Engineered TCR T-cell therapy targeting MAGE-A4; autologous T cells transduced to express a T-cell receptor recognizing MAGE-A4 peptide–HLA complexes on tumor cells.
Autologous T cells are transduced to express an affinity‑enhanced T‑cell receptor specific for an HLA‑A2–restricted MAGE‑A4 peptide. After infusion, these TCR‑T cells recognize the peptide–HLA complex on tumor cells, activate, and kill MAGE‑A4–expressing cancer cells via cytotoxic mechanisms (e.g., perforin/granzyme).
YES
DIRECT
Engineered TCR-T cells recognize the HLA-A2–restricted MAGE-A4 peptide–HLA complex on target cells and kill them via cytotoxic T-cell effector functions (perforin/granzyme-mediated apoptosis, plus Fas–FasL).
Engineered TCR T-cell therapy targeting MAGE-A4; autologous T cells transduced to express a T-cell receptor recognizing MAGE-A4 peptide–HLA complexes on tumor cells.
Autologous T cells are transduced to express an affinity‑enhanced T‑cell receptor specific for an HLA‑A2–restricted MAGE‑A4 peptide. After infusion, these TCR‑T cells recognize the peptide–HLA complex on tumor cells, activate, and kill MAGE‑A4–expressing cancer cells via cytotoxic mechanisms (e.g., perforin/granzyme).
NO
INDIRECT
Afamitresgene autoleucel TCR-T cells kill only cells presenting the MAGE-A4 peptide in HLA-A2 via T-cell cytotoxicity (perforin/granzyme). HLA-A2 expression alone is not sufficient for killing.
Engineered TCR T-cell therapy targeting NY-ESO-1; autologous T cells modified to express a T-cell receptor recognizing NY-ESO-1 peptide–HLA complexes on tumor cells.
Autologous T cells are transduced to express a high‑affinity TCR specific for NY‑ESO‑1/LAGE‑1 peptide–HLA complexes on tumor cells. After infusion, these TCR‑engineered T cells recognize antigen-presenting tumor cells and mediate cytotoxic killing and cytokine-driven anti-tumor responses.
YES
DIRECT
Engineered TCR T cells recognize NY-ESO-1 peptide–HLA complexes on tumor cells and directly kill them via CTL mechanisms (perforin/granzyme and Fas–FasL apoptosis).
Engineered TCR T-cell therapy targeting NY-ESO-1; autologous T cells modified to express a T-cell receptor recognizing NY-ESO-1 peptide–HLA complexes on tumor cells.
Autologous T cells are transduced to express a high‑affinity TCR specific for NY‑ESO‑1/LAGE‑1 peptide–HLA complexes on tumor cells. After infusion, these TCR‑engineered T cells recognize antigen-presenting tumor cells and mediate cytotoxic killing and cytokine-driven anti-tumor responses.
YES
DIRECT
Autologous TCR-engineered T cells recognize LAGE-1/NY-ESO-1 peptide–HLA complexes on tumor cells and induce CTL-mediated killing via perforin/granzyme and apoptosis pathways.
Antibody-drug conjugate targeting a tumor-associated cell-surface antigen; internalizes and releases a cytotoxic payload (e.g., topoisomerase I or microtubule-targeting warhead) to kill cancer cells.
IgG1 monoclonal antibody targeting nectin‑4 binds tumor cells, is internalized, and via a cleavable linker releases a topoisomerase I inhibitor payload that blocks DNA topoisomerase I, inhibiting DNA replication and inducing cell-cycle arrest and apoptosis in nectin‑4–expressing cancers.
YES
DIRECT
The ADC binds nectin-4 on tumor cells, is internalized, and a cleavable linker releases a topoisomerase I inhibitor that blocks DNA replication, leading to cell-cycle arrest and apoptosis of nectin-4–expressing cells.