Press Release
<< Back
Verastem Publishes Scientific Data Highlighting Potential Role of FAK Inhibition in Pancreatic and Breast Cancer
Preclinical Data Supportive of Ongoing Clinical Collaboration Trials Evaluating FAK Inhibition in Combination with Chemotherapeutic and Immunotherapeutic Agents
PLoS ONE Publication Highlights Potential Role of FAK Inhibition in Pancreatic Cancer
In a paper titled “The
Extracellular Matrix and Focal Adhesion Kinase Signaling Regulate Cancer
Stem Cell Function in Pancreatic Ductal Adenocarcinoma,”
The researchers show that the TME in PDAC is dramatically altered by several ECM proteins, including type I collagen. Type I collagen increases PDAC tumor-initiating potential, self-renewal and the frequency of cancer stem cells (CSCs) through the activation of FAK. While FAK overexpression increased tumor initiation, it was demonstrated that FAK inhibition reduced PDAC growth in vitro and in vivo. In an in vivo murine PDAC model, FAK inhibitor-treated tumors grew significantly slower than tumors in vehicle-treated control animals. In addition, tumor regression was enhanced by the addition of a FAK inhibitor to Gem-Pac and tumor regrowth was also significantly delayed in animals treated with the combination of a FAK inhibitor with Gem-Pac, as compared to Gem-Pac alone.
Oncotarget Publication Describing the Preferential Targeting of Cancer Stem Cells by FAK Inhibition in Breast Cancer Models
In a paper by
About the Tumor Microenvironment
The TME encompasses multiple tumor and non-tumor cell populations and an extracellular matrix that support cancer cell survival. This includes immunosuppressive regulatory T-cells, myeloid-derived suppressor cells, tumor-associated macrophages, cancer-associated fibroblasts, and extracellular matrix proteins that can hamper the entry and therapeutic benefit of cytotoxic T-cells and anti-cancer drugs. In addition to targeting the proliferative and survival signaling of cancer cells, Verastem’s product candidates, including duvelisib and defactinib, also target the TME to potentially improve response to therapy.
About Focal Adhesion Kinase and Defactinib
Defactinib (VS-6063) is an investigational inhibitor of Focal Adhesion
Kinase (FAK), a non-receptor tyrosine kinase encoded by the PTK-2 gene
that mediates oncogenic signaling in response to cellular adhesion and
growth factors.1 Based on the multi-faceted roles of FAK,
defactinib is used to treat cancer through modulation of the tumor
microenvironment, enhancement of anti-tumor immunity, and reduction of
cancer stem cells.2,3 Defactinib is currently being evaluated
in three separate clinical collaborations in combination with
immunotherapeutic agents for the treatment of several different cancer
types including pancreatic, ovarian, non-small cell lung cancer, and
mesothelioma. These studies are combination clinical trials with
pembrolizumab and avelumab from
About
This press release includes forward-looking statements about Verastem’s
strategy, future plans and prospects, including statements regarding
results of the Phase 2 DYNAMO® study, and Verastem’s PI3K/mTOR and FAK
programs generally, the structure of our planned and pending clinical
trials and the timeline and indications for clinical development,
including reporting top-line data, and regulatory submissions and, our
rights to develop or commercialize our product candidates. 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 expected, including for the
Phase 3 DUO study; that enrollment of clinical trials may take longer
than expected; that our product candidates will cause unexpected safety
events or result in an unmanageable safety profile as compared to their
level of efficacy; that duvelisib will be ineffective at treating
patients with lymphoid malignancies; that
References
1 Schaller M.D. and Parsons J.T. Focal adhesion kinase: an
integrin-linked protein tyrosine kinase. Trends Cell Biol. 1993 3:
258-62.
2 Jiang H et al. Targeting focal adhesion kinase
renders pancreatic cancers responsive to checkpoint immunotherapy. Nat
Med 2016:
3 Sulzmaier F.J. et al. FAK
in cancer: mechanistic findings and clinical applications. Nature Rev
Cancer. 2014 14: 598-610.
4www.clinicaltrials.gov,
NCT02546531
5 www.clinicaltrials.gov,
NCT02943317
6www.clinicaltrials.gov,
NCT02758587
View source version on businesswire.com: http://www.businesswire.com/news/home/20170725005355/en/
Source:
Verastem, Inc.
Brian Sullivan, 781-292-4214
Director,
Corporate Development
bsullivan@verastem.com