CP-07

CP-07 (20 nM; ATP 20 μM) exhibits an inhibition rate of 85.6% against CDK9/cyclin T1, with an IC₅₀ of 3.3 nM^[1].
CP-07 (6.17-500 nM; 12 h) induces degradation of the CDK9 protein in 22RV1 cells in a concentration-dependent manner, with a DC₅₀ of 43 nM; CDK9 is completely downregulated at 500 nM ^[1].
CP-07 (100 nM; 2-24 h) initiates the induction of CDK9 degradation in 22RV1 cells after 2 h of treatment, and achieves complete degradation at 12 h ^[1].
CP-07 (500 nM; 12 h) completely downregulates CDK9 in 22RV1 cells, while exhibiting minimal or no significant effects on the protein levels of CDK2, CDK4, CDK5, CDK6, and CDK7, demonstrating selectivity for CDK9 degradation^[1].
CP-07 (72 h) inhibits the growth/viability of 22RV1 cells, with an IC₅₀ of 0.06 μM (60 nM) reported in Table 1^[1].
CP-07 (14 days) inhibits the colony formation of 22RV1 cells in a concentration-dependent manner, and completely blocks colony formation at approximately 60 nM, exhibiting stronger effects than LWT-111 and flavopiridol^[1].
CP-07 (0.1-1.5 μM; 24 h) downregulates p-RNAPII-Ser2, Mcl-1 and c-Myc in a concentration-dependent manner in 22RV1 cells, and reduces the protein levels of cyclin T1, AR, ARv7 and PSA^[1].
CP-07 (0.1 μM)-induced CDK9 degradation can be blocked by pretreatment with LWT-111, Thalidomide (HY-14658), or the proteasome inhibitor MG132 (HY-13259), which supports that its CDK9 degradation is ligand-dependent and proteasome-dependent^[1].
CP-07 exhibits good water solubility, with a measured solubility of 53 μg/mL at pH 7.4 and 125 μg/mL at pH 6.0^[1].
CP-07 exhibits an in vitro half-life of 97 min in human liver microsomes, indicating moderate in vitro metabolic stability^[1].

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