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T-1A5 is a monoclonal antibody targeting the immune checkpoint molecule B7-H3 (CD276), specifically binding to the FG loop region of the protein. Developed by researchers at the University of Texas MD Anderson Cancer Center, T-1A5 is designed to block the immunomodulatory function of B7-H3, which is often overexpressed in acute myeloid leukemia (AML) and associated with poor prognosis. By blocking B7-H3, the antibody enhances natural killer (NK) cell-mediated cytotoxicity against AML cells. A human-mouse chimeric version, chT-1A5, has demonstrated the ability to induce antibody-dependent cell-mediated cytotoxicity (ADCC) in primary AML cells while sparing healthy peripheral blood mononuclear cells. In preclinical models, T-1A5 has shown significant inhibition of leukemia growth and extended survival, particularly when combined with NK cell therapy.
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