PKI 166 hydrochloride

PKI-166 hydrochloride is a potent, selective and orally bioavailable EGFR tyrosine kinase inhibitor, with an IC50 of 0.7 nM[1].

Research Areas >> Cancer

Signaling Pathways >> JAK/STAT Signaling >> EGFR

Signaling Pathways >> Protein Tyrosine Kinase/RTK >> EGFR

IC50: 0.7 nM (EGFR tyrosine kinase)[1]

Pretreatment with PKI-166 hydrochloride (0-0.5 μM; 1 hour) inhibits EGFR autophosphorylation in human pancreatic cancer cells[1]. PKI-166 hydrochloride (0.03 μM; 6 days) enhances the cytotoxicity mediated by gemcitabine[1]. Western Blot Analysis[1] Cell Line: L3.6pl cells Concentration: 0.01 μM, 0.05 μM, 0.5 μM Incubation Time: 1 hour Result: Inhibited EGFR autophosphorylation in a dose-dependent manner. Cell Cytotoxicity Assay[1] Cell Line: L3.6pl cells Concentration: 0.03 μM Incubation Time: 6 days Result: Enhanced the cytotoxicity mediated by gemcitabine.

PKI-166 hydrochloride (100 mg/kg; p.o.; daily; day 7-day 35 after xenograft) inhibits of pancreatic cancer growth[1]. Animal Model: Male athymic nude mice with L3.6pl cells xenograft (8–12 weeks)[1] Dosage: 100 mg/kg Administration: Oral administration; daily; from day 7 to day 35 after xenograft Result: Significantly decreased median tumor volume.

[1]. Bruns CJ, et al. Blockade of the epidermal growth factor receptor signaling by a novel tyrosine kinase inhibitor leads to apoptosis of endothelial cells and therapy of human pancreatic carcinoma. Cancer Res. 2000 Jun 1;60(11):2926-35.