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Effect of Ack1 tyrosine kinase inhibitor on ligand‐independent androgen receptor activity

Androgen receptor (AR) plays a critical role in the progression of both androgen‐dependent and androgen‐independent prostate cancer (AIPC). Ligand‐independent activation of AR in AIPC or castration resistant prostate cancer (CRPC) is often associated with poor prognosis. Recently, tyrosine kinase Ack1 has been shown to regulate AR activity by phosphorylating it at tyrosine 267 and this event was shown to be critical for AIPC growth. However, whether a small molecule inhibitor that can mitigate Ack1 activation is sufficient to abrogate AR activity on AR regulated promoters in androgen‐depleted environment is not known.