March 31, 2016 9:59am

This data shows that VSTM’s FAK inhibitor dramatically reduced tumor stroma and reduced numbers of immunosuppressive cells in pancreatic cancer models


 

VSTM presented preclinical data by it’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.

 

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

 

The Bottom Line: To date, single-agent immunotherapy has achieved limited clinical benefit for patients suffering from pancreatic cancer. 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. The data also supports the rationale for the P1 dose-escalation clinical study evaluating FAK inhibitor VS-6063 in combination with pembrolizumab and gemcitabine in patients with pancreatic cancer.

 

VSTM closed at $1.43 and is UP +$0.04 or +2.80%. The pre-open ranked the VSTM as a BUY pre the announcement referencing the total cash per share being “pegged” at $3.26 - BUY

 

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.