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A Chemical Genomic Analysis of Decoquinate, a Plasmodium falciparum Cytochrome b Inhibitor
Journal article   Open access   Peer reviewed

A Chemical Genomic Analysis of Decoquinate, a Plasmodium falciparum Cytochrome b Inhibitor

Tae-gyu Nam, Case W McNamara, Selina Bopp, Neekesh V Dharia, Stephan Meister, Ghislain M. C Bonamy, David M Plouffe, Nobutaka Kato, Susan McCormack, Badry Bursulaya, …
ACS chemical biology, v 6(11), pp 1214-1222
18 Nov 2011
PMID: 21866942
url
https://doi.org/10.1021/cb200105dView
Published, Version of Record (VoR) Open

Abstract

Decoquinate has single-digit nanomolar activity against in vitro blood stage Plasmodium falciparum parasites, the causative agent of human malaria. In vitro evolution of decoquinate-resistant parasites and subsequent comparative genomic analysis to the drug-sensitive parental strain revealed resistance was conferred by two nonsynonymous single nucleotide polymorphisms in the gene encoding cytochrome b . The resultant amino acid mutations, A122T and Y126C, reside within helix C in the ubiquinol-binding pocket of cytochrome b , an essential subunit of the cytochrome bc 1 complex. As with other cytochrome bc 1 inhibitors, such as atovaquone, decoquinate has low nanomolar activity against in vitro liver stage P. yoelii and provides partial prophylaxis protection when administered to infected mice at 50 mg kg –1 . In addition, transgenic parasites expressing yeast dihydroorotate dehydrogenase are >200-fold less sensitive to decoquinate, which provides additional evidence that this drug inhibits the parasite’s mitochondrial electron transport chain. Importantly, decoquinate exhibits limited cross-resistance to a panel of atovaquone-resistant parasites evolved to harbor various mutations in cytochrome b . The basis for this difference was revealed by molecular docking studies, in which both of these inhibitors were shown to have distinctly different modes of binding within the ubiquinol-binding site of cytochrome b .

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Biochemistry & Molecular Biology
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