A bispecific T-cell engager (BiTE) antibody that binds CD19 on B cells and CD3 on T cells to redirect cytotoxic T cells against CD19+ B cells and modulate aberrant humoral immunity.
A single‑chain bispecific antibody that binds CD19 on B cells and CD3 on T cells, forming an immunologic synapse that activates cytotoxic T cells to release perforin/granzymes and lyse CD19+ B cells, resulting in B‑cell depletion and modulation of humoral immunity.
YES
DIRECT
Blinatumomab bridges CD3+ T cells to CD19+ cells, forming an immunologic synapse that activates T-cell cytotoxicity (perforin/granzyme-mediated lysis) of CD19-expressing cells.
HER2-directed antibody–drug conjugate in which a humanized anti‑HER2 antibody is linked via a protease-cleavable vedotin linker to the microtubule inhibitor MMAE. Binding to HER2 triggers internalization and lysosomal release of MMAE, which inhibits tubulin polymerization, causing G2/M arrest and apoptosis, with potential bystander cytotoxicity to adjacent cells.
YES
DIRECT
ADC binds HER2, is internalized, linker is proteolytically cleaved to release MMAE, which inhibits tubulin polymerization causing G2/M arrest and apoptosis; released payload may also cause bystander killing of adjacent cells.
HER2-directed antibody–drug conjugate in which a humanized anti‑HER2 antibody is linked via a protease-cleavable vedotin linker to the microtubule inhibitor MMAE. Binding to HER2 triggers internalization and lysosomal release of MMAE, which inhibits tubulin polymerization, causing G2/M arrest and apoptosis, with potential bystander cytotoxicity to adjacent cells.
NO
INDIRECT
Disitamab vedotin targets HER2 on the cell surface, is internalized, and releases MMAE, which binds beta-tubulin to inhibit microtubule polymerization, causing G2/M arrest and apoptosis; beta-tubulin expression alone does not trigger targeting.
HER2-directed antibody–drug conjugate with a topoisomerase I inhibitor payload (DXd).
HER2-targeted monoclonal antibody linked via a cleavable linker to the topoisomerase I inhibitor deruxtecan (DXd). After HER2 binding and internalization, DXd is released to inhibit Top1–DNA complexes, blocking DNA replication and causing cell-cycle arrest and apoptosis; also mediates ADCC and a bystander killing effect.
YES
DIRECT
HER2-binding ADC is internalized and releases the topoisomerase I inhibitor deruxtecan, causing DNA damage/replication block, cell-cycle arrest and apoptosis; it also mediates ADCC and a bystander killing effect.
HER2-directed antibody–drug conjugate with a topoisomerase I inhibitor payload (DXd).
HER2-targeted monoclonal antibody linked via a cleavable linker to the topoisomerase I inhibitor deruxtecan (DXd). After HER2 binding and internalization, DXd is released to inhibit Top1–DNA complexes, blocking DNA replication and causing cell-cycle arrest and apoptosis; also mediates ADCC and a bystander killing effect.
NO
INDIRECT
Trastuzumab deruxtecan targets HER2, is internalized, and releases deruxtecan, which inhibits Top1 to cause DNA damage and apoptosis. DNA topoisomerase I expression alone does not result in targeting or direct killing.