A bispecific T‑cell–engaging monoclonal antibody (REGN5458) that binds BCMA on plasma cells and CD3 on T cells to redirect cytotoxic T‑cell activity against BCMA-expressing plasma cells in MGUS/smoldering myeloma.
Linvoseltamab (REGN5458) is a bispecific monoclonal antibody that binds BCMA on plasma cells and CD3 on T cells, bringing T cells into close proximity to BCMA+ cells to form an immune synapse. This triggers TCR/CD3-mediated T‑cell activation, cytokine release, and perforin/granzyme‑mediated cytotoxicity, selectively lysing BCMA‑expressing plasma cells.
Bispecific BCMA×CD3 antibody redirects and activates T cells against BCMA+ cells, causing perforin/granzyme-mediated cytolysis (with cytokine release) of the target cells.
Anti-CD20×CD3 bispecific IgG T-cell–engaging antibody that links CD20 on B cells to CD3 on T cells to activate cytotoxic T cells and kill CD20+ B cells.
Bispecific anti-CD20xCD3 IgG antibody that binds CD20 on B cells and CD3 on T cells, redirecting and activating cytotoxic T cells to form an immune synapse and kill CD20-positive B cells.
Bispecific antibody links CD20 on target B cells to CD3 on T cells, forming an immune synapse; activated T cells kill CD20+ cells via perforin/granzyme-mediated cytotoxicity.
Anti-CD20 monoclonal antibody mediating ADCC, complement-dependent cytotoxicity, and apoptosis of CD20+ B cells.
Chimeric anti‑CD20 monoclonal antibody that binds CD20 on B lymphocytes and induces B‑cell depletion via antibody‑dependent cellular cytotoxicity, complement‑dependent cytotoxicity, and direct apoptosis of CD20+ cells.
Binds CD20 on B cells and induces killing via Fc-mediated ADCC, complement-dependent cytotoxicity, and direct apoptosis of CD20+ cells.
Humanized IgG1 monoclonal antibody against HER2/ERBB2 that inhibits receptor signaling/dimerization and mediates ADCC.
Humanized IgG1 monoclonal antibody against HER2/ERBB2 that binds the extracellular receptor, inhibits HER2 signaling and dimerization, promotes receptor downregulation, and induces Fc-gamma receptor–mediated ADCC against HER2-overexpressing tumor cells.
Trastuzumab binds HER2 on tumor cells and its Fc engages Fc-gamma receptors on NK cells/other effectors to trigger ADCC (and phagocytosis), killing the cells; it also inhibits HER2 signaling.
Anti-EGFR chimeric monoclonal antibody that inhibits EGFR signaling and can induce antibody-dependent cellular cytotoxicity.
Cetuximab is a chimeric IgG1 monoclonal antibody that binds the extracellular domain of EGFR, blocking ligand binding and receptor dimerization, thereby inhibiting downstream signaling (e.g., RAS–RAF–MEK–ERK and PI3K–AKT) to reduce tumor cell proliferation and survival; it can also mediate antibody‑dependent cellular cytotoxicity (ADCC).
Cetuximab binds EGFR on target cells and its IgG1 Fc engages Fcγ receptor–bearing effector cells (e.g., NK cells, macrophages), triggering antibody‑dependent cellular cytotoxicity; complement-mediated lysis may also contribute.