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Headline : 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

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Tags : #bridge #biotherapeutics #launches #research #collaboration #emory #university #school #medicine #explore #combination #therapy #bbt877 #krasp53 #mutant #nsclc #patients #resistant #antipd1 #blockade



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SEONGNAM, South Korea and ATLANTA, March 28, 2024 /PRNewswire/ --ย Bridgeย 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.

Read more from the original article on here at www.prnewswire.com.


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