Chimeric monoclonal antibody against EGFR that inhibits downstream signaling (RAS/MAPK, PI3K/AKT) and mediates antibody‑dependent cellular cytotoxicity (ADCC).
Chimeric monoclonal antibody that binds the extracellular domain of EGFR, blocking ligand binding and receptor dimerization/activation, thereby inhibiting downstream RAS/MAPK and PI3K/AKT signaling and tumor cell proliferation; also mediates NK cell–dependent ADCC.
NO
INDIRECT
Cetuximab binds EGFR on tumor cells; its Fc engages CD16a on NK cells to trigger ADCC, leading NK cells to kill EGFR+ targets. CD16a-expressing cells are not killed.
Autologous T cells genetically engineered to express chimeric antigen receptors targeting CD19, CD20, and BCMA; upon antigen binding, CAR signaling (CD3ζ with costimulatory domains) activates T-cell proliferation, cytokine release, and cytotoxic killing of malignant B-lineage and plasma cells.
Autologous T cells are genetically engineered to express chimeric antigen receptors recognizing CD19, CD20, and BCMA; antigen binding activates CD3zeta and costimulatory signaling, inducing T-cell activation, proliferation, cytokine release, and perforin/granzyme-mediated cytotoxic killing of malignant B-lineage cells and plasma cells, with multi-antigen targeting to limit antigen escape.
YES
DIRECT
CAR-T cells recognize CD19 and, upon CAR signaling, induce T-cell cytotoxicity via perforin/granzyme-mediated lysis (and apoptosis) of CD19+ cells.
Autologous T cells genetically engineered to express chimeric antigen receptors targeting CD19, CD20, and BCMA; upon antigen binding, CAR signaling (CD3ζ with costimulatory domains) activates T-cell proliferation, cytokine release, and cytotoxic killing of malignant B-lineage and plasma cells.
Autologous T cells are genetically engineered to express chimeric antigen receptors recognizing CD19, CD20, and BCMA; antigen binding activates CD3zeta and costimulatory signaling, inducing T-cell activation, proliferation, cytokine release, and perforin/granzyme-mediated cytotoxic killing of malignant B-lineage cells and plasma cells, with multi-antigen targeting to limit antigen escape.
YES
DIRECT
CAR-T cells bind CD20 via the CAR; CD3ζ/costimulatory signaling activates T-cell cytotoxicity, causing perforin/granzyme-mediated lysis (and Fas/FasL apoptosis) of CD20+ cells.
Autologous T cells genetically engineered to express chimeric antigen receptors targeting CD19, CD20, and BCMA; upon antigen binding, CAR signaling (CD3ζ with costimulatory domains) activates T-cell proliferation, cytokine release, and cytotoxic killing of malignant B-lineage and plasma cells.
Autologous T cells are genetically engineered to express chimeric antigen receptors recognizing CD19, CD20, and BCMA; antigen binding activates CD3zeta and costimulatory signaling, inducing T-cell activation, proliferation, cytokine release, and perforin/granzyme-mediated cytotoxic killing of malignant B-lineage cells and plasma cells, with multi-antigen targeting to limit antigen escape.
YES
DIRECT
CAR-T cells recognize BCMA and, upon engagement, activate and kill BCMA+ cells via perforin/granzyme release (and death-receptor pathways).
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.
NO
INDIRECT
ATG depletes T cells by binding T-cell surface antigens (e.g., CD2, CD3, CD4, CD8) and inducing complement-mediated lysis, ADCC, and apoptosis; it does not specifically target HLA-B to kill HLA-B–expressing cells.