Antibody–drug conjugate targeting Nectin-4 that delivers the microtubule-disrupting payload MMAE to induce tumor cell death.
Nectin-4–targeted antibody–drug conjugate; the antibody binds Nectin-4 on tumor cells, is internalized, and a cleavable linker releases MMAE, which binds tubulin to inhibit microtubule polymerization, causing G2/M arrest and apoptotic cell death in Nectin-4–expressing tumors.
The ADC binds Nectin-4 on target cells, is internalized, and releases MMAE, which inhibits tubulin polymerization, causing G2/M arrest and apoptosis.
Anti-CD20 monoclonal antibody that induces ADCC/CDC and apoptosis of CD20-positive B cells.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B cells and depletes CD20-positive lymphocytes via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and direct induction of apoptosis.
Rituximab binds CD20 on B cells and eliminates them via Fc-mediated ADCC and complement-dependent cytotoxicity; it can also trigger apoptosis upon CD20 crosslinking.
Anti-CD20 monoclonal antibody that depletes CD20-positive B-cell blasts via complement-dependent cytotoxicity and antibody-dependent cellular cytotoxicity.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B cells and B-lymphoblasts, triggering complement-dependent cytotoxicity and antibody-dependent cellular cytotoxicity to deplete CD20-positive cells.
Rituximab binds CD20 on B cells and triggers complement-dependent cytotoxicity and Fc-mediated effector killing (ADCC/ADCP), directly eliminating CD20+ cells.
Autologous, gene-modified CAR T-cell therapy engineered to co-target CD19 and BCMA to deplete CD19+ B cells and BCMA+ plasmablasts/long-lived plasma cells, aiming to reset humoral immunity and reduce autoantibody production in lupus nephritis and IgG4-related disease.
Autologous gene‑modified T cells expressing dual CARs targeting CD19 and BCMA selectively recognize and kill CD19+ B cells and BCMA+ plasmablasts/long‑lived plasma cells, depleting pathogenic B‑lineage compartments to reduce autoantibody production and reset humoral immunity in autoimmune disease.
CD19-directed CAR T cells bind CD19 on target cells and kill them via T cell cytotoxicity (immune synapse formation, perforin/granzyme release, and apoptosis pathways such as Fas-FasL).
Autologous, gene-modified CAR T-cell therapy engineered to co-target CD19 and BCMA to deplete CD19+ B cells and BCMA+ plasmablasts/long-lived plasma cells, aiming to reset humoral immunity and reduce autoantibody production in lupus nephritis and IgG4-related disease.
Autologous gene‑modified T cells expressing dual CARs targeting CD19 and BCMA selectively recognize and kill CD19+ B cells and BCMA+ plasmablasts/long‑lived plasma cells, depleting pathogenic B‑lineage compartments to reduce autoantibody production and reset humoral immunity in autoimmune disease.
Anti-BCMA CAR T cells recognize BCMA on target cells and directly kill them via T-cell cytotoxic mechanisms (perforin/granzyme and Fas–FasL–mediated apoptosis).