PD168393

PD168393 is an potent, cell-permeable, irreversible EGFR inhibitor with IC50 of 0.70 nM, irreversibly alkylate Cys-773, inactive against insulin, PDGFR, FGFR and PKC. target: EGFRIC 50: 0.7 nM [1](1) PD 168393 inhibite EGFr autophosphorylation in A431 human epidermoid carcinoma cells with >9-fold greater potency than PD 174265.[1](2) PD 168393 decrease the production of TNF-α and phosphrylation of ERK1/2 and p38 induced by LPS in cardiomyocytes.[2](3) PD168393 completely inhibits AKT and ERK phosphorylation at concentrations as low as 0.03 umol/L.[3](4) PD168393 could induce apoptosis and inhibit cell growth in ErbB2 positive lung and breast cancer cell lines.[3](5) PD168393 disrupted MEK1/p44/42 ERK signaling in HaCaT cells as determined by inhibition of phospho-p44/42 ERK. [4]

Signaling Pathways >> Autophagy >> Autophagy

Research Areas >> Cancer

EGFR:0.7 nM (IC50)

[1]. Fry DW et al. Specific, irreversible inactivation of the epidermal growth factor receptor and erbB2, by a new class of tyrosine kinase inhibitor. Proc Natl Acad Sci U S A. 1998 Sep 29;95(20):12022-7.

[2]. Sun X et al. The activation of EGFR promotes myocardial tumor necrosis factor-α production and cardiac failure in endotoxemia. Oncotarget. 2015 Nov 3;6(34):35478-95.

[3]. Li G et al. Modulation of ErbB2 blockade in ErbB2-positive cancers: the role of ErbB2 Mutations and PHLDA1. PLoS One. 2014 Sep 19;9(9):e106349.

[4]. White KJ et al. Irritant activation of epithelial cells is mediated via protease-dependent EGFR activation. J Invest Dermatol. 2011 Feb;131(2):435-42.

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