TROP2-directed antibody–drug conjugate carrying a topoisomerase I inhibitor payload; binds TROP2 on tumor cells, is internalized, and releases the cytotoxic payload to induce DNA damage/replication stress with a bystander effect.
TROP2-targeted antibody–drug conjugate that binds TROP2 on tumor cells, is internalized, and releases a topoisomerase I inhibitor payload to induce DNA damage and replication stress, with a membrane-permeable bystander effect.
YES
DIRECT
Anti-TROP2 antibody-drug conjugate binds TROP2, is internalized, and releases a topoisomerase I inhibitor payload that causes DNA damage/replication stress, killing the target cell (with a bystander effect).
Gene-modified natural killer (NK) cells engineered to express an NKG2D-based chimeric antigen receptor (CAR) that recognizes NKG2D ligands (MICA, MICB, ULBP family) on tumor cells, activating NK cytotoxicity for treatment of relapsed/refractory multiple myeloma.
Gene‑modified NK cells expressing an NKG2D‑based CAR recognize stress‑induced NKG2D ligands (MICA, MICB, ULBP family) on tumor cells. CAR signaling activates NK cytotoxic functions, inducing degranulation (perforin/granzyme), cytokine‑mediated killing, and apoptosis of malignant cells, targeting relapsed/refractory multiple myeloma.
YES
DIRECT
NKG2D-CAR NK cells bind ULBP2 on target cells, triggering NK activation and degranulation (perforin/granzyme) leading to apoptotic cytolysis.
TROP2-directed antibody–drug conjugate carrying a topoisomerase I inhibitor payload; binds TROP2 on tumor cells, is internalized, and releases the cytotoxic payload to induce DNA damage/replication stress with a bystander effect.
TROP2-targeted antibody–drug conjugate that binds TROP2 on tumor cells, is internalized, and releases a topoisomerase I inhibitor payload to induce DNA damage and replication stress, with a membrane-permeable bystander effect.
NO
INDIRECT
The ADC binds TROP2 (not topoisomerase I), is internalized, and releases a topoisomerase I inhibitor that causes DNA damage/replication stress to kill TROP2+ cells (with possible bystander killing). Topoisomerase I is the intracellular payload target, not the directly targeted antigen.
A Nectin-4–targeting antibody–drug conjugate (ADC) that delivers the microtubule-disrupting cytotoxic payload MMAE to tumor cells.
Bulumtatug fuvedotin (9MW2821) targets Nectin-4 on tumor cells; after binding and internalization, the linker is cleaved to release MMAE, which inhibits tubulin polymerization, causing G2/M arrest and apoptotic cell death (with potential bystander cytotoxicity).
YES
DIRECT
The ADC binds Nectin-4, is internalized, and releases MMAE, which inhibits tubulin polymerization, causing G2/M arrest and apoptotic death (with possible bystander effect).
A Nectin-4–targeting antibody–drug conjugate (ADC) that delivers the microtubule-disrupting cytotoxic payload MMAE to tumor cells.
Bulumtatug fuvedotin (9MW2821) targets Nectin-4 on tumor cells; after binding and internalization, the linker is cleaved to release MMAE, which inhibits tubulin polymerization, causing G2/M arrest and apoptotic cell death (with potential bystander cytotoxicity).
NO
INDIRECT
This ADC binds Nectin-4 on tumor cells, is internalized, and releases MMAE; MMAE inhibits beta-tubulin polymerization, causing G2/M arrest and apoptosis. Beta-tubulin expression alone does not render cells directly targeted by the drug.