An intravenous chimeric IgG1 monoclonal antibody that binds soluble and transmembrane TNF-α, blocking TNFR1/2 signaling and NF-κB–driven inflammation; can induce apoptosis of activated T cells/monocytes and promote mucosal healing. Regimen: 10 mg/kg at week 0, then 5 mg/kg at weeks 2, 4, and 8; maintenance every 6 weeks from week 12.
Chimeric IgG1 monoclonal antibody that binds soluble and transmembrane TNF-α, neutralizing TNF and preventing engagement of TNFR1/2. This blocks downstream NF-κB–driven inflammatory signaling, reduces proinflammatory cytokines and adhesion molecule expression, and can trigger apoptosis of activated T cells/monocytes, promoting mucosal healing.
Binding to transmembrane TNF on activated immune cells triggers Fc-mediated ADCC and complement-dependent cytotoxicity, and tmTNF cross-linking induces reverse-signaling apoptosis.
Humanized IgG1 monoclonal antibody that binds HER2 extracellular domain II to block HER2 heterodimerization (especially with HER3), inhibiting downstream signaling (PI3K/AKT/MAPK) and promoting tumor cell death; also mediates antibody-dependent cellular cytotoxicity (ADCC).
Binds HER2 on target cells and recruits FcγR-expressing immune effectors (e.g., NK cells) to mediate ADCC; HER2 signaling blockade may also induce apoptosis.
Humanized IgG1 monoclonal antibody binding HER2 (domain IV); inhibits signaling and mediates ADCC; administered IV or SC.
Humanized IgG1 monoclonal antibody that binds HER2 (domain IV), inhibits HER2 signaling and proliferation, promotes receptor internalization and prevents extracellular domain shedding, and mediates Fc-dependent ADCC against HER2-overexpressing tumor cells.
Binds HER2 and engages Fc receptors on effector cells to trigger antibody-dependent cell-mediated cytotoxicity (ADCC) and phagocytosis; HER2 signaling blockade can also promote apoptosis.
HER2-directed antibody-drug conjugate delivering a topoisomerase I inhibitor payload (DXd) with bystander effect.
HER2-directed antibody-drug conjugate: trastuzumab binds HER2 on tumor cells and is internalized; a cleavable linker releases the DXd (exatecan derivative) topoisomerase I inhibitor, which traps Top1-DNA complexes to block DNA replication and induce cell-cycle arrest and apoptosis; also mediates ADCC and has a membrane-permeable payload that causes bystander killing.
Trastuzumab binds HER2 on target cells, is internalized, and releases the DXd topoisomerase I inhibitor, causing DNA damage/replication arrest and apoptosis; it also mediates Fc-dependent ADCC and bystander killing.
HER2-directed antibody-drug conjugate linking trastuzumab to DM1 (maytansinoid) microtubule inhibitor.
HER2-directed antibody-drug conjugate: trastuzumab binds ERBB2/HER2 and is internalized; lysosomal processing of the non-cleavable MCC linker releases active Lys-MCC-DM1, a maytansinoid microtubule inhibitor that causes mitotic arrest and apoptosis. Trastuzumab also inhibits HER2 signaling and can mediate ADCC.
ADC binds HER2 and is internalized; lysosomal processing releases the DM1 payload, a microtubule inhibitor, causing mitotic arrest and apoptosis in HER2+ cells (with additional ADCC from trastuzumab).