Rabbit-derived polyclonal IgG immunosuppressant that depletes and functionally modulates T lymphocytes via complement-dependent cytotoxicity, apoptosis, and Fc-mediated clearance; preferentially reduces autoreactive effector/memory T cells and may spare or promote regulatory T cells to attenuate islet autoimmunity.
Rabbit-derived polyclonal IgG (anti-thymocyte globulin) that binds multiple T-cell surface antigens (e.g., CD2/CD3/CD4/CD8), inducing T-cell depletion via complement-dependent cytotoxicity, apoptosis, and Fc receptor–mediated clearance; preferentially reduces autoreactive effector/memory T cells while relatively sparing or promoting regulatory T cells, thereby suppressing TCR-driven and cytokine-mediated immune responses and attenuating islet autoimmunity.
ATG antibodies bind CD3 on T cells and deplete them via complement-dependent cytotoxicity, Fc receptor–mediated ADCC/ADCP, and apoptosis.
Rabbit-derived polyclonal IgG immunosuppressant that depletes and functionally modulates T lymphocytes via complement-dependent cytotoxicity, apoptosis, and Fc-mediated clearance; preferentially reduces autoreactive effector/memory T cells and may spare or promote regulatory T cells to attenuate islet autoimmunity.
Rabbit-derived polyclonal IgG (anti-thymocyte globulin) that binds multiple T-cell surface antigens (e.g., CD2/CD3/CD4/CD8), inducing T-cell depletion via complement-dependent cytotoxicity, apoptosis, and Fc receptor–mediated clearance; preferentially reduces autoreactive effector/memory T cells while relatively sparing or promoting regulatory T cells, thereby suppressing TCR-driven and cytokine-mediated immune responses and attenuating islet autoimmunity.
ATG antibodies bind CD4 on T cells and induce complement-mediated lysis and Fc receptor–mediated ADCC/phagocytosis, leading to depletion/apoptosis of CD4+ cells.
Rabbit-derived polyclonal IgG immunosuppressant that depletes and functionally modulates T lymphocytes via complement-dependent cytotoxicity, apoptosis, and Fc-mediated clearance; preferentially reduces autoreactive effector/memory T cells and may spare or promote regulatory T cells to attenuate islet autoimmunity.
Rabbit-derived polyclonal IgG (anti-thymocyte globulin) that binds multiple T-cell surface antigens (e.g., CD2/CD3/CD4/CD8), inducing T-cell depletion via complement-dependent cytotoxicity, apoptosis, and Fc receptor–mediated clearance; preferentially reduces autoreactive effector/memory T cells while relatively sparing or promoting regulatory T cells, thereby suppressing TCR-driven and cytokine-mediated immune responses and attenuating islet autoimmunity.
ATG antibodies bind CD8 on T cells and induce depletion via complement-dependent lysis, Fc receptor–mediated ADCC/phagocytosis, and apoptosis.
Investigational immunotherapy; protocol suggests it is a CD137 (4-1BB) costimulatory agonist, likely a monoclonal antibody that activates cytotoxic T cells and NK cells.
ZL-1310 is an anti-DLL3 antibody-drug conjugate. It binds DLL3 on tumor cells (e.g., SCLC), is internalized, and delivers a linked cytotoxic payload that induces death of DLL3-expressing cells.
ADC binds DLL3 on tumor cells, is internalized, and releases a cytotoxic payload inside the cell, causing death of DLL3-expressing cells.
An autologous, genetically engineered anti-CD19 chimeric antigen receptor (CAR) T-cell therapy. Patient T cells are modified to express a CD19-specific CAR with CD28 costimulatory and CD3ζ signaling domains. Administered as a single infusion of CAR-positive viable T cells (target 2×10^6 cells/kg; maximum 2×10^8 cells). Upon CD19 engagement on B cells, CAR T cells activate cytotoxicity, proliferate, and release cytokines, leading to depletion of CD19+ lymphoma cells.
Autologous T cells are engineered to express a CD19-specific chimeric antigen receptor with CD28 costimulatory and CD3ζ signaling domains. Upon binding CD19 on B cells, the CAR T cells activate, proliferate, release cytokines, and kill target cells via cytotoxic mechanisms (perforin/granzyme), resulting in depletion of CD19+ lymphoma cells.
CD19-specific CAR T cells bind CD19 on target B cells, form an immunologic synapse, and kill via perforin/granzyme-mediated cytolysis and death-receptor apoptosis.