An international team of scientists has developed a malaria drug that tricks the immune system into destroying infected red blood cells while leaving healthy cells unharmed.

The compound comes with a pretty catchy name; (+)-SJ73, but the real achievement is the potential boost to anti-malarial drug development.

Malaria is caused by a parasite from the bite of an infected mosquito, and remains a major threat to the health of more than half the world's population, particularly children.

In Africa, a child dies of malaria every minute.

In their latest study, researchers from St Jude Children's Research Hospital in the US determined that (+)-SJ733 uses a previously-unknown mechanism to attack the parasite by enlisting the immune system to destroy malaria-infected red blood cells.

In a mouse model of malaria, a single dose killed 80 per cent of malaria parasites in just 24 hours. The parasite was below detectable levels after 48 hours.

The compound's speed and mode of action appear to work together to stop the development of drug-resistant parasites – a major sticking point of efforts to treat and block malaria transmission.

The exciting result has put the drug on a fast track to human trials, with safety trials planned as soon as possible.

“Our goal is to develop an affordable, fast-acting combination therapy that cures malaria with a single dose,” said corresponding author R Kiplin Guy, PhD, chair of the St Jude Department of Chemical Biology and Therapeutics.

“These results indicate that SJ733 and other compounds that act in a similar fashion are highly attractive additions to the global malaria eradication campaign, which would mean so much for the world's children, who are central to the mission of St Jude.”

The find came from a previous effort to sequence the genome of Plasmodium falciparum; the deadliest of the malaria parasites.

This data helped researchers discover that (+)-SJ733 actually disrupted activity of the ATP4 protein, which functions as a pump to regulate the sodium that malaria parasites depend on.

They found that inhibiting ATP4 set off a series of changes in malaria-infected red blood cells that marked them for destruction by the immune system.

The infected cells were seen to change shape and shrink in size while becoming more rigid and exhibiting other signs normally seen in aging red blood cells.

This caused the immune system to respond using the same mechanism it uses to clear out aging red blood cells.

“The data suggest that compounds targeting ATP4 induce physical changes in the infected red blood cells that allow the immune system or erythrocyte quality control mechanisms to recognize and rapidly eliminate infected cells,” co-atuhor Dr Joseph DeRisi said.

“This rapid clearance response depends on the presence of both the parasite and the investigational drug. That is important because it leaves uninfected red blood cells, also known as erythrocytes, unharmed.”

Plans are underway to move (+)-SJ733 from the laboratory into the clinic, with a human safety study is being led scientists at St Jude, the Swiss-based non-profit Medicines for Malaria Venture and Eisai Co, a Japanese pharmaceutical firm.

The latest paper is accessible here.