Ghavami Maryam, Merino Emilio F, Yao Zhong-Ke, Elahi Rubayet, Simpson Morgan E, Fernández-Murga Maria L, Butler Joshua H, Casasanta Michael A, Krai Priscilla M, Totrov Maxim M, Slade Daniel J, Carlier Paul R, Cassera Maria Belen
Department of Chemistry and Virginia Tech Center for Drug Discovery , Virginia Tech , Hahn Hall South, 800 West Campus Drive , Blacksburg , Virginia 24061 , United States.
Department of Biochemistry and Virginia Tech Center for Drug Discovery , Virginia Tech , Engel Hall, 340 West Campus Drive , Blacksburg , Virginia 24061 , United States.
ACS Infect Dis. 2018 Apr 13;4(4):549-559. doi: 10.1021/acsinfecdis.7b00159. Epub 2017 Nov 7.
Malaria continues to be one of the deadliest diseases worldwide, and the emergence of drug resistance parasites is a constant threat. Plasmodium parasites utilize the methylerythritol phosphate (MEP) pathway to synthesize isopentenyl pyrophosphate (IPP) and dimethylallyl pyrophosphate (DMAPP), which are essential for parasite growth. Previously, we and others identified that the Malaria Box compound MMV008138 targets the apicoplast and that parasite growth inhibition by this compound can be reversed by supplementation of IPP. Further work has revealed that MMV008138 targets the enzyme 2- C-methyl-d-erythritol 4-phosphate cytidylyltransferase (IspD) in the MEP pathway, which converts MEP and cytidine triphosphate (CTP) to cytidinediphosphate methylerythritol (CDP-ME) and pyrophosphate. In this work, we sought to gain insight into the structure-activity relationships by probing the ability of MMV008138 analogs to inhibit PfIspD recombinant enzyme. Here, we report PfIspD inhibition data for fosmidomycin (FOS) and 19 previously disclosed analogs and report parasite growth and PfIspD inhibition data for 27 new analogs of MMV008138. In addition, we show that MMV008138 does not target the recently characterized human IspD, reinforcing MMV008138 as a prototype of a new class of species-selective IspD-targeting antimalarial agents.
疟疾仍然是全球最致命的疾病之一,耐药寄生虫的出现是一个持续的威胁。疟原虫利用甲基赤藓糖醇磷酸(MEP)途径合成异戊烯基焦磷酸(IPP)和二甲基烯丙基焦磷酸(DMAPP),这些对寄生虫的生长至关重要。此前,我们和其他人发现疟疾盒化合物MMV008138靶向质体,并且补充IPP可以逆转该化合物对寄生虫生长的抑制作用。进一步的研究表明,MMV008138靶向MEP途径中的2-C-甲基-D-赤藓糖醇4-磷酸胞苷转移酶(IspD),该酶将MEP和三磷酸胞苷(CTP)转化为二磷酸胞苷甲基赤藓糖醇(CDP-ME)和焦磷酸。在这项工作中,我们试图通过探究MMV008138类似物抑制PfIspD重组酶的能力来深入了解构效关系。在此,我们报告了磷霉素(FOS)和19种先前公开的类似物的PfIspD抑制数据,并报告了MMV008138的27种新类似物的寄生虫生长和PfIspD抑制数据。此外,我们表明MMV008138不靶向最近鉴定的人类IspD,这进一步证明MMV008138是一类新型物种选择性IspD靶向抗疟药物的原型。