Arvinas Presents Preclinical Data on Protein Degrader, ARV-471, at the 2018 San Antonio Breast Cancer Symposium (SABCS)

ARV-471 Degraded Estrogen Receptor and Provided Improved Anti-Tumor Activity When Compared to SOC, Both as a Monotherapy and in Combination

NEW HAVEN, Conn., Dec. 07, 2018 (GLOBE NEWSWIRE) — Arvinas Inc. (Nasdaq: ARVN), a biotechnology company creating a new class of drugs based on targeted protein degradation, today presented positive preclinical data on the company’s lead clinical candidate, ARV-471, for advanced or metastatic ER-positive/HER2-negative breast cancer at the 2018 San Antonio Breast Cancer Symposium (SABCS), taking place December 4-8 in San Antonio, Texas (Poster P5-04-18; Session 5: Tumor Cell and Molecular Biology: Endocrine Therapy and Resistance). In this study, orally administered ARV-471 demonstrated improved potency and anti-tumor activity both as a monotherapy and in combination with a CDK4/6 inhibitor, compared to current standard of care treatment regimens. 

“We believe that ARV-471 has the potential to be the first oral protein degrader for the treatment of patients with metastatic ER-positive/HER2-negative breast cancer, when used either as a single-agent or in combination with other routinely used anti-cancer agents,” said John Houston, Ph.D., President and CEO of Arvinas. “This data reinforces our growing confidence that our PROTAC™ protein degraders have the potential to provide distinct advantages over existing approaches across a broad range of disease targets and to improve clinical outcomes over current standard of care. We continue to expect to initiate our Phase 1 clinical trial of ARV-471 in mid-2019.”

Key highlights from the poster “ARV-471, an oral estrogen receptor PROTAC degrader for breast cancer”:

  • Orally bioavailable ARV-471 demonstrated potent ERa degradation in wild-type and mutant ERa-expressing cell lines.
  • Oral administration of ARV-471 caused near-complete ERa degradation and resulted in tumor shrinkage in an orthotopic MCF7/estradiol breast cancer preclinical model; ARV-471 demonstrated superior tumor growth inhibition and ERa degradation compared to standard-of-care agent, fulvestrant.
  • Combination of ARV-471 and a CDK4/6 inhibitor demonstrated superior tumor growth inhibition when compared to the combination of fulvestrant and a CDK4/6 inhibitor.
  • ARV-471 inhibited growth of tamoxifen-resistant and ERa gene (ESR1) mutant tumors while also reducing tumor ERa levels.
  • ARV-471 displayed no ER agonist activity.

About Arvinas
Arvinas is a biopharmaceutical company dedicated to improving the lives of patients suffering from debilitating and life-threatening diseases through the discovery, development, and commercialization of therapies to degrade disease-causing proteins. Arvinas uses its proprietary technology platform to engineer proteolysis targeting chimeras, or PROTAC™ protein degraders, that are designed to harness the body’s own natural protein recycling system to selectively and efficiently degrade and remove disease-causing proteins. For more information, see www.arvinas.com.

Forward-Looking Statements
This press release contains forward-looking statements that involve substantial risks and uncertainties, including statements regarding the development and regulatory status of our product candidates, including the timing of our clinical trial for ARV-471. All statements, other than statements of historical facts, contained in this press release, including statements regarding our strategy, future operations, prospects, plans and objectives of management, are forward-looking statements. The words “anticipate,” “believe,” “estimate,” “expect,” “intend,” “may,” “might,” “plan,” “predict,” “project,” “target,” “potential,” “will,” “would,” “could,” “should,” “continue,” and similar expressions are intended to identify forward-looking statements, although not all forward-looking statements contain these identifying words.

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Arvinas Investor Contact
Randy Teel, VP Corporate Development
ir@arvinas.com

Arvinas Media Contact
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pr@arvinas.com