A Trop-2–directed antibody–drug conjugate (brand name Trodelvy) consisting of a humanized anti–Trop-2 IgG1 monoclonal antibody linked via a hydrolyzable linker to SN-38, the active metabolite of irinotecan and a topoisomerase I inhibitor. Binding to Trop-2 on tumor cells triggers internalization and intracellular release of SN-38, causing DNA damage and cell death with a bystander effect.
Trop-2-directed IgG1 antibody-drug conjugate linked via a hydrolyzable linker to SN-38 (a topoisomerase I inhibitor). Binding to Trop-2 on tumor cells triggers internalization and intracellular release of SN-38, which stabilizes Topo I-DNA complexes, causing DNA breaks, replication arrest, and apoptosis; the membrane-permeable payload produces a bystander killing effect.
YES
DIRECT
ADC binds Trop-2, is internalized, and releases SN-38 (topoisomerase I inhibitor) intracellularly, causing DNA damage, replication arrest, and apoptosis; the membrane-permeable payload can also cause bystander killing.
A Trop-2–directed antibody–drug conjugate (brand name Trodelvy) consisting of a humanized anti–Trop-2 IgG1 monoclonal antibody linked via a hydrolyzable linker to SN-38, the active metabolite of irinotecan and a topoisomerase I inhibitor. Binding to Trop-2 on tumor cells triggers internalization and intracellular release of SN-38, causing DNA damage and cell death with a bystander effect.
Trop-2-directed IgG1 antibody-drug conjugate linked via a hydrolyzable linker to SN-38 (a topoisomerase I inhibitor). Binding to Trop-2 on tumor cells triggers internalization and intracellular release of SN-38, which stabilizes Topo I-DNA complexes, causing DNA breaks, replication arrest, and apoptosis; the membrane-permeable payload produces a bystander killing effect.
YES
INDIRECT
The ADC binds Trop-2 on tumor cells, is internalized, and releases SN-38, which inhibits Topoisomerase I, stabilizing Topo I–DNA complexes and causing DNA damage, replication arrest, and apoptosis; the membrane-permeable payload can also cause bystander killing.
An antibody–drug conjugate targeting NaPi2b (SLC34A2) that, after binding and internalization into tumor cells, releases a topoisomerase I inhibitor payload (exatecan/camptothecan class) to inhibit topo I, cause replication-associated DNA breaks, and induce cell death; administered IV every 3 weeks.
Humanized IgG1 antibody–drug conjugate targeting NaPi2b (SLC34A2). After binding and internalization, a cleavable linker releases exatecan, a camptothecin-class topoisomerase I inhibitor, which blocks topo I, induces replication-associated DNA breaks, and triggers cell cycle arrest and apoptosis, with potential bystander killing of adjacent tumor cells.
YES
DIRECT
ADC binds NaPi2b, is internalized, and releases exatecan (topoisomerase I inhibitor) after linker cleavage, causing replication-associated DNA breaks, cell-cycle arrest, and apoptosis; can also cause bystander killing of neighboring cells.
An antibody–drug conjugate targeting NaPi2b (SLC34A2) that, after binding and internalization into tumor cells, releases a topoisomerase I inhibitor payload (exatecan/camptothecan class) to inhibit topo I, cause replication-associated DNA breaks, and induce cell death; administered IV every 3 weeks.
Humanized IgG1 antibody–drug conjugate targeting NaPi2b (SLC34A2). After binding and internalization, a cleavable linker releases exatecan, a camptothecin-class topoisomerase I inhibitor, which blocks topo I, induces replication-associated DNA breaks, and triggers cell cycle arrest and apoptosis, with potential bystander killing of adjacent tumor cells.
NO
INDIRECT
TUB-040 binds NaPi2b, is internalized, and releases exatecan that inhibits topoisomerase I to cause DNA damage and apoptosis (with possible bystander killing). DNA topoisomerase I is not the antigen recognized by the ADC, so its expression alone does not make cells direct targets.
Autologous/allogeneic T cells engineered with a lentiviral vector to express a CAR targeting Epstein-Barr virus GP350; IV dose-escalated infusion; designed for MHC-independent killing of GP350-expressing EBV-associated malignant cells.
Autologous/allogeneic T cells are lentivirally engineered to express a CAR that binds EBV GP350 on EBV-associated malignant cells, enabling MHC-independent recognition and activation of T-cell cytotoxicity (perforin/granzyme release) and cytokine-mediated tumor cell killing.
YES
DIRECT
CAR T cells bind GP350 on target cells in an MHC-independent manner, become activated, and kill the bound cells via perforin/granzyme-mediated cytolysis (and Fas/FasL apoptosis).