Chimeric anti-CD20 monoclonal antibody that depletes CD20+ B lymphocytes via complement activation, ADCC, and apoptosis, reducing pathogenic humoral activity and B–T cell interactions.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B lymphocytes and depletes them via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and apoptosis, reducing pathogenic humoral activity and B–T cell interactions.
YES
DIRECT
Rituximab binds CD20 on B cells and induces killing via complement-dependent cytotoxicity and Fc-mediated ADCC; crosslinking can also trigger apoptosis.
Chimeric IgG1 monoclonal antibody targeting EGFR; blocks ligand binding to inhibit downstream signaling (RAS/RAF/MEK/ERK, PI3K/AKT) and can induce ADCC against EGFR-expressing tumor cells.
Cetuximab is a chimeric IgG1 monoclonal antibody against EGFR that binds the receptor’s extracellular domain, blocking ligand binding and receptor dimerization/activation, thereby inhibiting downstream RAS/RAF/MEK/ERK and PI3K/AKT signaling to suppress tumor cell proliferation; its Fc region can also mediate antibody-dependent cellular cytotoxicity (ADCC) against EGFR-expressing cells.
YES
DIRECT
Cetuximab binds EGFR on target cells and its IgG1 Fc engages Fcγ receptor–bearing immune cells (e.g., NK cells) to mediate ADCC (and some CDC), resulting in lysis of EGFR-expressing cells.
Chimeric IgG1 monoclonal antibody targeting EGFR; blocks ligand binding to inhibit downstream signaling (RAS/RAF/MEK/ERK, PI3K/AKT) and can induce ADCC against EGFR-expressing tumor cells.
Cetuximab is a chimeric IgG1 monoclonal antibody against EGFR that binds the receptor’s extracellular domain, blocking ligand binding and receptor dimerization/activation, thereby inhibiting downstream RAS/RAF/MEK/ERK and PI3K/AKT signaling to suppress tumor cell proliferation; its Fc region can also mediate antibody-dependent cellular cytotoxicity (ADCC) against EGFR-expressing cells.
NO
INDIRECT
Cetuximab binds EGFR on tumor cells; its Fc engages FCGR3A (CD16a) on NK cells to trigger ADCC, which kills EGFR-positive cells, not the FCGR3A-expressing effector cells.
Polyclonal antibody preparation that depletes T cells to reduce graft rejection and GVHD.
Polyclonal anti–T-cell immunoglobulins that bind multiple T-cell surface antigens and deplete T cells via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and phagocytic clearance, producing immunosuppression to prevent graft rejection and GVHD.
YES
DIRECT
ATG contains antibodies against CD2; binding to CD2+ cells triggers complement-dependent lysis and Fc-mediated ADCC, with additional opsonization leading to phagocytic clearance.
Polyclonal antibody preparation that depletes T cells to reduce graft rejection and GVHD.
Polyclonal anti–T-cell immunoglobulins that bind multiple T-cell surface antigens and deplete T cells via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and phagocytic clearance, producing immunosuppression to prevent graft rejection and GVHD.
YES
DIRECT
ATG antibodies bind CD3 on T cells, opsonizing them and inducing complement-dependent cytotoxicity, Fc-mediated ADCC, and phagocytic clearance, depleting CD3+ cells.