Chimeric IgG1 anti-EGFR monoclonal antibody that blocks EGFR signaling and mediates ADCC.
Chimeric IgG1 monoclonal antibody targeting EGFR; binds the receptor’s extracellular domain to block ligand binding, activation, and dimerization, thereby inhibiting downstream RAS/MAPK and PI3K/AKT signaling and tumor cell proliferation. Its Fc region also engages Fcγ receptors to mediate antibody-dependent cellular cytotoxicity (ADCC) against EGFR-expressing cells.
NO
INDIRECT
Cetuximab binds EGFR on tumor cells; its Fc engages CD16A on NK cells to mediate ADCC, killing EGFR+ targets. CD16A-expressing cells act as effectors and are not killed.
Anti-CD38 IgG1 monoclonal antibody that binds CD38 on malignant plasma cells, inhibits CD38 ectoenzyme activity, induces Fc-mediated cytotoxicity (ADCC/ADCP/CDC) and direct apoptosis, and may reduce CD38+ immunosuppressive cells.
Humanized IgG1 anti-CD38 monoclonal antibody that binds CD38 on malignant plasma cells, inhibits CD38 ectoenzyme activity, and triggers Fc-mediated cytotoxicity (ADCC, ADCP, CDC) and direct apoptosis, depleting CD38+ tumor and immunosuppressive cells.
YES
DIRECT
Isatuximab binds CD38 on target cells and induces Fc-mediated ADCC (NK cells), ADCP (macrophages), CDC (complement), and can trigger direct apoptosis, killing CD38+ cells.
Anti-CD20 × anti-CD3 bispecific IgG T‑cell engager (REGN1979) that binds CD20 on B cells and CD3 on T cells to redirect cytotoxic T cells to kill malignant CD20+ B cells.
Bispecific anti‑CD20×CD3 monoclonal antibody that simultaneously binds CD20 on B cells and CD3 on T cells, physically bridging T cells to malignant CD20+ B cells to trigger T‑cell activation and cytotoxic killing (perforin/granzyme) of the target B cells.
YES
DIRECT
Odronextamab bridges CD20 on target B cells with CD3 on T cells, activating T cells to kill CD20+ cells via perforin/granzyme-mediated cytolysis.
Anti-CD20 × anti-CD3 bispecific IgG T‑cell engager (REGN1979) that binds CD20 on B cells and CD3 on T cells to redirect cytotoxic T cells to kill malignant CD20+ B cells.
Bispecific anti‑CD20×CD3 monoclonal antibody that simultaneously binds CD20 on B cells and CD3 on T cells, physically bridging T cells to malignant CD20+ B cells to trigger T‑cell activation and cytotoxic killing (perforin/granzyme) of the target B cells.
NO
INDIRECT
CD3 on T cells is engaged to activate and redirect T-cell killing toward CD20+ B cells; cytotoxicity occurs via perforin/granzyme-mediated lysis of CD20-expressing targets, not CD3+ cells.
An antibody–drug conjugate (ADC) comprising a humanized anti‑HER2 IgG1 (trastuzumab sequence) linked via a cleavable tetrapeptide to an exatecan‑derived topoisomerase I inhibitor (DXd). It binds HER2 (ERBB2), is internalized, and releases the payload to inhibit topoisomerase I, causing DNA damage and apoptosis; also provides HER2 signaling blockade, ADCC, and a membrane‑permeable bystander effect.
HER2-targeted antibody-drug conjugate: trastuzumab binds HER2 and is internalized; a cleavable tetrapeptide linker releases deruxtecan (DXd), a membrane-permeable topoisomerase I inhibitor that stabilizes Top1-DNA cleavage complexes, causing DNA damage, replication arrest, and apoptosis; also provides HER2 signaling blockade, mediates ADCC, and enables a bystander killing effect.
NO
INDIRECT
The ADC targets HER2, is internalized, and releases deruxtecan, which inhibits topoisomerase I to cause DNA damage and apoptosis; killing depends on HER2-mediated delivery (with possible bystander effect), not on topoisomerase I expression per se.