Plasmodium dihydrofolate reductase is a second enzyme target for the antimalarial action of triclosan

Research output: Contribution to journalArticle

  • External authors:
  • Elizabeth Bilsland
  • Liisa Van Vliet
  • Kevin Williams
  • Jack Feltham
  • Marta P. Carrasco
  • Wesley L. Fotoran
  • Eliana F.G. Cubillos
  • Gerhard Wunderlich
  • Morten Grøtli
  • Florian Hollfelder
  • Victoria Jackson
  • Stephen G. Oliver


Malaria, caused by parasites of the genus Plasmodium, leads to over half a million deaths per year, 90% of which are caused by Plasmodium falciparum. P. vivax usually causes milder forms of malaria; however, P. vivax can remain dormant in the livers of infected patients for weeks or years before re-emerging in a new bout of the disease. The only drugs available that target all stages of the parasite can lead to severe side effects in patients with glucose-6-phosphate dehydrogenase (G6PD) deficiency; hence, there is an urgent need to develop new drugs active against blood and liver stages of the parasite. Different groups have demonstrated that triclosan, a common antibacterial agent, targets the Plasmodium liver enzyme enoyl reductase. Here, we provide 4 independent lines of evidence demonstrating that triclosan specifically targets both wild-type and pyrimethamine-resistant P. falciparum and P. vivax dihydrofolate reductases, classic targets for the blood stage of the parasite. This makes triclosan an exciting candidate for further development as a dual specificity antimalarial, which could target both liver and blood stages of the parasite.

Bibliographical metadata

Original languageEnglish
Article number1038
JournalScientific Reports
Issue number1
Early online date18 Feb 2018
StatePublished - 2018