Humanized IgG1 monoclonal antibody targeting the HER2 extracellular dimerization domain (subdomain II); blocks HER2/HER3 dimerization, inhibiting downstream PI3K/AKT/MAPK signaling, and engages Fc-mediated ADCC to promote tumor cell killing.
YES
DIRECT
Pertuzumab binds HER2 on tumor cells and engages Fcγ receptors on immune effectors to trigger ADCC; blockade of HER2/HER3 signaling also promotes apoptosis.
Humanized IgG1 monoclonal antibody targeting the HER2 extracellular dimerization domain (subdomain II); blocks HER2/HER3 dimerization, inhibiting downstream PI3K/AKT/MAPK signaling, and engages Fc-mediated ADCC to promote tumor cell killing.
NO
INDIRECT
Pertuzumab binds HER2 on tumor cells; its Fc engages CD16a on NK cells to trigger ADCC, resulting in NK-mediated killing of HER2+ cells. CD16a-expressing immune cells are not killed.
A HER2-targeted antibody–drug conjugate composed of a humanized anti-HER2 monoclonal antibody linked via a cleavable linker to deruxtecan (DXd), a membrane-permeable topoisomerase I inhibitor. Binds HER2, is internalized, and releases DXd to inhibit topoisomerase I, causing DNA damage and a bystander effect; dosed 5.4 mg/kg IV every 3 weeks.
Humanized anti-HER2 monoclonal antibody linked via a cleavable linker to deruxtecan (DXd), a membrane-permeable topoisomerase I inhibitor. After binding HER2 on tumor cells, the ADC is internalized and the linker is cleaved in lysosomes to release DXd, which inhibits topoisomerase I, inducing DNA damage and apoptosis; the membrane-permeable payload produces a bystander killing effect in adjacent cells.
YES
DIRECT
ADC binds HER2, is internalized, and releases the DXd topoisomerase I inhibitor in lysosomes, causing DNA damage and apoptosis; the membrane‑permeable payload can also cause bystander killing.
A HER2-targeted antibody–drug conjugate composed of a humanized anti-HER2 monoclonal antibody linked via a cleavable linker to deruxtecan (DXd), a membrane-permeable topoisomerase I inhibitor. Binds HER2, is internalized, and releases DXd to inhibit topoisomerase I, causing DNA damage and a bystander effect; dosed 5.4 mg/kg IV every 3 weeks.
Humanized anti-HER2 monoclonal antibody linked via a cleavable linker to deruxtecan (DXd), a membrane-permeable topoisomerase I inhibitor. After binding HER2 on tumor cells, the ADC is internalized and the linker is cleaved in lysosomes to release DXd, which inhibits topoisomerase I, inducing DNA damage and apoptosis; the membrane-permeable payload produces a bystander killing effect in adjacent cells.
YES
INDIRECT
After HER2 binding and internalization, T-DXd releases the DXd payload, which inhibits DNA topoisomerase I in exposed cells, causing DNA damage and apoptosis; the membrane-permeable payload can also kill neighboring cells (bystander effect).
Allogeneic, gene-edited T-cell therapy engineered with a reverse, universal CAR displaying an extracellular peptide epitope; given as a single IV infusion to enable dose-tunable engagement of CD123+ AML cells when bridged by R-TM123.
Allogeneic, gene-edited T cells expressing a reverse, universal CAR that displays an extracellular peptide epitope. Anti-leukemia activity is adapter-dependent: the bispecific protein R-TM123 binds both the RevCAR epitope and CD123 on tumor cells, bridging the engineered T cells to CD123+ blasts to trigger CAR signaling and cytotoxic killing with dose-tunable control.
YES
DIRECT
R-TM123 bridges CD123 on target cells to the RevCAR on engineered T cells, activating CAR signaling and T cell–mediated killing (perforin/granzyme apoptosis) of CD123+ cells.