Anti-CD19 monoclonal antibody given IV that depletes CD19+ B-lineage cells (naive/memory B cells, plasmablasts, some plasma cells) via cytotoxic mechanisms, reducing AQP4-IgG and B-cell–mediated inflammation.
Humanized, afucosylated IgG1 anti‑CD19 monoclonal antibody that binds CD19 on B‑lineage cells (naive/memory B cells, plasmablasts, some plasma cells) and depletes them primarily via enhanced antibody‑dependent cellular cytotoxicity (and complement‑mediated lysis), thereby reducing AQP4‑IgG production and B‑cell–mediated inflammation.
YES
DIRECT
Inebilizumab binds CD19 on B-lineage cells and triggers Fc-mediated effector functions—enhanced ADCC by NK cells/macrophages and complement-dependent cytotoxicity (and phagocytosis)—leading to depletion of CD19+ cells.
Anti-TROP2 antibody–drug conjugate that delivers the topoisomerase I inhibitor SN-38 to TROP2-expressing tumor cells.
Anti-TROP2 monoclonal antibody–drug conjugate that binds TROP2 on tumor cells, is internalized, and releases the topoisomerase I inhibitor SN-38, which stabilizes topo I–DNA complexes causing DNA breaks, inhibition of DNA replication, and apoptosis; can produce a bystander effect in neighboring cells.
YES
DIRECT
Anti-TROP2 ADC binds TROP2, is internalized, and releases SN-38 (topoisomerase I inhibitor) causing topo I–DNA complex stabilization, DNA damage, replication arrest, and apoptosis; may also produce a bystander effect.
Anti-TROP2 antibody–drug conjugate that delivers the topoisomerase I inhibitor SN-38 to TROP2-expressing tumor cells.
Anti-TROP2 monoclonal antibody–drug conjugate that binds TROP2 on tumor cells, is internalized, and releases the topoisomerase I inhibitor SN-38, which stabilizes topo I–DNA complexes causing DNA breaks, inhibition of DNA replication, and apoptosis; can produce a bystander effect in neighboring cells.
NO
INDIRECT
Sacituzumab govitecan binds TROP2 (not topoisomerase I), is internalized, and releases SN-38, which inhibits topoisomerase I to cause DNA damage and apoptosis. Killing depends on TROP2-mediated delivery; topoisomerase I is the intracellular payload target, not the directly targeted antigen.
Genetically engineered natural killer (NK) cells expressing an anti-CD19 chimeric antigen receptor to recognize and eliminate CD19+ B cells via NK cytotoxic pathways, intended to deplete autoreactive B cells/plasmablasts in refractory ITP.
Genetically engineered natural killer (NK) cells expressing an anti-CD19 chimeric antigen receptor selectively bind CD19 on B cells/plasmablasts and eliminate them via NK cytotoxic pathways (perforin/granzyme release and death receptor signaling), depleting autoreactive B cells to reduce pathogenic autoantibody production in refractory ITP.
YES
DIRECT
Anti-CD19 CAR-expressing NK cells recognize CD19 on B cells and directly lyse them via CAR-triggered NK cytotoxic pathways (perforin/granzyme release and death receptor–mediated apoptosis).
IgG monoclonal antibodies targeting CD38 on myeloma cells, mediating ADCC/CDC and direct cytotoxicity.
Unconjugated IgG monoclonal antibodies that bind CD38 on myeloma cells and induce Fc-mediated effector functions (antibody-dependent cellular cytotoxicity, antibody-dependent cellular phagocytosis, complement-dependent cytotoxicity) and direct apoptotic signaling, resulting in depletion of CD38-positive tumor and immunosuppressive cells.
YES
DIRECT
Anti-CD38 IgG binds CD38 on target cells and recruits immune effectors via its Fc to mediate NK cell ADCC, macrophage ADCP, and complement-dependent cytotoxicity, and can also trigger apoptotic signaling, leading to depletion of CD38+ cells.