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).
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.
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.
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).
Autologous, gene-modified TCR-engineered T cells (TCR-T; T-Plex) expressing a high-affinity TCR specific for MAGE-A1 peptide presented by HLA-C*07:02; designed to recognize peptide–HLA on tumor cells and trigger TCR/CD3 signaling and cytotoxicity after lymphodepletion.
Autologous T cells are gene-modified to express a high-affinity TCR specific for the MAGE-A1 peptide presented by HLA-C*07:02. Binding to the peptide-HLA complex on tumor cells activates TCR/CD3 signaling and cytotoxic effector functions, resulting in selective killing of MAGE-A1-positive tumor cells (administered after lymphodepletion).
TCR-engineered autologous T cells bind the MAGE-A1 peptide presented by HLA-C*07:02 on tumor cells, activating TCR/CD3 signaling and inducing CTL effector killing via perforin/granzyme (and Fas/FasL) apoptosis.
Autologous, gene-modified TCR-engineered T cells (TCR-T; T-Plex) expressing a high-affinity TCR specific for HPV16 E7 peptide presented by HLA-A*02:01; mediates recognition of peptide–HLA on tumor cells and TCR/CD3-driven cytotoxic killing following lymphodepletion.
Autologous T cells are gene-modified to express a high-affinity TCR specific for the HPV16 E7 peptide presented by HLA-A*02:01. Recognition of the peptide–HLA complex on tumor cells triggers TCR/CD3 signaling, leading to T-cell activation, cytotoxic granule release, cytokine secretion, and targeted tumor cell killing after lymphodepletion.
TCR-engineered autologous T cells recognize the HPV16 E7 peptide presented by HLA-A*02:01 on tumor cells via TCR/CD3, leading to direct killing through perforin/granzyme (and Fas/FasL) cytotoxic pathways.
Autologous, gene-modified TCR-engineered T cells (TCR-T; T-Plex) expressing a high-affinity TCR specific for PRAME peptide presented by HLA-A*02:01; engages peptide–HLA on tumor cells to activate TCR/CD3 signaling and cytotoxicity post-lymphodepletion.
Autologous T cells are gene-modified to express a high-affinity TCR specific for the PRAME peptide presented by HLA-A*02:01. Upon binding the peptide–HLA complex on tumor cells, the engineered TCR engages CD3 to trigger TCR signaling, leading to T-cell activation, cytokine release, and cytotoxic killing of PRAME-expressing, HLA-A*02:01–positive cancer cells after lymphodepletion.
TCR-engineered autologous T cells recognize the PRAME peptide–HLA-A*02:01 complex via their TCR/CD3, activate, and directly kill target cells through perforin/granzyme-mediated cytolysis (and Fas–FasL apoptosis).