An intravenous antibody-drug conjugate (PADCEV; ASG-22CE) consisting of a monoclonal antibody targeting NECTIN-4 linked to the cytotoxic payload monomethyl auristatin E (MMAE). After binding NECTIN-4 on tumor cells and internalization, the linker is cleaved to release MMAE, a microtubule inhibitor that disrupts tubulin, induces G2/M arrest and apoptosis, and may enable bystander killing and ADCC.
Enfortumab vedotin is a monoclonal antibody targeting NECTIN-4 linked to the cytotoxic payload MMAE. After binding NECTIN-4 and internalization, the cleavable linker releases MMAE, which inhibits microtubule polymerization, causing G2/M arrest and apoptosis; it may also enable bystander killing and ADCC.
The ADC binds NECTIN-4 on target cells, is internalized, and releases MMAE, which inhibits microtubule polymerization causing G2/M arrest and apoptosis; may also enable bystander killing and ADCC.
TROP2-directed antibody–drug conjugate (Dato-DXd) delivering a deruxtecan topoisomerase I inhibitor payload to TROP2-positive tumor cells, causing DNA damage and bystander killing.
TROP2-directed antibody–drug conjugate: a humanized anti-TROP2 monoclonal antibody linked via a cleavable peptide to deruxtecan (DXd), a topoisomerase I inhibitor. After TROP2 binding and internalization, lysosomal cleavage releases DXd, which stabilizes the Topo I–DNA complex, causing DNA breaks, inhibiting replication, and inducing apoptosis, with a bystander killing effect.
The ADC binds TROP2 on target cells, is internalized, and lysosomal linker cleavage releases the DXd topoisomerase I inhibitor, causing DNA damage (Topo I–DNA complex stabilization), replication arrest, and apoptosis, with a bystander effect.
Autologous mRNA-engineered TCR-T cell therapy in which a patient’s T cells are transiently transfected with mRNA encoding HBV-specific T-cell receptors; infused cells recognize HBV peptides presented by HLA-A*02:01/A*11:01/A*24:02 on infected hepatocytes and mediate MHC class I–restricted cytotoxicity to reduce HBV-infected cells and antigen burden.
Autologous T cells are transiently transfected with mRNA encoding HBV-specific T-cell receptors; after infusion, they recognize HBV peptides presented by HLA-A*02:01/A*11:01/A*24:02 on infected hepatocytes and execute MHC class I–restricted cytotoxicity to reduce HBV-infected cells and antigen burden.
Engineered TCR-T cells recognize HBV peptide–HLA-A*02:01 on target cells and induce MHC I–restricted killing via perforin/granzyme-mediated apoptosis (and Fas–FasL).
Autologous mRNA-engineered TCR-T cell therapy in which a patient’s T cells are transiently transfected with mRNA encoding HBV-specific T-cell receptors; infused cells recognize HBV peptides presented by HLA-A*02:01/A*11:01/A*24:02 on infected hepatocytes and mediate MHC class I–restricted cytotoxicity to reduce HBV-infected cells and antigen burden.
Autologous T cells are transiently transfected with mRNA encoding HBV-specific T-cell receptors; after infusion, they recognize HBV peptides presented by HLA-A*02:01/A*11:01/A*24:02 on infected hepatocytes and execute MHC class I–restricted cytotoxicity to reduce HBV-infected cells and antigen burden.
Autologous TCR-engineered T cells recognize the HBV peptide–HLA-A*11:01 complex on infected cells and kill them via MHC I–restricted cytotoxic T lymphocyte mechanisms (perforin/granzyme-mediated apoptosis, Fas–FasL).
Autologous mRNA-engineered TCR-T cell therapy in which a patient’s T cells are transiently transfected with mRNA encoding HBV-specific T-cell receptors; infused cells recognize HBV peptides presented by HLA-A*02:01/A*11:01/A*24:02 on infected hepatocytes and mediate MHC class I–restricted cytotoxicity to reduce HBV-infected cells and antigen burden.
Autologous T cells are transiently transfected with mRNA encoding HBV-specific T-cell receptors; after infusion, they recognize HBV peptides presented by HLA-A*02:01/A*11:01/A*24:02 on infected hepatocytes and execute MHC class I–restricted cytotoxicity to reduce HBV-infected cells and antigen burden.
Engineered TCR-T cells recognize HBV peptide–HLA-A*24:02 complexes on infected cells and induce MHC I–restricted cytotoxicity via perforin/granzyme release and Fas–FasL–mediated apoptosis.