Antibody–drug conjugate targeting TROP2; after binding, it is internalized and releases a camptothecin/topoisomerase I inhibitor payload that induces DNA damage and apoptosis.
Humanized anti-TROP2 monoclonal antibody linked via a cleavable linker to the camptothecin/topoisomerase I inhibitor tirumotecan. After binding TROP2 on tumor cells and internalization (and/or extracellular pH-sensitive cleavage), the payload is released to inhibit topoisomerase I, causing DNA damage, replication arrest, and apoptosis, with a bystander effect on neighboring tumor cells.
NO
INDIRECT
The ADC targets TROP2 (not topoisomerase I) for delivery; after binding TROP2 and internalization or extracellular cleavage, tirumotecan is released and inhibits DNA topoisomerase I, causing DNA damage and apoptosis in TROP2-positive cells (with a bystander effect).
Autologous, genetically engineered TCR-T cell therapy expressing an HLA-A*11:01–restricted T cell receptor specific for the KRAS G12V neoantigen; administered after lymphodepletion with a single IV infusion to recognize KRAS G12V peptides on tumor HLA-A*11:01, expand (with low-dose IL-2 support), and mediate cytotoxic killing of tumor cells in advanced solid tumors.
Autologous T cells genetically engineered to express an HLA-A*11:01–restricted TCR specific for the KRAS G12V neoantigen; after lymphodepletion and low-dose IL-2 support, the infused cells recognize KRAS G12V peptides presented on tumor HLA-A*11:01, expand, and mediate cytotoxic killing of mutant KRAS–expressing tumor cells.
NO
INDIRECT
Killing requires engineered TCR-T cells to recognize the KRAS G12V peptide presented by HLA-A*11:01 and then lyse the cell via perforin/granzyme; HLA-A*11:01 expression alone is not sufficient for killing.
Antibody–drug conjugate targeting Tissue Factor (TF) and delivering the microtubule inhibitor MMAE.
Anti–tissue factor (TF) monoclonal antibody linked via a protease‑cleavable linker to the microtubule inhibitor monomethyl auristatin E (MMAE). After binding TF on tumor cells and internalization, MMAE is released to inhibit tubulin polymerization, causing G2/M arrest and apoptosis; TF binding may also interfere with TF–FVIIa signaling, contributing antiangiogenic/anticoagulant effects.
YES
DIRECT
ADC binds Tissue Factor on target cells, is internalized, and releases MMAE via protease cleavage; MMAE inhibits tubulin polymerization causing G2/M arrest and apoptosis of the TF-expressing cell.
Antibody–drug conjugate targeting Tissue Factor (TF) and delivering the microtubule inhibitor MMAE.
Anti–tissue factor (TF) monoclonal antibody linked via a protease‑cleavable linker to the microtubule inhibitor monomethyl auristatin E (MMAE). After binding TF on tumor cells and internalization, MMAE is released to inhibit tubulin polymerization, causing G2/M arrest and apoptosis; TF binding may also interfere with TF–FVIIa signaling, contributing antiangiogenic/anticoagulant effects.
NO
INDIRECT
Tisotumab vedotin targets tissue factor on cells, is internalized, and releases MMAE, which binds tubulin to inhibit polymerization, causing G2/M arrest and apoptosis. Tubulin is the intracellular payload target, not the antigen used for cell selection.
Autologous dual-target BCMA/CD19 chimeric antigen receptor T-cell (CAR-T) therapy produced via lentiviral transduction; single IV infusion to deplete CD19+ B cells and BCMA+ plasma cells in autoimmune kidney disease.
Autologous T cells are lentivirally engineered to express dual chimeric antigen receptors targeting CD19 and BCMA. On engagement with these antigens on B cells and plasma cells, the CAR-T cells become activated and kill targets via perforin/granzyme and death receptor pathways, depleting CD19+ B cells and BCMA+ plasmablasts/plasma cells to reduce pathogenic autoantibody production in autoimmune kidney disease.
YES
DIRECT
CAR-T cells bind CD19 via the CAR, become activated, and kill CD19+ cells through perforin/granzyme release and death receptor–mediated apoptosis.