Anti-EGFR monoclonal antibody that inhibits EGFR-mediated activation of RAS signaling.
Cetuximab is a chimeric monoclonal antibody that binds the extracellular domain of EGFR, blocking ligand binding and receptor dimerization, preventing EGFR activation and downstream RAS-MAPK and PI3K-AKT signaling, thereby inhibiting tumor cell proliferation; it can also trigger antibody-dependent cellular cytotoxicity.
Cetuximab coats EGFR+ cells and engages Fcγ receptors on NK cells/macrophages to induce antibody-dependent cellular cytotoxicity (and some complement-mediated lysis), while also blocking EGFR signaling (antiproliferative).
Fc-mediated ADCC: trastuzumab binds HER2 on tumor cells and its Fc engages Fcγ receptors on NK cells/macrophages, triggering cytolytic degranulation and lysis of HER2-positive cells (with minimal complement involvement).
Humanized IgG1 monoclonal antibody targeting HER2; binds domain II to block HER2 heterodimerization with HER3/EGFR, suppress ligand-dependent signaling, and enhance ADCC.
Humanized IgG1 monoclonal antibody against HER2 that binds extracellular domain II to prevent HER2 heterodimerization (especially with HER3/EGFR), blocking ligand‑dependent HER signaling (PI3K/AKT, MAPK), inhibiting tumor growth and promoting apoptosis; Fc region mediates antibody‑dependent cellular cytotoxicity (ADCC).
Pertuzumab binds HER2 and its Fc engages Fcγ receptor–bearing immune cells to mediate ADCC against HER2+ cells; blockade of HER2 heterodimerization also inhibits survival signaling and can induce apoptosis.
A HER2-targeted antibody–drug conjugate (RC48) that binds HER2 on tumor cells, is internalized, and releases the cytotoxic microtubule inhibitor MMAE via a cleavable linker to disrupt mitosis and induce apoptosis.
HER2-targeted antibody-drug conjugate: Disitamab binds HER2 on tumor cells, is internalized, and a cleavable linker releases monomethyl auristatin E (MMAE), which inhibits microtubule polymerization, causing G2/M arrest and apoptosis.
An ADC binds HER2 on tumor cells, is internalized, and releases MMAE via a cleavable linker; MMAE inhibits microtubule polymerization, causing G2/M arrest and apoptosis (with potential bystander effect).
Genetically engineered CAR T-cell therapy that expresses dual chimeric antigen receptors targeting CD19 and CD22 to recognize and kill malignant B-ALL cells; administered intravenously at 1.0×10^6–10.0×10^6 CAR T cells/kg.
Genetically engineered T cells expressing dual chimeric antigen receptors targeting CD19 and CD22; antigen binding triggers CAR signaling (CD3ζ with costimulatory domains) to activate, expand, and mediate cytotoxic killing of malignant B‑ALL cells, mitigating antigen escape seen with single‑antigen CARs.
CAR T cells bind CD19 via the CAR, activate, and directly lyse target cells through perforin/granzyme-mediated cytotoxicity (and Fas–FasL apoptosis).