Preclinically, EPI-7386 can inhibit both full-length and clinically relevant mutant and splice variant forms of AR, including forms of AR that are resistant to current antiandrogen treatments. ESSA’s novel approach has the potential to prevent or delay drug resistance, in addition to broadly inhibiting AR activity in earlier stages of disease.
ANITAC™ AR NTD Degraders
Leveraging ESSA’s scientific foundation in successfully targeting the N-terminal domain of the androgen receptor with a new class of small molecules called Anitens, ESSA is developing the first generation of ANITen bAsed Chimera (ANITAC™) degraders targeting the AR NTD. In preclinical models, the orally bioavailable ANITAC degraders can eliminate forms of AR protein found in castration-resistant prostate cancer that can potentially drive disease progression, including LBD mutants and LBD truncated splice variants.