Preliminary Results from Dose Escalation
Portion and Expansion Cohorts Investigating VS-6766 in Combination
with Defactinib in Patients with KRAS Mutant Advanced Solid Tumors
to be Highlighted in a Virtual Poster Presentation
Management to Host Investor Conference Call
Following the Virtual Poster Presentation to Discuss the Data
Verastem, Inc. (Nasdaq:VSTM) (also known as Verastem Oncology),
a biopharmaceutical company committed to developing and
commercializing new medicines for patients battling cancer, today
announced that an abstract highlighting preliminary results from
the ongoing investigator-initiated clinical study investigating
VS-6766, its RAF/MEK inhibitor, in combination with defactinib, its
FAK inhibitor, in patients with KRAS mutant advanced solid tumors
has been selected for a virtual poster presentation at the upcoming
American Association for Cancer Research (AACR) 2020 Virtual Annual
Meeting I, taking place April 27-28, 2020.
This ongoing study is an open label, dose escalation and
expansion study. The expansion cohorts are currently ongoing in
patients with KRAS mutant advanced solid tumors, including low
grade serous ovarian cancer (LGSOC), non-small cell lung cancer
(NSCLC) and colorectal cancer (CRC). Following the virtual data
presentation, Verastem Oncology will host an investor conference
call to discuss the presented data. The exact date and time of the
investor conference call will be announced soon.
“These early clinical results led to our decision to in-license
VS-6766 earlier this year and accelerate development of this
exciting combination program for patients with KRAS mutant
cancers,” said Brian Stuglik, Chief Executive Officer of Verastem
Oncology. “The synergy between VS-6766 and defactinib has been
encouraging and we look forward to sharing the data with the
medical and scientific communities later this month.”
Verastem Oncology plans to initiate discussions with regulatory
authorities during the first half of 2020, with the goal of
commencing a registration-directed trial investigating the
VS-6766/defactinib combination as soon as possible.
Other Abstracts Selected for Presentation at AACR 2020
Virtual Meeting I
Two additional abstracts also selected for presentation at the
April virtual meeting include: updated data from an ongoing
Investigator-initiated Phase 1 study investigating defactinib in
combination with pembrolizumab and gemcitabine in patients with
advanced pancreatic ductal adenocarcinoma (PDAC) (Wang-Gilliam, et
al); and preclinical research describing the synergistic antitumor
efficacy of duvelisib, the Company’s oral inhibitor of
phosphoinositide 3-kinase (PI3K)-delta and PI3K-gamma, in
combination with PD-1 blockade in solid tumor and lymphoma
models.
Details for the AACR 2020 Virtual Meeting I presentations are
as follows:
Title: Phase 1 study of the combination of a RAF-MEK
inhibitor CH5126766 and FAK inhibitor defactinib in an intermittent
dosing schedule with expansions in KRAS mutant cancers Lead
author: Udai Banerji, Institute of Cancer Research and The
Royal Marsden Poster #: CT143 Session: VPO.CT01 -
Phase I Clinical Trials Date and Time: Monday, April 27,
2020; 9:00 a.m. to 6:00 p.m. ET URL:
https://www.abstractsonline.com/pp8/#!/9045/presentation/10642
Title: Phase 1 study of defactinib combined with
pembrolizumab and gemcitabine in patients with advanced cancer:
Experiences of pancreatic ductal adenocarcinoma (PDAC) patients
Lead author: Andrea Wang-Gilliam, Washington University in
St. Louis Poster #: CT118 Session: VPO.CT01 - Phase I
Clinical Trials Date and Time: Monday, April 27, 2020; 9:00
a.m. to 6:00 p.m. ET URL:
https://www.abstractsonline.com/pp8/#!/9045/presentation/10617
Title: Synergistic antitumor efficacy of the dual
PI3K-δ/PI3K-γ inhibitor duvelisib with PD-1 blockade in solid tumor
and lymphoma models Lead author: Jonathan Pachter, Verastem
Oncology Abstract #: CT045 Session: VCTPL04 -
Immunotherapy Clinical Trials 2 Date and Time: Tuesday,
April 28, 2020; 3:15 – 3:25 p.m. ET URL:
https://www.abstractsonline.com/pp8/#!/9045/presentation/10754
About VS-6766
VS-6766 (formerly known as CH5126766, CKI27 and RO5126766) is a
unique inhibitor of the RAF/MEK signaling pathway. In contrast to
other MEK inhibitors in development, VS-6766 blocks both MEK kinase
activity and the ability of RAF to phosphorylate MEK. This unique
mechanism allows VS-6766 to block MEK signaling without the
compensatory activation of MEK that appears to limit the efficacy
of other inhibitors. The combination of VS-6766 and the focal
adhesion kinase (FAK) inhibitor defactinib is currently being
investigated in a Phase 1 dose escalation and expansion study. The
expansion cohorts are currently ongoing in patients with KRAS
mutant advanced solid tumors, including low grade serous ovarian
cancer (LGSOC), non-small cell lung cancer (NSCLC) and colorectal
cancer (CRC).3 The ongoing clinical study of the VS-6766/defactinib
combination is supported by single-agent Phase 2 studies which
investigated defactinib in KRAS mutant NSCLC4 and VS-6766 in KRAS
mutant NSCLC and LGSOC.5
About Defactinib
Defactinib is an oral small molecule inhibitor of FAK and PYK2
that is currently being evaluated as a potential combination
therapy for various solid tumors. The Company has received Orphan
Drug designation for defactinib in ovarian cancer and mesothelioma
in the US, EU and Australia. Preclinical research by Verastem
Oncology scientists and collaborators at world-renowned research
institutions has described the effect of FAK inhibition to enhance
immune response by decreasing immuno-suppressive cells, increasing
cytotoxic T cells, and reducing stromal density, which allows
tumor-killing immune cells to enter the tumor.1,2 Additionally, in
both preclinical and clinical studies, FAK activation has been
shown to occur as a potential resistance mechanism in response to
MEK inhibitor treatment, and synergy of a FAK inhibitor with a
RAF/MEK inhibitor has been shown in several preclinical models. The
combination of defactinib and VS-6766 is currently being
investigated in a Phase 1 dose escalation and expansion study. The
expansion cohorts are currently ongoing in patients with KRAS
mutant advanced solid tumors, including low grade serous ovarian
cancer (LGSOC), non-small cell lung cancer (NSCLC) and colorectal
cancer (CRC).3 The ongoing clinical study of the VS-6766/defactinib
combination is supported by single-agent Phase 2 studies which
investigated defactinib in KRAS mutant NSCLC4 and VS-6766 in KRAS
mutant NSCLC and LGSOC.5 Defactinib is also in clinical testing in
combination with pembrolizumab for treatment of patients with
pancreatic cancer, NSCLC and mesothelioma.6
About COPIKTRA® (duvelisib)
COPIKTRA is an oral inhibitor of phosphoinositide 3-kinase
(PI3K), and the first approved dual inhibitor of PI3K-delta and
PI3K-gamma, two enzymes known to help support the growth and
survival of malignant B-cells. PI3K signaling may lead to the
proliferation of malignant B-cells and is thought to play a role in
the formation and maintenance of the supportive tumor
microenvironment.7,8,9 COPIKTRA is indicated for the treatment of
adult patients with relapsed or refractory chronic lymphocytic
leukemia/small lymphocytic lymphoma (CLL/SLL) after at least two
prior therapies and relapsed or refractory follicular lymphoma (FL)
after at least two prior systemic therapies. COPIKTRA is also being
developed by Verastem Oncology for the treatment of peripheral
T-cell lymphoma (PTCL), for which it has received Fast Track status
and Orphan Drug Designation, and is being investigated in
combination with other agents through investigator-sponsored
studies.10 For more information on COPIKTRA, please visit
www.COPIKTRA.com. Information about duvelisib clinical trials can
be found on www.clinicaltrials.gov.
About Verastem Oncology
Verastem Oncology (Nasdaq: VSTM) is a commercial
biopharmaceutical company committed to the development and
commercialization of new medicines to improve the lives of patients
diagnosed with cancer. Our pipeline is focused on novel small
molecule drugs that inhibit critical signaling pathways in cancer
that promote cancer cell survival and tumor growth, including
phosphoinositide 3-kinase (PI3K), focal adhesion kinase (FAK) and
RAF/MEK inhibition.
Our first FDA approved product is available for the treatment of
patients with certain types of indolent non-Hodgkin’s lymphoma
(iNHL).
For more information, please visit www.verastem.com.
Forward-Looking Statements Notice
This press release includes forward-looking statements about
Verastem Oncology’s strategy, future plans and prospects, including
statements related to the opportunity to rapidly advance the
development of clinical programs through Verastem Oncology’s
expanded development pipeline and strengthened balance sheet, the
timing of top-line results for clinical trials, anticipated
reductions in operating expenses from Verastem Oncology’s strategic
realignment, the timing of commencing a registration-directed trial
for CH5126766 (VS-6766) and financial guidance estimates. 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.
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 and uncertainties, among other
things, regarding: the success in the development and potential
commercialization of our product candidates, including defactinib
in combination with CH5126766 (VS-6766); the occurrence of adverse
safety events and/or unexpected concerns that may arise from
additional data or analysis or result in unmanageable safety
profiles as compared to their levels of efficacy; our ability to
obtain, maintain and enforce patent and other intellectual property
protection for our product candidates; the scope, timing, and
outcome of any legal proceedings; decisions by regulatory
authorities regarding labeling and other matters that could affect
the availability or commercial potential of our product candidates;
whether preclinical testing of our product candidates and
preliminary or interim data from clinical trials will be predictive
of the results or success of ongoing or later clinical trials; that
the timing, scope and rate of reimbursement for our product
candidates is uncertain; that third-party payors (including
government agencies) may not reimburse; that there may be
competitive developments affecting our product candidates; that
data may not be available when expected; that enrollment of
clinical trials may take longer than expected; that our product
candidates will experience manufacturing or supply interruptions or
failures; that we will be unable to successfully initiate or
complete the clinical development and eventual commercialization of
our product candidates; that the development and commercialization
of our product candidates will take longer or cost more than
planned; that we or Chugai Pharmaceutical Co., Ltd. will fail to
fully perform under the CH5126766 (VS-6766) license agreement; that
we may not have sufficient cash to fund our contemplated
operations; that we may be unable to make additional draws under
our debt facility or obtain adequate financing in the future
through product licensing, co-promotional arrangements, public or
private equity, debt financing or otherwise; that we will be unable
to execute on our partnering strategies for defactinib in
combination with CH5126766 (VS-6766); that we will not pursue or
submit regulatory filings for our product candidates, and that our
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 the Company’s Quarterly Report on Form
10-Q for the quarterly period ended September 30, 2019, as filed
with the Securities and Exchange Commission (SEC) on October 30,
2019, its Annual Report on Form 10-K for the year ended December
31, 2018 as filed with the SEC on March 12, 2019 and in any
subsequent filings with the SEC. The forward-looking statements
contained in this press release reflect Verastem Oncology’s views
as of the date hereof, and the Company does not assume and
specifically disclaims any obligation to update any forward-looking
statements whether as a result of new information, future events or
otherwise, except as required by law.
References
1 Jiang H et al. Targeting focal adhesion kinase renders
pancreatic cancers responsive to checkpoint immunotherapy. Nat Med
2016: Aug 22(8) 851-60.
2 Sulzmaier F.J. et al. FAK in cancer: mechanistic findings and
clinical applications. Nature Rev Cancer. 2014 14: 598-610.
3 https://clinicaltrials.gov, NCT03875820
4 Gerber D. et al. Phase 2 study of the focal adhesion kinase
inhibitor defactinib (VS-6063) in previously treated advanced KRAS
mutant non-small cell lung cancer. Lung Cancer 2020: 139:60-67.
5 Chénard-Poirier, M. et al. Results from the biomarker-driven
basket trial of RO5126766 (CH5127566), a potent RAF/MEK inhibitor,
in RAS- or RAF-mutated malignancies including multiple myeloma.
Journal of Clinical Oncology 2017: 35.
10.1200/JCO.2017.35.15_suppl.2506.
6 www.clinicaltrials.gov, NCT02758587
7 Winkler D.G., Faia K.L., DiNitto J.P. et al. PI3K-delta and
PI3K-gamma inhibition by IPI-145 abrogates immune responses and
suppresses activity in autoimmune and inflammatory disease models.
Chem Biol 2013; 20:1-11.
8 Reif K et al. Cutting Edge: Differential Roles for
Phosphoinositide 3 kinases, p110-gamma and p110-delta, in
lymphocyte chemotaxis and homing. J Immunol 2004:173:2236-2240.
9 Schmid M et al. Receptor Tyrosine Kinases and TLR/IL1Rs
Unexpectedly activate myeloid cell PI3K, a single convergent point
promoting tumor inflammation and progression. Cancer Cell
2011;19:715-727.
10 www.clinicaltrials.gov, NCT03372057.
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version on businesswire.com: https://www.businesswire.com/news/home/20200413005493/en/
Investors:
John Doyle Vice President, Investor Relations & Finance +1
781-469-1546 jdoyle@verastem.com
Media:
Lisa Buffington Corporate Communications +1 781-292-4205
lbuffington@verastem.com
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