Genetically engineered T cells transduced via lentivirus to express a synthetic antigen receptor targeting LILRB4 (ILT3) on leukemic/myeloid cells, activating T-cell cytotoxicity; administered after lymphodepletion for R/R AML/CMML.
Autologous T cells are lentivirally engineered to express a synthetic/chimeric antigen receptor that recognizes LILRB4 (ILT3) on leukemic and immunosuppressive myeloid cells. Upon LILRB4 binding, the CAR activates T-cell signaling, leading to proliferation, cytokine release, and perforin/granzyme-mediated cytotoxicity, eliminating LILRB4-positive AML/CMML cells; lymphodepletion supports in vivo expansion and persistence.
LILRB4-targeted CAR-T cells bind LILRB4 on target cells and, upon activation, kill them via perforin/granzyme-mediated cytotoxicity (and apoptotic pathways).
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.
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.
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.
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.
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.
Chimeric anti-CD20 monoclonal antibody that depletes B cells via ADCC, CDC, and apoptosis.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B cells and depletes them via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and induction of apoptosis.
Rituximab binds CD20 on B cells and induces killing via antibody-dependent cellular cytotoxicity (Fc-mediated engagement of NK cells/macrophages), complement-dependent cytotoxicity, and can trigger apoptosis upon CD20 crosslinking.