Targeting Androgen Receptor Mutations in Metastatic Castration-Resistant Prostate Cancer with a Novel Androgen Biosynthesis Inhibitor.

Abstract

Multiple therapeutic advances in recent years have significantly improved outcomes for patients with metastatic prostate cancer, including utilization of combination androgen receptor (AR) pathway inhibitors and/or taxane chemotherapy in earlier, hormone-sensitive disease.¹ Unfortunately, patients typically still develop metastatic castration-resistant prostate cancer (mCRPC), the lethal form of disease with limited prognosis. Despite castration resistance, the majority of patients with mCRPC continue to have AR-dependent disease through a variety of mechanisms, including emergence of AR mutations, amplifications, splice variants, and persistent AR activation via alternative pathways of androgen production.².