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Study Published in Nature Medicine Highlights Potential Role of FAK Inhibition in Pancreatic Cancer
- FAK Inhibition Renders Previously Unresponsive Pancreatic Tumors Responsive to Chemo- and Immunotherapy –
- Preclinical Results Support Ongoing Phase 1 Clinical Trial in Patients with Pancreatic Cancer –
“The application of immunotherapy holds great promise to improve outcomes for patients with pancreatic cancer, as it has for melanoma and lung cancer patients,” said Dr. DeNardo. “To date, however, attempts at immunotherapy in PDAC have achieved limited clinical benefit when deployed as single agents. This is likely due in part to the presence of a uniquely immunosuppressive tumor microenvironment which is dominant in most human cases of PDAC. Major drivers of this pro-tumorigenic microenvironment include a highly fibrotic stroma and extensive infiltration by immunosuppressive cell populations. Thus, agents that can potentially overcome excessive fibrosis while altering immune suppression would be particularly attractive targets for PDAC.”
The paper, titled “Targeting Focal Adhesion Kinase Renders Pancreatic
Cancers Responsive to Checkpoint Immunotherapy,” (Jiang, et al.,
advanced online publication,
In this study, researchers show that FAK signaling is a key driver of fibrosis, immunosuppression and PDAC progression. It was then demonstrated that single-agent treatment with Verastem’s FAK inhibitor VS-4718 significantly limited tumor progression, resulting in a doubling of survival in an in vivo model of human PDAC. This slowing of tumor progression was associated with dramatically reduced tumor fibrosis, and a reduced number of tumor-infiltrating immunosuppressive cells. Given these findings, it was then hypothesized that the resulting effects of FAK inhibition on the TME may render PDAC tumors more sensitive to immunotherapy. Study results then demonstrated that FAK inhibition rendered previously unresponsive in vivo models responsive to T cell therapy and anti-PD1 antagonists. These data strongly support the ongoing clinical evaluation of FAK inhibitors in combination with checkpoint immunotherapy in patients with pancreatic cancer.
“FAK signaling has been shown to be important in several carcinomas,
including pancreatic tumors, but its compelling role in creating an
immunosuppressive tumor microenvironment is just emerging,” said
In early 2016,
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.
About
This press release includes forward-looking statements about Verastem’s
strategy, future plans and prospects, including statements regarding the
development and activity of Verastem’s product candidates, VS-6063 and
VS-4718, and Verastem’s FAK programs generally, the utility of FAK
inhibitors for the treatment of cancers, the structure of our planned
and pending clinical trials and the timeline for clinical development.
The words “anticipate,” “appear,” “believe,” “estimate,” “expect,”
“intend,” “may,” “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. Each
forward-looking statement is subject to risks and uncertainties that
could cause actual results to differ materially from those expressed or
implied in such statement. Applicable risks and uncertainties include
the risks that the preclinical testing of Verastem’s product candidates
and preliminary or interim data from clinical trials may not be
predictive of the results or success of ongoing or later clinical
trials, that data may not be available when we expect it to be, that
enrollment of clinical trials may take longer than expected, that our
product candidates will cause unexpected safety events, that
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Source:
Verastem, Inc.
Brian Sullivan, 781-292-4214
bsullivan@verastem.com