An intravenous antibody–drug conjugate (ADC) targeting a tumor-associated antigen. Following antigen binding and internalization, a cleavable linker releases a cytotoxic payload that kills tumor cells (via microtubule disruption and/or DNA damage); Fc-mediated immune effector functions may contribute. Dosed every 3 weeks.
TROP-2-targeted monoclonal antibody linked via a cleavable linker to a topoisomerase I inhibitor; after antigen binding and internalization, linker cleavage releases the payload to inhibit topoisomerase I, blocking DNA replication and inducing DNA damage, cell-cycle arrest, and apoptosis in TROP-2-expressing tumor cells; Fc-mediated effector functions may contribute.
NO
INDIRECT
The ADC binds TROP-2 (not DNA topoisomerase I), is internalized, and releases a topoisomerase I inhibitor that causes DNA damage and apoptosis in TROP-2–expressing cells. Cells expressing topoisomerase I alone are not directly targeted.
TROP2-directed antibody–drug conjugate that internalizes into TROP2-positive tumor cells to deliver a topoisomerase I inhibitor (DXd) payload, causing DNA damage and tumor cell death.
TROP2-directed antibody–drug conjugate that binds TROP2 on tumor cells, is internalized, and releases a lysosomally cleaved DXd (topoisomerase I inhibitor) payload, stabilizing the Topo I–DNA cleavable complex to induce DNA damage, inhibit replication, and trigger apoptosis in TROP2-expressing tumor cells.
YES
DIRECT
ADC binds TROP2 on tumor cells, is internalized, and releases a DXd topoisomerase I inhibitor payload that causes DNA damage and apoptosis of the TROP2-expressing cells.
TROP2-directed antibody–drug conjugate that internalizes into TROP2-positive tumor cells to deliver a topoisomerase I inhibitor (DXd) payload, causing DNA damage and tumor cell death.
TROP2-directed antibody–drug conjugate that binds TROP2 on tumor cells, is internalized, and releases a lysosomally cleaved DXd (topoisomerase I inhibitor) payload, stabilizing the Topo I–DNA cleavable complex to induce DNA damage, inhibit replication, and trigger apoptosis in TROP2-expressing tumor cells.
NO
INDIRECT
The ADC targets TROP2 on the cell surface, is internalized, and then releases a DXd payload that inhibits intracellular topoisomerase I, causing DNA damage and apoptosis; topoisomerase I itself is not the binding/selection target.
Cytokine immunotherapy that activates TNFR1/TNFR2 on tumor and tumor-associated endothelial cells to induce apoptosis/necrosis, disrupt tumor vasculature, increase vascular permeability, and enhance local immune responses.
Recombinant modified human TNF-alpha cytokine that binds TNFR1/TNFR2 on tumor cells and tumor-associated endothelial cells, inducing apoptotic/necrotic signaling, disrupting tumor vasculature and increasing vascular permeability, and enhancing local antitumor immune responses.
YES
DIRECT
TNF-α binds TNFR1 on target cells, triggering death‑domain signaling (TRADD/FADD) that activates caspase‑8–mediated apoptosis or, if caspases are inhibited, RIPK1/RIPK3‑dependent necroptosis; it also kills tumor-associated endothelium via the same pathway, disrupting tumor vasculature.
Cytokine immunotherapy that activates TNFR1/TNFR2 on tumor and tumor-associated endothelial cells to induce apoptosis/necrosis, disrupt tumor vasculature, increase vascular permeability, and enhance local immune responses.
Recombinant modified human TNF-alpha cytokine that binds TNFR1/TNFR2 on tumor cells and tumor-associated endothelial cells, inducing apoptotic/necrotic signaling, disrupting tumor vasculature and increasing vascular permeability, and enhancing local antitumor immune responses.
YES
DIRECT
rmhTNF binds TNFR2 (and TNFR1) on tumor and tumor-associated endothelial cells, triggering TNF-receptor signaling that induces apoptosis/necroptosis and vascular disruption.