| Description |
PKI-166 is a potent, selective and orally bioavailable EGFR tyrosine kinase inhibitor, with an IC50 of 0.7 nM[1].
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| Related Catalog |
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| Target |
IC50: 0.7 nM (EGFR tyrosine kinase)[1]
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| In Vitro |
Pretreatment with PKI-166 (0–0.5 μM; 1 hour) inhibits EGFR autophosphorylation in human pancreatic cancer cells[1]. PKI-166 (0.03μ M; 6 days) enhanced 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.
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| In Vivo |
PKI-166 (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.
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| References |
[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.
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