Bridge Biotherapeutics Launches a Research Collaboration with Emory University School of Medicine to Explore Combination Therapy of BBT-877 for KRAS/P53 Mutant NSCLC Patients Resistant to Anti-PD-1 Blockade

SEONGNAM, South Korea and ATLANTA, March 29, 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

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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