SNS-032 is primarily investigated for its potential in cancer therapy due to its ability to inhibit cyclin-dependent kinases (CDKs), specifically CDK2, CDK7, and CDK9. These enzymes play critical roles in regulating the cell cycle and transcription, and their dysregulation is commonly associated with tumor growth. By inhibiting CDK9, SNS-032 disrupts the transcription of key survival genes in cancer cells, such as those in the Bcl-2 family, leading to apoptosis. It has shown activity in preclinical studies against various hematological malignancies, including chronic lymphocytic leukemia (CLL) and multiple myeloma. Its mechanism makes it a candidate for targeting transcriptionally addicted cancers, especially those dependent on rapid gene expression for survival. Research continues to explore its efficacy, optimal dosing, and potential combinations with other anticancer agents.