An anti-HER2 antibody–drug conjugate that binds HER2 on tumor cells, is internalized, and releases the microtubule toxin MMAE to disrupt microtubules and induce apoptosis; can also trigger antibody-dependent cellular cytotoxicity (ADCC).
Humanized anti‑HER2 monoclonal antibody conjugated to the microtubule toxin MMAE. Upon binding HER2 on tumor cells, the complex is internalized and the linker is cleaved to release MMAE, which inhibits tubulin polymerization leading to G2/M arrest and apoptosis; the antibody Fc can also mediate ADCC.
YES
DIRECT
The anti-HER2 ADC binds HER2, is internalized, and releases MMAE to disrupt microtubules, causing G2/M arrest and apoptosis; its Fc can also trigger ADCC against HER2+ cells.
An anti-HER2 antibody–drug conjugate that binds HER2 on tumor cells, is internalized, and releases the microtubule toxin MMAE to disrupt microtubules and induce apoptosis; can also trigger antibody-dependent cellular cytotoxicity (ADCC).
Humanized anti‑HER2 monoclonal antibody conjugated to the microtubule toxin MMAE. Upon binding HER2 on tumor cells, the complex is internalized and the linker is cleaved to release MMAE, which inhibits tubulin polymerization leading to G2/M arrest and apoptosis; the antibody Fc can also mediate ADCC.
NO
INDIRECT
The ADC binds HER2 (not beta‑tubulin), is internalized, and releases MMAE, which inhibits beta‑tubulin–dependent microtubule polymerization to cause G2/M arrest and apoptosis; beta‑tubulin is the intracellular payload target, not the drug’s binding target.
A humanized anti-CEACAM5 antibody-drug conjugate that binds CEACAM5 on tumor cells, is internalized, and releases the camptothecin-class topoisomerase I inhibitor payload (tocentecan), causing DNA damage and tumor cell death.
Humanized anti-CEACAM5 antibody-drug conjugate that binds CEACAM5 on tumor cells, is internalized, and releases the camptothecin-class topoisomerase I inhibitor tocentecan, causing DNA damage and tumor cell death.
NO
INDIRECT
Cells are selected by CEACAM5 binding; after internalization the payload inhibits topoisomerase I, causing DNA damage and death. Topoisomerase I is not the targeting antigen that dictates which cells are killed.
Recombinant fusion protein immunotoxin (IL-3 linked to truncated diphtheria toxin) that targets CD123 (IL-3Rα) on AML cells, is internalized, and ADP-ribosylates EF-2 to halt protein synthesis and induce cell death.
IL-3–diphtheria toxin recombinant fusion that targets CD123 (IL-3R alpha) on leukemic cells; following receptor-mediated endocytosis, the diphtheria toxin domain ADP-ribosylates EF-2, halting protein synthesis and causing cell death.
YES
DIRECT
IL-3 moiety binds CD123, the fusion protein is internalized, and the diphtheria toxin domain ADP-ribosylates EF-2 to block protein synthesis, causing cell death.
Subcutaneous bispecific T‑cell–engaging antibody (BCMA×CD3) that redirects cytotoxic T cells to BCMA-expressing myeloma cells to induce lysis.
Bispecific antibody targeting BCMA on myeloma cells and CD3 on T cells; crosslinks T cells to BCMA-positive plasma cells to form an immune synapse, activate cytotoxic T lymphocytes, and induce perforin/granzyme-mediated tumor cell lysis.
YES
DIRECT
Elranatamab bridges CD3 on T cells to BCMA on target cells, forming an immune synapse and activating cytotoxic T cells to kill BCMA+ cells via perforin/granzyme-mediated lysis.