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.
Medlife has not independently confirmed the accuracy of these methods. They are for reference only.