Chimeric IgG1 monoclonal antibody against EGFR (HER1); blocks ligand binding and receptor activation, inhibiting downstream RAS/RAF/MEK/ERK and PI3K/AKT pathways and inducing NK cell–mediated ADCC.
Chimeric IgG1 monoclonal antibody against EGFR (HER1) that binds the receptor’s extracellular domain to block ligand binding and prevent receptor activation and dimerization, thereby inhibiting downstream RAS/RAF/MEK/ERK and PI3K/AKT signaling and tumor cell proliferation; its IgG1 Fc also induces NK cell–mediated ADCC.
Cetuximab binds EGFR on target cells and its IgG1 Fc engages NK cells (via FcγRIIIa) to mediate ADCC; it can also activate complement (CDC). EGFR blockade itself is antiproliferative.
An antibody–drug conjugate (Dato‑DXd; DS‑1062a) comprising a humanized IgG1 antibody targeting TROP2 linked via a cleavable linker to the cytotoxic payload DXd (a topoisomerase I inhibitor). After binding TROP2 and internalization, DXd is released to induce DNA damage, S‑phase arrest, apoptosis, and a bystander effect.
Humanized IgG1 antibody targeting TROP2 linked via a cleavable linker to DXd (an exatecan-derived topoisomerase I inhibitor). After TROP2 binding and internalization, lysosomal cleavage releases DXd, which stabilizes the topoisomerase I–DNA complex, causing DNA strand breaks, S-phase arrest, apoptosis, and a bystander cytotoxic effect.
ADC binds TROP2 on target cells, is internalized, and lysosomal cleavage releases the DXd topoisomerase I inhibitor, causing DNA damage (topo I–DNA complex stabilization), S‑phase arrest, and apoptosis; with a potential bystander effect.
Humanized monoclonal antibody targeting CD2; blocks the CD2–LFA-3 costimulatory interaction and depletes/modulates CD2+ lymphocytes, inhibiting T/NK cell activation and cytokine release to reduce neuroinflammation.
Humanized anti-CD2 monoclonal antibody that blocks the CD2–LFA-3 costimulatory interaction and depletes/modulates CD2+ T and NK lymphocytes, thereby suppressing T-cell activation and proinflammatory cytokine release to reduce neuroinflammation.
Anti-CD2 antibody binds CD2 on T/NK cells and depletes them via Fc-mediated ADCC and complement-dependent cytotoxicity (with possible apoptosis upon cross-linking).
MET-targeting antibody-drug conjugate designed to bind MET on tumor cells, inhibit HGF/MET signaling, and deliver cytotoxic activity to MET-positive cells.
Anti-MET (c-MET/HGFR) monoclonal antibody conjugated to the microtubule-disrupting payload MMAE. RC108 binds MET on tumor cells, inhibits HGF/MET signaling, is internalized, and releases MMAE intracellularly to disrupt tubulin polymerization, causing G2/M arrest and apoptosis in MET-positive cells.
Anti-MET ADC binds MET on target cells, is internalized, and releases MMAE intracellularly; MMAE inhibits tubulin polymerization causing G2/M arrest and apoptosis of MET-positive cells.
Third-generation, irreversible covalent EGFR tyrosine kinase inhibitor selective for mutant EGFR (including T790M), blocking EGFR signaling to inhibit proliferation and induce death of EGFR-mutant tumor cells and overcome T790M-mediated resistance.
Irreversible covalent inhibition of mutant EGFR (including T790M) blocks survival signaling (e.g., MAPK/PI3K-AKT), causing apoptosis of EGFR-mutant tumor cells.