Bispecific IgG1 monoclonal antibody targeting EGFR and LGR5; inhibits EGFR signaling, promotes receptor internalization, and mediates ADCC to eliminate EGFR+/LGR5+ HNSCC cells, including stem-like cells.
Bispecific IgG1 monoclonal antibody that binds EGFR and LGR5 on tumor cells to block EGFR signaling, promote receptor internalization/degradation, and leverage Fc-mediated ADCC to eliminate EGFR+/LGR5+ cancer cells, including stem-like populations.
IgG1 Fc engages immune effectors (e.g., NK cells) to mediate ADCC against tumor cells when the bispecific binds LGR5 (preferentially on EGFR+/LGR5+ cells), leading to targeted lysis.
Chimeric monoclonal antibody against EGFR that blocks ligand binding and mediates ADCC.
Chimeric IgG1 monoclonal antibody targeting EGFR; binds the extracellular domain to block ligand binding and prevent receptor activation/dimerization, inhibiting downstream signaling and tumor proliferation, while its Fc region mediates ADCC against EGFR-expressing cells.
Cetuximab binds EGFR on target cells and its IgG1 Fc engages FcγR+ effector cells (e.g., NK cells) to trigger ADCC and cell lysis; may also activate complement (CDC).
Antibody–drug conjugate targeting CD79b that delivers the microtubule inhibitor MMAE to B cells.
Monoclonal antibody targets CD79b on B cells and is internalized; a protease-cleavable linker releases the cytotoxic payload MMAE, which binds tubulin to inhibit microtubule polymerization, causing G2/M arrest and apoptosis of malignant B cells.
The ADC binds CD79b, is internalized, and releases MMAE intracellularly; MMAE inhibits tubulin polymerization, causing G2/M arrest and apoptosis of the target-expressing cells.
Anti-CD20 monoclonal antibody that mediates ADCC, complement-dependent cytotoxicity, and apoptosis of B cells.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B cells and depletes them via Fc-mediated effector functions (ADCC, complement-dependent cytotoxicity, phagocytosis) and by directly inducing apoptosis.
Rituximab binds CD20 on B cells and recruits immune effectors via its Fc to kill targets (NK-cell ADCC, complement-dependent cytotoxicity/MAC, and phagocytosis) and can also induce apoptosis upon CD20 cross-linking.
Anti–Trop-2 antibody–drug conjugate delivering SN-38 (topoisomerase I inhibitor).
Humanized anti-Trop-2 monoclonal antibody linked to SN-38; binds Trop-2 on tumor cells, is internalized, and releases SN-38, a topoisomerase I inhibitor that stabilizes topo I-DNA complexes to cause DNA breaks, inhibit replication, and induce apoptosis.
The anti–TROP‑2 ADC binds TROP‑2 on target cells, is internalized, and releases SN‑38, a topoisomerase I inhibitor that causes DNA damage (stabilized topo I–DNA complexes), blocking replication and inducing apoptosis.