SEONGNAM, South Korea and
ATLANTA, March 28, 2024 /PRNewswire/
-- Bridge Biotherapeutics (KQ288330), a South Korean
clinical-stage biotech company developing novel drugs for cancer,
fibrosis, and inflammation, announced a research collaboration with
Dr. Jessica M. Konen's Lab at
Emory University School of
Medicine.
The collaboration will explore the potential therapeutic
benefits of combination therapy of BBT-877, a novel autotaxin (ATX)
inhibitor, with anti-PD-1 immunotherapy for the treatment of
non-small cell lung cancer (NSCLC) in patients harboring KRAS and
P53 (KP) mutations who are resistant to anti-PD-1 blockade.
As a member of the cancer immunology research program at Winship
Cancer Institute of Emory University,
Dr. Konen's research has shown that autotaxin has a direct impact
on the body's immune response to tumors. Specifically, higher
levels of ATX expression are associated with a decrease in the
number of tumor-infiltrating CD8 T cells and an increase in
inflammatory gene signatures, including those related to the
cytolytic activity of CD8 T cells. Furthermore, an activated
tumor-immune microenvironment upregulates ATX and thus provides
opportunities for acquired resistance to anti-PD-1
treatment.[i]
From their in vitro studies, the company and the
laboratory found that BBT-877 induces CD4 and CD8 T cell
proliferation and activation markers, with a robust increase in CD8
T cells that express Granzyme B. The ongoing research collaboration
is dedicated to investigating the potential benefits of combining
BBT-877 with anti-PD-1 therapy as a treatment approach.
"We are excited to collaborate with Dr. Konen's team at
Emory University School of Medicine to
explore the potential of BBT-877 in overcoming resistance to
anti-PD-1 therapy in NSCLC patients with KRAS and P53 mutations as
a combination therapy with immuno-oncology agents," said
James Lee, CEO of Bridge
Biotherapeutics. "We believe that Dr. Konen's research on the role
of autotaxin in immunosuppression has the potential to
significantly improve treatment outcomes for those patients who are
resistant to anti-PD-1 therapy."
"This collaboration presents a promising opportunity to
translate our scientific understanding of autotaxin's role in
immunotherapy resistance into a novel therapeutic approach for
KRAS/P53 mutant NSCLC patients," said Dr. Jessica Konen, Department of Hematology and
Medical Oncology Instructor at Emory
University School of Medicine. "We are pleased to work with
Bridge Biotherapeutics to explore indication expansion into NSCLC
through a combination of BBT-877 with anti-PD-1 agent and
potentially offer new hope to those patients."
Under the terms of the collaboration, Bridge Biotherapeutics
will provide financial support and access to BBT-877, while Dr.
Jessica Konen's Lab will contribute
its expertise in immunology and oncology. Together, the two
entities will conduct preclinical studies to evaluate the
therapeutic potential of BBT-877 in enhancing anti-tumor
immunity.
About Bridge Biotherapeutics, Inc.
Bridge Biotherapeutics Inc., based in the Republic of Korea and
the U.S., is a publicly traded, clinical-stage biotech company
founded in 2015. Bridge Biotherapeutics is engaged in the discovery
and development of novel therapeutics, focusing on therapeutic
areas with high unmet needs, including fibrotic diseases and
cancers. The company is developing BBT-877, a novel autotaxin
inhibitor for the treatment of fibrotic diseases including
idiopathic pulmonary fibrosis (IPF), and BBT-207, a potent targeted
cancer therapy for non-small cell lung cancer (NSCLC) with EGFR
C797S mutations. Learn more at https://www.bridgebiorx.com/en/.
About Autotaxin
Autotaxin (ATX), a protein of approximately 900 amino acids
discovered in the early 1990s, is an important enzyme for
generating the lipid-signaling molecule, lysophosphatidic acid
(LPA). Autotaxin's lysophospholipase D activity converts
lysophosphatidylcholine (LPC) into LPA, which engages in signaling
via LPA receptors. LPA signaling results in cell proliferation,
migration, secretion of cytokines and chemokines, and reduction of
cell apoptosis. Ultimately, autotaxin has a pathogenic role in
processes of inflammation and fibrosis, making it an attractive
drug target.
[i] Konen, Jessica M et
al. "Autotaxin suppresses cytotoxic T cells via LPAR5 to promote
anti-PD-1 resistance in non-small cell lung cancer." The Journal of
clinical investigation vol. 133,17 e163128. 1 Sep. 2023,
doi:10.1172/JCI163128
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SOURCE Bridge Biotherapeutics, Inc.