Investigational antibody–drug conjugate carrying a topoisomerase I inhibitor payload; binds a tumor-associated antigen to deliver the cytotoxin intracellularly, causing DNA single-strand breaks/replication stress and tumor-cell apoptosis (possible bystander effect).
Nectin-4–targeted IgG1 antibody–drug conjugate with a cleavable linker delivering a topoisomerase I inhibitor payload; upon antigen binding and internalization, the payload is released to inhibit topoisomerase I, causing DNA single-strand breaks/replication stress, cell-cycle arrest, and apoptosis in nectin-4–expressing tumor cells (with potential bystander effect).
The ADC binds Nectin-4 on target cells, is internalized, and the cleavable linker releases a topoisomerase I inhibitor that causes DNA damage/replication stress, leading to cell-cycle arrest and apoptosis (with potential bystander effect).
Intravenous chimeric IgG1 anti‑EGFR monoclonal antibody that blocks EGFR ligand binding/signaling and triggers antibody‑dependent cellular cytotoxicity (ADCC).
Chimeric IgG1 monoclonal antibody targeting EGFR; binds the extracellular domain to block ligand binding and receptor dimerization/activation, inhibiting downstream MAPK signaling and tumor cell proliferation, with additional antitumor activity via Fc-mediated ADCC.
Cetuximab binds EGFR on target cells and its IgG1 Fc engages Fc gamma receptor–bearing effector cells (e.g., NK cells) to trigger ADCC (and some complement-mediated cytotoxicity), leading to lysis of EGFR+ cells; it also blocks EGFR signaling (anti-proliferative).
Autologous, fully human anti-CD19 CAR T-cell therapy that engineers patient T cells to target and lyse CD19+ B-lineage cells, depleting naïve/memory B cells and plasmablasts/early plasma cells to reduce B-cell antigen presentation, inflammatory cytokines, and autoantibody production.
Autologous T cells are engineered to express an anti‑CD19 chimeric antigen receptor (scFv–CD8α hinge/transmembrane–CD28 costimulatory–CD3ζ signaling). Upon reinfusion, these CAR T cells recognize CD19 on B-lineage cells and lyse CD19+ naïve and memory B cells and plasmablasts/early plasma cells, depleting B cells and reducing antigen presentation, proinflammatory cytokines, and autoantibody production.
Anti‑CD19 CAR T cells bind CD19 on target cells and kill them via T‑cell cytotoxic pathways (perforin/granzyme-mediated apoptosis, Fas/FasL).
B-cell–depleting monoclonal antibody that removes CD20+ B cells via ADCC, CDC, and apoptosis, generally sparing long-lived plasma cells.
Monoclonal antibody targeting CD20 on B cells that depletes CD20+ B cells via antibody-dependent cellular cytotoxicity (ADCC), complement-dependent cytotoxicity (CDC), and apoptosis, generally sparing long-lived plasma cells.
Binding to CD20 on B cells triggers Fc-mediated ADCC by NK cells/macrophages, activates complement (CDC), and can directly induce apoptosis, leading to depletion of CD20+ cells.