BSI-093

BSI-093 is a humanized anti-BTN3A monoclonal antibody capable of binding to BTN3A on the surface of tumor cells to mediate conformational changes in the BTN3A/BTN2A1 complex. This process deconstructs the resting-state BTN3A/BTN2A1 oligomers and exposes the Vγ9Vδ2 TCR binding site, thereby activating Vγ9Vδ2 T cells in a phosphoantigen (pAg)-independent manner and initiating Vγ9Vδ2 T cell-mediated antitumor immunity. Compared to conventional αβ T cells, the Vγ9Vδ2 T cell-mediated tumor immunity mediated by BSI-093 features MHC-independent recognition, which translates into better tolerability and a lower risk of off-target effects. In head-to-head comparisons, BSI-093 demonstrated superior in vitro killing activity and in vivo efficacy compared to ICT01 (ImCheck Therapeutics), a first-in-class anti-BTN3A antibody, while showing a wider therapeutic window in non-human primates (NHPs) and a potentially prolonged half-life achieved through engineering. BTN3A is overexpressed in a wide range of solid tumors (e.g., melanoma, urothelial carcinoma) and hematological malignancies (e.g., acute myeloid leukemia [AML]), offering broad application prospects for a large patient population. Currently, the project is advancing through IND-enabling studies at full speed, with the IND filing anticipated in the third quarter of 2026 (3Q 2026).