BOSTON--(BUSINESS WIRE)--Apr. 2, 2017--
Verastem, Inc. (NASDAQ: VSTM), focused on discovering and developing
drugs to treat cancer, today announced the oral presentation of data for
its lead focal adhesion kinase (FAK) inhibitor, defactinib, by the
Company’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 2017
American Association for Cancer Research (AACR) annual meeting in
Washington, DC.
In an oral presentation titled, “Reprogramming the tumor
microenvironment to improve responses to therapy,” Dr. DeNardo described
data demonstrating that FAK inhibition can enable efficacy of PD-1
inhibition in preclinical models of pancreatic cancer that, like the
clinical disease, are otherwise refractory to checkpoint inhibition. As
described in Dr. DeNardo’s presentation, a clinical trial is in
progress, which combines Verastem’s FAK inhibitor defactinib with
Merck’s PD-1 inhibitor pembrolizumab together with gemcitabine in
patients with advanced pancreatic ductal adenocarcinoma (PDAC). Initial
analysis of immune biomarkers from matched pairs of metastatic biopsies,
taken either pre or post treatment, from patients with PDAC has been
conducted in this study.
“Immunotherapeutic agents have shown little clinical benefit in
pancreatic cancer and this is likely due, at least in part, to the
presence of an immunosuppressive tumor microenvironment including a
dense stroma which may prevent T cell entry into, or function within,
tumor tissues,” said Dr. DeNardo. “Our initial biomarker data,
indicating an increase in activated proliferating cytotoxic T cells
together with a reduction in tumor-associated macrophages (TAMs) appear
promising. We are extremely interested to see whether these immune
changes that may shift the balance from immunosuppressive to
immunoreactive tumors, may translate into a clinical benefit for
pancreatic cancer patients who have few effective treatment options.”
Jonathan Pachter, PhD, Verastem’s Chief Scientific Officer, added,
“Pancreatic cancer has the highest mortality rate of all major cancers,
and the disease is still considered largely incurable. The data
presented today by Dr. DeNardo at AACR 2017 provide important support
and rationale for the ongoing clinical study evaluating Verastem’s lead
FAK inhibitor defactinib in combination with pembrolizumab and
gemcitabine in patients with pancreatic cancer.”
The ongoing Phase 1 clinical trial is being conducted at the Washington
University School of Medicine in St. Louis under the direction of Andrea
Wang-Gillam, MD, PhD, Clinical Director of the Gastrointestinal Oncology
Program with financial support from the Precision Medicine Research
Associates and the BJH Foundation. The trial, which is expected to
enroll approximately 50 patients, is currently completing its
dose-escalation portion.
Details for the oral symposium presentation at AACR 2017 are:
Title: Reprogramming the Tumor Microenvironment to Facilitate
Responses to Immunotherapy
Session: Major Symposium; SY14 –
Myelomonocytic Cells and Stroma as Therapeutic Targets
Location:
Room 206 – Level 2 Washington Convention Center
Date and time:
Sunday, April 2, 2017 from 2:05-2:30pm ET
A copy of the oral presentation slides will be available here
following the conclusion of Dr. DeNardo’s presentation and a webcast
will be available from AACR beginning on April 26, 2017.
About the Tumor Microenvironment
The tumor microenvironment 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 tumor
microenvironment to potentially improve a patient’s response to therapy.
About Defactinib
Defactinib is an investigational inhibitor of 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 combination with
immunotherapy for the treatment of pancreatic cancer, ovarian cancer,
non-small cell lung cancer, and mesothelioma, in three combination
clinical trials with pembrolizumab or avelumab from Merck & Co. and
Pfizer/Merck KGaA, respectively.4,5,6 Information about these
and additional clinical trials evaluating the safety and efficacy of
defactinib can be found on www.clinicaltrials.gov.
About Verastem, Inc.
Verastem, Inc. (NASDAQ:VSTM) is a biopharmaceutical company focused on
discovering and developing drugs to improve outcomes for patients with
cancer. Verastem is currently developing duvelisib, a dual inhibitor of
PI3K-delta and PI3K-gamma, which has successfully met its primary
endpoint in a Phase 2 study in iNHL and is currently being evaluated in
a Phase 3 clinical trial in patients with CLL. In addition, Verastem is
developing the FAK inhibitor defactinib, which is currently being
evaluated in three separate clinical collaborations in combination with
immunotherapeutic agents for the treatment of several different cancer
types, including pancreatic cancer, ovarian cancer and non-small cell
lung cancer, and mesothelioma. Verastem’s product candidates seek to
treat cancer by modulating the local tumor microenvironment, enhancing
anti-tumor immunity and reducing cancer stem cells. For more
information, please visit www.verastem.com.
Verastem forward-looking statements notice:
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 investigational product
candidates, including duvelisib and defactinib (VS-6063), and Verastem's
PI3K and FAK programs generally, the structure of our planned and
pending clinical trials and the timeline and indications for clinical
development, our rights to develop or commercialize our product
candidates and our ability to finance contemplated development
activities and fund operations for a specified period. The words
"anticipate," "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; 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 Verastem will be unable to successfully
initiate or complete the clinical development of its product candidates;
that the development of Verastem's product candidates will take longer
or cost more than planned; that Verastem may not have sufficient cash to
fund its contemplated operations; that Verastem will not pursue or
submit regulatory filings for its product candidates; and that
Verastem's product candidates will not receive regulatory approval,
become commercially successful products, or result in new treatment
options being offered to patients. Other risks and uncertainties include
those identified under the heading "Risk Factors" in Verastem's Annual
Report on Form 10-K for the year ended December 31, 2016 and in any
subsequent filings with the U.S. Securities and Exchange Commission. The
forward-looking statements contained in this press release reflect
Verastem's views as of the date of this release, and Verastem does not
undertake and specifically disclaims any obligation to update any
forward-looking statements.
1Schaller MD and Parsons JT. Focal adhesion kinase: an
integrin-linked protein tyrosine kinase. Trends Cell Biol. 1993 3:
258-62.
2Jiang H et al. Targeting focal adhesion kinase renders
pancreatic cancers responsive to checkpoint immunotherapy. Nat Med 2016:
Aug 22(8) 851-60.
3Sulzmaier FJ et al. FAK in cancer: mechanistic findings and
clinical applications. Nature Rev Cancer. 2014 14: 598-610.
4www.clinicaltrials.gov,
NCT02546531
5www.clinicaltrials.gov,
NCT02943317
6www.clinicaltrials.gov,
NCT02758587
View source version on businesswire.com: http://www.businesswire.com/news/home/20170402005084/en/
Source: Verastem, Inc.
Verastem, Inc.
Brian Sullivan, 781-292-4214
Director,
Corporate Development
bsullivan@verastem.com