BOSTON–(BUSINESS WIRE)– Verastem, Inc. (NASDAQ: VSTM) (Verastem Oncology or the Company),
focused on developing and commercializing drugs to improve the survival
and quality of life of cancer patients, today announced that Jonathan
Pachter, PhD, the Company’s Chief Scientific Officer, will give an oral
presentation and moderate a roundtable discussion at the 3rd
Annual Advances in Immuno-Oncology Congress being held May 24-25, 2018
in London, UK.
“The data that will be presented at the Immuno-Oncology Congress
demonstrate the unique potential of duvelisib, as a dual inhibitor of
PI3K-delta and PI3K-gamma, to enhance the efficacy of immune checkpoint
and co-stimulatory antibodies in preclinical models of both
hematological malignancies and solid tumors,” said Dr. Pachter. “These
results support continued research and lend particular importance as we
move toward the commercialization of duvelisib, Verastem’s lead
candidate an oral, dual inhibitor of PI3K-delta and PI3K-gamma. The
duvelisib New Drug Application (NDA) is currently under review by the
U.S. Food and Drug Administration (FDA) for the treatment of patients
with relapsed or refractory CLL/SLL, and accelerated approval for the
treatment of patients with relapsed or refractory follicular lymphoma. I
will also give an update on the scientific rationale and clinical
progress of our FAK inhibitor defactinib in combination with PD-1 and
PD-L1 inhibitors in solid tumors.”
Details for the presentation and round table discussion at the
Congress are as follows:
Oral Presentation Title: Immunological Effects of Clinical Stage
FAK & PI3K-Delta/Gamma Inhibitors
Date and time: Thursday, May 24, 2018 at
5:40 – 6:10 PM BST
Round Table Discussion Title: Novel Checkpoint Pathways &
Strategies for Combined Modality Treatment
Date and time:
Friday, May 25, 2018 at 7:30 – 8:00 AM BST
A copy of the oral presentation will be available here
following the presentation.
Duvelisib is a first-in-class
investigational oral, dual inhibitor of phosphoinositide 3-kinase
(PI3K)-delta and PI3K-gamma, two enzymes known to help support the
growth and survival of malignant B-cells and T-cells. PI3K signaling may
lead to the proliferation of malignant B- and T-cells and is thought to
play a role in the formation and maintenance of the supportive tumor
microenvironment.1,2,3 Duvelisib was evaluated in late- and
mid-stage extension trials, including DUO™, a randomized, Phase 3
monotherapy study in patients with relapsed or refractory chronic
lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL),4
and DYNAMO™, a single-arm, Phase 2 monotherapy study in patients with
refractory indolent non-Hodgkin lymphoma (iNHL).5 Both DUO
and DYNAMO achieved their primary endpoints. Verastem Oncology’s New
Drug Application (NDA) requesting the full approval of duvelisib for the
treatment of patients with relapsed or refractory CLL/SLL, and
accelerated approval for the treatment of patients with relapsed or
refractory follicular lymphoma (FL) was accepted for filing by the U.S.
Food and Drug Administration (FDA), granted Priority Review and assigned
a target action date of October 5, 2018. Duvelisib is also being
developed by Verastem Oncology for the treatment of peripheral T-cell
lymphoma (PTCL), and is being investigated in combination with other
agents through investigator-sponsored studies.6 Information
about duvelisib clinical trials can be found on www.clinicaltrials.gov.
Defactinib is an investigational inhibitor
of focal adhesion kinase (FAK), a non-receptor tyrosine kinase that
mediates oncogenic signaling in response to cellular adhesion and growth
factors.7 Based on the multi-faceted roles of FAK, defactinib
is used to treat cancer through modulation of the tumor microenvironment
and enhancement of anti-tumor immunity.8,9 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 cancer, ovarian cancer,
non-small cell lung cancer (NSCLC), and mesothelioma. These studies are
combination clinical trials with pembrolizumab and avelumab from Merck &
Co. and Pfizer/Merck KGaA, respectively.10,11,12 Information
about these and additional clinical trials evaluating the safety and
efficacy of defactinib can be found on www.clinicaltrials.gov.
About Verastem Oncology
Verastem, Inc. (Nasdaq:VSTM),
operating as Verastem Oncology, is a biopharmaceutical company focused
on developing and commercializing drugs to improve the survival and
quality of life of cancer patients. Verastem Oncology 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
indolent Non-Hodgkin Lymphoma (iNHL) and a Phase 3 clinical trial in
patients with chronic lymphocytic leukemia/small lymphocytic lymphoma
(CLL/SLL). Verastem Oncology’s New Drug Application (NDA) requesting the
full approval of duvelisib for the treatment of patients with relapsed
or refractory CLL/SLL, and accelerated approval for the treatment of
patients with relapsed or refractory follicular lymphoma (FL) was
accepted for filing by the U.S. Food and Drug Administration (FDA),
granted Priority Review and assigned a target action date of October 5,
2018. In addition, Verastem Oncology 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, non-small-cell lung cancer (NSCLC), and
mesothelioma. Verastem Oncology’s product candidates seek to treat
cancer by modulating the local tumor microenvironment and enhancing
anti-tumor immunity. For more information, please visit www.verastem.com.
1 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.
2 Reif K et al.
Cutting Edge: Differential Roles for Phosphoinositide 3 kinases,
p110-gamma and p110-delta, in lymphocyte chemotaxis and homing. J
3 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.
7 Schaller M.D. and Parsons
J.T. Focal adhesion kinase: an integrin-linked protein tyrosine kinase.
Trends Cell Biol. 1993 3: 258-62.
8 Jiang H et al.
Targeting focal adhesion kinase renders pancreatic cancers responsive to
checkpoint immunotherapy. Nat Med 2016: Aug 22(8) 851-60.
Sulzmaier F.J. et al. FAK in cancer: mechanistic findings and clinical
applications. Nature Rev Cancer. 2014 14: 598-610.
Verastem Oncology, Inc.
Marianne M. Lambertson, +1
Vice President, Corporate Communications
Source: Verastem, Inc.