Analysis of Drug Tyrosine Kinase Inhibitor

Added on - 28 May 2020

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Running head: TYROSINE KINASE INHIBITORSAnalysis of Drug Tyrosine Kinase InhibitorName of the Student:Name of the University:Author Note:
TYROSINE KINASE INHIBITORS1Table of contentsIntroduction......................................................................................................................................2Body.................................................................................................................................................4Conclusion.......................................................................................................................................8Reference.........................................................................................................................................9
TYROSINE KINASE INHIBITORS2IntroductionTyrosine Kinase inhibitor (TKI) is a drug that inhibits the action of the enzyme calledtyrosine kinase. This drug belongs to the class of medications that deal with chemotherapy.TKI’s have been made out of the understanding and knowledge of the cell cycle, DNA,molecular signaling pathways. Thus, TKI represent a change in the conventional methods ofcancer treatment. The drug tyrosine kinase inhibitor targets the enzyme tyrosine kinase. Tyrosinekinase is the major causal agent that triggers the action of the several proteins through thecascading signal pathways (Ng eta l. 2012).Tyrosine kinase inhibitors are also called tyrphostins (tyrosine phosphorylation inhibitor).The terms were first coined in a publication in the year 1988 which first revealed that the certaincompounds called kinase inhibitors, inhibited the catalytic activity of EFGR (Epidermal growthfactor receptor). In that particular publication the study was based on the step by step search andeffectively discover a molecular compound exhibiting small molecular weight and that acts toinhibit the phosphorylation of tyrosine. The search was based on the objective that the compoundmust be able to distinguish between the insulin receptor and the kinase domains of Epidermalgrowth factor receptor (Mesothelioma-aid.org, 2018). However, study even focused on the factorthat the searched compound must not be inhibitory to the protein kinases that phosphorylatethreonine and serine. However, later it was found that other than the naturally existing kinaseinhibitors, one can artificially synthesize the tyrphostins that can effectively differentiate amongthe protein kinase inhibitors like the HER2 and EGFR. The development of the tyrosine kinaseinhibitors was focused mainly on the different types of tyrosine kinases. The inhibitors werefound to be effectively working against the anti-leukemic agents and the anti-tumor agents(Hartman, Zhao and Agazie 2013). Depending upon the functions of these inhibitors different
TYROSINE KINASE INHIBITORS3types of drugs were developed. To act against the Chronic Myelogenous Leukemia (CML),Imatinib was developed. Later, Elotinib and Gefitinib were developed to aim for the EpidermalGrowth Receptor (EGF) receptors. in order to act against the receptors of fibroblast growthfactor, platelet-derived growth factor and vascular endothelial growth factor, a drug calledSunitinib was developed (Ng eta l. 2012)..The drugs that belong to the three different classes of tyrosine kinase inhibitors are asfollows:Type I inhibitors- Sunitinib is an orally administered drug and it competes with the ATPto bind at the socket of ATP of an activated kinase. This drug however lacks theselectivity, because there exist more than 500 kinases that exhibit the similarity in theATP-socket.Type II inhibitors- This class of inhibitors include nilotinib and imatinib that binds to thetwo different receptors on the kinase. The two regions are the ATP pocket and a regionadjacent to the to the ATP pocket which is accessible only when kinase is inactive. Thistype II inhibitor bind only when the kinases are in the inactive condition. Comparatively,the type II inhibitors exhibit more potentiality than the type I inhibitors.Type III inhibitors- these type of inhibitors acts more specifically, and are more selectivein nature than the other types. These TKIs are more complex to design and are not aseffective compared to the other two inhibitors (Roskoski 2016).The major difference between the chemotherapy and targeted therapy is that chemotherapycan kill the normal cells along with the infected cells. However, in targeted therapy normalcells survive the therapy. Chemotherapy drugs target the cancer cells that needs to divide andgrow, this affects the normal cells. Whereas, in the targeted therapy the defective proteins
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