SDS of cas: 98-97-5. Recently I am researching about CARDIAC-SPECIFIC KINASE; DUAL INHIBITORS; DESIGN; OVEREXPRESSION; MECHANISMS; DISEASE; CARDIOPROTECTION; ANTHOCYANINS; CLEAVAGE; AGENTS, Saw an article supported by the National Natural Science Foundation of ChinaNational Natural Science Foundation of China (NSFC) [21772131]; Fundamental Research Funds for the Science & Technology department of Sichuan Province [2019YFSY0004, 20GJHZ0179]. Published in ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER in ISSY-LES-MOULINEAUX ,Authors: Pang, HY; Wang, N; Chai, JL; Wang, XY; Zhang, YH; Bi, Z; Wu, WB; He, G. The CAS is 98-97-5. Through research, I have a further understanding and discovery of Pyrazine-2-carboxylic acid
Myocardial infarction (MI) injury is a highly lethal syndrome that has, until recently, suffered from a lack of clinically efficient targeted therapeutics. The cardiac troponin I interacting kinase (TNNI3K) exacerbates ischemia-reperfusion (IR) injury via oxidative stress, thereby promoting cardiomyocyte death. In this current study, we designed and synthesized 35 novel TNNI3K inhibitors with a pyrido[4,5]thieno [2,3-d] pyrimidine scaffold. In vitro results indicated that some of the inhibitors exhibited sub-micromolar TNNI3K inhibitory capacity and good kinase selectivity, as well as cytoprotective activity, in an oxygen-glucose deprivation (OGD) injury cardiomyocyte model. Furthermore, investigation of the mechanism of the representative derivative compound 6o suggested it suppresses pyroptosis and apoptosis in cardiomyocytes by interfering with p38MAPK activation, which was further confirmed in a murine myocardial infarction injury model. In vivo results indicate that compound 6o can markedly reduce myocardial infarction size and alleviate cardiac tissue damage in rats. In brief, our results provide the basis for further development of novel TNNI3K inhibitors for targeted MI therapy. (C) 2020 Elsevier Masson SAS. All rights reserved.
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Patent; Chevron Research Company; US4732894; (1988); A;,
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