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・ Tyrosinase
・ Tyrosine
・ Tyrosine (data page)
・ Tyrosine 2,3-aminomutase
・ Tyrosine aminotransferase
・ Tyrosine ammonia-lyase
・ Tyrosine decarboxylase
・ Tyrosine hydroxylase
・ Tyrosine kinase
・ Tyrosine kinase 2
・ Tyrosine N-monooxygenase
・ Tyrosine phenol-lyase
・ Tyrosine phosphorylation
・ Tyrosine sulfation
・ Tyrosine-ester sulfotransferase
Tyrosine-kinase inhibitor
・ Tyrosine-protein kinase BLK
・ Tyrosine-protein kinase CSK
・ Tyrosinemia
・ Tyrosinemia type II
・ Tyrosinemia type III
・ Tyrosine—arginine ligase
・ Tyrosine—tRNA ligase
・ Tyrosol
・ Tyrosylprotein sulfotransferase
・ Tyrothricin
・ Tyrotoxism
・ Tyrowo
・ TYRP1
・ Tyrrau Mawr


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Tyrosine-kinase inhibitor : ウィキペディア英語版
Tyrosine-kinase inhibitor

A tyrosine kinase inhibitor (TKI) is a pharmaceutical drug that inhibits tyrosine kinases. Tyrosine kinases are enzymes responsible for the activation of many proteins by signal transduction cascades. The proteins are activated by adding a phosphate group to the protein (phosphorylation), a step that TKIs inhibit. TKIs are typically used as anticancer drugs. For example, they have substantially improved outcomes in chronic myelogenous leukemia.
They are also called tyrphostins, the short name for “tyrosine phosphorylation inhibitor”, originally coined in a 1988 publication, which was the first description of compounds inhibiting the catalytic activity of the epidermal growth factor receptor (EGFR).
The 1988 study was the first demonstration of a systematic search and discovery of small-molecular-weight inhibitors of tyrosine phosphorylation, which do not inhibit protein kinases that phosphorylate serine or threonine residues and can discriminate between the kinase domains of the EGFR and that of the insulin receptor. It was further shown that in spite of the conservation of the tyrosine-kinase domains one can design and synthesize tyrphostins that discriminate between even closely related protein tyrosine kinases such as EGFR and its close relative HER2.
==Development of drugs==
Numerous TKIs aiming at various tyrosine kinases have been generated by the originators of these compounds and proven to be effective anti-tumor agents and anti-leukemic agents. Based on this work imatinib was developed against chronic myelogenous leukemia (CML) and later gefitinib and erlotinib aiming at the EGF receptor. Sunitinib, an inhibitor of the receptors for FGF, PDGF and VEGF is also based on early studies on TKIs aiming at VEGF receptors.

抄文引用元・出典: フリー百科事典『 ウィキペディア(Wikipedia)
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