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.
YES
DIRECT
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.
YES
DIRECT
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).
YES
DIRECT
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.
An autologous, gene-modified chimeric antigen receptor T-cell (CAR-T) therapy engineered to target GPRC5D on malignant plasma cells in relapsed/refractory multiple myeloma; CAR engagement activates T-cell signaling to drive activation, proliferation, cytokine release, and cytotoxic killing.
Autologous T cells engineered to express a chimeric antigen receptor specific for GPRC5D on malignant plasma cells; CAR engagement initiates CD3ζ/costimulatory signaling that activates and expands T cells, drives cytokine release, and induces cytotoxic killing of GPRC5D-positive multiple myeloma cells.
YES
DIRECT
CAR engagement of GPRC5D activates T cells (CD3ζ/co-stim), leading to perforin/granzyme release and Fas–FasL–mediated apoptosis of GPRC5D-positive cells.
Anti-HER2 antibody–drug conjugate (humanized IgG1 linked to MMAE) that binds HER2, is internalized, and releases MMAE to disrupt microtubules, causing mitotic arrest and apoptosis; may mediate ADCC and bystander effects.
Disitamab vedotin is an anti-HER2 antibody-drug conjugate (humanized IgG1 linked to MMAE). It binds HER2 on tumor cells, is internalized, and releases MMAE that binds tubulin and inhibits microtubule polymerization, causing G2/M arrest and apoptosis; it may also mediate ADCC and bystander killing.
YES
DIRECT
The anti-HER2 ADC binds HER2 on tumor cells, is internalized, and releases MMAE, which disrupts microtubules causing G2/M arrest and apoptosis; it may also trigger ADCC and bystander killing.