On January 21, 2016 Verastem, Inc. (NASDAQ:VSTM), focused on discovering and developing drugs to treat cancer, reported the presentation of preclinical data and participation in an expert panel at Immunotherapy World 2016 being held January 25-27, 2016 in Washington, DC (Press release, Verastem, JAN 21, 2016, View Source;p=RssLanding&cat=news&id=2131222 [SID:1234508838]).
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"Over the past couple of years, exciting data have emerged from several research groups demonstrating the importance of FAK inhibition in the immuno-oncology arsenal," said Dr. Jonathan Pachter, Verastem Head of Research. "Our presentation next week at Immunotherapy World 2016 will provide an overview of preclinical research to date demonstrating how FAK inhibition increases influx of cytotoxic T cells into tumors while reducing immuno-suppressive and stromal density barriers to anti-tumor immune attack. This creates a more favorable tumor microenvironment for the antitumor effects of immune checkpoint inhibitors and potentially other immunotherapies. Preclinical models have demonstrated extended survival with the combination of our FAK inhibitor with anti-PD-1 therapy, and we plan to test this hypothesis clinically in several tumor types and combinations in 2016. The first of such clinical trials was recently started at Washington University of Saint Louis in patients with advanced pancreatic cancer."
The Washington University of Saint Louis clinical trial is evaluating Verastem’s focal adhesion kinase (FAK) inhibitor VS-6063 in combination with Merck’s PD-1 inhibitor pembrolizumab and gemcitabine/Nab-paclitaxel in patients with pancreatic cancer. This clinical study is supported by a growing body of preclinical research suggesting that focal adhesion kinase (FAK) inhibition, when combined with PD-1 inhibitors, increases the anti-tumor activity of these immunotherapeutic agents. As published in the journal Cell (24 Sept 2015), FAK inhibition has been shown to increase cytotoxic (CD8+) T cells in tumors and decrease immunosuppressive T regulatory cells leading to full tumor regression. This is the first of several combination clinical trials Verastem expects to initiate this year.
Details for the Immunotherapy World 2016 events are as follows:
Oral Presentation
Title: FAK Inhibitors induce T cell-mediated tumor regression: Prospects for combination with checkpoint inhibitors
Date and time: Monday, January 25, 2016, 3:00 pm ET
Session: Focus Session 3: Next generation approaches to Immuno-oncology: Investigative Therapies, Tools and Tech
A copy of the oral presentation will be available following the presentation at http://bit.ly/R3M6wc
Expert Panel
Title: Moving beyond the first generation of immunotherapies
Date and time: Monday, January 25, 2016, 3:30 pm ET
Session: Focus Session 3: Next generation approaches to Immuno-oncology: Investigative Therapies, Tools and Tech
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 metastatic capability. VS-6063 (defactinib) and VS-4718 are orally available compounds designed to target cancer stem cells through the potent inhibition of FAK. Cancer stem cells are an underlying cause of tumor resistance to chemotherapy, recurrence and ultimate disease progression. Research has demonstrated that FAK activity is critical for the growth and survival of cancer stem cells. VS-6063 and VS-4718 are currently being studied in multiple clinical trials for their ability to improve patient survival through the targeting of cancer stem cells, potentiation of an immune response against cancer cells and reduction of the stromal density encapsulating a tumor.