An autologous CD19-directed CAR T-cell therapy in which a patient’s T cells are engineered ex vivo to express a chimeric antigen receptor targeting CD19, leading to T-cell activation, proliferation, cytokine release, and cytotoxic killing of CD19+ B cells; evaluated in relapsed/refractory CD19+ B-cell non-Hodgkin lymphoma.
Autologous T cells are engineered ex vivo to express a chimeric antigen receptor targeting CD19. CAR engagement with CD19 triggers CD3ζ/co-stimulatory signaling, leading to T-cell activation, proliferation, cytokine release, and perforin/granzyme-mediated killing of CD19+ malignant (and normal) B cells in an MHC-independent manner.
YES
DIRECT
CD19-directed CAR T cells bind CD19 on target cells; CAR signaling activates T cells to kill via perforin/granzyme-mediated cytolysis (MHC-independent).
TROP2-directed antibody–drug conjugate that delivers the topoisomerase I inhibitor SN-38 to tumor cells, causing DNA damage–induced cell death.
Humanized anti-TROP2 antibody linked to SN-38 (topoisomerase I inhibitor). After TROP2 binding and internalization, linker cleavage releases SN-38, which stabilizes topoisomerase I–DNA complexes, causing DNA breaks, inhibition of replication, and apoptosis (with potential bystander effect).
YES
DIRECT
Anti-TROP2 ADC binds TROP2, is internalized, and releases SN-38, a topoisomerase I inhibitor, causing DNA damage (Topo I–DNA complex stabilization), replication arrest, and apoptosis; may also cause a bystander effect.
TROP2-directed antibody–drug conjugate that delivers the topoisomerase I inhibitor SN-38 to tumor cells, causing DNA damage–induced cell death.
Humanized anti-TROP2 antibody linked to SN-38 (topoisomerase I inhibitor). After TROP2 binding and internalization, linker cleavage releases SN-38, which stabilizes topoisomerase I–DNA complexes, causing DNA breaks, inhibition of replication, and apoptosis (with potential bystander effect).
NO
INDIRECT
The ADC binds TROP2 on tumor cells, is internalized, and releases SN-38, which inhibits topoisomerase I to cause DNA damage and apoptosis; topoisomerase I is the intracellular payload target, not the antigen used for targeting.
Autologous, gene-modified TCR-engineered T cells (TCR-T; T-Plex) expressing a high-affinity TCR specific for MAGE-A1 peptide presented by HLA-A*02:01; administered after lymphodepletion to recognize peptide–HLA on tumor cells and induce TCR/CD3-mediated cytotoxic killing.
Autologous T cells are gene-modified to express a high-affinity TCR specific for the MAGE-A1 peptide presented by HLA-A*02:01. Upon encountering MAGE-A1 peptide–HLA complexes on tumor cells, the engineered T cells engage TCR/CD3 signaling, activate cytotoxic effector functions, and mediate targeted killing of MAGE-A1–expressing cancer cells after lymphodepletion.
YES
DIRECT
TCR-engineered autologous T cells recognize the MAGE-A1 peptide–HLA-A*02:01 complex via TCR/CD3 and directly kill target cells through CTL effector mechanisms (perforin/granzyme release and Fas–FasL-mediated apoptosis).
Investigational next-generation HER2-targeted antibody–drug conjugate that binds HER2, is internalized, and releases a cytotoxic payload to kill HER2-expressing tumor cells.
Humanized anti-HER2 monoclonal antibody linked via an enzyme-cleavable linker to a topoisomerase I inhibitor payload. After binding HER2 and internalization, the payload is released to inhibit DNA topoisomerase I, blocking DNA replication and inducing cell-cycle arrest and apoptosis in HER2-expressing tumor cells.
NO
INDIRECT
The ADC targets HER2 on the cell surface, is internalized, and releases a topoisomerase I inhibitor payload that blocks DNA replication and induces apoptosis in HER2-expressing cells; topoisomerase I is the intracellular enzymatic target, not the selection antigen.