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Structural Biology Studies reveal the Conformational Switching of Anaplastic Lymphoma Kinase (ALK) by Pyrazolylamine Derivatives
Dissertation

Structural Biology Studies reveal the Conformational Switching of Anaplastic Lymphoma Kinase (ALK) by Pyrazolylamine Derivatives

Tu, Chih-Hsiang
Doctor of Philosophy (PHD), 國立清華大學, 生物資訊與結構生物研究所
2016

Abstract

蛋白結晶學 間變性淋巴瘤激酶 第一型激酶抑制劑 第二型激酶抑制劑 Protein crystallography Anaplastic lymphoma kinase (ALK) Type-I kinase inhibitor Type-II kinase inhibitor
Studies have shown that anaplastic lymphoma kinase (ALK) chromosomal translocation, gene amplification and point mutations are associated with various human cancers. Hence, ALK has been proposed as a potential drug target in the treatment of cancers and the inhibition of irregularly activated ALK by small molecules constitutes a promising approach. Currently, most of ALK inhibitors are developed as the type-I kinase inhibitors. Although some of type-I inhibitors are FDA-approved and exhibit excellent drug potency, those are associated with some adverse effects. For this reason, continuous development of ALK inhibitors is needed. Type II kinase inhibitor is expected to be an alternative approach for the development of novel ALK inhibitors. However, only few researches have been devoted to type-II ALK inhibitor’s studies due to the limitations of the traditional enzymatic assay. Limited type-II ALK structural studies are available, which may also impede the development of the novel type-II ALK inhibitors. In our research, protein crystallography and structural biology studies of BPR-1J297 with ALK kinase domain revealed that BPR-1J297 adopts a type-IIA binding mode. BPR-1J297, distinct from others published type-IIA inhibitors, simultaneously causes the conformational change in activation loop, αC-helix, and juxtamembrane domain of ALK, which are all important domains for ALK autoinhibition, phosphorylation, activation, and downstream signal pathway regulation. The structure-activity relationship (SAR) of BPR-1J297 reveals that minor modifications to the chemical structure of BPR-1J297 led to significant differences in the ALK potency (or ligand efficiency) as well as alters the binding mode between type-I and type-II in ALK. In addition, biophysics studies were performed and that hydrophobic urea-substituted tail moiety endowed BPR-1J297 with slow association rate and dissociation rate, in consistent with the results in structure biology studies. To our knowledge, this is the first research comprehensively demonstrated that chemical modification in a small molecule structure can directly regulate the switch between the type I and type II binding modes, and induce dramatic conformational changes in protein structures. Structural biology studies of ALK in complex with BPR-1J297 and its analogues together with the physicochemical properties studies provide the insights on the future chemical structural optimization of pyrazolylamine series as potential ALK inhibitors in the treatment of cancer reagents.

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