The androgen receptor (AR) plays an essential role in controlling the effects of androgen hormones and cell growth in certain cancers including prostate and breast cancer. ESSA is developing drugs that selectively block transcription at the N-terminal domain.
The N-terminal domain controls the transcriptional activity of the AR, a critical function necessary for AR-driven cancer cell growth.
Cancer cell adaptations (such as mutations) maintain AR-driven tumor growth despite low circulating levels of androgen and despite the potential presence of anti-androgens. Furthermore, some truncated AR splice variants that lack a ligand-binding domain retain their activity independent of androgen and represent a resistance mechanism to existing hormone therapies.
