KI-ARv-03

KI-ARv-03 binds in the ATP-pocket of CDK9, forming critical interactions with hinge residues Glu107, His108, and the DFG-motif's Asp109^[1].
KI-ARv-03 (5 μM, 18 h) selectively suppressed AR-V7 transcripts in both VCaP-16 and 22Rv1 cells, an effect that translated to KLK3 downregulation only in VCaP-16 cells, with no impact on AR-FL^[1].
KI-ARv-03 (0-10 μM, 48-72 h) exhibits dose-dependent anti-proliferative activity (GR₅₀ = 1.52 μM in MV-4-11; GR₅₀ = 3.26 μM in 22Rv1) and induces more robust apoptosis in MV-4-11 AML cells, suggesting a heightened susceptibility of hematological cancers to CDK9 inhibition^[1].
KI-ARv-03 (0-40 μM, 1 h) directly engages CDK9 but not AR species, indicating it affects AR levels through impaired CDK9 enzymatic activity^[1].
KI-ARv-03 (0.5-10 μM, 1-48 h) dose-dependently reduces RNA Pol II (pSer2/pSer7), and time-dependently depletes AR-FL, AR-V7 and AR (pSer81) levels in 22Rv1 cells, consistent with its role in CDK9-mediated transcriptional regulation of the AR locus^[1].
KI-ARv-03 (5 μM, 6-24 h) triggers the depletion of AR protein through a proteasome-dependent pathway, as evidenced by rescue with MG132 (HY-13259), thereby linking CDK9 inhibition to AR protein stability^[1].
KI-ARv-03 (0-10 μM, 72-120 h) dose-dependently inhibits the proliferation of MOLT-4, PSN-1, and RH-4 cells, with IC₅₀ values ranging from 279.2 nM to 9.99 μM^[2].

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