Rabbit polyclonal anti-thymocyte globulin that depletes T cells to prevent rejection and GVHD.
Rabbit polyclonal anti-thymocyte IgG that binds multiple T-cell surface antigens and depletes T cells via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and apoptosis, producing immunosuppression to prevent rejection and GVHD.
YES
DIRECT
ATG antibodies bind CD5 on T cells and deplete them via complement-dependent cytotoxicity and Fc-mediated ADCC, with additional apoptosis induction.
Anti-CLDN18.2 monoclonal antibody that binds Claudin 18.2 on tumor cells and mediates immune cytotoxicity (ADCC/CDC).
Anti-CLDN18.2 antibody–drug conjugate that binds Claudin 18.2 on tumor cells, is internalized, and releases the MMAE payload via a cleavable linker. MMAE binds tubulin, inhibits microtubule polymerization, and induces G2/M arrest and apoptosis in CLDN18.2-expressing cells; Fc-mediated ADCC/CDC may also contribute.
NO
INDIRECT
LM-302 targets CLDN18.2 on tumor cells, is internalized, and releases MMAE; the payload then binds the vinca site on beta-tubulin to inhibit microtubule polymerization, causing G2/M arrest and apoptosis (ADCC/CDC may also contribute). Beta-tubulin is not the targeting antigen.
Allogeneic unmodified invariant natural killer T (iNKT) cell therapy; iNKT cells recognize glycolipid antigens via CD1d, secrete Th1 cytokines, and activate NK cells, CD8 T cells, and macrophages to kill tumor and remodel the tumor microenvironment.
Allogeneic, unmodified invariant NKT cells that recognize CD1d-presented glycolipid antigens and stress ligands via invariant TCR and NKG2D, secrete Th1 cytokines (e.g., IFN-γ), activate NK cells, CD8 T cells, and macrophages, and directly lyse tumor cells to remodel the tumor microenvironment.
YES
DIRECT
AgenT-797 iNKT cells express NKG2D, which binds ULBP2 on target cells, triggering iNKT activation and direct killing via perforin/granzyme (and potentially FasL/cytokine-mediated cytotoxicity).
Allogeneic unmodified invariant natural killer T (iNKT) cell therapy; iNKT cells recognize glycolipid antigens via CD1d, secrete Th1 cytokines, and activate NK cells, CD8 T cells, and macrophages to kill tumor and remodel the tumor microenvironment.
Allogeneic, unmodified invariant NKT cells that recognize CD1d-presented glycolipid antigens and stress ligands via invariant TCR and NKG2D, secrete Th1 cytokines (e.g., IFN-γ), activate NK cells, CD8 T cells, and macrophages, and directly lyse tumor cells to remodel the tumor microenvironment.
YES
DIRECT
AgenT-797 iNKT cells express NKG2D, which binds ULBP3 on stressed/tumor cells, triggering direct cytotoxicity via perforin/granzyme-mediated lysis and apoptosis.
Allogeneic unmodified invariant natural killer T (iNKT) cell therapy; iNKT cells recognize glycolipid antigens via CD1d, secrete Th1 cytokines, and activate NK cells, CD8 T cells, and macrophages to kill tumor and remodel the tumor microenvironment.
Allogeneic, unmodified invariant NKT cells that recognize CD1d-presented glycolipid antigens and stress ligands via invariant TCR and NKG2D, secrete Th1 cytokines (e.g., IFN-γ), activate NK cells, CD8 T cells, and macrophages, and directly lyse tumor cells to remodel the tumor microenvironment.
YES
DIRECT
AgenT-797 iNKT cells express NKG2D, which binds ULBP4 on target cells and triggers direct cytotoxic killing via perforin/granzyme release (with supportive Th1 cytokines).