On March 30, 2016 Verastem, Inc. (NASDAQ:VSTM), focused on discovering and developing drugs to treat cancer, reported the oral presentation of preclinical data by the Company’s scientific collaborator David G. DeNardo, PhD, Assistant Professor of Medicine, Division of Oncology, Department of Immunology, Washington University School of Medicine in St. Louis, at the Keystone Symposium on Cancer Pathophysiology being held March 28 – April 1, 2016 in Breckenridge, CO (Press release, Verastem, MAR 30, 2016, View Source;p=RssLanding&cat=news&id=2151878 [SID:1234510228]).
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"To date, single-agent immunotherapy has achieved limited clinical benefit for patients suffering from pancreatic cancer," said Dr. DeNardo. "This is thought to be due to abundance of tumor-associated immune-suppressive cells in pancreatic tumors along with the dense stroma that prevents T cell entry. Our data show that Verastem’s FAK inhibitor dramatically reduced tumor stroma and reduced numbers of immunosuppressive cells in pancreatic cancer models. Further, when the FAK inhibitor was combined with immune checkpoint antibodies, the tumors became highly responsive leading to a near tripling of survival times relative to checkpoint inhibitors alone."
Jonathan Pachter, PhD, Verastem Head of Research, added: "The data presented today by Dr. DeNardo at the Keystone Symposium provide important support and rationale for the ongoing Phase 1 dose-escalation clinical study evaluating Verastem’s FAK inhibitor VS-6063 in combination with pembrolizumab and gemcitabine in patients with pancreatic cancer."
Details for the presentation at the Keystone Symposium on Cancer Pathophysiology are as follows:
Oral Presentation
Title: Reprogramming the Tumor Microenvironment to Facilitate Responses to Immunotherapy
Session: Immune Cells I: Adaptive and Innate Immune Cells in the Tumor Microenvironment (TME)
Date and time: Wednesday, March 30, 2016 at 8:00 – 11:15 AM MT
A copy of the oral presentation will be available following the presentation at http://bit.ly/R3M6wc
About Focal Adhesion Kinase
Focal Adhesion Kinase (FAK) is a non-receptor tyrosine kinase encoded by the PTK-2 gene that is involved in cellular adhesion and, in cancer, metastatic capability. VS-6063 (defactinib) and VS-4718 are orally available compounds that are potent inhibitors of FAK. VS-6063 and VS-4718 utilize a multi-faceted approach to treat cancer by reducing cancer stem cells, enhancing anti-tumor immunity, and modulating the local tumor microenvironment. VS-6063 and VS-4718 are currently being studied in multiple clinical trials for patients with cancer.