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Cancer Cell ; 23(4): 477-88, 2013 Apr 15.
Article in English | MEDLINE | ID: mdl-23597562

ABSTRACT

Receptor tyrosine kinases (RTK) are targets for anticancer drug development. To date, only RTK inhibitors that block orthosteric binding of ligands and substrates have been developed. Here, we report the pharmacologic characterization of the chemical SSR128129E (SSR), which inhibits fibroblast growth factor receptor (FGFR) signaling by binding to the extracellular FGFR domain without affecting orthosteric FGF binding. SSR exhibits allosteric properties, including probe dependence, signaling bias, and ceiling effects. Inhibition by SSR is highly conserved throughout the animal kingdom. Oral delivery of SSR inhibits arthritis and tumors that are relatively refractory to anti-vascular endothelial growth factor receptor-2 antibodies. Thus, orally-active extracellularly acting small-molecule modulators of RTKs with allosteric properties can be developed and may offer opportunities to improve anticancer treatment.


Subject(s)
Protein Kinase Inhibitors/pharmacology , Receptors, Fibroblast Growth Factor/antagonists & inhibitors , Receptors, Fibroblast Growth Factor/metabolism , Small Molecule Libraries/pharmacology , Allosteric Regulation , Animals , Antibodies, Monoclonal/pharmacology , Arthritis, Experimental/drug therapy , Bone Resorption/drug therapy , Carcinoma, Lewis Lung/drug therapy , Carcinoma, Lewis Lung/metabolism , Carcinoma, Lewis Lung/pathology , Fibroblast Growth Factors/antagonists & inhibitors , Fibroblast Growth Factors/metabolism , HEK293 Cells , Human Umbilical Vein Endothelial Cells/cytology , Human Umbilical Vein Endothelial Cells/drug effects , Human Umbilical Vein Endothelial Cells/metabolism , Humans , Mice , Neovascularization, Pathologic/drug therapy , Pancreatic Neoplasms/drug therapy , Pancreatic Neoplasms/metabolism , Pancreatic Neoplasms/pathology , Phosphorylation/drug effects , Protein Kinase Inhibitors/metabolism , Receptor Protein-Tyrosine Kinases/antagonists & inhibitors , Signal Transduction , Xenograft Model Antitumor Assays
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