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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 ...
ALK inhibitors are anti-cancer drugs that act on tumours with variations of anaplastic lymphoma kinase (ALK) such as an EML4-ALK translocation. [1] They fall under the category of tyrosine kinase inhibitors , which work by inhibiting proteins involved in the abnormal growth of tumour cells.
Tyrosine kinase inhibitor (TKI) with selective activity against RET, VEGFR-2 and EGFR: Medullary thyroid cancer. Diarrhoea, hypertension, QT interval prolongation, depression, electrolyte anomalies, hypothyroidism and GI perforation (uncommon). 2.3 mTOR inhibitors: Everolimus: PO: mTOR inhibitor.
Intedanib is a multiple tyrosine kinase inhibitor and is the first drug to treat idiopathic pulmonary fibrosis. [4] Indol derivatives with 1-NH of 2-indolinone motif that is an H-bond donor, and 2-carbonyl oxygen that acts as an H-bond acceptor, bind with Glu915 and Cys917, respectively.
c-Met inhibitors are a class of small molecules that inhibit the enzymatic activity of the c-Met tyrosine kinase, the receptor of hepatocyte growth factor/scatter factor (HGF/SF). These inhibitors may have therapeutic application in the treatment of various types of cancers.
Inhibitors of tyrosine kinase are mainly used against some specific forms of cancer ... Non-receptor tyrosine kinase inhibitors (1 C, 25 P) R.
These inhibitors are used to treat cancers like non-small cell lung cancer, medullary thyroid carcinoma, and some types of colorectal and pancreatic cancer. RET inhibitors fall under the category of the tyrosine kinase inhibitors, which work by inhibiting proteins involved in the abnormal growth of cancer cells. Existing molecules fall in two ...
This abnormality was discovered by Peter Nowell in 1960 [1] and is a consequence of fusion between the Abelson tyrosine kinase gene at chromosome 9 and the break point cluster gene at chromosome 22, resulting in a chimeric oncogene and a constitutively active Bcr-Abl tyrosine kinase that has been implicated in the pathogenesis of CML. Compounds ...
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