HER2-targeted antibody-drug conjugate that delivers the microtubule toxin MMAE to tumor cells to induce apoptosis.
Disitamab vedotin is a HER2-targeted antibody–drug conjugate that binds HER2 on tumor cells, is internalized, and releases the cytotoxic payload MMAE via a cleavable linker. MMAE disrupts microtubules, causing G2/M arrest and apoptosis, with potential bystander killing due to membrane-permeable payload.
The ADC binds HER2 on target cells, is internalized, and releases the MMAE payload via a cleavable linker, inhibiting microtubules to cause G2/M arrest and apoptosis; the membrane-permeable payload can also cause bystander killing.
Personalized cellular immunotherapy using patient-derived tumor-resident T cells (primarily CD8+ and CD4+) expanded ex vivo and reinfused as a single IV infusion (e.g., 2.0×10^7 cells/kg) to recognize tumor/neoantigens via TCR–MHC interactions and mediate cytotoxicity through perforin/granzyme and cytokine release.
Autologous tumor-resident T cells (CD8+/CD4+) expanded ex vivo and reinfused; they recognize patient-specific tumor/neoantigens via native TCR–MHC I/II interactions and mediate cytotoxicity through perforin/granzyme release and cytokine secretion (e.g., IFN-γ, TNF-α), enhancing antitumor immunity within the tumor microenvironment.
Native TCR recognition of GPC3-derived peptide presented on MHC triggers TIL activation and cytotoxic granule release (perforin/granzyme) and death-receptor signaling, killing the target cell.
Chimeric IgG1 monoclonal antibody (Remicade) that binds soluble and transmembrane TNF-α, blocking TNFR1/TNFR2 signaling and downstream NF-κB–mediated inflammation; reduces pro-inflammatory cytokines (e.g., IL-1, IL-6), macrophage activation, and matrix metalloproteinases.
Chimeric IgG1 monoclonal antibody that binds soluble and transmembrane TNF-α, neutralizing TNF-α and blocking TNFR1/TNFR2 signaling, thereby suppressing NF-κB–mediated inflammatory pathways and reducing downstream pro‑inflammatory cytokines and tissue-destructive mediators.
Infliximab binds transmembrane TNF-α on cells and, via its IgG1 Fc, triggers ADCC and complement-dependent cytotoxicity; it can also induce apoptosis through reverse signaling in tmTNF-expressing cells.
CD30-directed antibody-drug conjugate that delivers the microtubule-disrupting agent MMAE to CD30-expressing tumor cells.
CD30-directed antibody-drug conjugate in which an anti-CD30 monoclonal antibody is linked via a protease-cleavable valine-citrulline linker to the cytotoxic agent MMAE. After binding to CD30-positive tumor cells and internalization, MMAE is released and binds tubulin, inhibiting microtubule polymerization and inducing G2/M arrest and apoptosis. The linker is stable in plasma, enhancing selectivity for CD30-expressing cells.
ADC binds CD30, is internalized, linker is cleaved to release MMAE, which inhibits tubulin, causing G2/M arrest and apoptosis of the CD30+ cell.
Anti-TIGIT Fc-enabled IgG1 monoclonal antibody that blocks TIGIT and can deplete TIGIT+ regulatory T cells, enhancing CD226 co-stimulation.
Fc-enabled anti-TIGIT IgG1 monoclonal antibody that blocks TIGIT interaction with CD155/CD112 to relieve inhibitory signaling and enhance CD226 (DNAM-1) co-stimulation on T and NK cells; additionally can deplete TIGIT+ regulatory T cells via Fc-mediated ADCC, collectively restoring antitumor immunity.
Fc-enabled IgG1 binds TIGIT on target cells and engages FcγR-expressing effectors (e.g., NK cells, macrophages) to mediate ADCC/ADCP, depleting TIGIT+ cells (notably TIGIT+ Tregs).