Type II, glycoengineered anti-CD20 IgG1 monoclonal antibody that depletes CD20+ B cells via ADCC/ADCP and direct cell death, reducing anti-PLA2R autoantibodies.
Type II, glycoengineered anti-CD20 IgG1 that binds CD20 on B cells and depletes CD20+ B cells via enhanced Fc gamma RIII–mediated ADCC/ADCP and direct cell death, reducing pathogenic anti-PLA2R autoantibodies.
NO
INDIRECT
Obinutuzumab does not target CD16b; its Fc engages FcγRIIIb on effector cells (e.g., neutrophils) to mediate ADCC/ADCP against CD20+ B cells, which are the cells killed (along with direct cell death upon CD20 binding). CD16b+ cells are effectors, not targets.
Anti-CD20 monoclonal antibody that depletes CD20+ B cells via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and apoptosis.
Chimeric anti‑CD20 monoclonal antibody that binds CD20 on B cells and depletes CD20+ cells via antibody‑dependent cellular cytotoxicity, complement‑dependent cytotoxicity, and induction of apoptosis.
YES
DIRECT
Rituximab binds CD20 on B cells and triggers Fc-mediated ADCC by NK cells/macrophages and complement-dependent cytotoxicity; it can also induce apoptosis upon CD20 cross‑linking.
Anti-CD38 monoclonal antibody mediating CDC, ADCC, ADCP, and apoptosis, and depleting CD38+ immunosuppressive cells.
Human IgG1k anti-CD38 monoclonal antibody that binds CD38 on malignant plasma cells and other CD38+ cells, inducing complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, antibody-dependent cellular phagocytosis, and apoptosis; also depletes CD38+ immunosuppressive cells (e.g., Tregs, Bregs, MDSCs), enhancing antitumor immunity.
YES
DIRECT
Anti-CD38 IgG1 binds CD38 on target cells and triggers Fc-mediated complement-dependent cytotoxicity (CDC), antibody-dependent cellular cytotoxicity (ADCC) by NK cells, antibody-dependent cellular phagocytosis (ADCP) by macrophages, and can induce apoptosis upon crosslinking.
Humanized anti-CD20 monoclonal antibody used as a high-efficacy disease-modifying therapy (DMT) to deplete CD20+ B cells in multiple sclerosis.
Humanized anti-CD20 IgG1 monoclonal antibody that binds CD20 on B lymphocytes and depletes them via antibody-dependent cellular cytotoxicity and complement-dependent cytotoxicity, reducing B-cell–mediated immune activity in multiple sclerosis.
YES
DIRECT
Ocrelizumab binds CD20 on B cells and triggers complement-dependent cytotoxicity and Fc-mediated ADCC (and phagocytosis), leading to lysis/depletion of CD20+ cells.
Humanized IgG1 monoclonal antibody targeting CCR4 that mediates antibody-dependent cellular cytotoxicity (ADCC) to deplete CCR4-positive malignant T cells and regulatory/Th2 T cells in CTCL (mycosis fungoides/Sézary syndrome).
Humanized IgG1 monoclonal antibody against CCR4 (CD194) that binds CCR4 on malignant T cells and CCR4+ Tregs/Th2 cells, blocks CCR4 chemokine signaling/trafficking, and induces Fc-mediated ADCC to deplete CCR4-positive cells, thereby reducing immunosuppressive Tregs and exerting antitumor activity in CTCL.
YES
DIRECT
IgG1 anti-CCR4 binds CCR4 on target cells and engages Fc-gamma receptor-bearing effector cells (e.g., NK cells) to mediate ADCC, killing CCR4+ cells; may also trigger complement-dependent cytotoxicity.