Institute of Molecular and Cellular Biosciences, The University of Tokyo, 1-1-1 Yayoi, Bunkyo-ku, Tokyo, 113-0032, Japan.
Angew Chem Int Ed Engl. 2017 Sep 11;56(38):11530-11533. doi: 10.1002/anie.201706529. Epub 2017 Aug 9.
Huntington's disease (HD) is an autosomal dominant neurodegenerative disorder caused by the aggregation of mutant huntingtin (mHtt), and removal of toxic mHtt is expected to be an effective therapeutic approach. We designed two small hybrid molecules (1 and 2) by linking a ligand for ubiquitin ligase (cellular inhibitor of apoptosis protein 1; cIAP1) with probes for mHtt aggregates, anticipating that these compounds would recruit cIAP1 to mHtt and induce selective degradation by the ubiquitin-proteasome system. The synthesized compounds reduced mHtt levels in HD patient fibroblasts and appear to be promising candidates for the development of a treatment for HD.
亨廷顿病(HD)是一种常染色体显性神经退行性疾病,由突变型亨廷顿蛋白(mHtt)聚集引起,去除毒性 mHtt 有望成为一种有效的治疗方法。我们通过连接泛素连接酶(细胞凋亡蛋白 1;cIAP1)的配体和 mHtt 聚集体的探针设计了两种小分子杂合分子(1 和 2),预计这些化合物将招募 cIAP1 到 mHtt 并通过泛素-蛋白酶体系统诱导选择性降解。合成的化合物降低了 HD 患者成纤维细胞中的 mHtt 水平,似乎是开发 HD 治疗方法的有前途的候选药物。