HOLON, Israel, Feb. 6, 2018 /PRNewswire/ -- Compugen Ltd.
(NASDAQ: CGEN), a leader in predictive discovery and development of
first-in-class therapeutics for cancer immunotherapy, today
announced the online publication of the discovery and validation of
the ILDR2 protein as a novel immune checkpoint and its use as an Fc
fusion protein for the treatment of autoimmune diseases in two
peer-reviewed papers in The Journal of Immunology.
Antibody-based therapeutics targeting ILDR2, designated by Compugen
as CGEN-15001T, for immuno-oncology were licensed to Bayer, while
Compugen retains the full rights to the fusion protein, designated
as CGEN-15001, consisting of the extracellular domain of ILDR2 and
an Fc domain, for potential use in autoimmune diseases.
ILDR2-Fc has a unique mechanism of action underlying its
ability to ameliorate autoimmunity, which combines immunomodulation
with regulation of immune homeostasis and with re-establishment of
immune tolerance.
"The publication of the discovery and functional validation of
ILDR2 and its potential therapeutic applications in a prestigious
peer-reviewed journal is a scientific recognition of the
significance of our findings. Compugen is the first to publish data
on ILDR2 as a new immune checkpoint with a potential therapeutic
role in autoimmune diseases and cancer immunotherapy, each
presenting first-in-class therapeutic opportunities," stated
Anat Cohen-Dayag, PhD, President and
CEO of Compugen. "This is the third novel immune checkpoint we
disclosed, following PVRIG and TIGIT. Similar to our discovery of
the PVRIG/PVRL2 pathway in immuno-oncology and its potential
clinical significance, here too, we identified a new pathway with
robust and diversified data supporting its mechanism-of-action and
broad therapeutic potential, both for the treatment of autoimmune
diseases and for cancer immunotherapy."
The publication1 led by Compugen's scientists,
describes the computational discovery approach leading to the
discovery of ILDR2 as a novel immune checkpoint. The experimental
validation of the role of this protein as a negative regulator of T
cell activity was established both internally at Compugen as well
as in collaboration with scientists from three leading academic
institutions. The publication reports the beneficial effects of
CGEN-15001 in an animal model of rheumatoid arthritis (RA), as well
as in a translational assay utilizing blood cells from RA patients,
that mimics the deleterious interactions of immune cells in the RA
synovium. The latter study was led by Prof. Iain B. McInnes, Muirhead Chair of Medicine and
Director of Institute of Infection, Immunity and Inflammation at
the University of Glasgow.
Prof. McInnes, co-author of the Compugen publication, said,
"These findings assign a new role to the ILDR2 protein, whose
immune-related function was not previously known, and uncover a
novel pathway involved in immune regulation. The expression pattern
of this protein, as well as its mechanism of action elucidated in
these two publications, involving the induction of immune tolerance
and restoration of immune homeostasis, offer a potential novel
treatment option for autoimmune and chronic inflammatory
conditions. Both traits are highly desired in a broad range of
autoimmune diseases and are not well addressed with currently
available therapies, which are often globally
immunosuppressive."
Preclinical research led by Compugen's scientists together with
Profs. Stephen Miller, Ph.D., and
Joseph R. Podojil, Ph.D., both from
the Department of Microbiology-Immunology and Interdepartmental
Immunobiology Center, Feinberg
School of Medicine, Northwestern
University2, and published in an
additional paper, demonstrates the potential of ILDR2-Fc fusion
protein to address autoimmune and inflammatory conditions as well
as the mechanism of action underlying this activity. The data show
the potent and long-lasting immunomodulatory activity of ILDR2-Fc
fusion protein in animal models of multiple sclerosis (R-EAE) and
type 1 diabetes, and its ability to promote engraftment in an
animal model of bone marrow transplantation. This work reveals the
mechanism of action of ILDR2-Fc in ameliorating autoimmunity
through regulation of immune homeostasis and re-establishment of
immune tolerance to the disease-causing antigen, by the induction
of regulatory T cells (Tregs).
Prof. Miller commented, "Our findings point to a compelling mode
of action for this Fc fusion protein in autoimmune diseases. In
animals, this protein induced a long-term response following a
short treatment duration through the promotion of regulatory T
cells activating an immune tolerance induction mechanism. We also
showed that this immune tolerance induction, addressing the
autoimmune disease, is specific to the antigen driving the
autoimmune disease and did not trigger a global non-specific
inhibition of immune responses, thus potentially maintaining the
immune response against infections and neo-malignancies."
- ILDR2 is a Novel B7-like Protein that Negatively Regulates T
Cell Responses (Hecht et al, JI, in press)
- ILDR2-Fc is a Novel Regulator of Immune Homeostasis and Inducer
of Antigen- Specific Immune Tolerance (Podojil et al, JI, in
press)
About Compugen
Compugen is a therapeutic discovery and
development company utilizing its broadly applicable predictive
discovery infrastructure to identify novel drug targets and develop
first-in-class therapeutics in the field of cancer immunotherapy.
The Company's therapeutic pipeline consists of immuno-oncology
programs against novel drug targets it has discovered, including T
cell immune checkpoints and myeloid target programs. Compugen's
business model is to selectively enter into collaborations for its
novel targets and related drug product candidates at various stages
of research and development. The Company is headquartered in
Israel, with R&D facilities in
both Israel and South San Francisco, CA. Compugen's shares are
listed on NASDAQ and the Tel Aviv Stock Exchange under the ticker
symbol CGEN. For additional information, please visit Compugen's
corporate website at http://www.cgen.com.
Forward-Looking Statement
This press release contains
"forward-looking statements" within the meaning of the Private
Securities Litigation Reform Act of 1995. Forward-looking
statements can be identified by the use of terminology such as
"will," "may," "expects," "anticipates," "believes," "potential,"
"plan," "goal," "estimate," "likely," "should," "confident," and
"intends," and describe opinions about possible future events.
These forward-looking statements involve known and unknown risks
and uncertainties that may cause the actual results, performance or
achievements of Compugen to be materially different from any future
results, performance or achievements expressed or implied by such
forward-looking statements. Among these risks: Compugen's business
model is substantially dependent on entering into collaboration
agreements with third parties and Compugen may not be successful in
generating adequate revenues or commercializing aspects of its
business model. Moreover, the development and commercialization of
therapeutic candidates involve many inherent risks, including
failure to progress to clinical trials or, if they progress to or
enter clinical trials, failure to receive regulatory approval.
These and other factors, including the ability to finance the
Company, are more fully discussed in the "Risk Factors" section of
Compugen's most recent Annual Report on Form 20-F as filed with the
Securities and Exchange Commission (SEC) as well as other documents
that may be subsequently filed by Compugen from time to time with
the SEC. In addition, any forward-looking statements represent
Compugen's views only as of the date of this release and should not
be relied upon as representing its views as of any subsequent date.
Compugen does not assume any obligation to update any
forward-looking statements unless required by law.
Company contact:
Elana
Holzman
Director, Investor Relations and Corporate Communications
Compugen Ltd.
Email: elanah@cgen.com
Tel: +972(3)-765-8124
Investor Relations contact:
Burns McClellan, Inc.
Jill Steier
Email: jsteier@burnsmc.com
Tel: +1-212-213-0006
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