Anti-GD2 IgG1 monoclonal antibody immunotherapy that binds GD2 on neuroblastoma cells and mediates Fc-dependent ADCC, ADCP, and CDC.
Anti-GD2 IgG1 monoclonal antibody that binds GD2 on neuroblastoma cells and triggers Fc-mediated effector functions—ADCC by NK cells, ADCP by macrophages—and complement-dependent cytotoxicity (CDC), leading to tumor cell lysis.
NO
INDIRECT
Naxitamab binds GD2 on tumor cells; its Fc engages CD16A on NK cells/macrophages to trigger ADCC/ADCP (and CDC) that kills GD2+ tumor cells, not the CD16A-expressing effector cells.
Anti-GD2 IgG1 monoclonal antibody immunotherapy that binds GD2 on neuroblastoma cells and mediates Fc-dependent ADCC, ADCP, and CDC.
Anti-GD2 IgG1 monoclonal antibody that binds GD2 on neuroblastoma cells and triggers Fc-mediated effector functions—ADCC by NK cells, ADCP by macrophages—and complement-dependent cytotoxicity (CDC), leading to tumor cell lysis.
NO
INDIRECT
Naxitamab binds GD2 on tumor cells; its Fc engages Fcγ receptors (including CD32A) on immune cells to drive ADCC/ADCP and complement activation, killing GD2-positive cells rather than CD32A-expressing cells.
Anti-GD2 IgG1 monoclonal antibody immunotherapy that binds GD2 on neuroblastoma cells and mediates Fc-dependent ADCC, ADCP, and CDC.
Anti-GD2 IgG1 monoclonal antibody that binds GD2 on neuroblastoma cells and triggers Fc-mediated effector functions—ADCC by NK cells, ADCP by macrophages—and complement-dependent cytotoxicity (CDC), leading to tumor cell lysis.
NO
INDIRECT
Naxitamab binds GD2 on tumor cells via its Fab; its Fc engages CD64 (FcγRI) on myeloid effector cells to drive ADCC/ADCP (and complement can lyse GD2+ cells). CD64+ cells serve as effectors and are not killed by the drug.
Anti-GD2 IgG1 monoclonal antibody immunotherapy that binds GD2 on neuroblastoma cells and mediates Fc-dependent ADCC, ADCP, and CDC.
Anti-GD2 IgG1 monoclonal antibody that binds GD2 on neuroblastoma cells and triggers Fc-mediated effector functions—ADCC by NK cells, ADCP by macrophages—and complement-dependent cytotoxicity (CDC), leading to tumor cell lysis.
NO
INDIRECT
Naxitamab targets GD2 on tumor cells, inducing ADCC/ADCP and CDC (via C1q binding to the antibody Fc) to lyse GD2+ cells; it does not target or kill C1q-expressing cells.
An autologous, genetically engineered BCMA-targeted CAR T-cell therapy designed to deplete BCMA-expressing plasmablasts and long-lived plasma cells to reduce pathogenic autoantibodies in refractory lupus nephritis and IgG4-related disease.
Autologous T cells are genetically engineered to express a BCMA-targeted chimeric antigen receptor. After infusion, these CAR T cells recognize and kill BCMA-expressing plasmablasts and long-lived plasma cells, depleting autoantibody-producing cells and reducing pathogenic antibodies in refractory lupus nephritis and IgG4-related disease.
YES
DIRECT
BCMA-targeted CAR T cells bind BCMA on plasmablasts/plasma cells and induce T-cell–mediated killing via perforin/granzyme release and death-receptor pathways.