On March 31, 2020 Arvinas, Inc. (Nasdaq: ARVN), a clinical-stage biotechnology company creating a new class of drugs based on targeted protein degradation, reported the acceptance of an abstract for presentation at the American Society of Clinical Oncology (ASCO) (Free ASCO Whitepaper) annual meeting being held virtually May 29 – June 2, 2020 (Press release, Arvinas, MAR 31, 2020, View Source [SID1234556032]). The presentation will include updated clinical data from the Arvinas’ Phase 1 dose escalation trial of ARV-110.
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ARV-110 is one of Arvinas’ two clinical-stage PROTAC protein degraders and is being developed for the treatment of men with metastatic castration-resistant prostate cancer. The second is ARV-471, which is in a Phase 1 dose escalation trial for patients with locally advanced or metastatic ER+/HER2- breast cancer. The next clinical update for ARV-471 is planned for the second half of 2020.
About ARV-110
ARV-110 is an orally bioavailable PROTAC protein degrader designed to selectively target and degrade the androgen receptor (AR). ARV-110 is being developed as a potential treatment for men with metastatic castration-resistant prostate cancer (mCRPC). Arvinas’ Phase 1 trial of ARV-110 is designed to assess its safety, tolerability, and pharmacokinetics, and includes measures of anti-tumor activity and pharmacodynamic readouts as secondary endpoints.
ARV-110 has demonstrated activity in preclinical models of AR mutation or overexpression, both common mechanisms of resistance to currently available AR-targeted therapies.
About ARV-471
ARV-471 is an orally bioavailable PROTAC protein degrader designed to specifically target and degrade the estrogen receptor (ER) for the treatment of patients with locally advanced or metastatic breast cancer. Arvinas’ Phase 1 trial of ARV-471 will assess its safety, tolerability, and pharmacokinetics, and will also include measures of anti-tumor activity and pharmacodynamic readouts as secondary endpoints.
In preclinical studies, ARV-471 demonstrated near-complete ER degradation in tumor cells, induced robust tumor shrinkage when dosed as a single agent in multiple ER-driven xenograft models, and showed superior anti-tumor activity when compared to a standard of care agent, fulvestrant, both as a single agent and in combination with a CDK4/6 inhibitor.