AIM-100 (2-10 μM; 48 hours) treatment not only inhibits Ack1 activation but also suppresses AKT tyrosine phosphorylation, leading to cell cycle arrest in the G1 phase. AIM-100 not only inhibits Ack1/AKT Tyr-phosphorylation but also suppressed growth of cell lines derived from pancreatic, breast, and lung tumors.
The Ack1 inhibitor AIM-100 not only inhibited Ack1 activity but also was able to suppress AR Tyr phosphorylation and its recruitment to the ataxia-telangiectasia mutated kinase (ATM) enhancer.
AIM-100 is able to suppress pTyr-AR phosphorylation, binding of androgen receptor (AR) to PSA, NKX3.1, and TMPRSS2 promoters, and inhibit AR transcription activity.