Prostate cancer is primarily driven by an activated androgen receptor (AR). The AR is composed of three domains: the ligand-binding domain (LBD) which binds to androgen hormones, the DNA-binding domain which binds to DNA in cells, and the N-terminal domain (NTD) which is necessary for AR gene transcription.

Currently approved antiandrogen treatments suppress AR activity by interfering with the production of androgens or preventing androgens from binding to the LBD. Over time, resistance develops at the DNA level (AR amplification; AR deletions, insertions, truncations and mutations) or RNA level (emergence of AR splice variants), resulting in a reactivated AR and disease progression.