FAQ

PF 04217903

Known as: MET Tyrosine Kinase Inhibitor PF-04217903, PF-04217903, PF04217903 
An orally bioavailabe, small-molecule tyrosine kinase inhibitor with potential antineoplastic activity. MET tyrosine kinase inhibitor PF-04217903… (More)
National Institutes of Health

Topic mentions per year

Topic mentions per year

2009-2017
02420092017

Related topics

Related topics

1 relation
Receptor Tyrosine Kinase Inhibition

Related mentions per year

Related mentions per year

2009-2017
20002005201020152020
PF 04217903
Receptor Tyrosine Kinase Inhibition

Papers overview

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2015
2015
Activating MET Kinase Rearrangements in Melanoma and Spitz Tumors
Oncogenic gene fusions have been identified in many cancers and many serve as biomarkers or targets for therapy. Here we identify… (More)
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2013
2013
Epithelial ovarian cancer-induced angiogenic phenotype of human omental microvascular endothelial cells may occur independently of VEGF signaling.
Epithelial ovarian cancer (EOC) metastasizes transcoelomically to the peritoneum and omentum, and despite surgery and… (More)
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2013
2013
Inhibition of c-Met reduces lymphatic metastasis in RIP-Tag2 transgenic mice.
Inhibition of VEGF signaling can promote lymph node metastasis in preclinical models, but the mechanism is not fully understood… (More)
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2012
2012
Sensitivity of selected human tumor models to PF-04217903, a novel selective c-Met kinase inhibitor.
The c-Met pathway has been implicated in a variety of human cancers for its critical role in tumor growth, invasion, and… (More)
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Highly Cited
2012
Highly Cited
2012
Suppression of tumor invasion and metastasis by concurrent inhibition of c-Met and VEGF signaling in pancreatic neuroendocrine tumors.
UNLABELLED Invasion and metastasis increase after the inhibition of VEGF signaling in some preclinical tumor models. In the… (More)
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2012
2012
A novel SND1-BRAF fusion confers resistance to c-Met inhibitor PF-04217903 in GTL16 cells through [corrected] MAPK activation.
Targeting cancers with amplified or abnormally activated c-Met (hepatocyte growth factor receptor) may have therapeutic benefit… (More)
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2012
2012
A Novel SND1-BRAF Fusion Confers Resistance to c-Met Inhibitor PF-04217903 in GTL16 Cells though MAPK Activation
Targeting cancers with amplified or abnormally activated c-Met (hepatocyte growth factor receptor) may have therapeutic benefit… (More)
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2012
2012
Discovery of a novel class of exquisitely selective mesenchymal-epithelial transition factor (c-MET) protein kinase inhibitors and identification of the clinical candidate 2-(4-(1-(quinolin-6…
The c-MET receptor tyrosine kinase is an attractive oncology target because of its critical role in human oncogenesis and tumor… (More)
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2011
2011
Prediction of oral pharmacokinetics of cMet kinase inhibitors in humans: physiologically based pharmacokinetic model versus traditional one-compartment model.
The objective of this study was to assess the physiologically based pharmacokinetic (PBPK) model for predicting plasma… (More)
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2009
2009
Enzymatic characterization of c-Met receptor tyrosine kinase oncogenic mutants and kinetic studies with aminopyridine and triazolopyrazine inhibitors.
The c-Met receptor tyrosine kinase (RTK) is a key regulator in cancer, in part, through oncogenic mutations. Eight clinically… (More)
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