Chimeric IgG1 monoclonal antibody against EGFR that blocks ligand binding and receptor activation, inhibiting downstream signaling (RAS/RAF/MEK/ERK and PI3K/AKT) and mediating antibody-dependent cellular cytotoxicity (ADCC).
Chimeric IgG1 monoclonal antibody against EGFR that binds the receptor’s extracellular domain, blocks ligand binding and receptor dimerization/activation, inhibiting downstream RAS/RAF/MEK/ERK and PI3K/AKT signaling; additionally mediates ADCC via Fcγ receptor–bearing effector cells.
YES
DIRECT
Cetuximab binds EGFR on target cells and engages Fcγ receptor–bearing effector cells (e.g., NK cells) to induce ADCC, killing the EGFR+ cells.
Chimeric IgG1 monoclonal antibody against EGFR that blocks ligand binding and receptor activation, inhibiting downstream signaling (RAS/RAF/MEK/ERK and PI3K/AKT) and mediating antibody-dependent cellular cytotoxicity (ADCC).
Chimeric IgG1 monoclonal antibody against EGFR that binds the receptor’s extracellular domain, blocks ligand binding and receptor dimerization/activation, inhibiting downstream RAS/RAF/MEK/ERK and PI3K/AKT signaling; additionally mediates ADCC via Fcγ receptor–bearing effector cells.
NO
INDIRECT
Cetuximab binds EGFR on tumor cells; its Fc engages CD16a on NK cells to trigger ADCC that kills EGFR+ targets. CD16a-expressing effector cells are not killed.
Allogeneic CD19-directed CAR T-cell therapy using donor T cells engineered to target CD19 on B cells, leading to T-cell activation and cytotoxic elimination of malignant B cells and minimal residual disease.
Allogeneic donor T cells engineered to express a CD19‑specific chimeric antigen receptor recognize CD19 on B cells, leading to T‑cell activation, proliferation, and cytotoxic elimination of malignant B cells to eradicate minimal residual disease.
YES
DIRECT
CD19-directed CAR T cells recognize CD19 on target B cells, activate, and kill them via T-cell cytotoxic mechanisms (perforin/granzyme release and Fas/FasL-mediated apoptosis).
Anti-CD52 monoclonal antibody that depletes CD52-positive immune cells (T, B, NK) to reduce rejection of allogeneic CAR T cells.
Unconjugated anti-CD52 monoclonal antibody that binds CD52 on T, B, and NK cells and depletes them via Fc-mediated effector functions (ADCC/CDC), achieving lymphodepletion to reduce host rejection of allogeneic CAR T cells.
YES
DIRECT
Unconjugated anti-CD52 mAb binds CD52 and triggers Fc-mediated ADCC and complement-dependent cytotoxicity, leading to lysis/depletion of CD52+ lymphocytes.
Actinium-225–macropa–pelgifatamab (225Ac‑pelgi), a PSMA-targeted radioimmunoconjugate in which the anti‑PSMA monoclonal antibody pelgifatamab is chelated via macropa to the alpha-emitter actinium‑225 to deliver targeted alpha radiation; administered IV every 6 weeks for mCRPC.
An anti‑PSMA monoclonal antibody (pelgifatamab) is chelated via macropa to the alpha‑emitter actinium‑225. After binding PSMA on prostate cancer cells, the conjugate delivers short‑range, high‑LET alpha radiation that induces lethal DNA double‑strand breaks, leading to targeted tumor cell death.
YES
DIRECT
Anti-PSMA antibody delivers actinium-225 alpha radiation to PSMA-expressing cells, causing high-LET DNA double-strand breaks and targeted cell death.