An antibody-drug conjugate carrying a topoisomerase I inhibitor payload; binds a tumor cell-surface antigen, is internalized, and releases the payload to induce DNA damage and tumor cell death.
An anti-nectin-4 IgG1 antibody-drug conjugate that binds nectin-4 on tumor cells, is internalized, and via a cleavable linker releases a topoisomerase I inhibitor payload. The payload inhibits topoisomerase I, disrupting DNA replication and causing DNA damage, cell-cycle arrest, and apoptosis in nectin-4–expressing cancer cells.
NO
INDIRECT
The ADC binds nectin-4 (not DNA topoisomerase I); after internalization it releases a topoisomerase I inhibitor that causes DNA damage and apoptosis in nectin-4–positive cells. Cells expressing topoisomerase I alone are not directly targeted or selectively killed.
Allogeneic cord blood–derived natural killer cells engineered with a TROP2-specific CAR and an IL-15 transgene to provide targeted NK cytotoxicity against TROP2-positive tumor cells and enhance NK survival and persistence.
Allogeneic cord blood–derived NK cells engineered with a TROP2-specific chimeric antigen receptor to direct antigen-specific NK cytotoxicity against TROP2-positive tumor cells; co-expression of IL-15 supports NK activation, survival, proliferation, and persistence in vivo.
YES
DIRECT
TROP2-specific CAR on NK cells binds TROP2 on target cells, activating NK cytotoxicity with degranulation (perforin/granzyme-mediated apoptosis) and death-receptor pathways; IL-15 supports NK activity and persistence.
An oncolytic adenovirus with replication driven by the survivin (BIRC5) promoter active in high-grade glioma cells; pk7 polylysine fiber modification enables CAR-independent entry via heparan sulfate proteoglycans, producing tumor-selective oncolysis and potential anti-tumor immune activation.
Engineered adenovirus that replicates selectively in survivin (BIRC5)-expressing glioma cells; pk7 polylysine fiber modification enables CAR-independent entry via heparan sulfate proteoglycans, leading to tumor-restricted viral replication, oncolysis, and secondary activation of anti-tumor immune responses.
YES
DIRECT
The adenovirus replicates only in cells with active survivin (BIRC5) promoter, leading to selective viral replication and lytic oncolysis of those cells.
An oncolytic adenovirus with replication driven by the survivin (BIRC5) promoter active in high-grade glioma cells; pk7 polylysine fiber modification enables CAR-independent entry via heparan sulfate proteoglycans, producing tumor-selective oncolysis and potential anti-tumor immune activation.
Engineered adenovirus that replicates selectively in survivin (BIRC5)-expressing glioma cells; pk7 polylysine fiber modification enables CAR-independent entry via heparan sulfate proteoglycans, leading to tumor-restricted viral replication, oncolysis, and secondary activation of anti-tumor immune responses.
NO
INDIRECT
HSPGs function as entry/attachment receptors for the pk7-modified adenovirus; cell killing occurs only when survivin (BIRC5) promoter activity enables viral replication and oncolysis. HSPG expression alone is insufficient for cytotoxicity.
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.
YES
DIRECT
The ADC binds TROP-2 on tumor cells, is internalized, and its cleavable linker releases a topoisomerase I inhibitor that blocks DNA replication, causing DNA damage, cell-cycle arrest, and apoptosis; Fc-mediated effector functions (e.g., ADCC/CDC) may also contribute.