Duligotuzumab

Duligotuzumab (0.01-25 μM; 72 h) inhibits proliferation of HER2-positive OE33, OE19, and NCI-N87 gastric cancer cell lines with IC₅₀ values of ≈0.1 to ≈0.5 μM over 72 h, but has no effect on HER2-negative MKN28 gastric cancer cells^[1].
Duligotuzumab (0.5 μM; 7 days) reduces colony formation in HER2-positive OE33, OE19, and NCI-N87 gastric cancer cell lines over 7 days^[1].
Duligotuzumab (0.5 μM; 72 h) reduces migration of HER2-positive OE33, OE19, and NCI-N87 gastric cancer cell lines over 72 h^[1].
Duligotuzumab (0.5 μM; 72 h) induces apoptosis in HER2-positive OE33, OE19, and NCI-N87 gastric cancer cell lines over 72 h, with an apoptotic rate of ≈35% in OE33 cells^[1].
Duligotuzumab (0.5 μM; 48 h) reduces phosphorylated HER2 and HER3 levels but does not alter total or phosphorylated AKT, MAPK, or total HER2 or HER3 protein levels in HER2-positive OE33 and OE19 gastric cancer cell lines^[1].
Duligotuzumab induces antibody-dependent cell-mediated cytotoxicity in EGFR-overexpressing cell lines, with activity comparable to cetuximab^[2].
Duligotuzumab binds to EGFR with a dissociation constant of 0.4 nM^[2].
Duligotuzumab enhances antiproliferative activity in cancer cells, overcomes EGFR resistance, and enhances radiation effects compared to monospecific HER antibodies, including in cetuximab-resistant cells^[3].
Duligotuzumab potently blocks EGFR and HER3 receptors and inhibits downstream HER/ErbB signaling pathways in an in vitro system^[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.