CDK9/CycT1 degrader-1

CDK9/CycT1 degrader-1 (compound 16) inhibits purified CDK9/cycT1 enzyme, with an inhibition rate of 19% at 10 nM and 74% at 100 nM; it also inhibits the proliferation of U-2932 cells, with an IC₅₀ of 45 nM^[1].
CDK9/CycT1 degrader-1 (1-1000 nM; 1-24 h) induces dose- and time-dependent degradation of CDK9, and downregulates cyclin T1 and Mcl-1 in U-2932 cells^[1].
CDK9/CycT1 degrader-1 (100 nM; 24 h) selectively degrades CDK9 (along with CDK1) in U-2932 cells, while exerting minimal effects on CDK2, CDK4 and CDK7^[1].
CDK9/CycT1 degrader-1 (10-1000 nM; 6 h) dose-dependently downregulates pSer2-RNAP2 (with no effect on pSer5-RNAP2) in U-2932 cells^[1].
CDK9/CycT1 degrader-1 (10-1000 nM; 6 h) downregulates the mRNA expression of Mcl-1 and c-Myc in a dose-dependent manner in U-2932 cells^[1].
CDK9/CycT1 degrader-1 (10-1000 nM; 24 h) induces apoptosis in U-2932 cells^[1].
CDK9/CycT1 degrader-1 (500 nM; 12 h, with 2 h pretreatment of 500 nM Bafilomycin A1 or 10 μM Hydroxychloroquine) degrades CDK9 via the autophagy-lysosomal pathway, which is confirmed by the reversed degradation effect in U-2932 cells treated with the autophagy inhibitors Bafilomycin A1 (HY-100558) or Hydroxychloroquine (HY-W031727)^[1].
CDK9/CycT1 degrader-1 (500 nM; 12 h, co-treated with 500 nM Bafilomycin A1) promotes the formation of a ternary complex between CDK9 and LC3B in U-2932 cells^[1].
CDK9/CycT1 degrader-1 (100 nM; 24 h) mediates CDK9 degradation in an LC3B-dependent manner, as evidenced by the blocked degradation in LC3B-knockout 293T cells compared with wild-type cells^[1].

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