New hope for advances in treating malaria

Apr 22, 2009

Researchers at the University of Leeds have developed chemicals which kill the most deadly malaria-causing parasite, Plasmodium falciparum - including those resistant to existing drugs.

The compounds work by preventing the enzyme dihydroorotate dehydrogenase (DHODH) - essential to the growth of the parasite - from working, which results in its death.

Says lead researcher Dr Glenn McConkey, from Leeds' Faculty of Biological Sciences: "Without this enzyme, Plasmodium falciparum is unable to grow and therefore it dies. The inhibitors developed at Leeds bind to the DHODH enzyme in the parasite and stop it functioning, preventing the proliferation of the parasites, which live in . In addition, our chemicals are equally effective against parasites that have developed resistance to drugs."

He adds: "DHODH in humans is not an essential enzyme, so by concentrating our studies on it we can develop chemical inhibitors that have a negative impact on the parasite without any major side-effects to the human host. In effect we are exploiting a biological difference, and this will allow us to develop potent, selective inhibitors."

According to the World Health Organisation (WHO), malaria kills a million people across the globe each year, with forty per cent of the world's population at risk of contracting the disease. WHO also estimates that a child dies from malaria every 30 seconds.

Dr McConkey says: "Our chemicals are particularly exciting as they kill malaria parasites at low concentrations, something that is important for medicines as they are massively diluted on entering the and, unlike many pharmaceutical products, we have a firm understanding of the molecular basis of their action. This project highlights the benefits of combining biological and chemistry disciplines."

Dr McConkey says the next stage of this research is to develop a larger collection of potent inhibitors and to see how these chemicals work alongside commonly used treatments.

"The parasites responsible for malaria have been very effective at developing resistance to existing drugs and efforts to find replacements are often stymied by the rate of resistance. Therefore it is essential that new products work effectively in combination with those already on the market," he says.

The research is published in the latest edition of the Journal of Medicinal Chemistry.

Source: University of Leeds (news : web)

Explore further: A new synthetic amino acid for an emerging class of drugs

add to favorites email to friend print save as pdf

Related Stories

Genome sequences of 2 malaria parasites defined

Oct 08, 2008

Professor Alan Cowman, Professor Brendan Crabb, Dr Paul Gilson and Dr Toby Sargeant are WEHI members of international research teams that have made significant discoveries about two deadly malaria parasites, Plasmodium kn ...

Research breakthrough to treat malaria

Feb 03, 2009

A team of Monash University researchers led by Professor James Whisstock has made a major breakthrough in the international fight against malaria, which claims the life of a child across the world every 30 seconds.

Researchers discover surprising drug that blocks malaria

Jan 16, 2007

Northwestern University researchers have discovered how malaria parasites persuade red blood cells to engulf them -- and how to block the invading parasites. The malaria marauders hack into the red cell's signaling system ...

Recommended for you

Scientists make diseased cells synthesize their own drug

24 minutes ago

In a new study that could ultimately lead to many new medicines, scientists from the Florida campus of The Scripps Research Institute (TSRI) have adapted a chemical approach to turn diseased cells into unique manufacturing ...

A new synthetic amino acid for an emerging class of drugs

Aug 31, 2014

Swiss scientists have developed a new amino acid that can be used to modify the 3-D structure of therapeutic peptides. Insertion of the amino acid into bioactive peptides enhanced their binding affinity up to 40-fold. Peptides ...

User comments : 0