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通过定量高通量筛选鉴定出的三类葡萄糖脑苷脂酶抑制剂是戈谢病的伴侣型先导化合物。

Three classes of glucocerebrosidase inhibitors identified by quantitative high-throughput screening are chaperone leads for Gaucher disease.

作者信息

Zheng Wei, Padia Janak, Urban Daniel J, Jadhav Ajit, Goker-Alpan Ozlem, Simeonov Anton, Goldin Ehud, Auld Douglas, LaMarca Mary E, Inglese James, Austin Christopher P, Sidransky Ellen

机构信息

NIH Chemical Genomics Center, National Human Genome Research Institute, National Institutes of Health, 9800 Medical Center Drive, MSC 3370, Bethesda, MD 20892-3370, USA.

出版信息

Proc Natl Acad Sci U S A. 2007 Aug 7;104(32):13192-7. doi: 10.1073/pnas.0705637104. Epub 2007 Aug 1.

Abstract

Gaucher disease is an autosomal recessive lysosomal storage disorder caused by mutations in the glucocerebrosidase gene. Missense mutations result in reduced enzyme activity that may be due to misfolding, raising the possibility of small-molecule chaperone correction of the defect. Screening large compound libraries by quantitative high-throughput screening (qHTS) provides comprehensive information on the potency, efficacy, and structure-activity relationships (SAR) of active compounds directly from the primary screen, facilitating identification of leads for medicinal chemistry optimization. We used qHTS to rapidly identify three structural series of potent, selective, nonsugar glucocerebrosidase inhibitors. The three structural classes had excellent potencies and efficacies and, importantly, high selectivity against closely related hydrolases. Preliminary SAR data were used to select compounds with high activity in both enzyme and cell-based assays. Compounds from two of these structural series increased N370S mutant glucocerebrosidase activity by 40-90% in patient cell lines and enhanced lysosomal colocalization, indicating chaperone activity. These small molecules have potential as leads for chaperone therapy for Gaucher disease, and this paradigm promises to accelerate the development of leads for other rare genetic disorders.

摘要

戈谢病是一种常染色体隐性溶酶体贮积症,由葡萄糖脑苷脂酶基因突变引起。错义突变导致酶活性降低,这可能是由于错误折叠所致,从而增加了小分子伴侣纠正该缺陷的可能性。通过定量高通量筛选(qHTS)对大型化合物库进行筛选,可直接从初筛中提供有关活性化合物的效力、功效和构效关系(SAR)的全面信息,有助于确定用于药物化学优化的先导化合物。我们使用qHTS快速鉴定出三种结构系列的强效、选择性、非糖葡萄糖脑苷脂酶抑制剂。这三种结构类别具有优异的效力和功效,重要的是,对密切相关的水解酶具有高选择性。初步的SAR数据用于选择在酶和细胞实验中均具有高活性的化合物。这些结构系列中的两个系列的化合物可使患者细胞系中的N370S突变型葡萄糖脑苷脂酶活性提高40 - 90%,并增强溶酶体共定位,表明具有伴侣活性。这些小分子有潜力作为戈谢病伴侣疗法的先导化合物,并且这种模式有望加速其他罕见遗传疾病先导化合物的开发。

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