TROP2-directed antibody-drug conjugate; a humanized anti-TROP2 monoclonal antibody that is internalized upon binding and releases a topoisomerase I inhibitor payload to induce DNA damage and cell death.
Humanized anti-TROP2 monoclonal antibody binds TROP2 on tumor cells, is internalized, and releases a topoisomerase I inhibitor payload that induces DNA damage and tumor cell death.
YES
INDIRECT
The ADC binds TROP2 on tumor cells, is internalized, and releases a topoisomerase I–inhibitor payload that inhibits DNA topoisomerase I, causing DNA damage and tumor cell death.
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.
YES
DIRECT
Polyclonal antibodies bind CD2 on T cells, triggering complement-dependent cytotoxicity and Fc-mediated effector functions (ADCC/phagocytosis) and apoptosis, leading to depletion of CD2+ 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.
YES
DIRECT
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.
YES
DIRECT
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.
YES
DIRECT
ATG antibodies bind CD8 on T cells and induce depletion via complement-dependent lysis, Fc receptor–mediated ADCC/phagocytosis, and apoptosis.