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Verastem (VSTM) Back with “game” as data supports inhibition targeting cancer stem cells

March 10, 2016 10:35am

FAK inhibition increases influx of cytotoxic T cells into tumors while reducing immuno-suppressive and stromal density barriers to anti-tumor immune attack in patients with advanced pancreatic cancer - BUY

Verastem (VSTM) presented pre-clinical data and participation in an expert panel at the Keystone Symposium on Stem Cells and Cancer being held March 6 – 10, 2016 in Breckenridge, CO.

VSTM’s presentation at the Keystone Symposium describes its current understanding of the role of PI3K/mTOR and FAK in the survival and tumor-initiating capability of cancer stem cells.

· Date and time: Thursday, March 10, 2016, 8:00 – 11:00 am PT

The Bottom Line: New data – early but, very positive from pre-clinical models presented demonstrate that FAK inhibition enhances the anti-tumor effect of adoptive T cell transfer.

These data suggest that the benefit of FAK inhibitor combination is likely to extend to various approaches that enhance cytotoxic T cell function, including combination with antibodies against PD-1 and PD-L1.

VSTM is now clinically testing this with the combination of VS-6063 and pembrolizumab at Washington University in Saint Louis in patients with advanced pancreatic cancer.

VSTM is also recently announced a clinical collaboration with Pfizer (PFE) and Merck KGaA (OTC: MKGAY) to combine VS-6063 and avelumab for the treatment of patients with ovarian cancer.”

VSTM is UP +$0.02 to $1.48, grossly oversold after “past events” - 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.

VS-5584 is an orally available compound that has demonstrated potent and highly selective activity against class 1 PI3K enzymes and dual inhibitory actions against mTORC1 and mTORC2. In preclinical studies, VS-5584 has been shown to reduce the percentage of cancer stem cells and induce tumor regression in chemotherapy-resistant models. VSTM is currently conducting a dose escalation trial of VS-5584 in patients with advanced solid tumors.

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