Antibody–drug conjugate targeting CD79b on B cells; internalization releases MMAE to disrupt microtubules, causing mitotic arrest and apoptosis; may also mediate ADCC.
Anti-CD79b antibody–drug conjugate; after binding CD79b on B cells, the complex is internalized and a protease-cleavable linker releases MMAE, which inhibits tubulin polymerization, causing G2/M arrest and apoptosis; Fc engagement may also mediate ADCC.
YES
DIRECT
ADC binds CD79b on B cells, is internalized, and releases MMAE, which inhibits tubulin polymerization causing G2/M arrest and apoptosis; Fc engagement may also trigger ADCC.
Antibody–drug conjugate targeting CD79b on B cells; internalization releases MMAE to disrupt microtubules, causing mitotic arrest and apoptosis; may also mediate ADCC.
Anti-CD79b antibody–drug conjugate; after binding CD79b on B cells, the complex is internalized and a protease-cleavable linker releases MMAE, which inhibits tubulin polymerization, causing G2/M arrest and apoptosis; Fc engagement may also mediate ADCC.
NO
INDIRECT
The ADC binds CD79b on B cells, is internalized, and releases MMAE, which binds the beta‑tubulin vinca site to block microtubule polymerization, causing G2/M arrest and apoptosis; Fc-mediated ADCC may also contribute.
Chimeric anti-CD20 monoclonal antibody that depletes B cells via ADCC, complement-dependent cytotoxicity, and direct apoptosis.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B cells and depletes them via antibody-dependent cellular cytotoxicity (ADCC), complement-dependent cytotoxicity (CDC), and direct induction of apoptosis.
YES
DIRECT
Rituximab binds CD20 on B cells and eliminates them via Fc-mediated ADCC by immune effectors, complement-dependent cytotoxicity (MAC formation), and direct pro-apoptotic signaling.
Intravenous anti-CD38 monoclonal antibody, 16 mg/kg weekly for 8 doses; binds CD38 on plasma cells (including long-lived autoreactive plasma cells/plasmablasts), depleting them via Fc-mediated effector functions (ADCC/CDC/ADCP) and apoptosis to reduce pathogenic anti-platelet autoantibodies in pediatric refractory/relapsed ITP.
Humanized anti‑CD38 monoclonal antibody that binds CD38 on plasma cells/plasmablasts and depletes them via Fc‑mediated effector functions (ADCC, CDC, ADCP) and apoptosis, reducing pathogenic anti‑platelet autoantibodies in ITP.
YES
DIRECT
Anti-CD38 mAb binds CD38 on target cells and depletes them via Fc-mediated ADCC (NK cells), complement-dependent cytotoxicity, antibody-dependent cellular phagocytosis, and apoptosis.
Autologous dendritic cell cancer vaccine engineered to present WT1 antigens via MHC I/II and surface-display the IL-15/IL-15Rα complex to enhance CD8+ T-cell and NK-cell activation, proliferation, cytotoxicity, and memory.
Autologous dendritic cells engineered to present WT1 antigens on MHC I/II and to surface-transpresent the IL-15/IL-15Ralpha complex, thereby priming and expanding WT1-specific CD8+ and CD4+ T cells and enhancing CD8+ T-cell and NK-cell activation, proliferation, cytotoxicity, survival, and memory via IL-15 signaling.
YES
INDIRECT
Dendritic-cell vaccination presents WT1 peptides and trans-presents IL-15 to prime/expand WT1-specific CD8+ T cells and activate NK cells. These effectors recognize WT1 peptide–MHC on tumor cells and kill them via perforin/granzyme (and Fas/FasL) pathways.