Reinvestigating the synthesis and efficacy of small benzimidazole derivatives as presequence protease enhancers.

Reinvestigating the synthesis and efficacy of small benzimidazole derivatives as presequence protease enhancers.
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DOI:
10.1016/j.ejmech.2019.111746
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发表时间:
2019-12
影响因子:
6.7
通讯作者:
Nan-Sheng Li;W. Liang;J. Piccirilli;Wei-Jen Tang
Nan-Sheng Li;W. Liang;J. Piccirilli;Wei-Jen Tang
中科院分区:
医学1区
文献类型:
--
作者:
Nan-Sheng Li;W. Liang;J. Piccirilli;Wei-Jen Tang

文献摘要

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前序列蛋白酶(PreP)是一种蛋白质稳定酶,在维持线粒体健康中起关键作用。PreP稳定性的缺陷与人类神经系统疾病有关,这种酶的活性改变调节小鼠阿尔茨海默病样病理学的进展。由于促进PreP蛋白水解活性的激动剂代表了一种有前途的治疗途径,我们试图确定苯并咪唑衍生物(3cand4c)作用的结构基础,这首先由Vangavaragu等人报道。(Eur. 76(2014)506 - 516)。然而,我们发现了用于合成3-环己基醛亚胺A的公开方法。然后,我们开发了一种替代的合成方法,并获得了3c,称为化合物C,和一种替代的苯并咪唑衍生物,称为化合物dB。我们测试了化合物A、B和C增强人PreP活性的能力。与以前的报道相反,我们观察到化合物A、B或C(3c)都没有调节人PreP的催化活性。在这里,我们报告了我们对所报道的苯并咪唑的错误鉴定和这些化合物对人PreP缺乏生物活性的发现。因此,用于基于PreP的疗法的PreP调节剂仍有待发现。
Presequence protease (PreP) is a proteostatic enzyme that plays a key role in the maintenance of mitochondrial health. Defects in PreP stability are associated with neurological disorders in humans, and altered activity of this enzyme modulates the progress of Alzheimer’s disease-like pathology in mice. As agonists that boost PreP proteolytic activity represent a promising therapeutic avenue, we sought to determine the structural basis for the action of benzimidazole derivatives (3cand4c), first reported by Vangavaragu et al. (Eur. J. Med. Chem. 76 (2014) 506–516) that enhance the activity of PreP. However, we found the published procedure for the synthesis of3cyielded aldimineAinstead. We then developed an alternative synthesis and obtained3c, termed compoundC,and an alternative benzimidazole derivative, termed compoundB. We tested compoundsA,BandCfor their ability to enhance the activities of human PreP. In contrast to the previous report, we observed that none of the compoundsA,B, orC(3c) modulated the catalytic activity of human PreP. Here we report our findings on the mis-identification of the reported benzimidazoles and the lack of biological activity of such compounds on human PreP. Thus, PreP modulators for PreP-based therapies remain to be discovered.