EGFR-targeting monoclonal antibody used as a safety 'off switch' to ablate EGFRt-tagged CAR T cells if needed.
Cetuximab is a chimeric IgG1 monoclonal antibody that binds the extracellular domain of EGFR, blocking ligand binding and receptor dimerization to inhibit downstream signaling and cell proliferation. Its Fc can recruit immune effector functions (e.g., ADCC/CDC). In this trial it is used as a safety off-switch by binding the truncated EGFR (EGFRt) tag on CAR T cells to enable their targeted elimination.
Cetuximab binds EGFR on the cell surface and its IgG1 Fc recruits immune effectors to mediate ADCC and complement-dependent cytotoxicity, killing EGFR-expressing cells (used here to ablate EGFRt-tagged CAR T cells).
EGFR-targeting monoclonal antibody used as a safety 'off switch' to ablate EGFRt-tagged CAR T cells if needed.
Cetuximab is a chimeric IgG1 monoclonal antibody that binds the extracellular domain of EGFR, blocking ligand binding and receptor dimerization to inhibit downstream signaling and cell proliferation. Its Fc can recruit immune effector functions (e.g., ADCC/CDC). In this trial it is used as a safety off-switch by binding the truncated EGFR (EGFRt) tag on CAR T cells to enable their targeted elimination.
Cetuximab binds the EGFRt tag and, via its Fc domain, engages immune effectors to kill tagged cells through ADCC and complement-mediated lysis (and phagocytosis).
Anti–TROP-2 antibody–drug conjugate that binds TROP-2 on tumor cells, is internalized, and releases a cytotoxic payload to kill TROP-2–expressing cancer cells.
An anti–TROP-2 IgG1 antibody–drug conjugate that binds TROP-2 on tumor cells, is internalized, and via a cleavable linker releases the exatecan-derived topoisomerase I inhibitor SHR9265, inhibiting DNA replication and inducing cell-cycle arrest and apoptosis in TROP-2–expressing cancer cells.
An anti–TROP-2 ADC binds TROP-2, is internalized, and releases an exatecan-derived topoisomerase I inhibitor (SHR9265) that inhibits DNA replication, causing cell-cycle arrest and apoptosis in TROP-2–expressing cells.
An intravenous CD70-targeted antibody-drug conjugate (ADC) comprising an anti-CD70 monoclonal antibody linked to a topoisomerase I inhibitor payload; binds CD70 on tumor cells, is internalized, and releases the cytotoxic payload to induce DNA damage and tumor cell death.
CD70-targeted monoclonal antibody linked to a topoisomerase I inhibitor; binds CD70 on tumor cells, is internalized, and releases the cytotoxic payload to inhibit topoisomerase I, causing DNA damage and tumor cell death.
The CD70-targeted ADC binds CD70 on CD70+ cells, is internalized, and releases a topoisomerase I inhibitor that induces DNA damage, leading to apoptosis of the target-expressing cells.
Glycoengineered type II anti-CD20 monoclonal antibody that targets CD20+ B cells, inducing direct cell death with enhanced ADCC/ADCP and complement-mediated cytotoxicity.
Glycoengineered type II anti-CD20 humanized IgG1 that binds CD20 on B cells and induces direct cell death and enhanced Fc-mediated effector functions (increased affinity for Fc-gamma RIIIa leading to stronger ADCC/ADCP), with some complement-mediated cytotoxicity.
Obinutuzumab binds CD20 on B cells, inducing direct cell death and recruiting immune effectors via FcγRIIIa for enhanced ADCC/ADCP, with some complement-mediated cytotoxicity (CDC).