 48h. Each column shows the % cells in Early G1, G1, S, G2, Late G2, and >4N, from bottom to top. FIGs.15A – 15D show SRSF3 inhibition assay data for Y-0309750. FIG.15A is a graph of the toxicity assay data for cells treated with Y-0309750 or SFI003 for 48h. FIG. 15B is a graph of the Cyclin D1 fold-increase versus inhibitor concentration for cells treated with Y-0309750 or SFI003 for 48h. FIG.15C is a chart of the cell cycle analysis versus inhibitor concentration for cells treated with Y-0309750 or SFI003 for 48h. Each column shows the % cells in Early G1, G1, S, G2, Late G2, and >4N, from bottom to top. FIG.15D shows cell cycle analysis data for cells treated with DMSO control, SFI003, and Y-0309750. FIGs.16A – 16D show SRSF3 inhibition assay data for Y-0309749. FIG.16A is a graph of the toxicity assay data for cells treated with Y-0309749 or SFI003 for 48h. FIG. 16B is a graph of the Cyclin D1 fold-increase versus inhibitor concentration for cells treated with Y-0309749 or SFI003 for 48h. FIG.16C is a chart of the cell cycle analysis versus inhibitor concentration for cells treated with Y-0309749 or SFI003 for 48h. Each column shows the % cells in Early G1, G1, S, G2, Late G2, and >4N, from bottom to top. FIG.16D shows cell cycle analysis data for cells treated with DMSO control, SFI003, and Y-0309749. FIGs.17A – 17D show SRSF3 inhibition assay data for Y-0309745. FIG.17A is a graph of the toxicity assay data for cells treated with Y-0309745 or SFI003 for 48h. FIG. 17B is a graph of the Cyclin D1 fold-increase versus inhibitor concentration for cells treated with Y-0309745 or SFI003 for 48h. FIG.17C is a chart of the cell cycle analysis versus inhibitor concentration for cells treated with Y-0309745 or SFI003 for 48h. Each column shows the % cells in Early G1, G1, S, G2, Late G2, and >4N, from bottom to top. FIG.17D shows cell cycle analysis data for cells treated with DMSO control, SFI003, and Y-0309745. FIGs.18A – 18B show SRSF3 inhibition assay data for Y-0309747. FIG.18A is a graph of the toxicity assay data for cells treated with Y-0309747 or SFI003 for 48h. FIG. Attorney Docket No.047162-7528WO1(02689) 18B is a graph of the Cyclin D1 fold-increase versus inhibitor concentration for cells treated with Y-0309747 or SFI003 for 48h. FIGs.19A – 19B show SRSF3 inhibition assay data for Y-0309751. FIG.19A is a graph of the toxicity assay data for cells treated with Y-0309751 or SFI003 for 48h. FIG. 19B is a graph of the Cyclin D1 fold-increase versus inhibitor concentration for cells treated with Y-0309751 or SFI003 for 48h. FIGs.20A – 20B show SRSF3 inhibition assay data for Y-0309748. FIG.20A is a graph of the toxicity assay data for cells treated with Y-0309748 or SFI003 for 48h. FIG. 20B is a graph of the Cyclin D1 fold-increase versus inhibitor concentration for cells treated with Y-0309748 or SFI003 for 48h. FIGs.21A – 21B show SRSF3 inhibition assay data for Y-0309746. FIG.21A is a graph of the toxicity assay data for cells treated with Y-0309746 or SFI003 for 48h. FIG. 21B is a graph of the Cyclin D1 fold-increase versus inhibitor concentration for cells treated with Y-0309746 or SFI003 for 48h. FIGs.22A – 22B show SRSF3 inhibition assay data for Y-0309741. FIG.22A is a graph of the toxicity assay data for cells treated with Y-0309741 or SFI003 for 48h. FIG. 22B is a graph of the Cyclin D1 fold-increase versus inhibitor concentration for cells treated with Y-0309741 or SFI003 for 48h. FIGs.23A – 23B show SRSF3 inhibition assay data for Y-0309742. FIG.23A is a graph of the toxicity assay data for cells treated with Y-0309742 or SFI003 for 48h. FIG. 23B is a graph of the Cyclin D1 fold-increase versus inhibitor concentration for cells treated with Y-0309742 or SFI003 for 48h. FIGs.24A – 24B show SRSF3 inhibition assay data for Y-0309743. FIG.24A is a graph of the toxicity assay data for cells treated with Y-0309743 or SFI003 for 48h. FIG. 24B is a graph of the Cyclin D1 fold-increase versus inhibitor concentration for cells treated with Y-0309743 or SFI003 for 48h. DETAILED DESCRIPTION Serine / arginine-rich splicing factor 3 (SRSF3) has been shown to be a direct regulator of p53, as downregulation of SRSF3 induces p53β, an alternatively spliced isoform of p53 that promotes cellular senescence (Tang, et al., Oncogene, 2013, 32(22): 2792–2798). The present disclosure relates in part to the discoveries, as demonstrated herein in Example 1, (i) that SCC cells express high SRSF3 and low p53β, (ii) that cells of keratoacanthoma (a subtype of SCC that can spontaneously regress) express approximately Attorney Docket No.047162-7528WO1(02689) 25% lower SRSF3 than SCC cells, and (iii) that keratinocytes treated with a small molecule inhibitor of SRSF3 (SFI003) show upregulation of six differentiation genes. Thus the present disclosure is directed primarily to pharmaceutical compositions, such as topical formulations, comprising an SRSF3 inhibitor and methods comprising the pharmaceutical compositions for treating squamous cell carcinoma. In one aspect, the present disclosure provides a method of treating or preventing squamous cell carcinoma (SCC) in a subject in need thereof, the method comprising administering to the subject a pharmaceutical composition comprising an effective amount of a serine / arginine-rich splicing factor 3 (SRSF3) inhibitor. In one aspect, the present disclosure provides a pharmaceutical composition comprising a serine / arginine-rich splicing factor 3 (SRSF3) inhibitor. In some aspects, the pharmaceutical composition comprising a serine / arginine-rich splicing factor 3 (SRSF3) inhibitor is for use in treating or preventing squamous cell carcinoma (SCC) in a subject in need thereof. In another aspect, the present disclosure provides novel compounds of Formula (II) . It is to be understood that the methods and compositions described in this disclosure are not limited to particular methods and experimental conditions disclosed herein as such methods and conditions may vary. It is also to be understood that the terminology used herein is for the purpose of describing particular embodiments only and is not intended to be limiting. Furthermore, the experiments described herein, unless otherwise indicated, use conventional chemical, molecular and cellular biological and immunological techniques within the skill of the art. Such techniques are well known to the skilled worker and are explained fully in the literature. See, e.g., Ausubel, et al., ed., Current Protocols in Molecular Biology, John Wiley & Sons, Inc., NY, N.Y. (1987-2008), including all supplements, Molecular Cloning: A Laboratory Manual (Fourth Edition) by Green and Sambrook, and Harlow et al., Antibodies: A Laboratory Manual, Chapter 14, Cold Spring Harbor Laboratory, Cold Spring Harbor (2013, 2nd edition). Attorney Docket No.047162-7528WO1(02689) Definitions Unless otherwise defined, scientific and technical terms used herein have the meanings that are commonly understood by those of ordinary skill in the art. In the event of any latent ambiguity, definitions provided herein take precedent over any dictionary or extrinsic definition. Unless otherwise required by context, singular terms shall include pluralities and plural terms shall include the singular. The use of “or” means “and / or” unless stated otherwise. The use of the term “including,” as well as other forms, such as “includes” and “included,” is not limiting. The present disclosure also contemplates other embodiments “comprising,” “consisting of” and “consisting essentially of” the embodiments or elements presented herein, whether explicitly set forth or not. Generally, the nomenclature used herein and the laboratory procedures in pharmaceutical science, organic chemistry, cell and tissue culture, molecular biology, immunology, microbiology, genetics and protein and nucleic acid chemistry and hybridization described herein is well-known and commonly used in the art. The methods and techniques provided herein are generally performed according to conventional methods well known in the art and as described in various general and more specific references that are cited and discussed throughout the present specification unless otherwise indicated. Enzymatic reactions and purification techniques are performed according to manufacturer’s specifications, as commonly accomplished in the art or as described herein. The nomenclatures used in connection with, and the laboratory procedures and techniques of, analytical chemistry, synthetic organic chemistry, and medicinal and pharmaceutical chemistry described herein are those well-known and commonly used in the art. Standard techniques are used for chemical syntheses, chemical analyses, pharmaceutical preparation, formulation, and delivery, and treatment of patients. It is also to be understood that the terminology used herein is for the purpose of describing particular embodiments only and is not intended to be limiting. That the disclosure may be more readily understood, select terms are defined below. The articles "a" and "an" are used herein to refer to one or to more than one (i.e. , to at least one) of the grammatical object of the article. By way of example, "an element" means one element or more than one element. "About" as used herein when referring to a measurable value such as an amount, a temporal duration, and the like, is meant to encompass variations of ±20% or ±10%, more preferably ±5%, even more preferably ±1%, and still more preferably ±0,1% from the specified value, as such variations are appropriate to perform the disclosed methods. Attorney Docket No.047162-7528WO1(02689) The term “alkyl” as used herein refers to straight chain and branched alkyl groups and cycloalkyl groups having from 1 to 40 carbon atoms, 1 to about 20 carbon atoms, 1 to 12 carbons or, in some embodiments, from 1 to 8 carbon atoms. Examples of straight chain alkyl groups include those with from 1 to 8 carbon atoms such as methyl, ethyl, n-propyl, n-butyl, n-pentyl, n-hexyl, n- heptyl, and n-octyl groups. Examples of branched alkyl groups include, but are not limited to, isopropyl, iso-butyl, sec-butyl, t-butyl, neopentyl, isopentyl, and 2,2-dimethylpropyl groups. As used herein, the term “alkyl” encompasses n-alkyl, isoalkyl, and anteisoalkyl groups as well as other branched chain forms of alkyl. Representative substituted alkyl groups can be substituted one or more times with any of the groups listed herein, for example, amino, hydroxy, cyano, carboxy, nitro, thio, alkoxy, and halogen groups. The term "alkenyl" as used herein refers to straight and branched chain and cyclic alkyl groups as defined herein, except that at least one double bond exists between two carbon atoms. Thus, alkenyl groups have from 2 to 40 carbon atoms, or 2 to about 20 carbon atoms, or 2 to 12 carbon atoms or, in some embodiments, from 2 to 8 carbon atoms. Examples include, but are not limited to vinyl, -CH=C=CCH2, -CH=CH(CH3), -CH=C(CH3)2, -C(CH3)=CH2, -C(CH3)=CH(CH3), - C(CH2CH3)=CH2, cyclohexenyl, cyclopentenyl, cyclohexadienyl, butadienyl, pentadienyl, and hexadienyl among others. The term "alkynyl" as used herein refers to straight and branched chain alkyl groups, except that at least one triple bond exists between two carbon atoms. Thus, alkynyl groups have from 2 to 40 carbon atoms, 2 to about 20 carbon atoms, or from 2 to 12 carbons or, in some embodiments, from 2 to 8 carbon atoms. Examples include, but are not limited to –C≡CH, -C≡C(CH3), - C≡C(CH2CH3), -CH2C≡CH, -CH2C≡C(CH3), and -CH2C≡C(CH2CH3) among others. The term "acyl" as used herein refers to a group containing a carbonyl moiety wherein the group is bonded via the carbonyl carbon atom. The carbonyl carbon atom is bonded to a hydrogen forming a "formyl" group or is bonded to another carbon atom, which can be part of an alkyl, aryl, aralkyl cycloalkyl, cycloalkylalkyl, heterocyclyl, heterocyclylalkyl, heteroaryl, heteroarylalkyl group or the like. An acyl group can include 0 to about 12, 0 to about 20, or 0 to about 40 additional carbon atoms bonded to the carbonyl group. An acyl group can include double or triple bonds within the meaning herein. An acryloyl group is an example of an acyl group. An acyl group can also include heteroatoms within the meaning herein. A nicotinoyl group (pyridyl-3-carbonyl) is an example of an acyl group within the meaning herein. Other examples include acetyl, benzoyl, phenylacetyl, pyridylacetyl, cinnamoyl, and acryloyl groups and the like. When the group containing the carbon atom that is bonded to the carbonyl carbon atom contains a halogen, the group is termed a "haloacyl" group. An example is a trifluoroacetyl group. The term "alkoxy" as used herein refers to an oxygen atom connected to an alkyl group, including a cycloalkyl group, as are defined herein. Examples of linear alkoxy groups include but are not limited to methoxy, ethoxy, propoxy, butoxy, pentyloxy, hexyloxy, and the like. Examples of Attorney Docket No.047162-7528WO1(02689) branched alkoxy include but are not limited to isopropoxy, sec-butoxy, tert-butoxy, isopentyloxy, isohexyloxy, and the like. Examples of cyclic alkoxy include but are not limited to cyclopropyloxy, cyclobutyloxy, cyclopentyloxy, cyclohexyloxy, and the like. An alkoxy group can include about 1 to about 12, about 1 to about 20, or about 1 to about 40 carbon atoms bonded to the oxygen atom, and can further include double or triple bonds, and can also include heteroatoms. For example, an allyloxy group or a methoxyethoxy group is also an alkoxy group within the meaning herein, as is a methylenedioxy group in a context where two adjacent atoms of a structure are substituted therewith. The term "amine" as used herein refers to primary, secondary, and tertiary amines having, e.g., the formula N(group)3wherein each group can independently be H or non-H, such as alkyl, aryl, and the like. Amines include but are not limited to R-NH2, for example, alkylamines, arylamines, alkylarylamines; R2NH wherein each R is independently selected, such as dialkylamines, diarylamines, aralkylamines, heterocyclylamines and the like; and R3N wherein each R is independently selected, such as trialkylamines, dialkylarylamines, alkyldiarylamines, triarylamines, and the like. The term "amine" also includes ammonium ions as used herein. The term "amino group" as used herein refers to a substituent of the form -NH2, -NHR, -NR2, -NR3+, wherein each R is independently selected, and protonated forms of each, except for -NR3+, which cannot be protonated. Accordingly, any compound substituted with an amino group can be viewed as an amine. An "amino group" within the meaning herein can be a primary, secondary, tertiary, or quaternary amino group. An "alkylamino" group includes a monoalkylamino, dialkylamino, and trialkylamino group. As used herein, “antibody” (Ab) is used in the broadest sense and specifically may include any immunoglobulin, whether natural or partly or wholly synthetically produced, including but not limited to monoclonal antibodies, polyclonal antibodies, multispecific antibodies (for example, bispecific antibodies and polyreactive antibodies), and antibody fragments. Thus, the term “antibody” as used in any context within this specification is meant to include, but not be limited to, any specific binding member, immunoglobulin class and / or isotype (e.g., IgG1, IgG2a, IgG2b, IgG3, IgG4, IgM, IgA1, IgA2, IgD, and IgE) and biologically relevant fragment or specific binding member thereof, including but not limited to Fab, F(ab′)2, scFv (single chain or related entity) and (scFv)2. The term “antibody fragments” as used herein may include those antibody fragments obtained using techniques readily known and available to those of ordinary skill in the art, as reviewed herein. Therefore, in addition to the definition for “antibody” presented supra, the term “antibody” may further encompass any polypeptide or protein comprising a portion of an intact antibody, such as the antigen binding or variable region of the intact antibody. These can be derived from natural sources, or they may be partly or wholly synthetically produced. Examples of Attorney Docket No.047162-7528WO1(02689) antibody fragments include, but are not limited to, Fab, Fab′, F(ab′)2, and Fv fragments; diabodies, and linear antibodies. As used herein, the term "antigen" refers to a molecule to which an antibody can selectively bind. The target antigen may be a protein, carbohydrate, nucleic acid, lipid, hapten, or other naturally occurring or synthetic compound. Preferably, the target antigen is a protein or fragment thereof or a complex of proteins. The term “aryl” as used herein refers to cyclic aromatic hydrocarbon groups that do not contain heteroatoms in the ring. Thus aryl groups include, but are not limited to, phenyl, azulenyl, heptalenyl, biphenyl, indacenyl, fluorenyl, phenanthrenyl, triphenylenyl, pyrenyl, naphthacenyl, chrysenyl, biphenylenyl, anthracenyl, and naphthyl groups. In some embodiments, aryl groups contain about 6 to about 14 carbons in the ring portions of the groups. Aryl groups can be unsubstituted or substituted, as defined herein. Representative substituted aryl groups can be mono- substituted or substituted more than once, such as, but not limited to, a phenyl group substituted at any one or more of 2-, 3-, 4-, 5-, or 6-positions of the phenyl ring, or a naphthyl group substituted at any one or more of 2- to 8-positions thereof. The term "aralkyl" as used herein refers to alkyl groups as defined herein in which a hydrogen or carbon bond of an alkyl group is replaced with a bond to an aryl group as defined herein. Representative aralkyl groups include benzyl and phenylethyl groups and fused (cycloalkylaryl)alkyl groups such as 4-ethyl-indanyl. Aralkenyl groups are alkenyl groups as defined herein in which a hydrogen or carbon bond of an alkyl group is replaced with a bond to an aryl group as defined herein. As used herein, the term “binding” refers to the adherence of molecules to one another, such as, but not limited to, enzymes to substrates, antibodies to antigens, DNA strands to their complementary strands. Binding occurs because the shape and chemical nature of parts of the molecule surfaces are complementary. A common metaphor is the “lock-and-key” used to describe how enzymes fit around their substrate. As used herein, the term "biological sample" refers to a sample obtained from an individual and used in a diagnostic or monitoring assay. Biological samples encompass, e.g., a clinical sample, cells in culture, cell supernatants, cell lysates, plasma, serum, biological fluid (e.g., urine), and tissue samples. The source of the biological sample may be solid tissue (e.g., from a fresh, frozen, and / or preserved organ, tissue sample, biopsy, or aspirate), blood or any blood constituents such as serum or plasma, bodily fluids (such as, e.g., urine, lymph, cerebral spinal fluid, amniotic fluid, peritoneal fluid, or interstitial fluid, semen), or cells from any time in gestation or development of the individual. The biological sample may contain compounds that are not naturally intermixed with the tissue in nature, such as preservatives, anticoagulants, buffers, fixatives, nutrients, or antibiotics. In certain Attorney Docket No.047162-7528WO1(02689) embodiments, the biological sample is a blood sample. In certain embodiments, the biological sample is whole blood. In certain embodiments, the biological sample is serum. In certain embodiments, the biological sample is plasma. As used herein, the terms “biomarker” or “marker” generally refers to a nucleic acid molecule, clinical indicator, protein, or other analyte that is associated with a disease. In various embodiments, a biomarker is differentially present in a biological sample obtained from a subject having or at risk of developing a disease or disorder (e.g., an disease or disorder related to abnormal ovarian reserve level) relative to a reference. A marker is differentially present if the mean or median level of the biomarker present in the sample is statistically different from the level present in a reference. A reference level may be, for example, the level present in a sample obtained from a healthy control subject or the level obtained from the subject at an earlier timepoint, i.e., prior to treatment. Common tests for statistical significance include, among others, t-test, ANOVA, Kruskal-Wallis, Wilcoxon, Mann-Whitney and odds ratio. Biomarkers, alone or in combination, provide measures of relative likelihood that a subject belongs to a phenotypic status of interest. The differential presence of a marker of the invention in a subject sample can be useful in characterizing the subject as having or at risk of developing a disease, for determining the stage or type of a disease (e.g., acute disease or chronic disease), for determining the prognosis of the subject, for evaluating therapeutic efficacy, or for selecting a treatment regimen. As used herein, the term “composition” or “pharmaceutical composition” refers to a mixture of at least one compound described herein with a pharmaceutically acceptable carrier. The pharmaceutical composition facilitates administration of the compound to a patient or subject. Multiple techniques of administering a compound exist in the art including, but not limited to, intravenous, oral, aerosol, parenteral, ophthalmic, pulmonary and topical administration. In this disclosure, “comprises,” “comprising,” “containing” and “having” and the like have the meaning ascribed to them in U.S. Patent law and mean “includes,” “including,” and the like; “consisting essentially of” or “consists essentially” likewise has the meaning ascribed in U.S. Patent law and the term is open-ended, allowing for the presence of more than that which is recited so long as basic or novel characteristics of that which is recited is not changed by the presence of more than that which is recited, but excludes prior art embodiments. The term “cycloalkyl” as used herein refers to cyclic alkyl groups such as, but not limited to, cyclopropyl, cyclobutyl, cyclopentyl, cyclohexyl, cycloheptyl, and cyclooctyl groups. In some embodiments, the cycloalkyl group can have 3 to about 8-12 ring members, whereas in other embodiments the number of ring carbon atoms range from 3 to 4, 5, 6, or 7. Cycloalkyl groups Attorney Docket No.047162-7528WO1(02689) further include polycyclic cycloalkyl groups such as, but not limited to, norbornyl, adamantyl, bornyl, camphenyl, isocamphenyl, and carenyl groups, and fused rings such as, but not limited to, decalinyl, and the like. Cycloalkyl groups also include rings that are substituted with straight or branched chain alkyl groups as defined herein. Representative substituted cycloalkyl groups can be mono-substituted or substituted more than once, such as, but not limited to, 2,2-, 2,3-, 2,4- 2,5- or 2,6-disubstituted cyclohexyl groups or mono-, di- or tri-substituted norbornyl or cycloheptyl groups, which can be substituted with, for example, amino, hydroxy, cyano, carboxy, nitro, thio, alkoxy, and halogen groups. The term “cycloalkenyl” alone or in combination denotes a cyclic alkenyl group. The term "heterocycloalkyl" as used herein refers to a cycloalkyl group as defined herein in which one or more carbon atoms in the ring are replaced by a heteroatom such as O, N, S, P, and the like, each of which may be substituted as described herein if an open valence is present, and each may be in any suitable stable oxidation state. As used herein, the term “disease” refers to a state of health of an animal wherein the animal cannot maintain homeostasis, and wherein if the disease is not ameliorated then the animal’s health continues to deteriorate. A “disease subtype” is a state of health of an animal wherein animals with the disease manifest different clinical features or symptoms. A “disorder” as used herein, is used interchangeably with “condition,” and refers to a state of health in an animal, wherein the animal is able to maintain homeostasis, but in which the animal’s state of health is less favorable than it would be in the absence of the disorder. Left untreated, a disorder does not necessarily cause a further decrease in the animal’s state of health. “Dynamic range” as used herein refers to range over which an assay readout is proportional to the amount of target molecule or analyte in the sample being analyzed. The dynamic range can be the range of linearity of the standard curve. As used herein, the term “effective amount” refers to the amount required to reduce or improve at least one symptom of a condition, disease, or disorder relative to an untreated patient or to practice the methods of the invention with a successful or enhanced outcome. The effective amount of active compound(s) used to practice the present invention varies depending upon the manner of administration, the age, body weight, and general health of the subject as well as requirements of the methods of the invention. The term “elevated” as used herein when applied to a gene, protein or chemical reaction means that the expression, activity or concentration of the gene, protein or reaction is higher compared to an appropriate control. The terms “halo,” “halogen,” or “halide” group, as used herein, by themselves or as part of another substituent, mean, unless otherwise stated, a fluorine, chlorine, bromine, or iodine atom. Attorney Docket No.047162-7528WO1(02689) The term “haloalkyl” group, as used herein, includes mono-halo alkyl groups, poly-halo alkyl groups wherein all halo atoms can be the same or different, and per-halo alkyl groups, wherein all hydrogen atoms are replaced by halogen atoms, such as fluoro. Examples of haloalkyl include trifluoromethyl, 1,1-dichloroethyl, 1,2-dichloroethyl, 1,3-dibromo-3,3-difluoropropyl, perfluorobutyl, and the like. The term “heteroaryl” as used herein refers to aromatic ring compounds containing 5 or more ring members, of which, one or more is a heteroatom such as, but not limited to, N, O, and S; for instance, heteroaryl rings can have 5 to about 8-12 ring members. A heteroaryl group is a variety of a heterocyclyl group that possesses an aromatic electronic structure. A heteroaryl group designated as a C2-heteroaryl can be a 5-ring with two carbon atoms and three heteroatoms, a 6-ring with two carbon atoms and four heteroatoms and so forth. Likewise a C4-heteroaryl can be a 5-ring with one heteroatom, a 6-ring with two heteroatoms, and so forth. The number of carbon atoms plus the number of heteroatoms sums up to equal the total number of ring atoms. Heteroaryl groups include, but are not limited to, groups such as pyrrolyl, pyrazolyl, triazolyl, tetrazolyl, oxazolyl, isoxazolyl, thiazolyl, pyridinyl, thiophenyl, benzothiophenyl, benzofuranyl, indolyl, azaindolyl, indazolyl, benzimidazolyl, azabenzimidazolyl, benzoxazolyl, benzothiazolyl, benzothiadiazolyl, imidazopyridinyl, isoxazolopyridinyl, thianaphthalenyl, purinyl, xanthinyl, adeninyl, guaninyl, quinolinyl, isoquinolinyl, tetrahydroquinolinyl, quinoxalinyl, and quinazolinyl groups. Heteroaryl groups can be unsubstituted, or can be substituted with groups as is discussed herein. Representative substituted heteroaryl groups can be substituted one or more times with groups such as those listed herein. Additional examples of aryl and heteroaryl groups include but are not limited to phenyl, biphenyl, indenyl, naphthyl (1-naphthyl, 2-naphthyl), N-hydroxytetrazolyl, N-hydroxytriazolyl, N-hydroxyimidazolyl, anthracenyl (1-anthracenyl, 2-anthracenyl, 3-anthracenyl), thiophenyl (2-thienyl, 3-thienyl), furyl (2-furyl, 3-furyl) , indolyl, oxadiazolyl, isoxazolyl, quinazolinyl, fluorenyl, xanthenyl, isoindanyl, benzhydryl, acridinyl, thiazolyl, pyrrolyl (2-pyrrolyl), pyrazolyl (3- pyrazolyl), imidazolyl (1-imidazolyl, 2-imidazolyl, 4-imidazolyl, 5-imidazolyl), triazolyl (1,2,3- triazol-1-yl, 1,2,3-triazol-2-yl 1,2,3-triazol-4-yl, 1,2,4-triazol-3-yl), oxazolyl (2-oxazolyl, 4-oxazolyl, 5-oxazolyl), thiazolyl (2-thiazolyl, 4-thiazolyl, 5-thiazolyl), pyridyl (2-pyridyl, 3-pyridyl, 4-pyridyl), pyrimidinyl (2-pyrimidinyl, 4-pyrimidinyl, 5-pyrimidinyl, 6-pyrimidinyl), pyrazinyl, pyridazinyl (3- pyridazinyl, 4-pyridazinyl, 5-pyridazinyl), quinolyl (2-quinolyl, 3-quinolyl, 4-quinolyl, 5-quinolyl, 6- quinolyl, 7-quinolyl, 8-quinolyl), isoquinolyl (1-isoquinolyl, 3-isoquinolyl, 4-isoquinolyl, 5- isoquinolyl, 6-isoquinolyl, 7-isoquinolyl, 8-isoquinolyl), benzo[b]furanyl (2-benzo[b]furanyl, 3- benzo[b]furanyl, 4-benzo[b]furanyl, 5-benzo[b]furanyl, 6-benzo[b]furanyl, 7-benzo[b]furanyl), 2,3- dihydro-benzo[b]furanyl (2-(2,3-dihydro-benzo[b]furanyl), 3-(2,3-dihydro-benzo[b]furanyl), 4-(2,3- dihydro-benzo[b]furanyl), 5-(2,3-dihydro-benzo[b]furanyl), 6-(2,3-dihydro-benzo[b]furanyl), 7-(2,3- dihydro-benzo[b]furanyl), benzo[b]thiophenyl (2-benzo[b]thiophenyl, 3-benzo[b]thiophenyl, Attorney Docket No.047162-7528WO1(02689) 4-benzo[b]thiophenyl, 5-benzo[b]thiophenyl, 6-benzo[b]thiophenyl, 7-benzo[b]thiophenyl), 2,3-dihydro-benzo[b]thiophenyl, (2-(2,3-dihydro-benzo[b]thiophenyl), 3-(2,3-dihydro- benzo[b]thiophenyl), 4-(2,3-dihydro-benzo[b]thiophenyl), 5-(2,3-dihydro-benzo[b]thiophenyl), 6- (2,3-dihydro-benzo[b]thiophenyl), 7-(2,3-dihydro-benzo[b]thiophenyl), indolyl (1-indolyl, 2-indolyl, 3-indolyl, 4-indolyl, 5-indolyl, 6-indolyl, 7-indolyl), indazole (1-indazolyl, 3-indazolyl, 4-indazolyl, 5-indazolyl, 6-indazolyl, 7-indazolyl), benzimidazolyl (1-benzimidazolyl, 2-benzimidazolyl, 4- benzimidazolyl, 5-benzimidazolyl, 6-benzimidazolyl, 7-benzimidazolyl, 8-benzimidazolyl), benzoxazolyl (1-benzoxazolyl, 2-benzoxazolyl), benzothiazolyl (1-benzothiazolyl, 2-benzothiazolyl, 4-benzothiazolyl, 5-benzothiazolyl, 6-benzothiazolyl, 7-benzothiazolyl), carbazolyl (1-carbazolyl, 2- carbazolyl, 3-carbazolyl, 4-carbazolyl), 5H-dibenz[b,f]azepine (5H-dibenz[b,f]azepin-1-yl, 5H- dibenz[b,f]azepine-2-yl, 5H-dibenz[b,f]azepine-3-yl, 5H-dibenz[b,f]azepine-4-yl, 5H- dibenz[b,f]azepine-5-yl), 10,11-dihydro-5H-dibenz[b,f]azepine (10,11-dihydro-5H- dibenz[b,f]azepine-1-yl, 10,11-dihydro-5H-dibenz[b,f]azepine-2-yl, 10,11-dihydro-5H- dibenz[b,f]azepine-3-yl, 10,11-dihydro-5H-dibenz[b,f]azepine-4-yl, 10,11-dihydro-5H- dibenz[b,f]azepine-5-yl), and the like. The term “heteroarylalkyl” as used herein refers to alkyl groups as defined herein in which a hydrogen or carbon bond of an alkyl group is replaced with a bond to a heteroaryl group as defined herein. The term “heterocyclylalkyl” as used herein refers to alkyl groups as defined herein in which a hydrogen or carbon bond of an alkyl group as defined herein is replaced with a bond to a heterocyclyl group as defined herein. Representative heterocyclyl alkyl groups include, but are not limited to, furan-2-yl methyl, furan-3-yl methyl, pyridine-3-yl methyl, tetrahydrofuran-2-yl ethyl, and indol-2-yl propyl. The term “heterocyclyl” as used herein refers to aromatic and non-aromatic ring compounds containing three or more ring members, of which one or more is a heteroatom such as, but not limited to, N, O, and S. Thus, a heterocyclyl can be a cycloheteroalkyl, or a heteroaryl, or if polycyclic, any combination thereof. In some embodiments, heterocyclyl groups include 3 to about 20 ring members, whereas other such groups have 3 to about 15 ring members. A heterocyclyl group designated as a C2-heterocyclyl can be a 5-ring with two carbon atoms and three heteroatoms, a 6-ring with two carbon atoms and four heteroatoms and so forth. Likewise a C4-heterocyclyl can be a 5-ring with one heteroatom, a 6-ring with two heteroatoms, and so forth. The number of carbon atoms plus the number of heteroatoms equals the total number of ring atoms. A heterocyclyl ring can also include one or more double bonds. A heteroaryl ring is an embodiment of a heterocyclyl group. The phrase “heterocyclyl group” includes fused ring species including those that include fused aromatic and non- aromatic groups. For example, a dioxolanyl ring and a benzdioxolanyl ring system (methylenedioxyphenyl ring system) are both heterocyclyl groups within the meaning herein. The phrase also includes polycyclic ring systems containing a heteroatom such as, but not limited to, Attorney Docket No.047162-7528WO1(02689) quinuclidyl. Heterocyclyl groups can be unsubstituted, or can be substituted as discussed herein. Heterocyclyl groups include, but are not limited to, pyrrolidinyl, piperidinyl, piperazinyl, morpholinyl, pyrrolyl, pyrazolyl, triazolyl, tetrazolyl, oxazolyl, isoxazolyl, thiazolyl, pyridinyl, thiophenyl, benzothiophenyl, benzofuranyl, dihydrobenzofuranyl, indolyl, dihydroindolyl, azaindolyl, indazolyl, benzimidazolyl, azabenzimidazolyl, benzoxazolyl, benzothiazolyl, benzothiadiazolyl, imidazopyridinyl, isoxazolopyridinyl, thianaphthalenyl, purinyl, xanthinyl, adeninyl, guaninyl, quinolinyl, isoquinolinyl, tetrahydroquinolinyl, quinoxalinyl, and quinazolinyl groups. Representative substituted heterocyclyl groups can be mono-substituted or substituted more than once, such as, but not limited to, piperidinyl or quinolinyl groups, which are 2-, 3-, 4-, 5-, or 6-substituted, or disubstituted with groups such as those listed herein. The term “hydrocarbon” or “hydrocarbyl” as used herein refers to a molecule or functional group that includes carbon and hydrogen atoms. The term can also refer to a molecule or functional group that normally includes both carbon and hydrogen atoms but wherein all the hydrogen atoms are substituted with other functional groups. As used herein, the term “hydrocarbyl” refers to a functional group derived from a straight chain, branched, or cyclic hydrocarbon, and can be alkyl, alkenyl, alkynyl, aryl, cycloalkyl, acyl, or any combination thereof. Hydrocarbyl groups can be shown as (Ca-Cb)hydrocarbyl, wherein a and b are integers and mean having any of a to b number of carbon atoms. For example, (C1-C4)hydrocarbyl means the hydrocarbyl group can be methyl (C1), ethyl (C2), propyl (C3), or butyl (C4), and (C0- Cb)hydrocarbyl means in certain embodiments there is no hydrocarbyl group. The term "independently selected from" as used herein refers to referenced groups being the same, different, or a mixture thereof, unless the context clearly indicates otherwise. Thus, under this definition, the phrase "X1, X2, and X3are independently selected from noble gases" would include the scenario where, for example, X1, X2, and X3are all the same, where X1, X2, and X3are all different, where X1and X2are the same but X3is different, and other analogous permutations. The term “monovalent” as used herein refers to a substituent connecting via a single bond to a substituted molecule. When a substituent is monovalent, such as, for example, F or Cl, it is bonded to the atom it is substituting by a single bond. The term “organic group” as used herein refers to any carbon-containing functional group. Examples can include an oxygen-containing group such as an alkoxy group, aryloxy group, aralkyloxy group, oxo(carbonyl) group; a carboxyl group including a carboxylic acid, carboxylate, and a carboxylate ester; a sulfur-containing group such as an alkyl and aryl sulfide group; and other heteroatom-containing groups. Non-limiting examples of organic groups include OR, OOR, OC(O)N(R)2, CN, CF3, OCF3, R, C(O), methylenedioxy, ethylenedioxy, N(R)2, SR, SOR, SO2R, SO2N(R)2, SO3R, C(O)R, C(O)C(O)R, C(O)CH2C(O)R, C(S)R, C(O)OR, OC(O)(R), C(O)N(R)2, OC(R)N(R)2, C(S)N(R)2, (CH2)0-2N(R)C(O)R, (CH2)0-2N(R)N(R)2, N(R)N(R)C(O)R, N(R)N(R)C(O)OR, N(R)N(R)CON(R)2, N(R)SO2(R), N(R)SOR2N(R)2, N(R)C(O)OR, N(R)C(O)R, Attorney Docket No.047162-7528WO1(02689) N(R)C(S)R, N(R)C(O)N(R)2, N(R)C(S)N(R)2, N(COR)COR, N(OR)R, C(=NH)N(R)2, C(O)N(OR)R, C(=NOR)R, and substituted or unsubstituted (C1-C100)hydrocarbyl, wherein R can be hydrogen (in examples that include other carbon atoms) or a carbon-based moiety, and wherein the carbon-based moiety can be substituted or unsubstituted. The phrase “inhibit,” as used herein, means to reduce a molecule, a reaction, an interaction, a gene, an mRNA, and / or a protein’s expression, stability, function or activity by a measurable amount or to prevent entirely. Inhibitors are compounds that, e.g., bind to, partially or totally block stimulation, decrease, prevent, delay activation, inactivate, desensitize, or down regulate a protein, a gene, and an mRNA stability, expression, function and activity, e.g., antagonists. As used herein, the term “SRSF3 inhibitor” refers to any molecule that decreases or entirely prevents the ability of SRSF3 to inhibit the inclusion of the p53β-unique exon in splicing of p53 pre-mRNA. As such, an SRSF3 inhibitor will result in an increase of the p53β isoform. As some SRSF3 inhibitors (e.g. amiodarone) do not increase the p53β isoform but do decrease levels of SRSF3, “SRSF3 inhibitor” also refers to any molecule that decreases levels of SRSF3, in particular the full-length SRSF3 isoform, but ultimately either the full- length SRSF3 isoform or the truncated SRSF3 isoform. As used herein, the term “endogenous” refers to any material from or produced inside an organism, cell, tissue or system. As used herein the term "immobilized" refers to bound directly or indirectly to a surface of, e.g., a device, including attachment by covalent binding or noncovalent binding (e.g., hydrogen bonding, ionic interactions, van der Waals forces, or hydrophobic interactions). As used herein “instructional material” includes a publication, a recording, a diagram, or any other medium of expression that can be used to communicate the usefulness of the device in a kit. The instructional material of the kit may, for example, be affixed to a container that contains the device of the invention or be shipped together with a container that contains the device. Alternatively, the instructional material may be shipped separately from the container with the intention that the recipient uses the instructional material and the device cooperatively. Delivery of the instructional material may be, for example, by physical delivery of the publication or other medium of expression communicating the usefulness of the kit, or may alternatively be achieved by electronic transmission, for example by means of a computer, such as by electronic mail, or download from a website. Attorney Docket No.047162-7528WO1(02689) “Label” and “detectable label” as used herein refer to a moiety attached to an antibody or an analyte to render the reaction between the antibody and the analyte detectable, and the antibody or analyte so labeled is referred to as “detectably labeled.” A label can produce a signal that is detectable by visual or instrumental means. Various labels include signal- producing substances, such as chromagens, fluorescent compounds, chemiluminescent compounds, radioactive compounds, and the like. Representative examples of labels include moieties that produce light, e.g., acridinium compounds, and moieties that produce fluorescence, e.g., fluorescein. Other labels are described herein. In this regard, the moiety, itself, may not be detectable but may become detectable upon reaction with yet another moiety. Use of the term “detectably labeled” is intended to encompass such labeling. Any suitable detectable label as is known in the art can be used. For example, the detectable label can be a radioactive label (such as3H,14C,32P,33P,35S,90Y,99Tc,111In,125I,131I,177Lu,166Ho, and153Sm), an enzymatic label (such as horseradish peroxidase, alkaline peroxidase, glucose 6-phosphate dehydrogenase, and the like), a chemiluminescent label (such as acridinium esters, thioesters, or sulfonamides; luminol, isoluminol, phenanthridinium esters, and the like), a fluorescent label (such as fluorescein ( e.g., 5-fluorescein, 6-carboxy- fluorescein, 3’6-carboxy-fluorescein, 5(6)-carboxy-fluorescein, 6-hexachloro-fluorescein, 6- tetrachloro-fluorescein, fluorescein isothiocyanate, and the like)), rhodamine, phycobiliproteins, R-phycoerythrin, quantum dots (e.g., zinc sulfide-capped cadmium selenide), a thermometric label, or an immuno-polymerase chain reaction label. An introduction to labels, labeling procedures and detection of labels is found in Polak and Van Noorden, Introduction to Immunocytochemistry, 2nd ed., Springer Verlag, N.Y. (1997), and in Haugland, Handbook of Fluorescent Probes and Research Chemicals (1996), which is a combined handbook and catalogue published by Molecular Probes, Inc., Eugene, Oregon. As used herein the term “level” is intended to refer to amount of a unit of a compound being measured, for example a protein. It is also intended to encompass “concentration” expressed as amount per volume or weight per volume and any other depiction of concentration as known in the art. “Linking sequence” or “linking peptide sequence” refers to a natural or artificial polypeptide sequence that is connected to one or more polypeptide sequences of interest (e.g., full-length, fragments, etc.). The term “connected” refers to the joining of the linking sequence to the polypeptide sequence of interest. Such polypeptide sequences are preferably joined by one or more peptide bonds. Linking sequences can have a length of from about 4 to about 50 amino acids. Preferably, the length of the linking sequence is from about 6 to about Attorney Docket No.047162-7528WO1(02689) 30 amino acids. Natural linking sequences can be modified by amino acid substitutions, additions, or deletions to create artificial linking sequences. Linking sequences can be used for many purposes, including in recombinant Fabs. Exemplary linking sequences include, but are not limited to: (i) Histidine (His) tags, such as a 6X His tag (aka His tag), are useful as linking sequences to facilitate the isolation and purification of polypeptides and antibodies of interest; (ii) Enterokinase cleavage sites, like 6X His tags, are used in the isolation and purification of proteins and antibodies of interest. Often, enterokinase cleavage sites are used together with 6X His tags in the isolation and purification of proteins and antibodies of interest. Various enterokinase cleavage sites are known in the art. (iii) Miscellaneous sequences can be used to link or connect the light and / or heavy chain variable regions of single chain variable region fragments. Examples of other linking sequences can be found in Bird et al., Science 242:423-426 (1988); Huston et al., PNAS USA 85: 5879-5883 (1988); and McCafferty et al., Nature 348: 552-554 (1990). Linking sequences also can be modified for additional functions, such as attachment of detectable labels or drugs or attachment to solid supports. In the context of the present disclosure, a monoclonal antibody, for example, can contain a linking sequence, such as a His tag, an enterokinase cleavage site, or both. As used herein, the term "pharmaceutical composition" or "composition" refers to a mixture of at least one compound useful within the invention with a pharmaceutically acceptable carrier. 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, intravenous, intradermal, transdermal, oral, aerosol, parenteral, ophthalmic, pulmonary and topical administration. As such, a pharmaceutical composition can be formulated for any one or more of such routes of administration. In certain embodiments, the pharmaceutical composition is a topical formulation. In certain embodiments, the pharmaceutical composition is formulated for intradermal administration. In certain embodiments, the pharmaceutical composition is formulated for transdermal administration. As used herein, the term "pharmaceutically acceptable" refers to a material, such as a carrier or diluent, which does not abrogate the biological activity or properties of the compound useful within the invention, and is relatively non-toxic, i.e., the material may be administered to a subject without causing undesirable biological effects or interacting in a deleterious manner with any of the components of the composition in which it is contained. As used herein, the term "pharmaceutically acceptable carrier" or “pharmaceutically acceptable excipient” means a pharmaceutically acceptable material, composition or carrier, Attorney Docket No.047162-7528WO1(02689) such as a liquid or solid filler, stabilizer, dispersing agent, suspending agent, diluent, excipient, thickening agent, solvent or encapsulating material, involved in carrying or transporting a compound useful within the invention within or to the subject such that it may perform its intended function. Typically, such constructs are carried or transported from one organ, or portion of the body, to another organ, or portion of the body. Each carrier must be "acceptable" in the sense of being compatible with the other ingredients of the formulation, including the compound useful within the invention, and not injurious to the subject. Some examples of materials that may serve as pharmaceutically acceptable carriers include: sugars, such as lactose, glucose and sucrose; starches, such as corn starch and potato starch; cellulose, and its derivatives, such as sodium carboxymethyl cellulose, ethyl cellulose and cellulose acetate; powdered tragacanth; malt; gelatin; talc; excipients, such as cocoa butter and suppository waxes; oils, such as peanut oil, cottonseed oil, safflower oil, sesame oil, olive oil, corn oil and soybean oil; glycols, such as propylene glycol; polyols, such as glycerin, sorbitol, mannitol and polyethylene glycol; esters, such as ethyl oleate and ethyl laurate; agar; buffering agents, such as magnesium hydroxide and aluminum hydroxide; surface active agents; alginic acid; pyrogen-free water; isotonic saline; Ringer's solution; ethyl alcohol; phosphate buffer solutions; and other non-toxic compatible substances employed in pharmaceutical formulations. As used herein, "pharmaceutically acceptable carrier" also includes any and all coatings, antibacterial and antifungal agents, and absorption delaying agents, and the like that are compatible with the activity of the compound useful within the invention, and are physiologically acceptable to the subject. Supplementary active compounds may also be incorporated into the compositions. The "pharmaceutically acceptable carrier" may further include a pharmaceutically acceptable salt of the compound useful within the invention. Other additional ingredients that may be included in the pharmaceutical compositions used in the practice of the invention are known in the art and described, for example in Remington's Pharmaceutical Sciences (Genaro, Ed., Mack Publishing Co., 1985, Easton, PA), which is incorporated herein by reference. As used herein, the language "pharmaceutically acceptable salt" refers to a salt of the administered compound prepared from pharmaceutically acceptable non-toxic acids and bases, including inorganic acids, inorganic bases, organic acids, inorganic bases, solvates, hydrates, and clathrates thereof. Suitable pharmaceutically acceptable acid addition salts may be prepared from an inorganic acid or from an organic acid. Examples of inorganic acids include hydrochloric, hydrobromic, hydriodic, nitric, carbonic, sulfuric (including sulfate and hydrogen sulfate), and phosphoric acids Attorney Docket No.047162-7528WO1(02689) (including hydrogen phosphate and dihydrogen phosphate). Appropriate organic acids may be selected from aliphatic, cycloaliphatic, aromatic, araliphatic, heterocyclic, carboxylic and sulfonic classes of organic acids, examples of which include formic, acetic, propionic, succinic, glycolic, gluconic, lactic, malic, tartaric, citric, ascorbic, glucuronic, maleic, malonic, saccharin, fumaric, pyruvic, aspartic, glutamic, benzoic, anthranilic, 4-hydroxybenzoic, phenylacetic, mandelic, embonic (pamoic), methanesulfonic, ethanesulfonic, benzenesulfonic, pantothenic, trifluoromethanesulfonic, 2- hydroxyethanesulfonic, p-toluenesulfonic, sulfanilic, cyclohexylaminosulfonic, stearic, alginic, β- hydroxybutyric, salicylic, galactaric and galacturonic acid. Suitable pharmaceutically acceptable base addition salts of compounds described herein include, for example, ammonium salts, metallic salts including alkali metal, alkaline earth metal and transition metal salts such as, for example, calcium, magnesium, potassium, sodium and zinc salts. Pharmaceutically acceptable base addition salts also include organic salts made from basic amines such as, for example, N,N'-dibenzylethylene-diamine, chloroprocaine, choline, diethanolamine, ethylenediamine, meglumine (N-methylglucamine) and procaine. All of these salts may be prepared from the corresponding compound by reacting, for example, the appropriate acid or base with the compound. As used herein, the terms “prevent,” “preventing,” “prevention,” and the like refer to reducing the probability of developing a disease or condition in a subject, who does not have, but is at risk of or susceptible to developing a disease, disorder, or condition. As used herein the terms “purified” or “biologically pure” refer to material that is free to varying degrees from components which normally accompany it as found in its native state. “Purify” denotes a degree of separation that is higher than isolation. A “purified” or “biologically pure” protein is sufficiently free of other materials such that any impurities do not materially affect the biological properties of the protein or cause other adverse consequences. That is, a nucleic acid or peptide of this invention is purified if it is substantially free of cellular material, viral material, or culture medium when produced by recombinant DNA techniques, or chemical precursors or other chemicals when chemically synthesized. Purity and homogeneity are typically determined using analytical chemistry techniques, for example, polyacrylamide gel electrophoresis or high-performance liquid chromatography. The term “purified” can denote that a nucleic acid or protein gives rise to essentially one band in an electrophoretic gel. For a protein that can be subjected to modifications, for example, phosphorylation or glycosylation, different modifications may give rise to different isolated proteins, which can be separately purified. “Quality control reagents” in the context of immunoassays and kits described herein, include, but are not limited to, calibrators, controls, and sensitivity panels. A “calibrator” or Attorney Docket No.047162-7528WO1(02689) “standard” typically is used (e.g., one or more, such as a plurality) in order to establish calibration (standard) curves for interpolation of the concentration of an analyte, such as an antibody or an analyte. Alternatively, a single calibrator, which is near a predetermined positive / negative cutoff, reference level or control level (e.g., “low,” “medium,” or “high” levels), can be used. Multiple calibrators (i.e., more than one calibrator or a varying amount of calibrator(s )) can be used in conjunction to comprise a “sensitivity panel.” As used herein the term “reference” is meant a standard or control value often used as a basis for comparison. The terms “reference” and “control” are used interchangeably herein. A “reference” or “control” means a value or level measured in a sample obtained from a suitable subject (a “reference subject”). A “reference” or “control” also means a value or level that is a composite of values or levels obtained from a group of reference subjects as described herein, or as generated by an algorithm using multiple measured values or levels. A “reference level” as used herein refers to an assay cutoff value that is used to assess diagnostic, prognostic, or therapeutic efficacy and that has been linked or is associated herein with various clinical parameters (e.g., presence of disease, stage of disease, severity of disease, progression, non-progression, or improvement of disease, etc.) This disclosure provides exemplary reference levels. However, it is well-known that reference levels may vary depending on the nature of the immunoassay (e.g., antibodies employed, reaction conditions, sample purity, etc.) and that assays can be compared and standardized. It further is well within the ordinary skill of one in the art to adapt the disclosure herein for other immunoassays to obtain immunoassay-specific reference levels for those other immunoassays based on the description provided by this disclosure. Whereas the precise value of the reference level may vary between assays, the findings as described herein should be generally applicable and capable of being extrapolated to other assays. "Risk assessment," "risk classification," "risk identification," or "risk stratification" of subjects (e.g., patients) as used herein refers to the evaluation of factors including biomarkers, to predict the risk of occurrence of future events including disease onset or disease progression, so that treatment decisions regarding the subject may be made on a more informed basis. "Sample," "test sample," "specimen," "sample from a subject," and "patient sample" as used herein may be used interchangeable and may be a sample of blood such as whole blood, tissue, urine, serum, plasma, amniotic fluid, cerebrospinal fluid, placental cells or tissue, endothelial cells, leukocytes, or monocytes. The sample can be used directly as obtained from a patient or can be pre-treated, such as by filtration, distillation, extraction, Attorney Docket No.047162-7528WO1(02689) concentration, centrifugation, inactivation of interfering components, addition of reagents, and the like, to modify the character of the sample in some manner as discussed herein or otherwise as is known in the art. As used herein the term “blood sample” refers to whole blood or blood that has been pre-treated and / or processed to obtain serum or plasma. "Sensitivity" of an assay as used herein refers to the proportion of subjects for whom the outcome is positive that are correctly identified as positive. "Specificity" of an assay as used herein refers to the proportion of subjects for whom the outcome is negative that are correctly identified as negative. As used herein the term “signal” refers to light intensity (e.g., light generated by fluorescence, bioluminescence, or phosphorescence), ionizing radiation, particle emission, magnetism, staining, or a product of a reaction involving an enzyme. Diffraction, absorbance, polarization, reflection, deflection, increases, decreases, or amplification of a signal may be indicative of an event (e.g., binding of a biomarker or biomarker complex to an antibody immobilized on the surface of a diffraction-based device). As used herein the term "single molecule detection" refers to the detection and / or measurement of a single molecule of an analyte in a test sample at very low levels of concentration (such as pg / mL or femtograrn / mL levels). A number of different single molecule analyzers or devices are known in the art and include nanopore and nanowell devices. Examples of nanopore devices are described in International Patent Publication No. WO 2016 / 161402, which is hereby incorporated by reference in its entirety. Examples of nanowell device are described in International Patent Publication No. WO 2016 / 161400, which is hereby incorporated by reference in its entirety. As used herein, the term “small molecule” refers to a non-peptidic, non-oligomeric organic compound either synthesized in the laboratory or found in nature. The term "solvent" as used herein refers to a liquid that can dissolve a solid, liquid, or gas. Non-limiting examples of solvents are silicones, organic compounds, water, alcohols, ionic liquids, and supercritical fluids. The term “substituted” as used herein in conjunction with a molecule or an organic group as defined herein refers to the state in which one or more hydrogen atoms contained therein are replaced by one or more non-hydrogen atoms. The term “functional group” or “substituent” as used herein refers to a group that can be or is substituted onto a molecule or onto an organic group. Examples of substituents or functional groups include, but are not limited to, a halogen (e.g., F, Cl, Br, and I); an oxygen atom in groups such as hydroxy groups, alkoxy groups, aryloxy groups, aralkyloxy groups, oxo(carbonyl) groups, carboxyl groups including carboxylic acids, carboxylates, and carboxylate esters; a sulfur atom in groups such as thiol groups, alkyl and aryl sulfide groups, sulfoxide groups, Attorney Docket No.047162-7528WO1(02689) sulfone groups, sulfonyl groups, and sulfonamide groups; a nitrogen atom in groups such as amines, hydroxyamines, nitriles, nitro groups, N-oxides, hydrazides, azides, and enamines; and other heteroatoms in various other groups. Non-limiting examples of substituents that can be bonded to a substituted carbon (or other) atom include F, Cl, Br, I, OR, OC(O)N(R)2, CN, NO, NO2, ONO2, azido, CF3, OCF3, R, O (oxo), S (thiono), C(O), S(O), methylenedioxy, ethylenedioxy, N(R)2, SR, SOR, SO2R, S(O)2R, S(O)3R, C(O)R, C(O)C(O)R, C(O)CH2C(O)R, C(S)R, C(O)OR, C(O)R, C(O)N(R)2, (CH2)0-2N(R)C(O)R, (CH2)0-2N(R)N(R)2, N(R)N(R)C(O)R, N(R)N(R)C(O)OR, N(R)N(R)CON(R)2, N(R)SO2R, N(R)SO2N(R)2, N(R)C(O)OR, N(R)C(O)R, N(R)C(S)R, N(R)C(O)N(R)2, N(R)C(S)N(R)2, N(COR)COR, N(OR)R, C(=NH)N(R)2, C(O)N(OR)R, and C(=NOR)R, wherein R can be hydrogen or a carbon-based moiety; for example, R can be hydrogen, (C1-C100)hydrocarbyl, alkyl, acyl, cycloalkyl, aryl, aralkyl, heterocyclyl, heteroaryl, or heteroarylalkyl; or wherein two R groups bonded to a nitrogen atom or to adjacent nitrogen atoms can together with the nitrogen atom or atoms form a heterocyclyl. The term “substrate” as used herein refers to a chemical or small organic molecule that is the target or subject of a chemical process such as enzymatic catalysis. As used herein the term “specifically binds” refers to an antibody or fragment thereof that recognizes and binds an antigen, but that does not substantially recognize or bind to other molecules in a biological sample. Specific recognition of an antigen by an antibody may be assayed by using, e.g., light diffraction devices with an immobilized capture surface or using standard techniques known to one of skill in the art, such as immunoprecipitation, Western blotting, and ELISA. "Solid phase" or "solid support" as used interchangeably herein, refers to any material that can be used to attach and / or attract and immobilize (1) one or more capture agents or capture specific binding partners, or (2) one or more detection agents or detection specific binding partners. The solid phase can be chosen for its intrinsic ability to attract and immobilize a capture agent. Alternatively, the solid phase can have affixed thereto a linking agent that has the ability to attract and immobilize the (1) capture agent or capture specific binding partner, or (2) detection agent or detection specific binding partner. For example, the linking agent can include a charged substance that is oppositely charged with respect to the capture agent (e.g., capture specific binding partner) or detection agent (e.g., detection specific binding partner) itself or to a charged substance conjugated to the (1) capture agent or capture specific binding partner or (2) detection agent or detection specific binding partner. In general, the linking agent can be any binding partner (preferably specific) that is immobilized on (attached to) the solid phase and that has the ability to immobilize the (1) capture agent or capture specific binding partner, or (2) detection agent or detection specific Attorney Docket No.047162-7528WO1(02689) binding partner through a binding reaction. The linking agent enables the indirect binding of the capture agent to a solid phase material before the performance of the assay or during the performance of the assay. For examples, the solid phase can be plastic, derivatized plastic, magnetic, or non-magnetic metal, glass or silicon, including, for example, a test tube, microtiter well, sheet, bead, microparticle, chip, and other configurations known to those of ordinary skill in the art. As used herein the terms “subject,” “individual,” “patient,” and the like are used interchangeably herein, and refer to any vertebrate, including, but not limited to, a mammal (e.g., a human, cow, pig, camel, llama, horse, goat, rabbit, sheep, hamsters, guinea pig, cat, dog, rat, mouse, a non-human primate (for example, a monkey, such as a cynomolgous or rhesus monkey, chimpanzee, etc.)) or cells thereof, whether in vitro or in situ, amenable to the methods described herein. In some embodiments, the term “subject” refers to a mammal, including a human or non-human mammal. The term “subject” may refer to a human or other animal which is the object of treatment, observation, or experiment (e.g., a patient). As used herein the terms “therapeutic” and “therapy” refers to a treatment and / or prophylaxis. A therapeutic effect is obtained by suppression, remission, or eradication of a disease state. As used herein, the terms “treat,” “treating,” “treatment,” and the like refer to ameliorating and / or reducing or improving a disease or condition and / or symptom associated therewith. It will be appreciated that, although not precluded, treating a disease or condition does not require that the disease, condition or symptoms associated therewith be completely ameliorated or eliminated. The term also refers to ameliorating and / or reducing the severity of a disease or condition or symptoms associated with such disease or condition prior to affliction with the disease or condition. Such prevention or reduction of the severity of a disease or condition prior to affliction refers to administration of a pharmaceutical composition to a subject that is not at the time of administration afflicted with the disease. “Preventing” and “prevent” also refer to preventing the recurrence of a disease or condition or of one or more symptoms associated with such disease or condition. Ranges provided herein are understood to be shorthand for all of the values within the range. For example, a range of 1 to 50 is understood to include any number, combination of numbers, or sub-range from the group consisting 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 30, 31, 32, 33, 34, 35, 36, 37, 38, 39, 40, 41, 42, 43, 44, 45, 46, 47, 48, 49, or 50. Attorney Docket No.047162-7528WO1(02689) The recitation of an embodiment for a variable or aspect herein includes that embodiment as any single embodiment or in combination with any other embodiments or portions thereof. Methods In one aspect, the present disclosure provides a method for treating a cutaneous disease or disorder characterized by abnormalities in differentiation in a subject in need thereof, the method comprising administering to the subject a pharmaceutical composition comprising an effective amount of a serine / arginine-rich splicing factor 3 (SRSF3) inhibitor. In certain embodiments, the cutaneous disease or disorder characterized by abnormalities in differentiation is squamous cell carcinoma, ichthyosis, porokeratosis, chronic wounds, psoriasis, keratoacanthoma, or other disorders of keratinocyte differentiation. In one aspect, the present disclosure provides a method of treating or preventing squamous cell carcinoma (SCC) in a subject in need thereof, the method comprising administering to the subject a pharmaceutical composition comprising an effective amount of a serine / arginine-rich splicing factor 3 (SRSF3) inhibitor. In certain embodiments, the pharmaceutical composition is a topical formulation that is administered to the skin of the subject. In some embodiments, the topical formulation comprises a gel or an ointment. In certain embodiments, the pharmaceutical composition is formulated for intradermal administration. In certain embodiments, the pharmaceutical composition is formulated for transdermal administration. In certain embodiments, the pharmaceutical composition may be formulated and used systemically (e.g. oral or intravenous). In certain embodiments, the SRSF3 inhibitor is a small molecule having molecular mass less than about 600 g / mol. In certain embodiments, the SRSF3 inhibitor is characterized by an effective level of skin permeability and / or is formulated (e.g., in a topical formulation and / or formulated for intradermal or transdermal delivery) to exhibit an effective level of skin permeability. The SRSF3 inhibitor refers to any molecule that decreases or entirely prevents the ability of SRSF3 to inhibit the inclusion of the p53β-unique exon in splicing of p53 pre- mRNA. As such, an SRSF3 inhibitor will result in an increase of the p53β isoform. The Attorney Docket No.047162-7528WO1(02689) SRSF3 inhibitor also refers to any molecule that decreases levels of full-length or truncated SRSF3. In certain embodiments, the SRSF3 inhibitor reduces SRSF3 amount or activity in SCC cells by at least about 10%, at least about 15%, at least about 20%, at least about 25%, at least about 30%, at least about 35%, at least about 40%, at least about 45%, at least about 50%, at least about 55%, at least about 60%, at least about 65%, at least about 70%, at least about 75%, at least about 80%, at least about 85%, at least about 90%, at least about 95%, or at least about 100% compared to SRSF3 amount or activity in SCC cells in the absence of the SRSF3 inhibitor. In certain embodiments, the SRSF3 inhibitor induces terminal differentiation of SCC cells. In certain embodiments, the SRSF3 inhibitor is a compound of Formula (I) or a salt, stereoisomer, or isotopologue thereof: , wherein: ; AA B A the group consisting of H, CN, NO2, OR , N(R )(R ), SR , C(=O)RA, C(=O)ORA, C(=O)N(RA)(RB), S(=O)RA, S(=O)2RA, S(=O)N(RA)(RB), S(=O)2N(RA)(RB), P(=O)(ORA)(ORB), halogen, optionally substituted C1-C6 alkyl, optionally substituted C3-C8cycloalkyl, optionally substituted C2-C8heterocycloalkyl, optionally substituted C6-C10 aryl, and optionally substituted C2-C8 heteroaryl; R4is selected from the group consisting of H and optionally substituted C1-C6alkyl; R5is selected from the group consisting of H and optionally substituted C1-C6 alkyl; R6is selected from the group consisting of H, optionally substituted C1-C6alkyl, optionally substituted C3-C8 cycloalkyl, optionally substituted C2-C8 heterocycloalkyl, optionally substituted C6-C10aryl, and optionally substituted C2-C8heteroaryl; Attorney Docket No.047162-7528WO1(02689) R7a, R7b, and R7c, if present, are each independently selected from the group consisting of H, CN, NO2, ORA, N(RA)(RB), C(=O)RA, C(=O)ORA, C(=O)N(RA)(RB), S(=O)RA, S(=O)2RA, S(=O)N(RA)(RB), S(=O)2N(RA)(RB), P(=O)(ORA)(ORB), halogen, substituted C2-C8heteroaryl, wherein R7aand R7bcan combine with the atoms to which they are bound to form an optionally substituted C6-C10aryl or optionally substituted C2-C8 heteroaryl; X1selected from the group consisting of N and CR7c; Z1is CR8aor N, Z2is CR8bor N, Z3is CR8cor N, Z4is CR8dor N, and Z5is CR8eor N, wherein no more than two of Z1, Z2, Z3, Z4, and Z5are N; R8a, R8b, R8c, R8d, and R8e, if present, are each independently selected from the group consisting of H, CN, NO2, ORA, N(RA)(RB), SRA, halogen, optionally substituted C1-C6alkyl, optionally substituted C3-C8 cycloalkyl, optionally substituted C2-C8 heterocycloalkyl, optionally substituted C6-C10aryl, and optionally substituted C2-C8heteroaryl; each occurrence of RAand RB, if present, is independently selected from the group consisting of H, optionally substituted C1-C6alkyl, optionally substituted C3-C8cycloalkyl, optionally substituted C2-C8 heterocycloalkyl, optionally substituted C6-C10 aryl, optionally substituted C2-C8heteroaryl, C(=O)RC, C(=O)ORC, C(=O)N(RC)(RD), S(=O)RC, S(=O)2RC, S(=O)N(RC)(RD), S(=O)2N(RC)(RD), and P(=O)(ORC)(ORD); each occurrence of RCand RD, if present, is independently selected from the group consisting of H, optionally substituted C1-C6 alkyl, optionally substituted C3-C8 cycloalkyl, optionally substituted C2-C8heterocycloalkyl, optionally substituted C6-C10aryl, and optionally substituted C2-C8 heteroaryl. In some embodiments, at least one of the following applies: (a) R7a, R7b, and R7c, if present, are each independently selected from the group consisting of H, CN, NO2, ORA, N(RA)(RB), C(=O)RA, C(=O)ORA, C(=O)N(RA)(RB), S(=O) halogen, optionally substituted C2-C8heterocycloalkyl, optionally substituted C6-C10aryl, and optionally substituted C2-C8heteroaryl; Attorney Docket No.047162-7528WO1(02689) (b) R7aand R7bcan combine with the atoms to which they are bound to form a substituted C6-C10aryl or optionally substituted C2-C8heteroaryl; (c) R7aand R7bcan combine with the atoms to which they are bound to form unsubstituted phenyl, and R8c, if present, is selected from the group consisting of H, CN, NO2, SRA, NH(substituted C1-C6alkyl), NH(optionally substituted C2-C6alkyl), halogen, optionally substituted C1-C6alkyl, substituted C1-C6alkoxy, optionally substituted C2-C6alkoxy, optionally substituted C3-C8cycloalkyl, optionally substituted C2-C8heterocycloalkyl, optionally substituted C6-C10aryl, and optionally substituted C2-C8heteroaryl; (d) R7aand R7bcan combine with the atoms to which they are bound to form unsubstituted phenyl, R8cis N(RA)(RB), and RAis C(=O)RC; and (e) R8cis N(RA)(RB), and RAis C(=O)RC. In some embodiments, R6is H. In some embodiments, one of the following applies: (a) R7aand R7bare each independently selected from the group consisting of H and CH3; or (b) R7aand R7bcombine with the atoms to which they are bound to form . In some embodiments, X1is selected from the group consisting of N and CH. , (a) Z1is CR8a, Z2is N, Z3is CR8c, Z4is CR8d, and Z5is CR8e; or (b) Z1is CR8a, Z2is CR8b, Z3is CR8c, Z4is CR8d, and Z5is CR8e. In some embodiments, R8a, R8b, R8d, and R8eare each independently H. In some embodiments, R8cis selected from the group consisting of O(C1-C6alkyl), O(C1-C6 haloalkyl), S(C1-C6 alkyl), NH(C1-C6 alkyl), and N(C1-C6 alkyl)C(=O)(C1-C6 haloalkyl), optionally wherein R8cis selected from the group consisting of OCH3, OCF3, SCH3, NHCH3, and N(CH3)C(=O)CF3. Attorney Docket No.047162-7528WO1(02689) In some embodiments, R2is selected from the group consisting of , . In some embodiments, R5is CH3. In some embodiments, the compound of formula (I) is selected from the group consisting of: (E)-2-(2-(1-(1H-benzo[d]imidazol-2-yl)ethylidene)hydrazineyl)-4-(4- methoxyphenyl)thiazole; (E)-4-(2-(2-(1-(1H-benzo[d]imidazol-2-yl)ethylidene)hydrazineyl)thiazol-4-yl)-N- methylaniline; (E)-2-(2-(1-(1H-pyrrol-2-yl)ethylidene)hydrazineyl)-4-(4-methoxyphenyl)thiazole; (E)-2-(2-(1-(1H-imidazol-2-yl)ethylidene)hydrazineyl)-4-(4-methoxyphenyl)thiazole; (E)-2-(2-(1-(1H-pyrrol-2-yl)ethylidene)hydrazineyl)-4-(6-methoxypyridin-3- yl)thiazole; (E)-2-(2-(1-(4,5-dimethyl-1H-imidazol-2-yl)ethylidene)hydrazineyl)-4-(6- methoxypyridin-3-yl)thiazole; (E)-2-(2-(1-(1H-imidazol-2-yl)ethylidene)hydrazineyl)-4-(6-methoxypyridin-3- yl)thiazole; (E)-2-(2-(1-(1H-benzo[d]imidazol-2-yl)ethylidene)hydrazineyl)-4-(4- (trifluoromethoxy)phenyl)thiazole; (E)-2-(2-(1-(1H-imidazol-2-yl)ethylidene)hydrazineyl)-4-(4- (trifluoromethoxy)phenyl)thiazole; (E)-2-(2-(1-(1H-benzo[d]imidazol-2-yl)ethylidene)hydrazineyl)-4-(4- (methylthio)phenyl)thiazole; (E)-2-(2-(1-(1H-imidazol-2-yl)ethylidene)hydrazineyl)-4-(4- (methylthio)phenyl)thiazole; (E)-4-(2-(2-(1-(1H-imidazol-2-yl)ethylidene)hydrazineyl)thiazol-4-yl)-N- methylaniline; (E)-N-(4-(2-(2-(1-(1H-benzo[d]imidazol-2-yl)ethylidene)hydrazineyl)thiazol-4- yl)phenyl)-2,2,2-trifluoro-N-methylacetamide; and Attorney Docket No.047162-7528WO1(02689) (E)-N-(4-(2-(2-(1-(1H-imidazol-2-yl)ethylidene)hydrazineyl)thiazol-4-yl)phenyl)- 2,2,2-trifluoro-N-methylacetamide. In certain embodiments, the SRSF3 inhibitor is the compound of Formula (I), wherein the compound of Formula (I) is SFI003, or a salt, solvate, stereoisomer, isotopologue, or tautomer thereof. The IUPAC name for SFI003 is N-[(E)-1-(1H-benzimidazol-2- yl)ethylideneamino]-4-(4-methoxyphenyl)-1,3-thiazol-2-amine. The chemical structure of SFI003 is: ethylidene)hydrazineyl)-4-(4- methoxyphenyl)thiazole, or a salt, solvate, stereoisomer, isotopologue, or tautomer thereof. In some embodiments, the SRSF3 inhibitor is selected from the group consisting of: (a) SFI003, or a salt, solvate, stereoisomer, isotopologue, or tautomer thereof; (b) (E)-N-(4-(2-(2-(1-(1H-benzo[d]imidazol-2-yl)ethylidene)hydrazineyl)thiazol- 4-yl)phenyl)-2,2,2-trifluoro-N-methylacetamide), or a salt, solvate, stereoisomer, isotopologue, or tautomer thereof; (c) (E)-4-(2-(2-(1-(1H-benzo[d]imidazole-2-yl)ethylidene)hydrazineyl)thiazol-4- yl)-N-methylaniline), or a salt, solvate, stereoisomer, isotopologue, or tautomer thereof; and (d) (E)-2-(2-(1-(1H-benzo[d]imidazol-2-yl)ethylidene)hydrazineyl)-4-(4- (trifluoromethoxy)phenyl)thiazole), or a salt, solvate, stereoisomer, isotopologue, or tautomer thereof. In some embodiments, the SRSF3 inhibitor is the compound of Formula (I), wherein the compound of Formula (I) is: i.e., hydrazineyl)-4-(4-methoxyphenyl)thiazole, or a salt, solvate, stereoisomer, isotopologue, or tautomer thereof. Attorney Docket No.047162-7528WO1(02689) In some embodiments, the SRSF3 inhibitor is the compound of Formula (I), wherein the compound of Formula (I) is: i.e., hydrazineyl)-4-(4-methoxyphenyl)thiazole, or a salt, or tautomer thereof. In some embodiments, the SRSF3 inhibitor is the compound of Formula (I), wherein the compound of Formula (I) is: i.e., hydrazineyl)-4-(6-methoxypyridin-3-yl)thiazole, or a salt, solvate, stereoisomer, isotopologue, or tautomer thereof. In some embodiments, the SRSF3 inhibitor is the compound of Formula (I), wherein the compound of Formula (I) is: i.e., 2-yl)ethylidene)hydrazineyl)-4-(6- methoxypyridin-3-yl)thiazole, or a salt, solvate, stereoisomer, isotopologue, or tautomer thereof. In some embodiments, the SRSF3 inhibitor is the compound of Formula (I), wherein the compound of Formula (I) is: Attorney Docket No.047162-7528WO1(02689) i.e., (E)-2-(2-(1-(1H-imidazol-2-yl)ethylidene)hydrazineyl)-4-(6-methoxypyridin-3- yl)thiazole, or a salt, solvate, stereoisomer, isotopologue, or tautomer thereof. In some embodiments, the SRSF3 inhibitor is the compound of Formula (I), wherein the compound of Formula (I) is: i.e., hydrazineyl)-4-(4- stereoisomer, isotopologue, or tautomer thereof. In some embodiments, the SRSF3 inhibitor is the compound of Formula (I), wherein the compound of Formula (I) is: i.e., hydrazineyl)-4-(4- (trifluoromethoxy)phenyl)thiazole, or a salt, solvate, stereoisomer, isotopologue, or tautomer thereof. In some embodiments, the SRSF3 inhibitor is the compound of Formula (I), wherein the compound of Formula (I) is: i.e., ethylidene)hydrazineyl)-4-(4- (methylthio)phenyl)thiazole, or a salt, solvate, stereoisomer, isotopologue, or tautomer thereof. In some embodiments, the SRSF3 inhibitor is the compound of Formula (I), wherein the compound of Formula (I) is: Attorney Docket No.047162-7528WO1(02689) i.e., hydrazineyl)-4-(4-(methylthio)phenyl)thiazole, or a or tautomer thereof. In some embodiments, the SRSF3 inhibitor is the compound of Formula (I), wherein the compound of Formula (I) is: i.e., 2-yl)ethylidene)hydrazineyl)thiazol-4-yl)-N- methylaniline, or a salt, solvate, stereoisomer, isotopologue, or tautomer thereof. In some embodiments, the SRSF3 inhibitor is the compound of Formula (I), wherein the compound of Formula (I) is: i.e., ethylidene)hydrazineyl)thiazol-4-yl)-N-methylaniline, or a salt, solvate, stereoisomer, isotopologue, or tautomer thereof. In some embodiments, the SRSF3 inhibitor is the compound of Formula (I), wherein the compound of Formula (I) is: (i.e., ethylidene)hydrazineyl)thiazol-4- yl)phenyl)-2,2,2-trifluoro-N-methylacetamide), or a salt, solvate, stereoisomer, isotopologue, or tautomer thereof. Attorney Docket No.047162-7528WO1(02689) In some embodiments, the SRSF3 inhibitor is the compound of Formula (I), wherein the compound of Formula (I) is: (i.e., hydrazineyl)thiazol-4-yl)phenyl)-2,2,2- , stereoisomer, isotopologue, or tautomer thereof. In certain embodiments, the SRSF3 inhibitor is amiodarone, or a salt, solvate, stereoisomer, isotopologue, or tautomer thereof. In certain embodiments, the SRSF3 inhibitor is digoxin, or a salt, solvate, stereoisomer, isotopologue, or tautomer thereof. In certain embodiments, the SRSF3 inhibitor is the only anticancer agent administered to the subject. In certain embodiments, the method further comprises administering to the subject at least one additional agent or therapy useful for treating or preventing the SCC. In some embodiments, the additional agent or therapy comprises surgical resection of at least one SCC lesion. In certain embodiments, the SCC is early-stage cutaneous SCC. In certain embodiments, the subject has multiple simultaneous SCC lesions In certain embodiments, the subject is a mammal. In certain embodiments, the subject is a human. Compounds invention provides compounds of Formula (II). In some embodiments, the compound is an SRSF3 inhibitor. In one aspect, the invention provides a compound of Formula (II), or a salt, stereoisomer, or isotopologue thereof: , wherein: Attorney Docket No.047162-7528WO1(02689) ; the group consisting of H, CN, NO2, ORA, N(RA)(RB), SRA, C(=O) N(RA)(RB), S(=O)RA, S(=O)2RA, S(=O)N(RA)(RB), S(=O)2N(RA)(RB), P(=O)(ORA)(ORB), halogen, optionally substituted C1-C6 alkyl, optionally substituted C3-C8cycloalkyl, optionally substituted C2-C8heterocycloalkyl, optionally substituted C6-C10 aryl, and optionally substituted C2-C8 heteroaryl; R4is selected from the group consisting of H and optionally substituted C1-C6alkyl; R5is selected from the group consisting of H and optionally substituted C1-C6 alkyl; R6is selected from the group consisting of H, optionally substituted C1-C6alkyl, optionally substituted C3-C8 cycloalkyl, optionally substituted C2-C8 heterocycloalkyl, optionally substituted C6-C10aryl, and optionally substituted C2-C8heteroaryl; R7a, R7b, and R7c, if present, are each independently selected from the group consisting of H, CN, NO2, ORA, N(RA)(RB), C(=O)RA, C(=O)ORA, C(=O)N(RA)(RB), S(=O) , halogen, substituted C2-C8 heterocycloalkyl, optionally substituted C6-C10 aryl, and optionally substituted C2-C8heteroaryl, wherein R7aand R7bcan combine with the atoms to which they are bound to form an optionally substituted C6-C10 aryl or optionally substituted C2-C8heteroaryl; X1selected from the group consisting of N and CR7c; Z1is CR8aor N, Z2is CR8bor N, Z3is CR8cor N, Z4is CR8dor N, and Z5is CR8eor N, wherein no more than two of Z1, Z2, Z3, Z4, and Z5are N; R8a, R8b, R8c, R8d, and R8e, if present, are each independently selected from the group consisting of H, CN, NO2, ORA, N(RA)(RB), SRA, halogen, optionally substituted C1-C6alkyl, optionally substituted C3-C8 cycloalkyl, optionally substituted C2-C8 heterocycloalkyl, optionally substituted C6-C10aryl, and optionally substituted C2-C8heteroaryl; each occurrence of RAand RB, if present, is independently selected from the group consisting of H, optionally substituted C1-C6alkyl, optionally substituted C3-C8cycloalkyl, Attorney Docket No.047162-7528WO1(02689) optionally substituted C2-C8 heterocycloalkyl, optionally substituted C6-C10 aryl, optionally substituted C2-C8heteroaryl, C(=O)RC, C(=O)ORC, C(=O)N(RC)(RD), S(=O)RC, S(=O)2RC, S(=O)N(RC)(RD), S(=O)2N(RC)(RD), and P(=O)(ORC)(ORD); each occurrence of RCand RD, if present, is independently selected from the group consisting of H, optionally substituted C1-C6 alkyl, optionally substituted C3-C8 cycloalkyl, optionally substituted C2-C8heterocycloalkyl, optionally substituted C6-C10aryl, and optionally substituted C2-C8 heteroaryl; wherein the compound of formula (II) is not a compound selected from the group consisting of: (E)-4-(2-(2-(1-(1H-benzo[d]imidazol-2-yl)ethylidene)hydrazineyl)thiazol-4-yl)-N- methylaniline; and (E)-2-(2-(1-(1H-benzo[d]imidazol-2-yl)ethylidene)hydrazineyl)-4-(4- methoxyphenyl)thiazole. In some embodiments, at least one of the following applies: (a) R7a, R7b, and R7c, if present, are each independently selected from the group consisting of H, CN, NO2, ORA, N(RA)(RB), C(=O)RA, C(=O)ORA, C(=O)N(RA)(RB), S(=O)RA, S(=O)2RA, S(=O)N(RA)(RB), S(=O)2N(RA)(RB), P(=O)(ORA)(ORB), halogen, optionally substituted C1-C6alkyl, optionally substituted C3-C8cycloalkyl, optionally substituted C2-C8heterocycloalkyl, optionally substituted C6-C10aryl, and optionally substituted C2-C8heteroaryl; (b) R7aand R7bcan combine with the atoms to which they are bound to form a substituted C6-C10aryl or optionally substituted C2-C8heteroaryl; (c) R7aand R7bcan combine with the atoms to which they are bound to form unsubstituted phenyl, and R8c, if present, is selected from the group consisting of H, CN, NO2, SRA, NH(substituted C1-C6alkyl), NH(optionally substituted C2-C6alkyl), halogen, optionally substituted C1-C6alkyl, substituted C1-C6alkoxy, optionally substituted C2-C6alkoxy, optionally substituted C3-C8cycloalkyl, optionally substituted C2-C8heterocycloalkyl, optionally substituted C6-C10aryl, and optionally substituted C2-C8heteroaryl; (d) R7aand R7bcan combine with the atoms to which they are bound to form unsubstituted phenyl, R8cis N(RA)(RB), and RAis C(=O)RC; and (e) R8cis N(RA)(RB), and RAis C(=O)RC. In some embodiments, R6is H. In some embodiments, one of the following applies: Attorney Docket No.047162-7528WO1(02689) (a) R7aand R7bare each independently selected from the group consisting of H and CH3; or (b) R7aand R7bcombine with the atoms to which they are bound to form . In some embodiments, X1is selected from the group consisting of N and In some embodiments, R1is selected from the group consisting , . one of the following applies: N, Z3is CR8c, Z4is CR8d, and Z5is CR8e; or (b) Z1is CR8a, Z2is CR8b, Z3is CR8c, Z4is CR8d, and Z5is CR8e. In some embodiments, R8a, R8b, R8d, and R8eare each independently H. In some embodiments, R8cis selected from the group consisting of O(C1-C6alkyl), O(C1-C6 haloalkyl), S(C1-C6 alkyl), NH(C1-C6 alkyl), and N(C1-C6 alkyl)C(=O)(C1-C6 haloalkyl), optionally wherein R8cis selected from the group consisting of OCH3, OCF3, SCH3, NHCH3, and N(CH3)C(=O)CF3. In some embodiments, R2is selected from the group consisting , . In some embodiments, R4is H. In some embodiments, R5is CH3. In some embodiments, the compound of formula (II) is selected from the group consisting of: (E)-2-(2-(1-(1H-pyrrol-2-yl)ethylidene)hydrazineyl)-4-(4-methoxyphenyl)thiazole; (E)-2-(2-(1-(1H-imidazol-2-yl)ethylidene)hydrazineyl)-4-(4-methoxyphenyl)thiazole; (E)-2-(2-(1-(1H-pyrrol-2-yl)ethylidene)hydrazineyl)-4-(6-methoxypyridin-3- yl)thiazole; (E)-2-(2-(1-(4,5-dimethyl-1H-imidazol-2-yl)ethylidene)hydrazineyl)-4-(6- methoxypyridin-3-yl)thiazole; Attorney Docket No.047162-7528WO1(02689) (E)-2-(2-(1-(1H-imidazol-2-yl)ethylidene)hydrazineyl)-4-(6-methoxypyridin-3- yl)thiazole; (E)-2-(2-(1-(1H-benzo[d]imidazol-2-yl)ethylidene)hydrazineyl)-4-(4- (trifluoromethoxy)phenyl)thiazole; (E)-2-(2-(1-(1H-imidazol-2-yl)ethylidene)hydrazineyl)-4-(4- (trifluoromethoxy)phenyl)thiazole; (E)-2-(2-(1-(1H-benzo[d]imidazol-2-yl)ethylidene)hydrazineyl)-4-(4- (methylthio)phenyl)thiazole; (E)-2-(2-(1-(1H-imidazol-2-yl)ethylidene)hydrazineyl)-4-(4- (methylthio)phenyl)thiazole; (E)-4-(2-(2-(1-(1H-imidazol-2-yl)ethylidene)hydrazineyl)thiazol-4-yl)-N- methylaniline; (E)-N-(4-(2-(2-(1-(1H-benzo[d]imidazol-2-yl)ethylidene)hydrazineyl)thiazol-4- yl)phenyl)-2,2,2-trifluoro-N-methylacetamide; and (E)-N-(4-(2-(2-(1-(1H-imidazol-2-yl)ethylidene)hydrazineyl)thiazol-4-yl)phenyl)- 2,2,2-trifluoro-N-methylacetamide. In some embodiments, the compound of formula (II) is: i.e., hydrazineyl)-4-(4-methoxyphenyl)thiazole, or a salt, solvate, stereoisomer, isotopologue, or tautomer thereof. In some embodiments, the compound of formula (II) is: i.e., hydrazineyl)-4-(4-methoxyphenyl)thiazole, or a salt, solvate, stereoisomer, isotopologue, or tautomer thereof. In some embodiments, the compound of formula (II) is: Attorney Docket No.047162-7528WO1(02689) i.e., hydrazineyl)-4-(6-methoxypyridin-3-yl)thiazole, or a or tautomer thereof. In some embodiments, the compound of formula (II) is: i.e., 2-yl)ethylidene)hydrazineyl)-4-(6- or a solvate, stereoisomer, isotopologue, or tautomer thereof. In some embodiments, the compound of formula (II) is: i.e., hydrazineyl)-4-(6-methoxypyridin-3- yl)thiazole, or a salt, solvate, stereoisomer, isotopologue, or tautomer thereof. In some embodiments, the compound of formula (II) is: i.e., hydrazineyl)-4-(4- (trifluoromethoxy)phenyl)thiazole, or a salt, solvate, stereoisomer, isotopologue, or tautomer thereof. In some embodiments, the compound of formula (II) is: Attorney Docket No.047162-7528WO1(02689) i.e., hydrazineyl)-4-(4- salt, solvate, stereoisomer, isotopologue, or tautomer thereof. In some embodiments, the compound of formula (II) is: i.e., ethylidene)hydrazineyl)-4-(4- (methylthio)phenyl)thiazole, or a salt, solvate, stereoisomer, isotopologue, or tautomer thereof. In some embodiments, the compound of formula (II) is: i.e., hydrazineyl)-4-(4-(methylthio)phenyl)thiazole, or a salt, solvate, stereoisomer, isotopologue, or tautomer thereof. In some embodiments, the compound of formula (II) is: i.e., ethylidene)hydrazineyl)thiazol-4-yl)-N-methylaniline, or a salt, solvate, stereoisomer, isotopologue, or tautomer thereof. In some embodiments, the SRSF3 inhibitor is the compound of Formula (II), wherein the compound of Formula (II) is: Attorney Docket No.047162-7528WO1(02689) (i.e., ethylidene)hydrazineyl)thiazol-4- yl) , a salt, solvate, stereoisomer, isotopologue, or tautomer thereof. In some embodiments, the SRSF3 inhibitor is the compound of Formula (II), wherein the compound of Formula (II) is: (i.e., hydrazineyl)thiazol-4-yl)phenyl)-2,2,2- , or a stereoisomer, isotopologue, or tautomer thereof. In some embodiments, the compound of Formula (II) is an SRSF3 inhibitor. In some embodiments, the compound of Formula (II) is an SRSF3 inhibitor selected from the group consisting of: (a) (E)-N-(4-(2-(2-(1-(1H-benzo[d]imidazol-2-yl)ethylidene)hydrazineyl)thiazol- 4-yl)phenyl)-2,2,2-trifluoro-N-methylacetamide), or a salt, solvate, stereoisomer, isotopologue, or tautomer thereof; (b) (E)-4-(2-(2-(1-(1H-benzo[d]imidazole-2-yl)ethylidene)hydrazineyl)thiazol-4- yl)-N-methylaniline), or a salt, solvate, stereoisomer, isotopologue, or tautomer thereof; and (c) (E)-2-(2-(1-(1H-benzo[d]imidazol-2-yl)ethylidene)hydrazineyl)-4-(4- (trifluoromethoxy)phenyl)thiazole), or a salt, solvate, stereoisomer, isotopologue, or tautomer thereof. Pharmaceutical Compositions In one aspect, the present disclosure provides a pharmaceutical composition comprising a serine / arginine-rich splicing factor 3 (SRSF3) inhibitor. In some embodiments, the pharmaceutical composition is for use in a method of treating or preventing squamous cell carcinoma (SCC) as described herein. Attorney Docket No.047162-7528WO1(02689) In certain embodiments, the pharmaceutical composition is a topical formulation (e.g., for administration to the skin). In some embodiments, the topical formulation comprises a gel or an ointment. In certain embodiments, the pharmaceutical composition is formulated for intradermal administration. In certain embodiments, the pharmaceutical composition is formulated for transdermal administration. In certain embodiments, the pharmaceutical composition may be formulated and used systemically (e.g. oral or intravenous). In certain embodiments, the SRSF3 inhibitor is a small molecule having molecular mass less than about 600 g / mol. In certain embodiments, the SRSF3 inhibitor is characterized by an effective level of skin permeability and / or is formulated (e.g., in a topical formulation and / or formulated for intradermal or transdermal delivery) to exhibit an effective level of skin permeability. The SRSF3 inhibitor refers to any molecule that decreases or entirely prevents the ability of SRSF3 to inhibit the inclusion of the p53β-unique exon in splicing of p53 pre- mRNA. As such, an SRSF3 inhibitor will result in an increase of the p53β isoform. As some SRSF3 inhibitors (e.g. amiodarone) do not increase the p53β isoform but do decrease levels of SRSF3, “SRSF3 inhibitor” also refers to any molecule that decreases levels of SRSF3, in particular the full-length SRSF3 isoform, but ultimately either the full-length SRSF3 isoform or the truncated SRSF3 isoform. In certain embodiments, the SRSF3 inhibitor reduces SRSF3 amount or activity in SCC cells by at least about 10%, at least about 15%, at least about 20%, at least about 25%, at least about 30%, at least about 35%, at least about 40%, at least about 45%, at least about 50%, at least about 55%, at least about 60%, at least about 65%, at least about 70%, at least about 75%, at least about 80%, at least about 85%, at least about 90%, at least about 95%, or at least about 100% compared to SRSF3 amount or activity in SCC cells in the absence of the SRSF3 inhibitor. In certain embodiments, the SRSF3 inhibitor induces terminal differentiation of SCC cells. In certain embodiments, the SRSF3 inhibitor is a compound of Formula (I), or a salt, stereoisomer, or isotopologue thereof: Attorney Docket No.047162-7528WO1(02689) , wherein: ; the group consisting of H, CN, NO2, ORA, N(RA)(RB), SRA, C(=O) N(RA)(RB), S(=O)RA, S(=O)2RA, S(=O)N(RA)(RB), S(=O)2N(RA)(RB), P(=O)(ORA)(ORB), halogen, optionally substituted C1-C6 alkyl, optionally substituted C3-C8cycloalkyl, optionally substituted C2-C8heterocycloalkyl, optionally substituted C6-C10 aryl, and optionally substituted C2-C8 heteroaryl; R4is selected from the group consisting of H and optionally substituted C1-C6alkyl; R5is selected from the group consisting of H and optionally substituted C1-C6 alkyl; R6is selected from the group consisting of H, optionally substituted C1-C6 alkyl, optionally substituted C3-C8cycloalkyl, optionally substituted C2-C8heterocycloalkyl, optionally substituted C6-C10 aryl, and optionally substituted C2-C8 heteroaryl; R7a, R7b, and R7c, if present, are each independently selected from the group consisting of H, CN, NO2, ORA, N(RA)(RB), C(=O)RA, C(=O)ORA, C(=O)N(RA)(RB), S(=O) , halogen, optionally substituted C2-C8heterocycloalkyl, optionally substituted C6-C10aryl, and optionally substituted C2-C8 heteroaryl, wherein R7aand R7bcan combine with the atoms to which they are bound to form an optionally substituted C6-C10 aryl or optionally substituted C2-C8heteroaryl; X1selected from the group consisting of N and CR7c; Z1is CR8aor N, Z2is CR8bor N, Z3is CR8cor N, Z4is CR8dor N, and Z5is CR8eor N, wherein no more than two of Z1, Z2, Z3, Z4, and Z5are N; Attorney Docket No.047162-7528WO1(02689) R8a, R8b, R8c, R8d, and R8e, if present, are each independently selected from the group consisting of H, CN, NO2, ORA, N(RA)(RB), SRA, halogen, optionally substituted C1-C6alkyl, substituted C2-C8 heterocycloalkyl, optionally substituted C6-C10aryl, and optionally substituted C2-C8heteroaryl; each occurrence of RAand RB, if present, is independently selected from the group consisting of H, optionally substituted C1-C6alkyl, optionally substituted C3-C8cycloalkyl, optionally substituted C2-C8 heterocycloalkyl, optionally substituted C6-C10 aryl, optionally substituted C2-C8heteroaryl, C(=O)RC, C(=O)ORC, C(=O)N(RC)(RD), S(=O)RC, S(=O)2RC, S(=O)N(RC)(RD), S(=O)2N(RC)(RD), and P(=O)(ORC)(ORD); each occurrence of RCand RD, if present, is independently selected from the group consisting of H, optionally substituted C1-C6alkyl, optionally substituted C3-C8cycloalkyl, optionally substituted C2-C8 heterocycloalkyl, optionally substituted C6-C10 aryl, and optionally substituted C2-C8heteroaryl. In some embodiments, at least one of the following applies: (a) R7a, R7b, and R7c, if present, are each independently selected from the group consisting of H, CN, NO2, ORA, N(RA)(RB), C(=O)RA, C(=O)ORA, C(=O)N(RA)(RB), S(=O)RA, S(=O)2RA, S(=O)N(RA)(RB), S(=O)2N(RA)(RB), P(=O)(ORA)(ORB), halogen, optionally substituted C1-C6alkyl, optionally substituted C3-C8cycloalkyl, optionally substituted C2-C8heterocycloalkyl, optionally substituted C6-C10aryl, and optionally substituted C2-C8heteroaryl; (b) R7aand R7bcan combine with the atoms to which they are bound to form a substituted C6-C10aryl or optionally substituted C2-C8heteroaryl; (c) R7aand R7bcan combine with the atoms to which they are bound to form unsubstituted phenyl, and R8c, if present, is selected from the group consisting of H, CN, NO2, SRA, NH(substituted C1-C6alkyl), NH(optionally substituted C2-C6alkyl), halogen, optionally substituted C1-C6alkyl, substituted C1-C6alkoxy, optionally substituted C2-C6alkoxy, optionally substituted C3-C8cycloalkyl, optionally substituted C2-C8heterocycloalkyl, optionally substituted C6-C10aryl, and optionally substituted C2-C8heteroaryl; (d) R7aand R7bcan combine with the atoms to which they are bound to form unsubstituted phenyl, R8cis N(RA)(RB), and RAis C(=O)RC; and (e) R8cis N(RA)(RB), and RAis C(=O)RC. In some embodiments, R6is H. In some embodiments, one of the following applies: Attorney Docket No.047162-7528WO1(02689) (a) R7aand R7bare each independently selected from the group consisting of H and CH3; or (b) R7aand R7bcombine with the atoms to which they are bound to form . In some embodiments, X1is selected from the group consisting of N and In some embodiments, R1is selected from the group consisting , . one of the following applies: N, Z3is CR8c, Z4is CR8d, and Z5is CR8e; or (b) Z1is CR8a, Z2is CR8b, Z3is CR8c, Z4is CR8d, and Z5is CR8e. In some embodiments, R8a, R8b, R8d, and R8eare each independently H. In some embodiments, R8cis selected from the group consisting of O(C1-C6alkyl), O(C1-C6 haloalkyl), S(C1-C6 alkyl), NH(C1-C6 alkyl), and N(C1-C6 alkyl)C(=O)(C1-C6 haloalkyl), optionally wherein R8cis selected from the group consisting of OCH3, OCF3, SCH3, NHCH3, and N(CH3)C(=O)CF3. In some embodiments, R2is selected from the group consisting , . In some embodiments, R4is H. In some embodiments, R5is CH3. In some embodiments, the compound of formula (I) is selected from the group consisting of: (E)-2-(2-(1-(1H-benzo[d]imidazol-2-yl)ethylidene)hydrazineyl)-4-(4- methoxyphenyl)thiazole; (E)-4-(2-(2-(1-(1H-benzo[d]imidazol-2-yl)ethylidene)hydrazineyl)thiazol-4-yl)-N- methylaniline; (E)-2-(2-(1-(1H-pyrrol-2-yl)ethylidene)hydrazineyl)-4-(4-methoxyphenyl)thiazole; (E)-2-(2-(1-(1H-imidazol-2-yl)ethylidene)hydrazineyl)-4-(4-methoxyphenyl)thiazole; Attorney Docket No.047162-7528WO1(02689) (E)-2-(2-(1-(1H-pyrrol-2-yl)ethylidene)hydrazineyl)-4-(6-methoxypyridin-3- yl)thiazole; (E)-2-(2-(1-(4,5-dimethyl-1H-imidazol-2-yl)ethylidene)hydrazineyl)-4-(6- methoxypyridin-3-yl)thiazole; (E)-2-(2-(1-(1H-imidazol-2-yl)ethylidene)hydrazineyl)-4-(6-methoxypyridin-3- yl)thiazole; (E)-2-(2-(1-(1H-benzo[d]imidazol-2-yl)ethylidene)hydrazineyl)-4-(4- (trifluoromethoxy)phenyl)thiazole; (E)-2-(2-(1-(1H-imidazol-2-yl)ethylidene)hydrazineyl)-4-(4- (trifluoromethoxy)phenyl)thiazole; (E)-2-(2-(1-(1H-benzo[d]imidazol-2-yl)ethylidene)hydrazineyl)-4-(4- (methylthio)phenyl)thiazole; (E)-2-(2-(1-(1H-imidazol-2-yl)ethylidene)hydrazineyl)-4-(4- (methylthio)phenyl)thiazole; (E)-4-(2-(2-(1-(1H-imidazol-2-yl)ethylidene)hydrazineyl)thiazol-4-yl)-N- methylaniline (E)-N-(4-(2-(2-(1-(1H-benzo[d]imidazol-2-yl)ethylidene)hydrazineyl)thiazol-4- yl)phenyl)-2,2,2-trifluoro-N-methylacetamide; and (E)-N-(4-(2-(2-(1-(1H-imidazol-2-yl)ethylidene)hydrazineyl)thiazol-4-yl)phenyl)- 2,2,2-trifluoro-N-methylacetamide. In certain embodiments, the SRSF3 inhibitor is the compound of Formula (I), wherein the compound of Formula (I) is SFI003, or a salt, solvate, stereoisomer, isotopologue, or tautomer thereof. The IUPAC name for SFI003 is N-[(E)-1-(1H-benzimidazol-2- yl)ethylideneamino]-4-(4-methoxyphenyl)-1,3-thiazol-2-amine. The chemical structure of SFI003 is shown: -2- 2- ethylidene)hydrazineyl)-4-(4- methoxyphenyl)thiazole, or a salt, solvate, stereoisomer, isotopologue, or tautomer thereof. In some embodiments, the SRSF3 inhibitor is selected from the group consisting of: (a) SFI003, or a salt, solvate, stereoisomer, isotopologue, or tautomer thereof; Attorney Docket No.047162-7528WO1(02689) (b) (E)-N-(4-(2-(2-(1-(1H-benzo[d]imidazol-2-yl)ethylidene)hydrazineyl)thiazol- 4-yl)phenyl)-2,2,2-trifluoro-N-methylacetamide), or a salt, solvate, stereoisomer, isotopologue, or tautomer thereof; (c) (E)-4-(2-(2-(1-(1H-benzo[d]imidazole-2-yl)ethylidene)hydrazineyl)thiazol-4- yl)-N-methylaniline), or a salt, solvate, stereoisomer, isotopologue, or tautomer thereof; and (d) (E)-2-(2-(1-(1H-benzo[d]imidazol-2-yl)ethylidene)hydrazineyl)-4-(4- (trifluoromethoxy)phenyl)thiazole), or a salt, solvate, stereoisomer, isotopologue, or tautomer thereof. In some embodiments, the SRSF3 inhibitor is the compound of Formula (I), wherein the compound of Formula (I) is: i.e., hydrazineyl)-4-(4-methoxyphenyl)thiazole, or a salt, solvate, stereoisomer, isotopologue, or tautomer thereof. In some embodiments, the SRSF3 inhibitor is the compound of Formula (I), wherein the compound of Formula (I) is: i.e., hydrazineyl)-4-(4-methoxyphenyl)thiazole, or a salt, solvate, stereoisomer, isotopologue, or tautomer thereof. In some embodiments, the SRSF3 inhibitor is the compound of Formula (I), wherein the compound of Formula (I) is: Attorney Docket No.047162-7528WO1(02689) i.e., (E)-2-(2-(1-(1H-pyrrol-2-yl)ethylidene)hydrazineyl)-4-(6-methoxypyridin-3-yl)thiazole, or a salt, solvate, stereoisomer, isotopologue, or tautomer thereof. In some embodiments, the SRSF3 inhibitor is the compound of Formula (I), wherein the compound of Formula (I) is: i.e., 2-yl)ethylidene)hydrazineyl)-4-(6- solvate, stereoisomer, isotopologue, or tautomer thereof. In some embodiments, the SRSF3 inhibitor is the compound of Formula (I), wherein the compound of Formula (I) is: i.e., hydrazineyl)-4-(6-methoxypyridin-3- yl)thiazole, or a salt, solvate, stereoisomer, isotopologue, or tautomer thereof. In some embodiments, the SRSF3 inhibitor is the compound of Formula (I), wherein the compound of Formula (I) is: i.e., hydrazineyl)-4-(4- (trifluoromethoxy)phenyl)thiazole, or a salt, solvate, stereoisomer, isotopologue, or tautomer thereof. In some embodiments, the SRSF3 inhibitor is the compound of Formula (I), wherein the compound of Formula (I) is: Attorney Docket No.047162-7528WO1(02689) i.e., hydrazineyl)-4-(4- salt, solvate, stereoisomer, isotopologue, or tautomer thereof. In some embodiments, the SRSF3 inhibitor is the compound of Formula (I), wherein the compound of Formula (I) is: i.e., ethylidene)hydrazineyl)-4-(4- (methylthio)phenyl)thiazole, or a salt, solvate, stereoisomer, isotopologue, or tautomer thereof. In some embodiments, the SRSF3 inhibitor is the compound of Formula (I), wherein the compound of Formula (I) is: i.e., hydrazineyl)-4-(4-(methylthio)phenyl)thiazole, or a salt, solvate, stereoisomer, isotopologue, or tautomer thereof. In some embodiments, the SRSF3 inhibitor is the compound of Formula (I), wherein the compound of Formula (I) is: Attorney Docket No.047162-7528WO1(02689) i.e., (E)-4-(2-(2-(1-(1H-benzo[d]imidazol-2-yl)ethylidene)hydrazineyl)thiazol-4-yl)-N- methylaniline, or a salt, solvate, stereoisomer, isotopologue, or tautomer thereof. In some embodiments, the SRSF3 inhibitor is the compound of Formula (I), wherein the compound of Formula (I) is: i.e., ethylidene)hydrazineyl)thiazol-4-yl)-N-methylaniline, or a or tautomer thereof. In some embodiments, the SRSF3 inhibitor is the compound of Formula (I), wherein the compound of Formula (I) is: (i.e., ethylidene)hydrazineyl)thiazol-4- yl)phenyl)-2,2,2-trifluoro-N-methylacetamide), or a salt, solvate, stereoisomer, isotopologue, or tautomer thereof. In some embodiments, the SRSF3 inhibitor is the compound of Formula (I), wherein the compound of Formula (I) is: (i.e., hydrazineyl)thiazol-4-yl)phenyl)-2,2,2- trifluoro-N-methylacetamide), or a salt, solvate, stereoisomer, isotopologue, or tautomer thereof. In certain embodiments, the SRSF3 inhibitor is amiodarone, or a salt, solvate, stereoisomer, isotopologue, or tautomer thereof.. In certain embodiments, the SRSF3 inhibitor is digoxin, or a salt, solvate, stereoisomer, isotopologue, or tautomer thereof.. Attorney Docket No.047162-7528WO1(02689) Synthesis of SRSF3 inhibitors The SRSF3 inhibitor compounds disclosed herein can be synthesized by conventional techniques of chemistry which are known in the art. In certain embodiments, the SRSF3 inhibitor is synthesized following Scheme I: Scheme I, Step 1 - Synthesis of compounds of formula I-3, e.g., 1-(1H- benzo[d]imidazol-2-yl)ethan-1-ol: Reflux a mixture of o-phenylenediamine (1 equiv) and lactic acid (2 equiv) in 4 M HCl for 1 h. After cooling to room temperature, adjust the pH to 8 using NaOH solution, resulting in the precipitation of a solid. Collect the solid by filtration and recrystallize it from ethanol to afford 1-(benzimidazole-2-ethyl)-1-ol. Scheme I, Step 2 – Synthesis of compounds of formula I-4, e.g., 1-(1H- benzo[d]imidazol-2-yl)ethan-1-one: Dissolve 1-(benzimidazole-2-ethyl)-1-ol in acetic acid and heat to 90 °C under reflux. Add chromic acid (2.5 equiv), prepared by dissolving CrO3 in a minimal amount of water and adding acetic acid dropwise, to the reaction mixture. Reflux the mixture at 105 °C for 30 min. After cooling to room temperature, add a large volume of water, extract the mixture with ethyl acetate, and dry the combined organic layers over anhydrous Na₂SO₄. Remove the solvent under reduced pressure to obtain 1-(benzimidazole- 2-ethyl)-1-ketone as a yellow to brown powder. Scheme I, Step 3 – Synthesis of compounds of formula I-6, e.g., (E)-2-(1-(1H- benzo[d]imidazol-2-yl)ethylidene)hydrazine-1-carbothioamide: Add 1-(benzimidazole-2- Attorney Docket No.047162-7528WO1(02689) ethyl)-1-one and thiosemicarbazide in a molar ratio of 1:1 to 20 mL of ethanol. Add 1 mL of glacial acetic acid to the reaction mixture and reflux at 80 °C for 5 h, monitoring the progress by TLC. After completion of the reaction, cool the mixture to room temperature, resulting in the precipitation of a white solid. Collect the solid by filtration and recrystallize it from ethanol to obtain the product. Scheme I, Step 4 – Synthesis of compounds of formula I-8, e.g., (E)-2-(2-(1-(1H- benzo[d]imidazole-2-yl)ethylidene)hydrazineyl)-4-phenylthiazole: Add 2-(1-(1H-imidazol- 2-yl)ethylidene)hydrazine-1-carbothioamide and 2-bromoacetophenone in a molar ratio of 1:1 to 20 mL of ethanol. Add two drops of glacial acetic acid and stir the mixture at room temperature while monitoring the progress of the reaction by TLC. After the reaction is complete, filter the mixture to isolate the solid product. Recrystallize the solid from ethanol to obtain the product as a yellow solid. Transdermal permeation enhancement and strategies When a substance reaches intact skin, there are three potential entry pathways to the viable tissue: across the continuous stratum corneum, through the hair follicles with their associated sebaceous glands and via the sweat ducts. Some biological factors have influence on transdermal permeation (e.g., skin condition, skin age, blood flow, and skin metabolism) as well as physicochemical factors (e.g., skin hydration, temperature, pH, diffusion coefficient, drug concentration, partition coefficient, molecular size, and shape). Most active agents do not permeate the skin in therapeutic amounts. Substances that are administered across the skin are of low molecular mass (usually <500 Da) and are very lipophilic in nature at low dosages. Hydrophilic substances generally exhibit poor skin permeability (10− 7to 10− 8cm / s), about one or more orders of magnitude lower than hydrophobic solutes (Azagury, Khoury, Enden, & Kost, 2014). The skin barrier and its relative impermeability have led to the development of a number of enhancements to chemical and physical approaches known in the art. The chemical approaches comprise methods that produce the active at very high thermodynamic activity. One chemical method is based on solvent loss, which may occur as a result of its evaporation or its diffusion into the skin. Moreover, the system matrix may take up water from the skin, leading to altering its solubility properties such that the permeant becomes supersaturated. The close-to-saturation state of the active agent can cause stability issues, and permeation rates from systems change with time. Attorney Docket No.047162-7528WO1(02689) It is common to use solvents that permeate into the skin and act essentially as a carrier for the active agent. These solvents can be ethanol, dimethyl sulfoxide, propylene glycol, glycerin, polyethylene glycol, urea, dimethyl acetamide, sodium lauryl sulfate, the poloxamers, Spans, Tweens, lecithin, terpenes, and many others, which can co-diffuse with the active agent, enabling its passage through the stratum corneum. Another chemical approach is based on the presence of a component (e.g., surfactant- like substance) that permeates into the intercellular lipids, where it intercalates and disrupts their structure. This action led to creating a region where diffusion is faster and permeation through the stratum corneum is improved. These enhancers can have irritant properties and need to be selected considering the reversibility of barrier function affection. It is very important that they do not disrupt the membranes of the viable cells in the deeper layers of the skin, where they could elicit adverse effects. They are divided into chemical groups such as sulfoxides, pyrrolidones, fatty acids, alcohols, surfactants, metabolic interventions, and the only material specifically designed to enhance transdermal mass transport, Azone (Williams & Barry, 2004). These three chemical approaches can be used simultaneously, so that in a combination of enhancers, one acts as a good solvent and one that disrupts the lipid structure. Several physical strategies for skin penetration enhancement, like stripping of the stratum corneum, heating, iontophoresis, electroporation, ultrasound, and microneedles, have also been studied. With the high advance in the development of biotechnological products, and the need to deliver peptides, oligonucleotides and their analogs, it is difficult to use conventional chemical enhancer methods. In addition, most peptides are charged and contribute to the iontophoresis approach to be used. Iontophoresis is a technique of the nineteenth century, by which the charged active agent moves through the skin membrane using an electrical field. It involves the application of a small electric current (up to 0.5 mA / cm2) to a drug reservoir, wetting the surface of the skin with the same charged electrode as the solute of interest. The process is dominated by the physicochemical properties of the active agent and considers the pH of the stratum corneum (4–5 to physiological). If the pKa of the permeant is between these values, charge reversal can occur, and the potential difference drives the active agent into the skin. Moreover, due to viscous forces, the entire solution undergoes a convective flow that carries non-charged particles as well. This process is referred to as electro-osmosis and can facilitate the absorption of uncharged hydrophilic substances. A number of actives have been Attorney Docket No.047162-7528WO1(02689) submitted to iontophoretic delivery, such as lidocaine, amino acids, peptides, proteins, dexamethasone, verapamil, and propranolol. Electroporation involves the application of a pulsating electrical field at high voltage (> 50 V, typically 1–100 ms) to the skin, causing the formation of transient aqueous pores in the stratum corneum, through which molecular transport is attainable. This technology was originally used to transfect cells with macromolecules such as DNA. In the skin, electroporation leads to enhanced permeability, mainly attributed to electrophoretic movement and diffusion through the newly created aqueous pathways. To differentiate from iontophoresis, which directly acts on the drug molecule to propel it into the skin, electroporation acts mainly on the skin to increase its permeability. Transdermal delivery mediated by ultrasound is also named phonophoresis or sonophoresis. Sonophoresis has relatively higher cavitation and improves the transport of substances through the skin and into the soft tissue during or following the influence of an ultrasonic perturbation (20 kHz–1 MHz) (Azagury et al., 2014). The fundamental mechanism by which sonophoresis enables transdermal delivery is still not clearly understood or characterized. There are proposed mechanisms such as thermal effects by absorption of ultrasound energy and cavitation effects caused by collapse and oscillation of cavitation bubbles in the ultrasound field. Between these two effects, cavitation is believed to be the predominant mechanism responsible for sonophoresis. The barrier function of the skin can also be physically breached by “shooting” particles through it using high velocities or by ablating the stratum corneum by precisely controlled laser technology. Laser cell-ablation to remove the stratum corneum barrier has been investigated as a means of enhancing transdermal drug delivery. Lasers such as erbium—yttrium–aluminum–garnet (YAG)—have been found to increase skin permeability. Molecular size, lipophilicity and sequence of peptides were found to play important roles in modulating delivery enhancement. Radio-frequency cell ablation is a physical approach by which cell ablation is performed by placing an array of microelectrodes on the skin and passing an alternating electrical current at radio frequency (100–500 kHz). The ions in the cells adjacent to the microelectrodes vibrate as they try to follow the change in electrical current direction. These vibrations generate heat, which causes water evaporation, cell ablation and possibly damage of deeper skin layers (Azagury et al., 2014). The microchannels are formed by placing a closely spaced array of tiny electrodes with very precise dimensions against the skin. The alternating electrical current transfers through each of the microelectrodes, ablates the cells Attorney Docket No.047162-7528WO1(02689) underneath each electrode and forms microscopic passages in the stratum corneum and in the outer dermis. Microneedles can also be developed to pierce the skin to allow delivery to carefully controlled depths. They create a physical pathway through the upper epidermis to increase skin permeability. The device is designed containing some microneedles that, when applied to the skin surface, pierce the outer epidermis layer deep enough to increase skin permeability and allow delivery of the active agent. Because the microneedles reach only sites that contain no nerves, they do not cause any pain through the sensory receptors of the dermis. The main materials used to prepare microneedles are silicon and biodegradable materials such as carboxymethyl cellulose, solid maltose, polylactic acid (PLA), poly(lactic-co-glycolic acid) (PLGA), and polyvinylpyrrolidone. Microneedles (MNs) are an innovative strategy for transdermal drug delivery. It can be described as a combination of a hypodermic needle and a transdermal patch. The base plate has MN arrays attached perpendicular to it. The length of each MN ranges from 0.25 to 1 mm. Materials like metal, ceramic, glass, silicon, and polymers are used for making MNs. Skin is an absorptive organ and its structure can be divided into three layers—epidermis, dermis, and subcutis. It contains various cells such as T lymphocytes, Langerhans cells, mast cells, keratinocytes, macrophages, and dendritic cells—all of which are important for the immune system. Langerhans cells are antigen-presenting cells (APCs) that take up antigens, transporting them to the draining lymph nodes. Mast cells can act as APCs themselves or transmit signals that can mobilize dendritic cells in the skin toward the drainage of lymph nodes. Capillary permeability and leukocyte diapedesis into the skin get increased when ECs are activated by proinflammatory mediators. The responses of CD4+ and CD8+ T cells in the draining lymph nodes are directly or indirectly induced by dendritic cells, leading to the preparation and expansion of adaptive immunity. The primed and expanded B and T cells can supply systemic protection by occupying the skin and other distal epithelial tissues. Transdermal drug delivery can bypass the first-pass effect and lead to sustained drug release. However, the stratum corneum which is the outermost layer of skin, acts as a barrier to effective drug delivery. Topical creams have poor bioavailability as only 10%–20% of the loaded drug is able to cross the skin barrier. Hypodermic needles have high bioavailability and fast onset of action but poor patient compliance due to the pain caused. Further, skilled professionals are needed to administer the drug as patients do not have the expertise to inject it themselves. Transdermal patches are painless, but their bioavailability is low as the molecules need to Attorney Docket No.047162-7528WO1(02689) cross the stratum corneum. Since the superficial dermis contains a capillary bed and accompanying lymphatic capillaries, the onset of action is quick with microneedles (MNs). There is higher control with MN compositions which leads to accurate doses. Due to their small size and length, MNs are painless and safe to use. The patch application does not require professional knowledge. The overall size of the medication package is reduced as MN patches combine the functioning of the drug formulation, needle, and syringe. This also results in an overall reduction or elimination of sharps waste. The MN’s enhanced solid-state formulation eliminates the requirement for a cold-chain system. Costs are also saved in terms of manufacturing, logistics, and dose sparing. With MN delivery, the drug is delivered via the topical route through diffusion. The skin is briefly disturbed in MN delivery. The device is manufactured by assembling hundreds of MNs in arrays on a small patch—similar to a commercially available transdermal patch. This enables it to administer enough drug to provide the desired therapeutic response. The device can go around the barrier layer by piercing the stratum corneum. The medicine is inserted directly into the epidermis or higher dermis layer, which subsequently goes into the systemic circulation and brings about a healing effect once it makes it to the target region. Administration / Dosage / Formulations The regimen of administration may affect what constitutes an effective amount. The therapeutic formulations may be administered to the subject either prior to or after the onset of a disease state. Further, several divided dosages, as well as staggered dosages may be administered daily or sequentially, or the dose may be continuously infused, or may be a bolus injection. Further, the dosages of the therapeutic formulations may be proportionally increased or decreased as indicated by the exigencies of the therapeutic or prophylactic situation. Administration of the compositions described herein to a patient, preferably a mammal, more preferably a human, may be carried out using known procedures, at dosages and for periods of time effective to treat a disease state in the patient. An effective amount of the therapeutic compound necessary to achieve a therapeutic effect may vary according to factors such as the state of the disease or disorder in the patient; the age, sex, and weight of the patient; and the ability of the therapeutic compound to treat a disease state in the patient. Dosage regimens may be adjusted to provide the optimum therapeutic response. For example, several divided doses may be administered daily or the dose may be proportionally reduced as indicated by the exigencies of the therapeutic situation. A non-limiting example of an Attorney Docket No.047162-7528WO1(02689) effective dose range for a therapeutic compound described herein is from about 1 and 5,000 mg / kg of body weight / per day. One of ordinary skill in the art would be able to study the relevant factors and make the determination regarding the effective amount of the therapeutic compound without undue experimentation. Actual dosage levels of the active ingredients in the pharmaceutical compositions described herein may be varied so as to obtain an amount of the active ingredient that is effective to achieve the desired therapeutic response for a particular patient, composition, and mode of administration, without being toxic to the patient. In particular, the selected dosage level depends upon a variety of factors including the activity of the particular compound employed, the time of administration, the rate of excretion of the compound, the duration of the treatment, other drugs, compounds or materials used in combination with the compound, the age, sex, weight, condition, general health and prior medical history of the patient being treated, and like factors well, known in the medical arts. A medical doctor, e.g., physician or veterinarian, having ordinary skill in the art may readily determine and prescribe the effective amount of the pharmaceutical composition required. For example, the physician or veterinarian could start doses of the compounds described herein employed in the pharmaceutical composition at levels lower than that required in order to achieve the desired therapeutic effect and gradually increase the dosage until the desired effect is achieved. In particular embodiments, it is especially advantageous to formulate the compound in dosage unit form for ease of administration and uniformity of dosage. Dosage unit form as used herein refers to physically discrete units suited as unitary dosages for the patients to be treated; each unit containing a predetermined quantity of therapeutic compound calculated to produce the desired therapeutic effect in association with the required pharmaceutical vehicle. The dosage unit forms of the compound(s) described herein are dictated by and directly dependent on (a) the unique characteristics of the therapeutic compound and the particular therapeutic effect to be achieved, and (b) the limitations inherent in the art of compounding / formulating such a therapeutic compound. In certain embodiments, the compositions described herein are formulated using one or more pharmaceutically acceptable excipients or carriers. In certain embodiments, the pharmaceutical compositions described herein comprise a therapeutically effective amount of a compound described herein and a pharmaceutically acceptable carrier. Attorney Docket No.047162-7528WO1(02689) The carrier may 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 may 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. Prevention of the action of microorganisms may be achieved by various antibacterial and antifungal agents, for example, parabens, chlorobutanol, phenol, ascorbic acid, thimerosal, and the like. In many cases, it is preferable to include isotonic agents, for example, sugars, sodium chloride, or polyalcohols such as mannitol and sorbitol, in the composition. Prolonged absorption of the injectable compositions may be brought about by including in the composition an agent which delays absorption, for example, aluminum monostearate or gelatin. In certain embodiments, the compositions described herein are administered to the patient in dosages that range from one to five times per day or more. In other embodiments, the compositions described herein are administered to the patient in range of dosages that include, but are not limited to, once every day, every two, days, every three days to once a week, and once every two weeks. It is readily apparent to one skilled in the art that the frequency of administration of the various combination compositions described herein varies from individual to individual depending on many factors including, but not limited to, age, disease or disorder to be treated, gender, overall health, and other factors. Thus, administration of the compounds and compositions described herein should not be construed to be limited to any particular dosage regime and the precise dosage and composition to be administered to any patient is determined by the attending physician taking all other factors about the patient into account. The compound(s) described herein for administration may be in the range of from about 1 µg to about 10,000 mg, about 20 µg to about 9,500 mg, about 40 µg to about 9,000 mg, about 75 µg to about 8,500 mg, about 150 µg to about 7,500 mg, about 200 µg to about 7,000 mg, about 350 µg to about 6,000 mg, about 500 µg to about 5,000 mg, about 750 µg to about 4,000 mg, about 1 mg to about 3,000 mg, about 10 mg to about 2,500 mg, about 20 mg to about 2,000 mg, about 25 mg to about 1,500 mg, about 30 mg to about 1,000 mg, about 40 mg to about 900 mg, about 50 mg to about 800 mg, about 60 mg to about 750 mg, about 70 mg to about 600 mg, about 80 mg to about 500 mg, and any and all whole or partial increments therebetween. In some embodiments, the dose of a compound described herein is from about 1 mg and about 2,500 mg. In some embodiments, a dose of a compound described herein used in Attorney Docket No.047162-7528WO1(02689) compositions described herein is less than about 10,000 mg, or less than about 8,000 mg, or less than about 6,000 mg, or less than about 5,000 mg, or less than about 3,000 mg, or less than about 2,000 mg, or less than about 1,000 mg, or less than about 500 mg, or less than about 200 mg, or less than about 50 mg. Similarly, in some embodiments, a dose of a second compound as described herein is less than about 1,000 mg, or less than about 800 mg, or less than about 600 mg, or less than about 500 mg, or less than about 400 mg, or less than about 300 mg, or less than about 200 mg, or less than about 100 mg, or less than about 50 mg, or less than about 40 mg, or less than about 30 mg, or less than about 25 mg, or less than about 20 mg, or less than about 15 mg, or less than about 10 mg, or less than about 5 mg, or less than about 2 mg, or less than about 1 mg, or less than about 0.5 mg, and any and all whole or partial increments thereof. In various embodiments, the compound(s) described herein can be administered to a subject in an amount ranging from about 0.01 mg / kg to about 200 mg / kg, or about 0.5 mg / kg to about 190 mg / kg, or about 0.75 mg / kg to about 180 mg / kg, or about 1 mg / kg to about 170 mg / kg, or about 1.5 mg / kg to about 160 mg / kg, or about 2 mg / kg to about 150 mg / kg, or about 2.5 mg / kg to about 140 mg / kg, or about 3 mg / kg to about 130 mg / kg, or about 3.5 mg / kg to about 120 mg / kg, or about 4 mg / kg to about 110 mg / kg, or about 4.5 mg / kg to about 100 mg / kg, or about 5 mg / kg to about 95 mg / kg, or about 5.5 mg / kg to about 90 mg / kg, or about 6 mg / kg to about 85 mg / kg, or about 6.5 mg / kg to about 80 mg / kg, or about 7 mg / kg to about 75 mg / kg, or about 7.5 mg / kg to about 70 mg / kg, or about 8 mg / kg to about 65 mg / kg, or about 8.5 mg / kg to about 60 mg / kg, or about 9 mg / kg to about 55 mg / kg or about 9.5 mg / kg to about 50 mg / kg, or about 10 mg / kg to about 45 mg / kg. In various embodiments, the compound(s) described herein can be administered to a subject in an amount that is less than, equal to, or greater than about 0.01 mg / kg, 0.05 mg / kg, 0.1 mg / kg, 0.25 mg / kg, 0.5 mg / kg, 0.75 mg / kg, 1 mg / kg, 1.5 mg / kg, 2 mg / kg, 2.5 mg / kg, 3 mg / kg, 3.5 mg / kg, 4 mg / kg, 4.5 mg / kg, 5 mg / kg, 5.5 mg / kg, 6 mg / kg, 6.5 mg / kg, 7 mg / kg, 7.5 mg / kg, 8 mg / kg, 8.5 mg / kg, 9 mg / kg, 9.5 mg / kg, 10 mg / kg, 12 mg / kg, 14 mg / kg, 16 mg / kg, 18 mg / kg, 20 mg / kg, 25 mg / kg, 30 mg / kg, 35 mg / kg, 40 mg / kg, 45 mg / kg, 50 mg / kg, 55 mg / kg, 60 mg / kg, 65 mg / kg, 70 mg / kg, 75 mg / kg, 80 mg / kg, 85 mg / kg, 90 mg / kg, 100 mg / kg, 105 mg / kg, 110 mg / kg, 115 mg / kg, 120 mg / kg, 125 mg / kg, 130 mg / kg, 140 mg / kg, 145 mg / kg, 150 mg / kg, 155 mg / kg, 160 mg / kg, 170 mg / kg, 175 mg / kg, 180 mg / kg, 185 mg / kg, 190 mg / kg, 195 mg / kg, or 200 mg / kg. In certain embodiments, a composition as described herein is a packaged pharmaceutical composition comprising a container holding a therapeutically effective Attorney Docket No.047162-7528WO1(02689) amount of a compound described herein, alone or in combination with a second pharmaceutical agent; and instructions for using the compound to treat, prevent, or reduce one or more symptoms of a disease state or disorder in a patient. Formulations may be employed in admixtures with conventional excipients, i.e., pharmaceutically acceptable organic or inorganic carrier substances suitable for oral, parenteral, nasal, intravenous, subcutaneous, enteral, or any other suitable mode of administration, known to the art. The pharmaceutical preparations may be sterilized and if desired mixed with auxiliary agents, e.g., lubricants, preservatives, stabilizers, wetting agents, emulsifiers, salts for influencing osmotic pressure buffers, coloring, flavoring and / or aromatic substances and the like. They may also be combined where desired with other active agents, e.g., other analgesic agents. Routes of administration of any of the compositions described herein include oral, nasal, rectal, intravaginal, parenteral, buccal, sublingual or topical. The compounds for use in the compositions described herein can be formulated for administration by any suitable route, such as for oral or parenteral, for example, transdermal, transmucosal (e.g., sublingual, lingual, (trans)buccal, (trans)urethral, vaginal (e.g., trans- and perivaginally), (intra)nasal and (trans)rectal), intravesical, intrapulmonary, intraduodenal, intragastrical, intrathecal, subcutaneous, intramuscular, intradermal, intra-arterial, intravenous, intrabronchial, inhalation, and topical administration. Suitable compositions and dosage forms include, for example, tablets, capsules, caplets, pills, gel caps, troches, dispersions, suspensions, solutions, syrups, granules, beads, transdermal patches, gels, powders, pellets, magmas, lozenges, creams, pastes, plasters, lotions, discs, suppositories, liquid sprays for nasal or oral administration, dry powder or aerosolized formulations for inhalation, compositions and formulations for intravesical administration and the like. It should be understood that the formulations and compositions described herein are not limited to the particular formulations and compositions that are described herein. Dosing The therapeutically effective amount or dose of a compound described herein depends on the age, sex and weight of the patient, the current medical condition of the patient and the progression of a disease state in the patient being treated. The skilled artisan is able to determine appropriate dosages depending on these and other factors. Attorney Docket No.047162-7528WO1(02689) A suitable dose of a compound described herein can be in the range of from about 0.01 mg to about 5,000 mg per day, such as from about 0.1 mg to about 1,000 mg, for example, from about 1 mg to about 500 mg, such as about 5 mg to about 250 mg per day. The dose may be administered in a single dosage or in multiple dosages, for example from 1 to 4 or more times per day. When multiple dosages are used, the amount of each dosage may be the same or different. For example, a dose of 1 mg per day may be administered as two 0.5 mg doses, with about a 12-hour interval between doses. It is understood that the amount of compound dosed per day may be administered, in non-limiting examples, every day, every other day, every 2 days, every 3 days, every 4 days, or every 5 days. For example, with every other day administration, a 5 mg per day dose may be initiated on Monday with a first subsequent 5 mg per day dose administered on Wednesday, a second subsequent 5 mg per day dose administered on Friday, and so on. In the case wherein the patient’s status does improve, upon the doctor’s discretion the administration of the compound(s) described herein is optionally given continuously; alternatively, the dose of drug being administered is temporarily reduced or temporarily suspended for a certain length of time (i.e., a “drug holiday”). The length of the drug holiday optionally varies between 2 days and 1 year, including by way of example only, 2 days, 3 days, 4 days, 5 days, 6 days, 7 days, 10 days, 12 days, 15 days, 20 days, 28 days, 35 days, 50 days, 70 days, 100 days, 120 days, 150 days, 180 days, 200 days, 250 days, 280 days, 300 days, 320 days, 350 days, or 365 days. The dose reduction during a drug holiday includes from 10%-100%, including, by way of example only, 10%, 15%, 20%, 25%, 30%, 35%, 40%, 45%, 50%, 55%, 60%, 65%, 70%, 75%, 80%, 85%, 90%, 95%, or 100%. Once improvement of the patient’s conditions has occurred, a maintenance dose is administered if necessary. Subsequently, the dosage or the frequency of administration, or both, is reduced to a level at which the improved disease is retained. In certain embodiments, patients require intermittent treatment on a long-term basis upon any recurrence of symptoms and / or infection. The compounds described herein can be formulated in unit dosage form. The term “unit dosage form” refers to physically discrete units suitable as unitary dosage for patients undergoing treatment, with each unit containing a predetermined quantity of active material calculated to produce the desired therapeutic effect, optionally in association with a suitable pharmaceutical carrier. The unit dosage form may be for a single daily dose or one of multiple daily doses (e.g., about 1 to 4 or more times per day). When multiple daily doses are used, the unit dosage form may be the same or different for each dose. Attorney Docket No.047162-7528WO1(02689) Toxicity and therapeutic efficacy of such therapeutic regimens are optionally determined in cell cultures or experimental animals, including, but not limited to, the determination of the LD50 (the dose lethal to 50% of the population) and the ED50 (the dose therapeutically effective in 50% of the population). The dose ratio between the toxic and therapeutic effects is the therapeutic index, which is expressed as the ratio between LD50 and ED50. The data obtained from cell culture assays and animal studies are optionally used in formulating a range of dosage for use in human. The dosage of such compounds lies preferably within a range of circulating concentrations that include the ED50with minimal toxicity. The dosage optionally varies within this range depending upon the dosage form employed and the route of administration utilized. It should be understood that the method, the compositions and the kits that would be useful in the present invention are not limited to the particular formulations set forth in the examples. The following examples are put forth so as to provide those of ordinary skill in the art with a complete disclosure and description of how to make and use the cells, expansion and culture methods, protein purification methods, and therapeutic methods of the invention, and are not intended to limit the scope of what the inventor regards as his invention. The practice of the present invention employs, unless otherwise indicated, conventional techniques of chemistry, molecular biology (including recombinant techniques), microbiology, cell biology, biochemistry and immunology, which are well within the purview of the skilled artisan. Such techniques are explained fully in the literature, such as, “Molecular Cloning: A Laboratory Manual”, second edition (Sambrook, 1989); “Oligonucleotide Synthesis” (Gait, 1984); “Animal Cell Culture” (Freshney, 1987); “Methods in Enzymology” “Handbook of Experimental Immunology” (Weir, 1996); “Gene Transfer Vectors for Mammalian Cells” (Miller and Calos, 1987); “Current Protocols in Molecular Biology” (Ausubel, 1987); “PCR: The Polymerase Chain Reaction”, (Mullis, 1994); “Current Protocols in Immunology” (Coligan, 1991). These techniques are applicable to the production of the polynucleotides and polypeptides of the invention, and, as such, may be considered in making and practicing the invention. Particularly useful techniques for particular embodiments will be discussed in the sections that follow. It is to be understood that, wherever values and ranges are provided herein, the description in range format is merely for convenience and brevity and should not be construed as an inflexible limitation on the scope of the invention. Accordingly, all values and ranges encompassed by these values and ranges are meant to be encompassed within the scope of the present invention. Moreover, all values that fall within these ranges, as well as Attorney Docket No.047162-7528WO1(02689) the upper or lower limits of a range of values, are also contemplated by the present application. The description of a range should be considered to have specifically disclosed all the possible sub-ranges as well as individual numerical values within that range and, when appropriate, partial integers of the numerical values within ranges. For example, description of a range such as from 1 to 6 should be considered to have specifically disclosed sub-ranges such as from 1 to 3, from 1 to 4, from 1 to 5, from 2 to 4, from 2 to 6, from 3 to 6 etc., as well as individual numbers within that range, for example, 1, 2, 2.7, 3, 4, 5, 5.3, and 6. This applies regardless of the breadth of the range. The contents of the articles, patents, and patent applications, and all other documents and electronically available information mentioned or cited herein, are hereby incorporated by reference in their entirety to the same extent as if each individual publication was specifically and individually indicated to be incorporated by reference. Applicants reserve the right to physically incorporate into this application any and all materials and information from any such articles, patents, patent applications, or other physical and electronic documents. While the present invention has been described with reference to the specific embodiments thereof, it should be understood by those skilled in the art that various changes may be made and equivalents may be substituted without departing from the true spirit and scope of the invention. It will be readily apparent to those skilled in the art that other suitable modifications and adaptations of the methods described herein may be made using suitable equivalents without departing from the scope of the embodiments disclosed herein. In addition, many modifications may be made to adapt a particular situation, material, composition of matter, process, process step or steps, to the objective, spirit and scope of the present invention. All such modifications are intended to be within the scope of the claims appended hereto. Having now described certain embodiments in detail, the same will be more clearly understood by reference to the following examples, which are included for purposes of illustration only and are not intended to be limiting. The following examples further illustrate aspects of the present invention. However, they are in no way a limitation of the teachings or disclosure of the present invention as set forth herein. EXAMPLES The invention is now described with reference to the following Examples. These Examples are provided for the purpose of illustration only and the invention should in no way Attorney Docket No.047162-7528WO1(02689) be construed as being limited to these Examples, but rather should be construed to encompass any and all variations which become evident as a result of the teachings provided herein. Example 1 Materials and Methods In vivo self-regression of squamous cell carcinoma (keratoacanthoma type) with genetic analysis Tumors clinically compatible with squamous cell carcinoma were subjected to a partial (25%) biopsy from 12 to 3 o’clock. These tumors were then followed for one month’s time, if the initial biopsy results were compatible with squamous cell carcinoma. If at follow- up, the tumor was regressing (overall, flattening out and >50% smaller), then the tumor was classified as keratoacanthoma. If at follow-up the tumor was not regressing, then the tumor was classified as squamous cell carcinoma (i.e., not self-regressing). Regardless of classification as regressing or non-regressing squamous cell carcinoma, tumors were sequenced, at the initial time point and the follow-up time point, via high-density, genome- wide single nucleotide polymorphism genotyping as well as paired whole-exome sequencing using blood leukocytes as the control. Regions of lesional tissue used for DNA sequencing were selected for > 50% tumor cells. Exome data were used to analyze tissue-specific somatic mutations, excluding variants in control datasets. Sanger sequencing was further used to verify mutation status on laser capture microdissected tissues (Lim, et al, J Invest Dermatol, 2016;136:1737) p53β expression Tumors compatible with keratoacanthoma as well as normal flanking epidermis were stained with KJC8 antibody that specifically detects the expression of p53β isoforms. “KJC8 detects the epitope (DQTSFQKENC) present in p53β, Δ40p53β, Δ133p53β and Δ 160p53β. A 20 µg / mL dilution of KJC8 was used on formalin-fixed, paraffin-embedded samples. Samples were processed in xylene, then absolute ethanol. Endogenous peroxidase was quenched with 3% H202 / methanol for 10 min, with slides washed in phosphate buffered saline (PBS). Slides were treated in microwave using citrate at pH 6.0 for 25 min at 95°C. Slides were then cooled, transferred to PBS, blocked with 10% bovine serum albumin / PBS for 1 hour at 37°C. Excess was blotted off with incubation of primary antibody using Van Gogh diluent (BioCare) overnight at 4°C. Slides were washed with PBS / Tween 0.05% for 4 min. A secondary antibody (Envision Dual link; Dako, Carpinteria, California, USA) was Attorney Docket No.047162-7528WO1(02689) applied for 30 min. Subsequent washing was with PBS-T and PBS before application of diaminobenzidine until color developed with washing in H20 before counterstaining with Mayer’s haematoxylin. Staining of <10% of the tumor was considered negative. Staining of >50% of the tumor was considered positive as previously described (Ko, et al, J Clin Pathol, 2018;71:1120). Propensity score matching For evaluation of systemic SRSF3 inhibition, using a publicly available dataset, individuals on digoxin or amiodarone (both SRSF3 inhibitors) were compared with individuals on beta-blockers and assessed for the likelihood of developing squamous cell carcinoma over time. SRSF3 expression in squamous cell carcinoma vs. keratoacanthoma The expression of SRSF3 in squamous cell carcinoma and keratoacanthoma was evaluated using publicly available RNA-seq data (Srivastava, et al, Cancer Res, 2022;82:3143). Human tissue samples For evaluation of SRSF3 inhibition by SFI003, two-dimensional and three- dimensional keratinocyte models were assessed for differentiation genes (early: K1 and MAF; late: IVL, LCE3D, CASP14, FLG) at 48 hours after treatment with 10 micromolar of SFI003 vs vehicle (0.1% DMSO). SRSF3 mRNA levels were measured in keratinocytes as well as 4 squamous cell carcinoma cell lines (A431, Cal27, SCCIC1, SCC13). Human organoids were also treated with vehicle (DMSO) vs SFI003, with assessment of differentiation and proliferation. In brief, all cells were maintained at appropriate temperatures and conditions. Primary human keratinocytes from freshly discarded surgical specimens were cultured in necessary conditions. Human skin organoids were derived from keratinocytes seeded onto devitalized human dermis and cultured at the air-liquid interface. For histopathologic analysis, human skin organoids were processed, embedded, and mounted onto slides that were then incubated under appropriate conditions with primary and secondary antibodies. Attorney Docket No.047162-7528WO1(02689) Results Although early stage SCC accounts for greater than 95% of SCC cases, there is currently no approved medical treatment and the existing standard of care is surgical excision (FIG.1). Excision therapy has several drawbacks including high morbidity and cost for the patient and high cost to the healthcare system. For example, at least two appointments are needed and there can be long wait times to schedule the appointments. Additionally, excision can lead to scarring, bleeding, and infection. Further, many SCC patients present with multiple SCC lesions at the same time, but simultaneous excision surgery is not feasible (FIG.2). As such, a medical treatment for early stage SCC is needed which would be safer and less costly than excision therapy. The tumor suppressor protein p53 is knows as the guardian of the genome. It is negatively regulated by MDM2 which involves many complex interactions (FIG.3)(Nag, et al., J Biomed Res, 2013;27:254). It is well-known that the gene encoding p53 is the most frequently mutated gene in human cancers (FIG.4). A splicing variant of p53 known as the p53 beta isoform (p53β) leads to cancer regression (FIG.4)( Camus, et al, Cell Cycle, 2012;11:1646; Fujita, et al., Nat Cell Biol, 2009;11:1135). In keratoacanthoma (a self- regressing form of squamous cell carcinoma), tumors in the growth stage (at the initial time point) had mutations in TP53 as well as NOTCH genes by whole exome sequencing. Keratoacanthoma tumors that were regressing no longer had mutations in TP53 as well as NOTCH genes by whole exome sequencing. Specifically, TP53 was mutated in the C- terminal domain at a splice site for p53β; this mutation is not the typical mutation found in cancers, including non-regressing squamous cell carcinoma, as the typical mutations are found in the DNA-binding domain. Serine / arginine-rich splicing factor 3 (SRSF3) modulates the splicing of numerous genes, is upregulated in various types of human cancers, and can promote cell neoplastic transformation when overexpressed. Additionally, SRSF3 has been shown to be a direct regulator of p53. Specifically, knockdown of SRSF3 in human fibroblasts resulted in increased p53β that promotes cellular senescence (FIG.5)(Tang, et al., Oncogene, 2013, 32(22): 2792–2798). More recently, a small molecule inhibitor of SRSF3 (SFI003) was synthesized and shown to promote differentiation of colorectal cancer cells and to exhibit potent antitumor efficacy in vitro and in vivo, by driving apoptosis of CRC cells via the SRSF3 / DHCR24 / reactive oxygen species (ROS) axis (FIG.6)(Zhang, et al., Cell Death Discov., 2022, 8, Article Number 238). Attorney Docket No.047162-7528WO1(02689) In order to assess the effect of systemic SRSF3 inhibition on SCC incidence, data were analyzed from the Eversana 2010-present database of anonymized medical records. Specifically, the incidence of SCC in patients with a history of atrial fibrillation or heart failure was examined because certain patients received digoxin or amiodarone, which are known SRSF3 inhibitors. SCC incidence in patients treated with digoxin (n = 4149) was compared to SCC incidence in patients who never received digoxin but received beta- blockers (n=100,000, downsampled). Propensity score matching was performed to control for baseline confounders, inclusive of age, gender, race year of inclusion, comorbidities, diagnostic, procedure, and medication codes, and empirical candidate covariates. Statistical methods including logistic regression and LASSO regularization were used. After propensity score matching, n=4135 in each group. Similar methods were used for patients on amiodarone (n=9,579) with a history of atrial fibrillation or heart failure. After propensity score matching, n=9,197 for amiodarone-treated patients vs. beta-blocker-treated patients. The analysis shows that, with systemic SRSF3 inhibition, more individuals are free of SCC (FIG.7). Keratoacanthoma is a subtype of squamous cell cancer that grows rapidly but is also known to spontaneously regress. As demonstrated herein, tissue biopsies of keratoacanthoma and self-regressing keratoacanthoma reveal terminal differentiation in the self-regressed keratoacanthoma tissues (FIG.8). TP53 and NOTCH1 / 2 mutations were present in the non- regressing stage and absent in the regressing stage. A specific TP53 mutation is associated with a regressing tumor, with increased levels of p53β. While it is difficult to target mutated p53, p53β is targetable via SRSF3 protein. Previously, it was shown that p53β expression is increased in regressing tumors and terminally differentiating keratinocytes (FIGs.9A – 9D) (Ko, et al, J Clin Pathol, 2018;71:1120). In contrast, as demonstrated herein, SCC tissues show high levels of SRSF3 and low levels of p53β (FIG.10). Additionally as demonstrated herein, SRSF3 levels are approximately 25% lower in keratoacanthoma cells compared to SRSF3 levels SCC cells (FIG.11). Next, SFI003 was used in two-dimensional and three-dimensional keratinocyte models, which were examined using fluorescence microscopy. The results show upregulation of six differentiation genes (K1, MAF, IVL, LCE3D, CASP14, and FLG)(FIG.12). Together, the data disclosed herein strongly support the idea as contemplated herein that inhibitors of SRSF3, such as SFI003, can be used to treat or prevent squamous cell carcinoma. Attorney Docket No.047162-7528WO1(02689) Example 2 Materials and Methods Novel small molecule inhibitors of SRSF3 were designed using the known SRSF3 inhibitor SFI003 as a starting compound. Homology modeling and molecular docking of SFI003 to SRSF3 (FIG.13) was previously described (Zhang, et al., Cell Death Discov., 2022, 8, Article Number 238) as follows: The well-prepared and minimized SRSF3 homology model was constructed by using Discover Studio. The three-dimensional structures of SRSF3 were evaluated according to the probability density function value or DOPE score in view of atomic statistical potential energy. Based on the optimal three-dimensional structure of SRSF3, we then applied Glide molecular docking software to screen small molecule compounds from the databases (ChemDiv, ChemBridge, Specs, etc.) using different precision scoring functions (HTVS, SP, and XP). The physiochemical properties of SFI003 are as follows: Property (SciFinder) Value Freely Rotatable Bonds 4 H Acceptors 6 H Donors 2 H Donor / Acceptor Sum 8 logP (predicted) 4.592 ± 0.479 Molecular Weight 363.44 pKa (predicted) 10.39 To design novel small molecule inhibitors of SRSF3, focus was placed on modifications that would be preferred for topical administration, i.e., compounds were designed to penetrate the skin while minimizing systemic exposure. As such, the following guidelines were followed: given the relationship between molecular properties and skin permeability, there have emerged certain (Lipinski-like) ‘rules’ that a drug must satisfy, in addition to potent pharmacological activity, to become a feasible candidate for TDD (transdermal drug delivery): (a) modest molecular weight (MW < 400 to 500 Da), (b) a balanced lipophilicity (log{octanol–water partition coefficient}, log P, ideally around 2 to 3), Attorney Docket No.047162-7528WO1(02689) and (c) a measurable solubility both in oil and in water (given that TDD requires both breaching the lipophilic stratum corneum and resorption into the aqueous central compartment of the systemic circulation (Wiedersberg and Guy, 2014, Journal of Controlled Release, 190: 150-156). As such, small modifications of SFI003 were introduced at the solvent exposed portion and / or non-essential (for binding) parts of SFI003, using the molecular docking of SFI003 (FIG.13) as a guide, to both decrease the molecular weight and decrease the log P. For example, adding nitrogen to certain positions of SFI003 is expected to decrease log P and / or increase hydrophilicity. Additionally, replacing the aryl methoxy group of SFI003 with suitable bioisosteres is predicted to improve metabolic stability while maintaining the desired pharmacological properties. Immunofluorescence-based SRSF3 or DHCR24 protein levels are not a suitable readout of SRSF3 activity and its inhibition by drugs. As such, immunofluorescence-based Cyclin D1 protein level quantification was developed as a cell-based readout of SRSF3 activity. Cell cycle analysis was also performed (DNA content quantification based on DAPI- stained images). Results The following compounds were designed which are predicted to be inhibitors of SRSF3. The compounds are also predicted to have an effective level of skin permeability. = 313.38; Log P = 2.63 (ChemDraw prediction) (E)-2- -4-(4-methoxyphenyl)thiazole. Referred to herein as Y-0309741. = 312.39; Log P = 3.22 (ChemDraw prediction) (E)-2- -4-(4-methoxyphenyl)thiazole. Referred to herein as Y-0309742. Attorney Docket No.047162-7528WO1(02689) = 313.38; Log P = 2.6 (ChemDraw prediction) (i.e., hydrazineyl)-4-(6-methoxypyridin-3- yl) . = 342.42; Log P = 3.05 (ChemDraw (i.e., (E)-2-(2-(1-(4,5-dimethyl-1H-imidazol-2-yl)ethylidene)hydrazineyl)-4-(6- methoxypyridin-3-yl)thiazole). = 314.37; Log P = 2.0 (ChemDraw prediction) (i.e., hydrazineyl)-4-(6-methoxypyridin-3- yl)thiazole). Referred to herein as Y-0309744. Log P = 5.76 (ChemDraw prediction) (i.e., ethylidene)hydrazineyl)-4-(4- (trifluoromethoxy)phenyl)thiazole). Referred to herein as Y-0309745. Attorney Docket No.047162-7528WO1(02689) Log P = 4.28 (ChemDraw prediction) (i.e., hydrazineyl)-4-(4- . to herein as Y-0309746. Log P = 4.67 (ChemDraw prediction) (i.e., yl)ethylidene)hydrazineyl)-4-(4- (methylthio)phenyl)thiazole). Log P = 3.19 (ChemDraw prediction) (i.e., hydrazineyl)-4-(4- (methylthio)phenyl)thiazole). Referred to herein as Y-0309747. Log P = 3.73 (ChemDraw prediction) (i.e., 2-yl)ethylidene)hydrazineyl)thiazol-4-yl)-N- methylaniline). Referred to herein as Y-0309749. Attorney Docket No.047162-7528WO1(02689) Log P = 2.25 (ChemDraw prediction) (i.e., ethylidene)hydrazineyl)thiazol-4-yl)-N- . as 0309748. Log P = 4.52 (ChemDraw prediction) (i.e., ethylidene)hydrazineyl)thiazol-4- yl)phenyl)-2,2,2-trifluoro-N-methylacetamide). Referred to herein as Y-0309750. Log P = 3.04 (ChemDraw prediction) (i.e., (E)- N-(4- thiazol-4-yl)phenyl)-2,2,2-trifluoro- N-methylacetamide). Referred to herein as Y-0309751. Next, several of the compounds were tested for their ability to inhibit SRSF3. Specifically, cells were treated with inhibitor at various concentrations for 48 hours and cell viability was assessed. An immunofluorescence-based Cyclin D1 protein level quantification assay was developed as a cell-based readout of SRSF3 activity. Additionally, for certain inhibitors, cell cycle analysis was also performed (DNA content quantification based on DAPI-stained images). Dose-dependent toxicity, accumulation of Cyclin D1 (aberrant splicing, non- functional protein assumed), and S / G2 / M arrest were observed when cells were treated with the known SRSF3 inhibitor SFI003 (FIGs.14A – 14C). The novel compound Y-0309750 unexpectedly shows toxicity, cyclin D1 increase, and G2 arrest very similar to the SFI003 parent compound (FIGs.15A—15D). The IC50 for Y-0309750 was measured to be 9.8 uM compared to 8.7 uM for SFI003 (FIG.15A). The novel compound Y-0309749 also shows toxicity, cyclin D1 increase and G2 arrest, albeit the activity is slightly lower compared to the Attorney Docket No.047162-7528WO1(02689) SFI003 parent compound (FIGs.16A – 16D). The novel compound Y-0309745 shows toxicity similar to SFI003, and also shows cyclin D1 increase and G2 arrest, but these activities are lower compared to SFI003 (FIGs.17A – 17D). Some of the remaining compounds tested were toxic, but did not affect Cyclin D1 levels. As such, the toxicity is likely non-specific. The data for Y-0309747 are shown in FIGs.18A – 18B. The data for Y-0309751 are shown in FIGs.19A – 19B. The data for Y- 0309748 are shown in FIGs.20A – 20B. The data for Y-0309746 are shown in FIGs.21A – 21B. The data for Y-0309741 are shown in FIGs.22A – 22B. The data for Y-0309742 are shown in FIGs.23A – 23B. The data for Y-0309743 are shown in FIGs.24A – 24B. The data for Y-0309744 are shown in FIGs.25A – 25B. Overall, the most active compound showing SRSF3 inhibition is Y-0309750. Other compounds showing strong SRSF3 inhibition include Y-0309749 and Y-0309745. Other compounds with detectable SRSF3 inhibition activity include Y-0309747, Y-0309751, and Y-0309748. The compounds which do not appear to be SRSF3 inhibitors based on these data include Y-0309741, Y-0309742, Y-0309743, Y-0309744, and Y-0309746. Based on these results, it is concluded that the fused benzene ring (i.e., of SFI003, Y-0309750, Y-0309749, and Y-0309745) is essential for strong SRSF3 inhibition. Additionally, replacing the methoxy group of SFI003 with trifluoromethyl or methylamine leads to a modest decrease in inhibition activity. Enumerated embodiments: The following exemplary embodiments are provided, the numbering of which is not to be construed as designating levels. Embodiment 1: A method of treating or preventing squamous cell carcinoma (SCC) in a subject in need thereof, the method comprising administering to the subject a pharmaceutical composition comprising an effective amount of a serine / arginine-rich splicing factor 3 (SRSF3) inhibitor. Embodiment 2: The method of embodiment 1, wherein the pharmaceutical composition is a topical formulation that is administered to the skin of the subject. Embodiment 3: The method of embodiment 1 or embodiment 2, wherein the SRSF3 inhibitor is a small molecule having molecular mass less than about 600 g / mol. Attorney Docket No.047162-7528WO1(02689) Embodiment 4: The method of any one of embodiments 1-3, wherein the SRSF3 inhibitor is characterized by an effective level of skin permeability and / or is formulated in a topical formulation to exhibit an effective level of skin permeability. Embodiment 5: The method of any one of embodiments 1-4, wherein the SRSF3 inhibitor reduces SRSF3 amount or activity in SCC cells by at least about 10%, at least about 15%, at least about 20%, at least about 25%, at least about 30%, at least about 35%, at least about 40%, at least about 45%, at least about 50%, at least about 55%, at least about 60%, at least about 65%, at least about 70%, at least about 75%, at least about 80%, at least about 85%, at least about 90%, at least about 95%, or at least about 100% compared to SRSF3 amount or activity in SCC cells in the absence of the SRSF3 inhibitor. Embodiment 6: The method of any one of embodiments 1-5, wherein the SRSF3 inhibitor induces terminal differentiation of SCC cells. Embodiment 7: The method of any one of embodiments 1-6, wherein the SRSF3 inhibitor is a compound of Formula (I), or a salt, stereoisomer, or isotopologue thereof: , wherein: ; the group consisting of H, CN, NO2, ORA, N(RA)(RB), SRA, C(=O)RA, C(=O)ORA, C(=O)N(RA)(RB), S(=O)RA, S(=O)2RA, S(=O)N(RA)(RB), S(=O)2N(RA)(RB), P(=O)(ORA)(ORB), halogen, optionally substituted C1-C6 alkyl, optionally substituted C3-C8 cycloalkyl, optionally substituted C2-C8 heterocycloalkyl, optionally substituted C6-C10 aryl, and optionally substituted C2-C8heteroaryl; Attorney Docket No.047162-7528WO1(02689) R4is selected from the group consisting of H and optionally substituted C1-C6 alkyl; R5is selected from the group consisting of H and optionally substituted C1-C6 alkyl; R6is selected from the group consisting of H, optionally substituted C1-C6 alkyl, optionally substituted C3-C8cycloalkyl, optionally substituted C2-C8heterocycloalkyl, optionally substituted C6-C10 aryl, and optionally substituted C2-C8 heteroaryl; R7a, R7b, and R7c, if present, are each independently selected from the group consisting of H, CN, NO2, ORA, N(RA)(RB), C(=O)RA, C(=O)ORA, C(=O)N(RA)(RB), S(=O) halogen, optionally substituted C2-C8 heteroaryl, wherein R7aand R7bcan combine with the atoms to which they are bound to form an optionally substituted C6-C10 aryl or optionally substituted C2-C8heteroaryl; X1selected from the group consisting of N and CR7c; Z1is CR8aor N, Z2is CR8bor N, Z3is CR8cor N, Z4is CR8dor N, and Z5is CR8eor N, wherein no more than two of Z1, Z2, Z3, Z4, and Z5are N; R8a, R8b, R8c, R8d, and R8e, if present, are each independently selected from the group consisting of H, CN, NO2, ORA, N(RA)(RB), SRA, halogen, optionally substituted C1-C6 alkyl, optionally substituted C3-C8 cycloalkyl, optionally substituted C2-C8heterocycloalkyl, optionally substituted C6-C10aryl, and optionally substituted C2-C8 heteroaryl; each occurrence of RAand RB, if present, is independently selected from the group consisting of H, optionally substituted C1-C6 alkyl, optionally substituted C3-C8 cycloalkyl, optionally substituted C2-C8 heterocycloalkyl, optionally substituted C6- C10 aryl, optionally substituted C2-C8 heteroaryl, C(=O)RC, C(=O)ORC, C(=O)N(RC)(RD), S(=O)RC, S(=O)2RC, S(=O)N(RC)(RD), S(=O)2N(RC)(RD), and the group consisting of H, optionally substituted C1-C6alkyl, optionally substituted C3-C8 Attorney Docket No.047162-7528WO1(02689) cycloalkyl, optionally substituted C2-C8 heterocycloalkyl, optionally substituted C6- C10aryl, and optionally substituted C2-C8heteroaryl. Embodiment 8: The method of embodiment 7, wherein the SRSF3 inhibitor is a compound of Formula (I), wherein at least one of the following applies: (a) R7a, R7b, and R7c, if present, are each independently selected from the group consisting of H, CN, NO2, ORA, N(RA)(RB), C(=O)RA, C(=O)ORA, C(=O)N(RA) S S S N S2N , P(=O)(ORA) substituted C3- optionally substituted C6-C10aryl, and optionally substituted C2-C8heteroaryl; (b) R7aand R7bcan combine with the atoms to which they are bound to form a substituted C6-C10aryl or optionally substituted C2-C8heteroaryl; (c) R7aand R7bcan combine with the atoms to which they are bound to form unsubstituted phenyl, and R8c, if present, is selected from the group consisting of H, CN, NO2, SRA, NH(substituted C1-C6 alkyl), NH(optionally substituted C2-C6alkyl), halogen, optionally substituted C1-C6alkyl, substituted C1-C6alkoxy, optionally substituted C2-C6 alkoxy, optionally substituted C3-C8 cycloalkyl, optionally substituted C2-C8heterocycloalkyl, optionally substituted C6-C10 aryl, and optionally substituted C2-C8 heteroaryl; (d) R7aand R7bcan combine with the atoms to which they are bound to form unsubstituted phenyl, R8cis N(RA)(RB), and RAis C(=O)RC; and (e) R8cis N(RA)(RB), and RAis C(=O)RC. Embodiment 9: The method of embodiment 7 or 8, wherein R6is H. Embodiment 10: The method of any one of embodiments 7-9, wherein one of the following applies: (a) R7aand R7bare each independently selected from the group consisting of H and CH3; or (b) R7aand R7bcombine with the atoms to which they are bound to . Attorney Docket No.047162-7528WO1(02689) Embodiment 11: The method of any one of embodiments 7-10, wherein X1is selected from the group consisting of N and CH. Embodiment 12: The method of any one of embodiments 7-11, wherein R1is selected from . the following applies: (a) Z1is CR8a, Z2is N, Z3is CR8c, Z4is CR8d, and Z5is CR8e; or (b) Z1is CR8a, Z2is CR8b, Z3is CR8c, Z4is CR8d, and Z5is CR8e. Embodiment 14: The method of any one of embodiments 7-13, wherein R8a, R8b, R8d, and R8eare each independently H. Embodiment 15: The method of any one of embodiments 7-14, wherein R8cis selected from the group consisting of O(C1-C6 alkyl), O(C1-C6 haloalkyl), S(C1-C6 alkyl), NH(C1-C6 alkyl), and N(C1-C6 alkyl)C(=O)(C1-C6 haloalkyl), optionally wherein R8cis selected from the group consisting of OCH3, OCF3, SCH3, NHCH3, and N(CH3)C(=O)CF3. Embodiment 16: The method of any one of embodiments 7-15, wherein R2is selected from , Embodiment 17: The method of any one of embodiments 7-16, wherein R3is H. Embodiment 18: The method of any one of embodiments 7-17, wherein R4is H. Embodiment 19: The method of any one of embodiments 7-18, wherein R5is CH3. Attorney Docket No.047162-7528WO1(02689) Embodiment 20: The method of any one of embodiments 7-19, wherein the compound of formula (I) is selected from the group consisting of: (E)-2-(2-(1-(1H-benzo[d]imidazol-2-yl)ethylidene)hydrazineyl)-4-(4- methoxyphenyl)thiazole; (E)-4-(2-(2-(1-(1H-benzo[d]imidazol-2-yl)ethylidene)hydrazineyl)thiazol-4- yl)-N-methylaniline; (E)-2-(2-(1-(1H-pyrrol-2-yl)ethylidene)hydrazineyl)-4-(4- methoxyphenyl)thiazole; (E)-2-(2-(1-(1H-imidazol-2-yl)ethylidene)hydrazineyl)-4-(4- methoxyphenyl)thiazole; (E)-2-(2-(1-(1H-pyrrol-2-yl)ethylidene)hydrazineyl)-4-(6-methoxypyridin-3- yl)thiazole; (E)-2-(2-(1-(4,5-dimethyl-1H-imidazol-2-yl)ethylidene)hydrazineyl)-4-(6- methoxypyridin-3-yl)thiazole; (E)-2-(2-(1-(1H-imidazol-2-yl)ethylidene)hydrazineyl)-4-(6-methoxypyridin- 3-yl)thiazole; (E)-2-(2-(1-(1H-benzo[d]imidazol-2-yl)ethylidene)hydrazineyl)-4-(4- (trifluoromethoxy)phenyl)thiazole; (E)-2-(2-(1-(1H-imidazol-2-yl)ethylidene)hydrazineyl)-4-(4- (trifluoromethoxy)phenyl)thiazole; (E)-2-(2-(1-(1H-benzo[d]imidazol-2-yl)ethylidene)hydrazineyl)-4-(4- (methylthio)phenyl)thiazole; (E)-2-(2-(1-(1H-imidazol-2-yl)ethylidene)hydrazineyl)-4-(4- (methylthio)phenyl)thiazole; (E)-4-(2-(2-(1-(1H-imidazol-2-yl)ethylidene)hydrazineyl)thiazol-4-yl)-N- methylaniline; (E)-N-(4-(2-(2-(1-(1H-benzo[d]imidazol-2-yl)ethylidene)hydrazineyl)thiazol- 4-yl)phenyl)-2,2,2-trifluoro-N-methylacetamide; and (E)-N-(4-(2-(2-(1-(1H-imidazol-2-yl)ethylidene)hydrazineyl)thiazol-4- yl)phenyl)-2,2,2-trifluoro-N-methylacetamide. Embodiment 21: The method of any one of embodiments 1-20, wherein the SRSF3 inhibitor is selected from the group consisting of: (a) SFI003, or a salt, solvate, stereoisomer, isotopologue, or tautomer thereof; Attorney Docket No.047162-7528WO1(02689) (b) (E)-N-(4-(2-(2-(1-(1H-benzo[d]imidazol-2-yl)ethylidene)hydrazineyl)thiazol- 4-yl)phenyl)-2,2,2-trifluoro-N-methylacetamide), or a salt, solvate, stereoisomer, isotopologue, or tautomer thereof; (c) (E)-4-(2-(2-(1-(1H-benzo[d]imidazole-2-yl)ethylidene)hydrazineyl)thiazol-4- yl)-N-methylaniline), or a salt, solvate, stereoisomer, isotopologue, or tautomer thereof; and (d) (E)-2-(2-(1-(1H-benzo[d]imidazol-2-yl)ethylidene)hydrazineyl)-4-(4- (trifluoromethoxy)phenyl)thiazole), or a salt, solvate, stereoisomer, isotopologue, or tautomer thereof. Embodiment 22: The method of any one of embodiments 1-21, wherein the SRSF3 inhibitor is the only anticancer agent administered to the subject. Embodiment 23: The method of any one of embodiments 1-22, further comprising administering to the subject at least one additional agent or therapy useful for treating or preventing the SCC, optionally wherein the additional agent or therapy comprises surgical resection of at least one SCC lesion. Embodiment 24: The method of any one of embodiments 1-23, wherein the topical formulation comprises a gel or an ointment. Embodiment 25: The method of any one of embodiments 1-24, wherein the SCC is early- stage cutaneous SCC. Embodiment 26: The method of any one of embodiments 1-25, wherein the subject has multiple simultaneous SCC lesions. Embodiment 27: The method of any one of embodiments 1-26, wherein the subject is a mammal. Embodiment 28: The method of any one of embodiments 1-27, wherein the subject is a human. Attorney Docket No.047162-7528WO1(02689) Embodiment 29: A pharmaceutical composition comprising a serine / arginine-rich splicing factor 3 (SRSF3) inhibitor, for use in the method of any one of embodiments 1-28. Embodiment 30: A pharmaceutical composition comprising a serine / arginine-rich splicing factor 3 (SRSF3) inhibitor. Embodiment 31: The pharmaceutical composition of embodiment 30, wherein the pharmaceutical composition is a topical formulation for administration to skin. Embodiment 32: The pharmaceutical composition of embodiment 30 or embodiment 31, wherein the SRSF3 inhibitor is a small molecule having molecular mass less than about 600 g / mol. Embodiment 33: The pharmaceutical composition of and one of embodiments 30-32, wherein the SRSF3 inhibitor is characterized by an effective level of skin permeability and / or is formulated in a topical formulation to exhibit an effective level of skin permeability. Embodiment 34: The pharmaceutical composition of any one of embodiments 30-33, wherein the SRSF3 inhibitor reduces SRSF3 amount or activity in squamous cell carcinoma (SCC) cells by at least about 10%, at least about 15%, at least about 20%, at least about 25%, at least about 30%, at least about 35%, at least about 40%, at least about 45%, at least about 50%, at least about 55%, at least about 60%, at least about 65%, at least about 70%, at least about 75%, at least about 80%, at least about 85%, at least about 90%, at least about 95%, or at least about 100% compared to SRSF3 amount or activity in SCC cells in the absence of the SRSF3 inhibitor. Embodiment 35: The pharmaceutical composition of any one of embodiments 30-34, wherein the SRSF3 inhibitor induces terminal differentiation of SCC cells. Embodiment 36: The pharmaceutical composition of any one of embodiments 30-35, wherein the topical formulation comprises a gel or an ointment. Attorney Docket No.047162-7528WO1(02689) Embodiment 37: The pharmaceutical composition of any one of embodiments 30-36, wherein the SRSF3 inhibitor is a compound of Formula (I), or a salt, stereoisomer, or isotopologue thereof: , wherein: ; the group consisting of H, CN, NO2, ORA, N(RA)(RB), SRA , C(=O)N(RA)(RB), S(=O)RA, S(=O)2RA, S(=O)N(RA)(RB), S(=O)2N(RA)(RB), P(=O)(ORA)(ORB), halogen, optionally substituted C1-C6alkyl, optionally substituted C3-C8cycloalkyl, optionally substituted C2-C8 heterocycloalkyl, optionally substituted C6-C10 aryl, and optionally substituted C2-C8heteroaryl; R4is selected from the group consisting of H and optionally substituted C1-C6 alkyl; R5is selected from the group consisting of H and optionally substituted C1-C6 alkyl; R6is selected from the group consisting of H, optionally substituted C1-C6 alkyl, optionally substituted C3-C8cycloalkyl, optionally substituted C2-C8heterocycloalkyl, optionally substituted C6-C10 aryl, and optionally substituted C2-C8 heteroaryl; R7a, R7b, and R7c, if present, are each independently selected from the group consisting of H, CN, NO2, ORA, N(RA)(RB), C(=O)RA, C(=O)ORA, C(=O)N(RA)(RB), S(=O)RA, S(=O)2RA, S(=O)N(RA)(RB), S(=O)2N(RA)(RB), P(=O)(ORA)(ORB), halogen, optionally substituted C1-C6alkyl, optionally substituted C3-C8cycloalkyl, optionally substituted C2-C8 heterocycloalkyl, optionally substituted C6-C10 aryl, and optionally substituted C2-C8 heteroaryl, Attorney Docket No.047162-7528WO1(02689) wherein R7aand R7bcan combine with the atoms to which they are bound to form an optionally substituted C6-C10aryl or optionally substituted C2-C8 heteroaryl; X1selected from the group consisting of N and CR7c; Z1is CR8aor N, Z2is CR8bor N, Z3is CR8cor N, Z4is CR8dor N, and Z5is CR8eor N, wherein no more than two of Z1, Z2, Z3, Z4, and Z5are N; R8a, R8b, R8c, R8d, and R8e, if present, are each independently selected from the group consisting of H, CN, NO2, ORA, N(RA)(RB), SRA, halogen, optionally substituted C1-C6 alkyl, optionally substituted C3-C8 cycloalkyl, optionally substituted C2-C8heterocycloalkyl, optionally substituted C6-C10aryl, and optionally substituted C2-C8 heteroaryl; each occurrence of RAand RB, if present, is independently selected from the group consisting of H, optionally substituted C1-C6 alkyl, optionally substituted C3-C8 cycloalkyl, optionally substituted C2-C8heterocycloalkyl, optionally substituted C6- C10 aryl, optionally substituted C2-C8 heteroaryl, C(=O)RC, C(=O)ORC, C(=O)N(RC)(RD), S(=O)RC, S(=O)2RC, S(=O)N(RC)(RD), S(=O)2N(RC)(RD), and P(=O)(ORC)(ORD); each occurrence of RCand RD, if present, is independently selected from the group consisting of H, optionally substituted C1-C6 alkyl, optionally substituted C3-C8 cycloalkyl, optionally substituted C2-C8heterocycloalkyl, optionally substituted C6- C10 aryl, and optionally substituted C2-C8 heteroaryl. Embodiment 38: The pharmaceutical composition of embodiment 37, wherein the SRSF3 inhibitor is a compound of Formula (I), wherein at least one of the following applies: (a) R7a, R7b, and R7c, if present, are each independently selected from the group consisting of H, CN, NO2, ORA, N(RA)(RB), C(=O)RA, C(=O)ORA, C(=O)N(RA) , P(=O)(ORA) substituted C3-C8 cycloalkyl, optionally substituted C2-C8 heterocycloalkyl, optionally substituted C6-C10 aryl, and optionally substituted C2-C8 heteroaryl; (b) R7aand R7bcan combine with the atoms to which they are bound to form a substituted C6-C10 aryl or optionally substituted C2-C8 heteroaryl; Attorney Docket No.047162-7528WO1(02689) (c) R7aand R7bcan combine with the atoms to which they are bound to form unsubstituted phenyl, and R8c, if present, is selected from the group consisting of H, CN, NO2, SRA, NH(substituted C1-C6 alkyl), NH(optionally substituted C2-C6alkyl), halogen, optionally substituted C1-C6alkyl, substituted C1-C6alkoxy, optionally substituted C2-C6 alkoxy, optionally substituted C3-C8 cycloalkyl, optionally substituted C2-C8heterocycloalkyl, optionally substituted C6-C10 aryl, and optionally substituted C2-C8 heteroaryl; (d) R7aand R7bcan combine with the atoms to which they are bound to form unsubstituted phenyl, R8cis N(RA)(RB), and RAis C(=O)RC; and (e) R8cis N(RA)(RB), and RAis C(=O)RC. Embodiment 39: The pharmaceutical composition of embodiment 37 or 38, wherein the SRSF3 inhibitor is the compound of Formula (I), wherein R6is H. Embodiment 40: The pharmaceutical composition of any one of embodiments 37-39, wherein the SRSF3 inhibitor is the compound of Formula (I), wherein one of the following applies: (a) R7aand R7bare each independently selected from the group consisting of H and CH3; or (b) R7aand R7bcombine with the atoms to which they are bound to . Embodiment 41: The pharmaceutical composition of any one of embodiments 37-40, wherein the SRSF3 inhibitor is the compound of Formula (I), wherein X1is selected from the group consisting of N and CH. Embodiment 42: The pharmaceutical composition of any one of embodiments 37-41, wherein the SRSF3 inhibitor is the compound of Formula (I), wherein R1is selected from the H N group . Attorney Docket No.047162-7528WO1(02689) Embodiment 43: The pharmaceutical composition of any one of embodiments 37-42, wherein the SRSF3 inhibitor is the compound of Formula (I), wherein one of the following applies: (a) Z1is CR8a, Z2is N, Z3is CR8c, Z4is CR8d, and Z5is CR8e; or (b) Z1is CR8a, Z2is CR8b, Z3is CR8c, Z4is CR8d, and Z5is CR8e. Embodiment 44: The pharmaceutical composition of any one of embodiments 37-43, wherein the SRSF3 inhibitor is the compound of Formula (I), wherein R8a, R8b, R8d, and R8eare each independently H. Embodiment 45: The pharmaceutical composition of any one of embodiments 37-44, wherein the SRSF3 inhibitor is the compound of Formula (I), wherein R8cis selected from the group consisting of O(C1-C6alkyl), O(C1-C6haloalkyl), S(C1-C6alkyl), NH(C1-C6alkyl), and N(C1-C6 alkyl)C(=O)(C1-C6 haloalkyl), optionally wherein R8cis selected from the group consisting of OCH3, OCF3, SCH3, NHCH3,and N(CH3)C(=O)CF3. Embodiment 46: The pharmaceutical composition of any one of embodiments 37-45, wherein the SRSF3 inhibitor is the compound of Formula (I), wherein R2is selected from the , Embodiment 47: The pharmaceutical composition of any one of embodiments 37-46, wherein the SRSF3 inhibitor is the compound of Formula (I), wherein R3is H. Embodiment 48: The pharmaceutical composition of any one of embodiments 37-47, wherein the SRSF3 inhibitor is the compound of Formula (I), wherein R4is H. Embodiment 49: The pharmaceutical composition of any one of embodiments 37-48, wherein the SRSF3 inhibitor is the compound of Formula (I), wherein R5is CH3. Attorney Docket No.047162-7528WO1(02689) Embodiment 50: The pharmaceutical composition of any one of embodiments 37-49, wherein the SRSF3 inhibitor is the compound of Formula (I), wherein the compound of formula (I) is selected from the group consisting of: (E)-2-(2-(1-(1H-benzo[d]imidazol-2-yl)ethylidene)hydrazineyl)-4-(4- methoxyphenyl)thiazole; (E)-4-(2-(2-(1-(1H-benzo[d]imidazol-2-yl)ethylidene)hydrazineyl)thiazol-4- yl)-N-methylaniline; (E)-2-(2-(1-(1H-pyrrol-2-yl)ethylidene)hydrazineyl)-4-(4- methoxyphenyl)thiazole; (E)-2-(2-(1-(1H-imidazol-2-yl)ethylidene)hydrazineyl)-4-(4- methoxyphenyl)thiazole; (E)-2-(2-(1-(1H-pyrrol-2-yl)ethylidene)hydrazineyl)-4-(6-methoxypyridin-3- yl)thiazole; (E)-2-(2-(1-(4,5-dimethyl-1H-imidazol-2-yl)ethylidene)hydrazineyl)-4-(6- methoxypyridin-3-yl)thiazole; (E)-2-(2-(1-(1H-imidazol-2-yl)ethylidene)hydrazineyl)-4-(6-methoxypyridin- 3-yl)thiazole; (E)-2-(2-(1-(1H-benzo[d]imidazol-2-yl)ethylidene)hydrazineyl)-4-(4- (trifluoromethoxy)phenyl)thiazole; (E)-2-(2-(1-(1H-imidazol-2-yl)ethylidene)hydrazineyl)-4-(4- (trifluoromethoxy)phenyl)thiazole; (E)-2-(2-(1-(1H-benzo[d]imidazol-2-yl)ethylidene)hydrazineyl)-4-(4- (methylthio)phenyl)thiazole; (E)-2-(2-(1-(1H-imidazol-2-yl)ethylidene)hydrazineyl)-4-(4- (methylthio)phenyl)thiazole; (E)-4-(2-(2-(1-(1H-imidazol-2-yl)ethylidene)hydrazineyl)thiazol-4-yl)-N- methylaniline; (E)-N-(4-(2-(2-(1-(1H-benzo[d]imidazol-2-yl)ethylidene)hydrazineyl)thiazol- 4-yl)phenyl)-2,2,2-trifluoro-N-methylacetamide; and (E)-N-(4-(2-(2-(1-(1H-imidazol-2-yl)ethylidene)hydrazineyl)thiazol-4- yl)phenyl)-2,2,2-trifluoro-N-methylacetamide. Embodiment 51: The pharmaceutical composition of any one of embodiments 37-50, wherein the SRSF3 inhibitor is selected from the group consisting of: Attorney Docket No.047162-7528WO1(02689) (a) SFI003, or a salt, solvate, stereoisomer, isotopologue, or tautomer thereof; (b) (E)-N-(4-(2-(2-(1-(1H-benzo[d]imidazol-2-yl)ethylidene)hydrazineyl)thiazol- 4-yl)phenyl)-2,2,2-trifluoro-N-methylacetamide), or a salt, solvate, stereoisomer, isotopologue, or tautomer thereof; (c) (E)-4-(2-(2-(1-(1H-benzo[d]imidazole-2-yl)ethylidene)hydrazineyl)thiazol-4- yl)-N-methylaniline), or a salt, solvate, stereoisomer, isotopologue, or tautomer thereof; and (d) (E)-2-(2-(1-(1H-benzo[d]imidazol-2-yl)ethylidene)hydrazineyl)-4-(4- (trifluoromethoxy)phenyl)thiazole), or a salt, solvate, stereoisomer, isotopologue, or tautomer thereof. Embodiment 52: A compound of Formula (II), or a salt, stereoisomer, or isotopologue thereof: , wherein: ; AA B the group consisting of H, CN, NO2, OR , N(R )(R ), SRA, C(=O)RA, C(=O)ORA, C(=O)N(RA)(RB), S(=O)RA, S(=O)2RA, S(=O)N(RA)(RB), S(=O)2N(RA)(RB), P(=O)(ORA)(ORB), halogen, optionally substituted C1-C6alkyl, optionally substituted C3-C8cycloalkyl, optionally substituted C2-C8 heterocycloalkyl, optionally substituted C6-C10 aryl, and optionally substituted C2-C8heteroaryl; R4is selected from the group consisting of H and optionally substituted C1-C6 alkyl; R5is selected from the group consisting of H and optionally substituted C1-C6 alkyl; Attorney Docket No.047162-7528WO1(02689) R6is selected from the group consisting of H, optionally substituted C1-C6 alkyl, optionally substituted C3-C8cycloalkyl, optionally substituted C2-C8heterocycloalkyl, optionally substituted C6-C10 aryl, and optionally substituted C2-C8 heteroaryl; R7a, R7b, and R7c, if present, are each independently selected from the group consisting of H, CN, NO2, ORA, N(RA)(RB), C(=O)RA, C(=O)ORA, C(=O)N(RA)(RB), S(=O)RA, S(=O)2RA, S(=O)N(RA)(RB), S(=O)2N(RA)(RB), P(=O)(ORA)(ORB), halogen, optionally substituted C2-C8 heteroaryl, wherein R7aand R7bcan combine with the atoms to which they are bound to form an optionally substituted C6-C10 aryl or optionally substituted C2-C8heteroaryl; X1selected from the group consisting of N and CR7c; Z1is CR8aor N, Z2is CR8bor N, Z3is CR8cor N, Z4is CR8dor N, and Z5is CR8eor N, wherein no more than two of Z1, Z2, Z3, Z4, and Z5are N; R8a, R8b, R8c, R8d, and R8e, if present, are each independently selected from the group consisting of H, CN, NO2, ORA, N(RA)(RB), SRA, halogen, optionally substituted C1-C6 alkyl, optionally substituted C3-C8 cycloalkyl, optionally substituted C2-C8heterocycloalkyl, optionally substituted C6-C10aryl, and optionally substituted C2-C8 heteroaryl; each occurrence of RAand RB, if present, is independently selected from the group consisting of H, optionally substituted C1-C6 alkyl, optionally substituted C3-C8 cycloalkyl, optionally substituted C2-C8heterocycloalkyl, optionally substituted C6- C10 aryl, optionally substituted C2-C8 heteroaryl, C(=O)RC, C(=O)ORC, C(=O)N(RC)(RD), S(=O)RC, S(=O)2RC, S(=O)N(RC)(RD), S(=O)2N(RC)(RD), and P(=O)(ORC)(ORD); each occurrence of RCand RD, if present, is independently selected from the group consisting of H, optionally substituted C1-C6 alkyl, optionally substituted C3-C8 cycloalkyl, optionally substituted C2-C8 heterocycloalkyl, optionally substituted C6- C10aryl, and optionally substituted C2-C8heteroaryl; wherein the compound of formula (II) is not a compound selected from the group consisting of: Attorney Docket No.047162-7528WO1(02689) (E)-4-(2-(2-(1-(1H-benzo[d]imidazol-2-yl)ethylidene)hydrazineyl)thiazol-4- yl)-N-methylaniline; and (E)-2-(2-(1-(1H-benzo[d]imidazol-2-yl)ethylidene)hydrazineyl)-4-(4- methoxyphenyl)thiazole. Embodiment 53: The compound of embodiment 52, wherein at least one of the following applies: (a) R7a, R7b, and R7c, if present, are each independently selected from the group consisting of H, CN, NO2, ORA, N(RA)(RB), C(=O)RA, C(=O)ORA, C(=O)N(RA) N , P(=O)(ORA) substituted C3- optionally substituted C6-C10aryl, and optionally substituted C2-C8heteroaryl; (b) R7aand R7bcan combine with the atoms to which they are bound to form a substituted C6-C10aryl or optionally substituted C2-C8heteroaryl; (c) R7aand R7bcan combine with the atoms to which they are bound to form unsubstituted phenyl, and R8c, if present, is selected from the group consisting of H, CN, NO2, SRA, NH(substituted C1-C6 alkyl), NH(optionally substituted C2-C6alkyl), halogen, optionally substituted C1-C6alkyl, substituted C1-C6alkoxy, optionally substituted C2-C6 alkoxy, optionally substituted C3-C8 cycloalkyl, optionally substituted C2-C8heterocycloalkyl, optionally substituted C6-C10 aryl, and optionally substituted C2-C8 heteroaryl; (d) R7aand R7bcan combine with the atoms to which they are bound to form unsubstituted phenyl, R8cis N(RA)(RB), and RAis C(=O)RC; and (e) R8cis N(RA)(RB), and RAis C(=O)RC. Embodiment 54: The compound of embodiment 52 or 53, wherein, R6is H. Embodiment 55: The compound of any one of embodiments 52-54, wherein one of the following applies: (a) R7aand R7bare each independently selected from the group consisting of H and CH3; or (b) R7aand R7bcombine with the atoms to which they are bound to . Attorney Docket No.047162-7528WO1(02689) Embodiment 56: The compound of any one of embodiments 52-55, wherein X1is selected from the group consisting of N and CH. Embodiment 57: The compound of any one of embodiments 52-56, wherein R1is selected H N . the following applies: (a) Z1is CR8a, Z2is N, Z3is CR8c, Z4is CR8d, and Z5is CR8e; or (b) Z1is CR8a, Z2is CR8b, Z3is CR8c, Z4is CR8d, and Z5is CR8e. Embodiment 59: The compound of any one of embodiments 52-58, wherein R8a, R8b, R8d, and R8eare each independently H. Embodiment 60: The compound of any one of embodiments 52-59, wherein R8cis selected from the group consisting of O(C1-C6 alkyl), O(C1-C6 haloalkyl), S(C1-C6 alkyl), NH(C1-C6 alkyl), and N(C1-C6 alkyl)C(=O)(C1-C6 haloalkyl), optionally wherein R8cis selected from the group consisting of OCH3, OCF3, SCH3, NHCH3, and N(CH3)C(=O)CF3. Embodiment 61: The compound of any one of embodiments 52-60, wherein R2is selected from the group consisting of , . Embodiment 62: The compound of any one of embodiments 52-61, wherein R3is H. Embodiment 63: The compound of any one of embodiments 52-62, wherein R4is H. Attorney Docket No.047162-7528WO1(02689) Embodiment 64: The compound of any one of embodiments 52-63, wherein R5is CH3. Embodiment 65: The compound of any one of embodiments 52-64, wherein the compound of formula (II) is selected from the group consisting of: (E)-2-(2-(1-(1H-pyrrol-2-yl)ethylidene)hydrazineyl)-4-(4- methoxyphenyl)thiazole; (E)-2-(2-(1-(1H-imidazol-2-yl)ethylidene)hydrazineyl)-4-(4- methoxyphenyl)thiazole; (E)-2-(2-(1-(1H-pyrrol-2-yl)ethylidene)hydrazineyl)-4-(6-methoxypyridin-3- yl)thiazole; (E)-2-(2-(1-(4,5-dimethyl-1H-imidazol-2-yl)ethylidene)hydrazineyl)-4-(6- methoxypyridin-3-yl)thiazole; (E)-2-(2-(1-(1H-imidazol-2-yl)ethylidene)hydrazineyl)-4-(6-methoxypyridin- 3-yl)thiazole; (E)-2-(2-(1-(1H-benzo[d]imidazol-2-yl)ethylidene)hydrazineyl)-4-(4- (trifluoromethoxy)phenyl)thiazole; (E)-2-(2-(1-(1H-imidazol-2-yl)ethylidene)hydrazineyl)-4-(4- (trifluoromethoxy)phenyl)thiazole; (E)-2-(2-(1-(1H-benzo[d]imidazol-2-yl)ethylidene)hydrazineyl)-4-(4- (methylthio)phenyl)thiazole; (E)-2-(2-(1-(1H-imidazol-2-yl)ethylidene)hydrazineyl)-4-(4- (methylthio)phenyl)thiazole; (E)-4-(2-(2-(1-(1H-imidazol-2-yl)ethylidene)hydrazineyl)thiazol-4-yl)-N- methylaniline; (E)-N-(4-(2-(2-(1-(1H-benzo[d]imidazol-2-yl)ethylidene)hydrazineyl)thiazol- 4-yl)phenyl)-2,2,2-trifluoro-N-methylacetamide; and (E)-N-(4-(2-(2-(1-(1H-imidazol-2-yl)ethylidene)hydrazineyl)thiazol-4- yl)phenyl)-2,2,2-trifluoro-N-methylacetamide. Embodiment 66: The compound of any one of embodiments 52-65, wherein the compound of Formula (II) is an SRSF3 inhibitor selected from the group consisting of: (a) (E)-N-(4-(2-(2-(1-(1H-benzo[d]imidazol-2-yl)ethylidene)hydrazineyl)thiazol- 4-yl)phenyl)-2,2,2-trifluoro-N-methylacetamide), or a salt, solvate, stereoisomer, isotopologue, or tautomer thereof; Attorney Docket No.047162-7528WO1(02689) (b) (E)-4-(2-(2-(1-(1H-benzo[d]imidazole-2-yl)ethylidene)hydrazineyl)thiazol-4- yl)-N-methylaniline), or a salt, solvate, stereoisomer, isotopologue, or tautomer thereof; and (c) (E)-2-(2-(1-(1H-benzo[d]imidazol-2-yl)ethylidene)hydrazineyl)-4-(4- (trifluoromethoxy)phenyl)thiazole), or a salt, solvate, stereoisomer, isotopologue, or tautomer thereof. Other Embodiments The recitation of a listing of elements in any definition of a variable herein includes definitions of that variable as any single element or combination (or subcombination) of listed elements. The recitation of an embodiment herein includes that embodiment as any single embodiment or in combination with any other embodiments or portions thereof. The disclosures of each and every patent, patent application, and publication cited herein are hereby incorporated herein by reference in their entirety. While this invention has been disclosed with reference to specific embodiments, it is apparent that other embodiments and variations of this invention may be devised by others skilled in the art without departing from the true spirit and scope of the invention. The appended claims are intended to be construed to include all such embodiments and equivalent variations.

Claims

1. Attorney Docket No.047162-7528WO1(02689) CLAIMS What is claimed is:

1. A method of treating or preventing squamous cell carcinoma (SCC) in a subject in need thereof, the method comprising administering to the subject a pharmaceutical composition comprising an effective amount of a serine / arginine-rich splicing factor 3 (SRSF3) inhibitor.

2. The method of claim 1, wherein the pharmaceutical composition is a topical formulation that is administered to the skin of the subject.

3. The method of claim 1 or claim 2, wherein the SRSF3 inhibitor is a small molecule having molecular mass less than about 600 g / mol.

4. The method of any one of claims 1-3, wherein the SRSF3 inhibitor is characterized by an effective level of skin permeability and / or is formulated in a topical formulation to exhibit an effective level of skin permeability.

5. The method of any one of claims 1-4, wherein the SRSF3 inhibitor reduces SRSF3 amount or activity in SCC cells by at least about 10%, at least about 15%, at least about 20%, at least about 25%, at least about 30%, at least about 35%, at least about 40%, at least about 45%, at least about 50%, at least about 55%, at least about 60%, at least about 65%, at least about 70%, at least about 75%, at least about 80%, at least about 85%, at least about 90%, at least about 95%, or at least about 100% compared to SRSF3 amount or activity in SCC cells in the absence of the SRSF3 inhibitor.

6. The method of any one of claims 1-5, wherein the SRSF3 inhibitor induces terminal differentiation of SCC cells.

7. The method of any one of claims 1-6, wherein the SRSF3 inhibitor is a compound of Formula (I), or a salt, stereoisomer, or isotopologue thereof:Attorney Docket No.047162-7528WO1(02689) , wherein:; the group consisting of H, CN, NO2, ORA, N(RA)(RB), SRA, C(=O)N(RA)(RB), S(=O)RA, S(=O)2RA, , halogen, optionally optionally substitutedand optionally substituted C2-C8 heteroaryl; R4is selected from the group consisting of H and optionally substituted C1-C6alkyl; R5is selected from the group consisting of H and optionally substituted C1-C6alkyl; R6is selected from the group consisting of H, optionally substituted C1-C6alkyl, optionally substituted C3-C8 cycloalkyl, optionally substituted C2-C8 heterocycloalkyl, optionally substituted C6-C10aryl, and optionally substituted C2-C8heteroaryl; R7a, R7b, and R7c, if present, are each independently selected from the group consisting of H, CN, NO2, ORA, N(RA)(RB), C(=O)RA, C(=O)ORA, C(=O)N(RA)(RB), S(=O) halogen,optionally substituted C2-C8heterocycloalkyl, optionally substituted C6-C10aryl, and optionally substituted C2-C8 heteroaryl, wherein R7aand R7bcan combine with the atoms to which they are bound to form an optionally substituted C6-C10 aryl or optionally substituted C2-C8 heteroaryl; X1selected from the group consisting of N and CR7c;Attorney Docket No.047162-7528WO1(02689) Z1is CR8aor N, Z2is CR8bor N, Z3is CR8cor N, Z4is CR8dor N, and Z5is CR8eor N, wherein no more than two of Z1, Z2, Z3, Z4, and Z5are N; R8a, R8b, R8c, R8d, and R8e, if present, are each independently selected from the group consisting of H, CN, NO2, ORA, N(RA)(RB), SRA, halogen, optionally substituted C1-C6alkyl, optionally substituted C3-C8cycloalkyl, optionally substituted C2-C8 heterocycloalkyl, optionally substituted C6-C10 aryl, and optionally substituted C2-C8heteroaryl; each occurrence of RAand RB, if present, is independently selected from the group consisting of H, optionally substituted C1-C6 alkyl, optionally substituted C3-C8 cycloalkyl, optionally substituted C2-C8heterocycloalkyl, optionally substituted C6- C10 aryl, optionally substituted C2-C8 heteroaryl, C(=O)RC, C(=O)ORC, C(=O)N(RC)(RD), S(=O)RC, S(=O)2RC, S(=O)N(RC)(RD), S(=O)2N(RC)(RD), and P(=O)(ORC)(ORD); each occurrence of RCand RD, if present, is independently selected from the group consisting of H, optionally substituted C1-C6 alkyl, optionally substituted C3-C8 cycloalkyl, optionally substituted C2-C8heterocycloalkyl, optionally substituted C6- C10 aryl, and optionally substituted C2-C8 heteroaryl.

8. The method of claim 7, wherein the SRSF3 inhibitor is a compound of Formula (I), wherein at least one of the following applies: (a) R7a, R7b, and R7c, if present, are each independently selected from the group consisting of H, CN, NO2, ORA, N(RA)(RB), C(=O)RA, C(=O)ORA, C(=O)N(RA) , P(=O)(ORA)substituted C3-C8 cycloalkyl, optionally substituted C2-C8 heterocycloalkyl, optionally substituted C6-C10aryl, and optionally substituted C2-C8heteroaryl; (b) R7aand R7bcan combine with the atoms to which they are bound to form a substituted C6-C10 aryl or optionally substituted C2-C8 heteroaryl; (c) R7aand R7bcan combine with the atoms to which they are bound to form unsubstituted phenyl, and R8c, if present, is selected from the group consisting of H, CN, NO2, SRA, NH(substituted C1-C6alkyl), NH(optionally substituted C2-C6 alkyl), halogen, optionally substituted C1-C6 alkyl, substituted C1-C6 alkoxy, optionally substituted C2-C6alkoxy, optionally substituted C3-C8Attorney Docket No.047162-7528WO1(02689) cycloalkyl, optionally substituted C2-C8 heterocycloalkyl, optionally substituted C6-C10aryl, and optionally substituted C2-C8heteroaryl; (d) R7aand R7bcan combine with the atoms to which they are bound to form unsubstituted phenyl, R8cis N(RA)(RB), and RAis C(=O)RC; and (e) R8cis N(RA)(RB), and RAis C(=O)RC.

9. The method of claim 7 or 8, wherein R6is H.

10. The method of any one of claims 7-9, wherein one of the following applies: (a) R7aand R7bare each independently selected from the group consisting of H and CH3; or (b) R7aand R7bcombine with the atoms to which they are bound to .

11. The method of any one of claims 7-10, wherein X1is selected from the group consisting of N and CH.

12. The method of any one of claims 7-11, wherein R1is selected from the group .

13. The method of any one of claims 7-12, wherein one of the following applies: (a) Z1is CR8a, Z2is N, Z3is CR8c, Z4is CR8d, and Z5is CR8e; or (b) Z1is CR8a, Z2is CR8b, Z3is CR8c, Z4is CR8d, and Z5is CR8e.

14. The method of any one of claims 7-13, wherein R8a, R8b, R8d, and R8eare each independently H.

15. The method of any one of claims 7-14, wherein R8cis selected from the group consisting of O(C1-C6alkyl), O(C1-C6haloalkyl), S(C1-C6alkyl), NH(C1-C6alkyl), and N(C1-C6 alkyl)C(=O)(C1-C6 haloalkyl), optionally wherein R8cis selected from the group consisting of OCH3, OCF3, SCH3, NHCH3, and N(CH3)C(=O)CF3.Attorney Docket No.047162-7528WO1(02689) 16. The method of any one of claims 7-15, wherein R2is selected from the group ,17. The method of any one of claims 7-16, wherein is H.

18. The method of any one of claims 7-17, wherein R4is H.

19. The method of any one of claims 7-18, wherein R5is CH3.

20. The method of any one of claims 7-19, wherein the compound of formula (I) is selected from the group consisting of: (E)-2-(2-(1-(1H-benzo[d]imidazol-2-yl)ethylidene)hydrazineyl)-4-(4- methoxyphenyl)thiazole; (E)-4-(2-(2-(1-(1H-benzo[d]imidazol-2-yl)ethylidene)hydrazineyl)thiazol-4- yl)-N-methylaniline; (E)-2-(2-(1-(1H-pyrrol-2-yl)ethylidene)hydrazineyl)-4-(4- methoxyphenyl)thiazole; (E)-2-(2-(1-(1H-imidazol-2-yl)ethylidene)hydrazineyl)-4-(4- methoxyphenyl)thiazole; (E)-2-(2-(1-(1H-pyrrol-2-yl)ethylidene)hydrazineyl)-4-(6-methoxypyridin-3- yl)thiazole; (E)-2-(2-(1-(4,5-dimethyl-1H-imidazol-2-yl)ethylidene)hydrazineyl)-4-(6- methoxypyridin-3-yl)thiazole; (E)-2-(2-(1-(1H-imidazol-2-yl)ethylidene)hydrazineyl)-4-(6-methoxypyridin- 3-yl)thiazole; (E)-2-(2-(1-(1H-benzo[d]imidazol-2-yl)ethylidene)hydrazineyl)-4-(4- (trifluoromethoxy)phenyl)thiazole; (E)-2-(2-(1-(1H-imidazol-2-yl)ethylidene)hydrazineyl)-4-(4- (trifluoromethoxy)phenyl)thiazole;Attorney Docket No.047162-7528WO1(02689) (E)-2-(2-(1-(1H-benzo[d]imidazol-2-yl)ethylidene)hydrazineyl)-4-(4- (methylthio)phenyl)thiazole; (E)-2-(2-(1-(1H-imidazol-2-yl)ethylidene)hydrazineyl)-4-(4- (methylthio)phenyl)thiazole; (E)-4-(2-(2-(1-(1H-imidazol-2-yl)ethylidene)hydrazineyl)thiazol-4-yl)-N- methylaniline; (E)-N-(4-(2-(2-(1-(1H-benzo[d]imidazol-2-yl)ethylidene)hydrazineyl)thiazol- 4-yl)phenyl)-2,2,2-trifluoro-N-methylacetamide; and (E)-N-(4-(2-(2-(1-(1H-imidazol-2-yl)ethylidene)hydrazineyl)thiazol-4- yl)phenyl)-2,2,2-trifluoro-N-methylacetamide.

21. The method of any one of claims 1-20, wherein the SRSF3 inhibitor is selected from the group consisting of: (a) SFI003, or a salt, solvate, stereoisomer, isotopologue, or tautomer thereof; (b) (E)-N-(4-(2-(2-(1-(1H-benzo[d]imidazol-2-yl)ethylidene)hydrazineyl)thiazol- 4-yl)phenyl)-2,2,2-trifluoro-N-methylacetamide), or a salt, solvate, stereoisomer, isotopologue, or tautomer thereof; (c) (E)-4-(2-(2-(1-(1H-benzo[d]imidazole-2-yl)ethylidene)hydrazineyl)thiazol-4- yl)-N-methylaniline), or a salt, solvate, stereoisomer, isotopologue, or tautomer thereof; and (d) (E)-2-(2-(1-(1H-benzo[d]imidazol-2-yl)ethylidene)hydrazineyl)-4-(4- (trifluoromethoxy)phenyl)thiazole), or a salt, solvate, stereoisomer, isotopologue, or tautomer thereof.

22. The method of any one of claims 1-21, wherein the SRSF3 inhibitor is the only anticancer agent administered to the subject.

23. The method of any one of claims 1-22, further comprising administering to the subject at least one additional agent or therapy useful for treating or preventing the SCC, optionally wherein the additional agent or therapy comprises surgical resection of at least one SCC lesion.

24. The method of any one of claims 1-23, wherein the topical formulation comprises a gel or an ointment.Attorney Docket No.047162-7528WO1(02689) 25. The method of any one of claims 1-24, wherein the SCC is early-stage cutaneous SCC.

26. The method of any one of claims 1-25, wherein the subject has multiple simultaneous SCC lesions.

27. The method of any one of claims 1-26, wherein the subject is a mammal.

28. The method of any one of claims 1-27, wherein the subject is a human.

29. A pharmaceutical composition comprising a serine / arginine-rich splicing factor 3 (SRSF3) inhibitor, for use in the method of any one of claims 1-28.

30. A pharmaceutical composition comprising a serine / arginine-rich splicing factor 3 (SRSF3) inhibitor.

31. The pharmaceutical composition of claim 30, wherein the pharmaceutical composition is a topical formulation for administration to skin.

32. The pharmaceutical composition of claim 30 or claim 31, wherein the SRSF3 inhibitor is a small molecule having molecular mass less than about 600 g / mol.

33. The pharmaceutical composition of any one of claims 30-32, wherein the SRSF3 inhibitor is characterized by an effective level of skin permeability and / or is formulated in a topical formulation to exhibit an effective level of skin permeability.

34. The pharmaceutical composition of any one of claims 30-33, wherein the SRSF3 inhibitor reduces SRSF3 amount or activity in squamous cell carcinoma (SCC) cells by at least about 10%, at least about 15%, at least about 20%, at least about 25%, at least about 30%, at least about 35%, at least about 40%, at least about 45%, at least about 50%, at least about 55%, at least about 60%, at least about 65%, at least about 70%, at least about 75%, at least about 80%, at least about 85%, at least about 90%, atAttorney Docket No.047162-7528WO1(02689) least about 95%, or at least about 100% compared to SRSF3 amount or activity in SCC cells in the absence of the SRSF3 inhibitor.

35. The pharmaceutical composition of any one of claims 30-34, wherein the SRSF3 inhibitor induces terminal differentiation of SCC cells.

36. The pharmaceutical composition of any one of claims 30-35, wherein the topical formulation comprises a gel or an ointment.

37. The pharmaceutical composition of any one of claims 30-36, wherein the SRSF3 inhibitor is a compound of Formula (I), or a salt, stereoisomer, or isotopologue thereof: , wherein:; AA Bthe group consisting of H, CN, NO2, OR , N(R )(R ), SRA, C(=O)RA, C(=O)ORA, C(=O)N(RA)(RB), S(=O)RA, S(=O)2RA, S(=O)N(RA)(RB), S(=O)2N(RA)(RB), P(=O)(ORA)(ORB), halogen, optionally substituted C1-C6 alkyl, optionally substituted C3-C8 cycloalkyl, optionally substituted C2-C8heterocycloalkyl, optionally substituted C6-C10aryl, and optionally substituted C2-C8 heteroaryl; R4is selected from the group consisting of H and optionally substituted C1-C6alkyl; R5is selected from the group consisting of H and optionally substituted C1-C6alkyl; R6is selected from the group consisting of H, optionally substituted C1-C6 alkyl, optionally substituted C3-C8cycloalkyl, optionally substituted C2-C8Attorney Docket No.047162-7528WO1(02689) heterocycloalkyl, optionally substituted C6-C10 aryl, and optionally substituted C2-C8 heteroaryl; R7a, R7b, and R7c, if present, are each independently selected from the group consisting of H, CN, NO2, ORA, N(RA)(RB), C(=O)RA, C(=O)ORA, C(=O)N(RA)(RB),optionally substituted C2-C8heteroaryl, wherein R7aand R7bcan combine with the atoms to which they are bound to form an optionally substituted C6-C10 aryl or optionally substituted C2-C8heteroaryl; X1selected from the group consisting of N and CR7c; Z1is CR8aor N, Z2is CR8bor N, Z3is CR8cor N, Z4is CR8dor N, and Z5is CR8eor N, wherein no more than two of Z1, Z2, Z3, Z4, and Z5are N; R8a, R8b, R8c, R8d, and R8e, if present, are each independently selected from the group consisting of H, CN, NO2, ORA, N(RA)(RB), SRA, halogen, optionally substituted C1-C6 alkyl, optionally substituted C3-C8 cycloalkyl, optionally substituted C2-C8heterocycloalkyl, optionally substituted C6-C10aryl, and optionally substituted C2-C8 heteroaryl; each occurrence of RAand RB, if present, is independently selected from the group consisting of H, optionally substituted C1-C6 alkyl, optionally substituted C3-C8 cycloalkyl, optionally substituted C2-C8heterocycloalkyl, optionally substituted C6- C10 aryl, optionally substituted C2-C8 heteroaryl, C(=O)RC, C(=O)ORC, C(=O)N(RC)(RD), S(=O)RC, S(=O)2RC, S(=O)N(RC)(RD), S(=O)2N(RC)(RD), and P(=O)(ORC)(ORD); each occurrence of RCand RD, if present, is independently selected from the group consisting of H, optionally substituted C1-C6 alkyl, optionally substituted C3-C8 cycloalkyl, optionally substituted C2-C8 heterocycloalkyl, optionally substituted C6- C10 aryl, and optionally substituted C2-C8 heteroaryl.

38. The pharmaceutical composition of claim 37, wherein the SRSF3 inhibitor is a compound of Formula (I), wherein at least one of the following applies:Attorney Docket No.047162-7528WO1(02689) (a) R7a, R7b, and R7c, if present, are each independently selected from the group consisting of H, CN, NO2, ORA, N(RA)(RB), C(=O)RA, C(=O)ORA, C(=O)N(RA)(RB), S(=O)RA, S(=O)2RA, S(=O)N(RA)(RB), S(=O)2N(RA)(RB), P(=O)(ORA) substituted C3-optionally substituted C6-C10aryl, and optionally substituted C2-C8heteroaryl; (b) R7aand R7bcan combine with the atoms to which they are bound to form a substituted C6-C10aryl or optionally substituted C2-C8heteroaryl; and (c) R7aand R7bcan combine with the atoms to which they are bound to form unsubstituted phenyl, and R8c, if present, is selected from the group consisting of H, CN, NO2, SRA, NH(substituted C1-C6alkyl), NH(optionally substituted C2-C6 alkyl), halogen, optionally substituted C1-C6 alkyl, substituted C1-C6 alkoxy, optionally substituted C2-C6alkoxy, optionally substituted C3-C8cycloalkyl, optionally substituted C2-C8 heterocycloalkyl, optionally substituted C6-C10aryl, and optionally substituted C2-C8heteroaryl; (d) R7aand R7bcan combine with the atoms to which they are bound to form unsubstituted phenyl, R8cis N(RA)(RB), and RAis C(=O)RC; and (e) R8cis N(RA)(RB), and RAis C(=O)RC.

39. The pharmaceutical composition of claim 37 or 38, wherein the SRSF3 inhibitor is the compound of Formula (I), wherein R6is H.

40. The pharmaceutical composition of any one of claims 37-39, wherein the SRSF3 inhibitor is the compound of Formula (I), wherein one of the following applies: (a) R7aand R7bare each independently selected from the group consisting of H and CH3; or (b) R7aand R7bcombine with the atoms to which they are bound to .

41. The pharmaceutical composition of any one of claims 37-40, wherein the SRSF3 inhibitor is the compound of Formula (I), wherein X1is selected from the group consisting of N and CH.Attorney Docket No.047162-7528WO1(02689) 42. The pharmaceutical composition of any one of claims 37-41, wherein the SRSF3 inhibitor is the compound of Formula (I), wherein R1is selected from the group H N .

43. Thewherein the SRSF3 inhibitor is the compound of Formula (I), wherein one of the following applies: (a) Z1is CR8a, Z2is N, Z3is CR8c, Z4is CR8d, and Z5is CR8e; or (b) Z1is CR8a, Z2is CR8b, Z3is CR8c, Z4is CR8d, and Z5is CR8e.

44. The pharmaceutical composition of any one of claims 37-43, wherein the SRSF3 inhibitor is the compound of Formula (I), wherein R8a, R8b, R8d, and R8eare each independently H.

45. The pharmaceutical composition of any one of claims 37-44, wherein the SRSF3 inhibitor is the compound of Formula (I), wherein R8cis selected from the group consisting of O(C1-C6 alkyl), O(C1-C6 haloalkyl), S(C1-C6 alkyl), NH(C1-C6 alkyl), and N(C1-C6 alkyl)C(=O)(C1-C6 haloalkyl), optionally wherein R8cis selected from the group consisting of OCH3, OCF3, SCH3, NHCH3, and N(CH3)C(=O)CF3.

46. The pharmaceutical composition of any one of claims 37-45, wherein the SRSF3 inhibitor is the compound of Formula (I), wherein R2is selected from the group ,47. The pharmaceutical composition of any one of claims 37-46, wherein the SRSF3 inhibitor is the compound of Formula (I), wherein R3is H.

48. The pharmaceutical composition of any one of claims 37-47, wherein the SRSF3 inhibitor is the compound of Formula (I), wherein R4is H.Attorney Docket No.047162-7528WO1(02689) 49. The pharmaceutical composition of any one of claims 37-48, wherein the SRSF3 inhibitor is the compound of Formula (I), wherein R5is CH3.

50. The pharmaceutical composition of any one of claims 37-49, wherein the SRSF3 inhibitor is the compound of Formula (I), wherein the compound of formula (I) is selected from the group consisting of: (E)-2-(2-(1-(1H-benzo[d]imidazol-2-yl)ethylidene)hydrazineyl)-4-(4- methoxyphenyl)thiazole; (E)-4-(2-(2-(1-(1H-benzo[d]imidazol-2-yl)ethylidene)hydrazineyl)thiazol-4- yl)-N-methylaniline; (E)-2-(2-(1-(1H-pyrrol-2-yl)ethylidene)hydrazineyl)-4-(4- methoxyphenyl)thiazole; (E)-2-(2-(1-(1H-imidazol-2-yl)ethylidene)hydrazineyl)-4-(4- methoxyphenyl)thiazole; (E)-2-(2-(1-(1H-pyrrol-2-yl)ethylidene)hydrazineyl)-4-(6-methoxypyridin-3- yl)thiazole; (E)-2-(2-(1-(4,5-dimethyl-1H-imidazol-2-yl)ethylidene)hydrazineyl)-4-(6- methoxypyridin-3-yl)thiazole; (E)-2-(2-(1-(1H-imidazol-2-yl)ethylidene)hydrazineyl)-4-(6-methoxypyridin- 3-yl)thiazole; (E)-2-(2-(1-(1H-benzo[d]imidazol-2-yl)ethylidene)hydrazineyl)-4-(4- (trifluoromethoxy)phenyl)thiazole; (E)-2-(2-(1-(1H-imidazol-2-yl)ethylidene)hydrazineyl)-4-(4- (trifluoromethoxy)phenyl)thiazole; (E)-2-(2-(1-(1H-benzo[d]imidazol-2-yl)ethylidene)hydrazineyl)-4-(4- (methylthio)phenyl)thiazole; (E)-2-(2-(1-(1H-imidazol-2-yl)ethylidene)hydrazineyl)-4-(4- (methylthio)phenyl)thiazole; (E)-4-(2-(2-(1-(1H-imidazol-2-yl)ethylidene)hydrazineyl)thiazol-4-yl)-N- methylaniline; (E)-N-(4-(2-(2-(1-(1H-benzo[d]imidazol-2-yl)ethylidene)hydrazineyl)thiazol- 4-yl)phenyl)-2,2,2-trifluoro-N-methylacetamide; andAttorney Docket No.047162-7528WO1(02689) (E)-N-(4-(2-(2-(1-(1H-imidazol-2-yl)ethylidene)hydrazineyl)thiazol-4- yl)phenyl)-2,2,2-trifluoro-N-methylacetamide.

51. The pharmaceutical composition of any one of claims 37-50, wherein the SRSF3 inhibitor is selected from the group consisting of: (a) SFI003, or a salt, solvate, stereoisomer, isotopologue, or tautomer thereof; (b) (E)-N-(4-(2-(2-(1-(1H-benzo[d]imidazol-2-yl)ethylidene)hydrazineyl)thiazol- 4-yl)phenyl)-2,2,2-trifluoro-N-methylacetamide), or a salt, solvate, stereoisomer, isotopologue, or tautomer thereof; (c) (E)-4-(2-(2-(1-(1H-benzo[d]imidazole-2-yl)ethylidene)hydrazineyl)thiazol-4- yl)-N-methylaniline), or a salt, solvate, stereoisomer, isotopologue, or tautomer thereof; and (d) (E)-2-(2-(1-(1H-benzo[d]imidazol-2-yl)ethylidene)hydrazineyl)-4-(4- (trifluoromethoxy)phenyl)thiazole), or a salt, solvate, stereoisomer, isotopologue, or tautomer thereof.

52. A compound of Formula (II), or a salt, stereoisomer, or isotopologue thereof: , wherein:;the group consisting of H, CN, NO2, ORA, N(RA)(RB), SRA, C(=O)RA, C(=O)ORA, C(=O)N(RA)(RB), S(=O)RA, S(=O)2RA, S(=O)N(RA)(RB), S(=O)2N(RA)(RB), P(=O)(ORA)(ORB), halogen, optionally substituted C1-C6alkyl, optionally substituted C3-C8cycloalkyl, optionally substituted C2-C8 heterocycloalkyl, optionally substituted C6-C10 aryl, and optionally substituted C2-C8heteroaryl;Attorney Docket No.047162-7528WO1(02689) R4is selected from the group consisting of H and optionally substituted C1-C6 alkyl; R5is selected from the group consisting of H and optionally substituted C1-C6 alkyl; R6is selected from the group consisting of H, optionally substituted C1-C6 alkyl, optionally substituted C3-C8cycloalkyl, optionally substituted C2-C8heterocycloalkyl, optionally substituted C6-C10 aryl, and optionally substituted C2-C8 heteroaryl; R7a, R7b, and R7c, if present, are each independently selected from the group consisting of H, CN, NO2, ORA, N(RA)(RB), C(=O)RA, C(=O)ORA, C(=O)N(RA)(RB), S(=O) halogen,optionally substituted C2-C8 heteroaryl, wherein R7aand R7bcan combine with the atoms to which they are bound to form an optionally substituted C6-C10 aryl or optionally substituted C2-C8heteroaryl; X1selected from the group consisting of N and CR7c; Z1is CR8aor N, Z2is CR8bor N, Z3is CR8cor N, Z4is CR8dor N, and Z5is CR8eor N, wherein no more than two of Z1, Z2, Z3, Z4, and Z5are N; R8a, R8b, R8c, R8d, and R8e, if present, are each independently selected from the group consisting of H, CN, NO2, ORA, N(RA)(RB), SRA, halogen, optionally substituted C1-C6 alkyl, optionally substituted C3-C8 cycloalkyl, optionally substituted C2-C8heterocycloalkyl, optionally substituted C6-C10aryl, and optionally substituted C2-C8 heteroaryl; each occurrence of RAand RB, if present, is independently selected from the group consisting of H, optionally substituted C1-C6 alkyl, optionally substituted C3-C8 cycloalkyl, optionally substituted C2-C8 heterocycloalkyl, optionally substituted C6- C10 aryl, optionally substituted C2-C8 heteroaryl, C(=O)RC, C(=O)ORC, C(=O)N(RC)(RD), S(=O)RC, S(=O)2RC, S(=O)N(RC)(RD), S(=O)2N(RC)(RD), andthe group consisting of H, optionally substituted C1-C6alkyl, optionally substituted C3-C8Attorney Docket No.047162-7528WO1(02689) cycloalkyl, optionally substituted C2-C8 heterocycloalkyl, optionally substituted C6- C10aryl, and optionally substituted C2-C8heteroaryl; wherein the compound of formula (II) is not a compound selected from the group consisting of: (E)-4-(2-(2-(1-(1H-benzo[d]imidazol-2-yl)ethylidene)hydrazineyl)thiazol-4- yl)-N-methylaniline; and (E)-2-(2-(1-(1H-benzo[d]imidazol-2-yl)ethylidene)hydrazineyl)-4-(4- methoxyphenyl)thiazole.

53. The compound of claim 52, wherein at least one of the following applies: (a) R7a, R7b, and R7c, if present, are each independently selected from the group consisting of H, CN, NO2, ORA, N(RA)(RB), C(=O)RA, C(=O)ORA, C(=O)N(RA)(RB), S(=O)RA, S(=O)2RA, S(=O)N(RA)(RB), S(=O)2N(RA)(RB), P(=O)(ORA)(ORB), halogen, optionally substituted C1-C6 alkyl, optionally substituted C3-C8cycloalkyl, optionally substituted C2-C8heterocycloalkyl, optionally substituted C6-C10 aryl, and optionally substituted C2-C8 heteroaryl; (b) R7aand R7bcan combine with the atoms to which they are bound to form a substituted C6-C10 aryl or optionally substituted C2-C8 heteroaryl; and (c) R7aand R7bcan combine with the atoms to which they are bound to form unsubstituted phenyl, and R8c, if present, is selected from the group consisting of H, CN, NO2, SRA, NH(substituted C1-C6alkyl), NH(optionally substituted C2-C6 alkyl), halogen, optionally substituted C1-C6 alkyl, substituted C1-C6 alkoxy, optionally substituted C2-C6alkoxy, optionally substituted C3-C8cycloalkyl, optionally substituted C2-C8 heterocycloalkyl, optionally substituted C6-C10aryl, and optionally substituted C2-C8heteroaryl; (d) R7aand R7bcan combine with the atoms to which they are bound to form unsubstituted phenyl, R8cis N(RA)(RB), and RAis C(=O)RC; and (e) R8cis N(RA)(RB), and RAis C(=O)RC.

54. The compound of claim 52 or 53, wherein, R6is H.

55. The compound of any one of claims 52-54, wherein one of the following applies: (a) R7aand R7bare each independently selected from the group consisting of H and CH3; orAttorney Docket No.047162-7528WO1(02689) (b) R7aand R7bcombine with the atoms to which they are bound to form .

56. The compound of any one of claims 52-55, wherein X1is selected from consisting of N and CH.

57. The compound of any one of claims 52-56, wherein R1is selected from the group .

58. The following applies: (a) Z1is CR8a, Z2is N, Z3is CR8c, Z4is CR8d, and Z5is CR8e; or (b) Z1is CR8a, Z2is CR8b, Z3is CR8c, Z4is CR8d, and Z5is CR8e.

59. The compound of any one of claims 52-58, wherein R8a, R8b, R8d, and R8eare each independently H.

60. The compound of any one of claims 52-59, wherein R8cis selected from the group consisting of O(C1-C6 alkyl), O(C1-C6 haloalkyl), S(C1-C6 alkyl), NH(C1-C6 alkyl), and N(C1-C6alkyl)C(=O)(C1-C6haloalkyl), optionally wherein R8cis selected from the group consisting of OCH3, OCF3, SCH3, NHCH3, and N(CH3)C(=O)CF3.

61. The compound of any one of claims 52-60, wherein R2is selected from the group ,62. The compound of any one of claims 52-61, wherein R3is H.

63. The compound of any one of claims 52-62, wherein R4is H.Attorney Docket No.047162-7528WO1(02689) 64. The compound of any one of claims 52-63, wherein R5is CH3.

65. The compound of any one of claims 52-64, wherein the compound of formula (II) is selected from the group consisting of: (E)-2-(2-(1-(1H-pyrrol-2-yl)ethylidene)hydrazineyl)-4-(4- methoxyphenyl)thiazole; (E)-2-(2-(1-(1H-imidazol-2-yl)ethylidene)hydrazineyl)-4-(4- methoxyphenyl)thiazole; (E)-2-(2-(1-(1H-pyrrol-2-yl)ethylidene)hydrazineyl)-4-(6-methoxypyridin-3- yl)thiazole; (E)-2-(2-(1-(4,5-dimethyl-1H-imidazol-2-yl)ethylidene)hydrazineyl)-4-(6- methoxypyridin-3-yl)thiazole; (E)-2-(2-(1-(1H-imidazol-2-yl)ethylidene)hydrazineyl)-4-(6-methoxypyridin- 3-yl)thiazole; (E)-2-(2-(1-(1H-benzo[d]imidazol-2-yl)ethylidene)hydrazineyl)-4-(4- (trifluoromethoxy)phenyl)thiazole; (E)-2-(2-(1-(1H-imidazol-2-yl)ethylidene)hydrazineyl)-4-(4- (trifluoromethoxy)phenyl)thiazole; (E)-2-(2-(1-(1H-benzo[d]imidazol-2-yl)ethylidene)hydrazineyl)-4-(4- (methylthio)phenyl)thiazole; (E)-2-(2-(1-(1H-imidazol-2-yl)ethylidene)hydrazineyl)-4-(4- (methylthio)phenyl)thiazole; (E)-4-(2-(2-(1-(1H-imidazol-2-yl)ethylidene)hydrazineyl)thiazol-4-yl)-N- methylaniline; (E)-N-(4-(2-(2-(1-(1H-benzo[d]imidazol-2-yl)ethylidene)hydrazineyl)thiazol- 4-yl)phenyl)-2,2,2-trifluoro-N-methylacetamide; and (E)-N-(4-(2-(2-(1-(1H-imidazol-2-yl)ethylidene)hydrazineyl)thiazol-4- yl)phenyl)-2,2,2-trifluoro-N-methylacetamide.

66. The compound of any one of claims 52-65, wherein the compound of Formula (II) is an SRSF3 inhibitor selected from the group consisting of: (a) (E)-N-(4-(2-(2-(1-(1H-benzo[d]imidazol-2-yl)ethylidene)hydrazineyl)thiazol- 4-yl)phenyl)-2,2,2-trifluoro-N-methylacetamide), or a salt, solvate, stereoisomer, isotopologue, or tautomer thereof;Attorney Docket No.047162-7528WO1(02689) (b) (E)-4-(2-(2-(1-(1H-benzo[d]imidazole-2-yl)ethylidene)hydrazineyl)thiazol-4- yl)-N-methylaniline), or a salt, solvate, stereoisomer, isotopologue, or tautomer thereof; and (c) (E)-2-(2-(1-(1H-benzo[d]imidazol-2-yl)ethylidene)hydrazineyl)-4-(4- (trifluoromethoxy)phenyl)thiazole), or a salt, solvate, stereoisomer, isotopologue, or tautomer thereof.

Images