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Asher Bio Presents New Data Demonstrating Preclinical Proof-of-Concept for AB359, a Highly Selective CD8-Targeted IL-2 Therapy, for Chronic Hepatitis B (HBV) at AASLD 2022

Excerpt from the Press Release:

SOUTH SAN FRANCISCO, Calif.–(BUSINESS WIRE)–Asher Biotherapeutics, Inc. (Asher Bio), a biotechnology company focused on developing therapies to precisely engage specific immune cells to fight cancer, chronic viral infection and autoimmune disease, today announced new preclinical data demonstrating proof-of-concept for AB359 as a novel immunotherapy approach for chronic HBV. AB359 is Asher Bio’s CD8-targeted interleukin-2 (IL-2) immunotherapy for the treatment of chronic viral infection. The data will be presented in a poster presentation at the American Association for the Study of Liver Disease (AASLD) 2022 Annual Meeting, being held in Washington, DC, on November 4-8, 2022.

“We are pleased to share these foundational preclinical data for AB359, demonstrating the broad applicability of our cis-targeting approach to potentially overcome key shortcomings of cytokine therapeutics and immunotherapies across a range of therapeutic areas, including oncology and now chronic viral infection,” said Andy Yeung, Ph.D., Chief Technology Officer and Co-founder of Asher Bio. “Chronic HBV is a major global health burden, which affects over 250 million people worldwide. Existing antiviral standard of care medicines, however, are indicated for only a subset of patients and offer low cure rates. Using our modular cis-targeting platform, we developed AB359 to selectively activate CD8+ T cells, which are important for clearing viruses, but become dysfunctional in patients with chronic HBV. We look forward to continuing to advance AB359 through preclinical development.”

CD8+ T cells have been shown to be involved in clearing some viral infections, including HBV. While functional HBV-reactive CD8+ T cells are detectable in HBV patients that clear viral infection, they are challenging to detect in patients with chronic HBV, suggesting the responses of CD8+ T cells against HBV antigens may be deficient in chronically infected patients

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