CDK9 degrader-1

CDK9 degrader-1 (AZ-9) (48 h) potently inhibits HCT116 cell viability with a GI₅₀ of 0.72 μM, an effect dependent on CDK9 degradation^[1].
CDK9 degrader-1 (0.1875-12 μM) dose-dependently degrades CDK9 with a DC₅₀ of 0.4073 μM and Cyclin T1 with a DC₅₀ of 1.215 μM in HCT116 cells^[1].
CDK9 degrader-1 (1 μM; 0-24 h) induces time-dependent degradation of CDK9 in HCT116 cells, with significant effects starting at 8 h, while Cyclin T1 degradation is not significant after 24 h^[1].
CDK9 degrader-1 (3 μM; 24 h pretreatment, followed by 0-24 h in drug-free medium) induces persistent degradation of CDK9 in HCT116 cells, with effects lasting up to 24 h after wash-out^[1].
CDK9 degrader-1 (0.75-12 μM) selectively degrades CDK9 and Cyclin T1 without affecting CDK2, CDK4, or CDK6 in HCT116, HT-29, DLD-1, RKO, and MOLM-13 cells^[1].
CDK9 degrader-1 (1-6 μM; 24-48 h) downregulates CDK9 downstream signaling in HCT116 cells, reducing anti-apoptotic protein levels and inducing caspase 3-mediated apoptosis^[1].
CDK9 degrader-1 (1 μM; 8 h pretreatment, 48 h incubation) induces degradation of CDK9 and Cyclin T1 in HCT116 cells via the autophagy-lysosome pathway^[1].
CDK9 degrader-1 (1 μM; 48 h) promotes degradation of CDK9 and Cyclin T1 in HCT116 cells by enhancing the interaction between CDK9 and ATG101, which is essential for the autophagy-lysosome pathway-mediated degradation^[1].
CDK9 degrader-1 (1-3 μM; 24-48 h) induces autophagy-lysosome pathway activation in HCT116 cells, increasing autophagosome formation and lysosome fusion to mediate CDK9 degradation^[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.