Polyclonal antibody preparation that depletes T cells for GVHD prophylaxis.
Polyclonal IgG directed against multiple T-cell antigens that binds and depletes T cells via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and induction of apoptosis, leading to immunosuppression and GVHD prophylaxis.
YES
DIRECT
ATG contains antibodies that bind CD25 on T cells, leading to complement-dependent lysis, Fc-mediated ADCC, and apoptosis of CD25+ cells.
Polyclonal antibody preparation that depletes T cells for GVHD prophylaxis.
Polyclonal IgG directed against multiple T-cell antigens that binds and depletes T cells via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and induction of apoptosis, leading to immunosuppression and GVHD prophylaxis.
YES
DIRECT
Polyclonal anti–T-cell IgG binds CD28 on T cells and induces complement-dependent cytotoxicity, Fc-mediated ADCC, and apoptosis, depleting CD28+ cells.
Polyclonal antibody preparation that depletes T cells for GVHD prophylaxis.
Polyclonal IgG directed against multiple T-cell antigens that binds and depletes T cells via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and induction of apoptosis, leading to immunosuppression and GVHD prophylaxis.
YES
DIRECT
Polyclonal antibodies bind CD45 on T cells and deplete them via complement-dependent cytotoxicity and Fc-mediated ADCC, with additional induction of apoptosis.
Polyclonal antibody preparation that depletes T cells for GVHD prophylaxis.
Polyclonal IgG directed against multiple T-cell antigens that binds and depletes T cells via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and induction of apoptosis, leading to immunosuppression and GVHD prophylaxis.
NO
INDIRECT
Antithymocyte globulin binds multiple T‑cell antigens (not ICAM‑1) and depletes T cells via complement-dependent cytotoxicity, ADCC, and apoptosis; ICAM‑1–expressing cells are not directly targeted or killed by the drug.
Autologous gene-modified T cells engineered to express a CAR targeting BCMA, depleting BCMA-positive plasma cells/plasmablasts to reduce pathogenic autoantibody production in MDR-SRNS.
Autologous T cells are genetically engineered to express a chimeric antigen receptor specific for BCMA. On recognizing BCMA on plasma cells/plasmablasts, the CAR-T cells become activated and kill these BCMA-positive cells via cytotoxic mechanisms, depleting antibody-secreting cells and reducing pathogenic autoantibody production in MDR-SRNS.
YES
DIRECT
CAR-T cells bind BCMA on target cells and induce cytotoxic T-cell killing via perforin/granzyme-mediated lysis and apoptosis (and Fas–FasL pathways).