Review demonstrates therapeutic mechanisms of CDK9 inhibition across refractory tumors, suggesting biomarker-guided combinations enhance clinical translational efficacy.
Key Points
To review the molecular biology of the CDK9/P-TEFb pathway and evaluate emerging therapeutic strategies, including selective inhibitors, targeted degraders, and rational drug combinations in oncology.
Synthesized molecular mechanisms of the CDK9/positive transcription elongation factor b (P-TEFb) axis in regulating RNA polymerase II and super-enhancer-driven oncogenic networks.
Evaluated pharmacological profiles of selective small-molecule CDK9 inhibitors, proteolysis-targeting chimera (PROTAC) degraders, predictive biomarkers, and resistance mechanisms.
CDK9 inhibition selectively suppresses transcriptional addiction, triggering apoptosis, epigenetic derepression, and favorable remodeling of the tumor microenvironment.
Therapeutic success in refractory malignancies relies on biomarker-driven patient selection, optimizing the therapeutic window, and combining CDK9 targeted agents to counteract adaptive resistance.