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.
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.
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.
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.
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.
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.
Autologous/allogeneic T cells transduced with a lentiviral vector encoding a CD33-specific CAR; IV infusion with dose escalation; targets CD33+ myeloid blasts in AML and related myeloid malignancies.
Autologous/allogeneic T cells are lentivirally engineered to express a CD33‑specific chimeric antigen receptor. The CAR enables MHC‑independent recognition of CD33 on myeloid blasts, triggering T‑cell activation and expansion, release of perforin/granzymes and inflammatory cytokines, and subsequent cytotoxic clearance of CD33+ AML and related myeloid malignancy cells.
CD33-directed CAR T cells bind CD33 on target cells, activate, and kill them via perforin/granzyme-mediated cytolysis (with cytokine-mediated effects).