The Journal of infectious diseases · 2014
Diversity-oriented synthesis probe targets Plasmodium falciparum cytochrome b ubiquinone reduction site and synergizes with oxidation site inhibitors.
СтатьяПоддержка NIH: внешняя программаПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
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Lukens Amanda K, Heidebrecht Richard W, Mulrooney Carol, Beaudoin Jennifer A, Comer Eamon, Duvall Jeremy R, Fitzgerald Mark E, Masi Daniela, Galinsky Kevin, Scherer Christina A, Palmer Michelle, Munoz Benito, Foley Michael, Schreiber Stuart L, Wiegand Roger C, Wirth Dyann F
Аннотация
BACKGROUND: The emergence and spread of drug resistance to current antimalarial therapies remains a pressing concern, escalating the need for compounds that demonstrate novel modes of action. Diversity-Oriented Synthesis (DOS) libraries bridge the gap between conventional small molecule and natural product libraries, allowing the interrogation of more diverse chemical space in efforts to identify probes of novel parasite pathways.
METHODS: We screened and optimized a probe from a DOS library using whole-cell phenotypic assays. Resistance selection and whole-genome sequencing approaches were employed to identify the cellular target of the compounds.
RESULTS: We identified a novel macrocyclic inhibitor of Plasmodium falciparum with nanomolar potency and identified the reduction site of cytochrome b as its cellular target. Combination experiments with reduction and oxidation site inhibitors showed synergistic inhibition of the parasite.
CONCLUSIONS: The cytochrome b oxidation center is a validated antimalarial target. We show that the reduction site of cytochrome b is also a druggable target. Our results demonstrating a synergistic relationship between oxidation and reduction site inhibitors suggests a future strategy for new combination therapies in the treatment of malaria.
METHODS: We screened and optimized a probe from a DOS library using whole-cell phenotypic assays. Resistance selection and whole-genome sequencing approaches were employed to identify the cellular target of the compounds.
RESULTS: We identified a novel macrocyclic inhibitor of Plasmodium falciparum with nanomolar potency and identified the reduction site of cytochrome b as its cellular target. Combination experiments with reduction and oxidation site inhibitors showed synergistic inhibition of the parasite.
CONCLUSIONS: The cytochrome b oxidation center is a validated antimalarial target. We show that the reduction site of cytochrome b is also a druggable target. Our results demonstrating a synergistic relationship between oxidation and reduction site inhibitors suggests a future strategy for new combination therapies in the treatment of malaria.
Предметные рубрики MeSH
AntimalarialsBase SequenceCatalytic DomainCytochromes bDrug DiscoveryDrug ResistanceDrug SynergismEnzyme InhibitorsHigh-Throughput Nucleotide SequencingHigh-Throughput Screening AssaysHumansLactams, MacrocyclicMalaria, FalciparumMolecular Sequence DataOxidation-ReductionPhenylurea CompoundsPlasmodium falciparumProtozoan ProteinsSmall Molecule LibrariesUbiquinoneBenzenesulfonamides