Harnessing a parasite’s vulnerability

Away from its bustling cities, Vietnam is a bucolic paradise of shimmering gold rice paddies, cone-hatted farmers and quietly grazing water buffalo. But its natural beauty belies a hard truth of rural life: When villagers get sick, their first recourse is often a concrete infirmary nestled in the jungle, with a garden of medicinal plants, a couple of metal beds and a handful of basic commercial medicines. 

And when patients are infected with malaria (Plasmodium falciparum), even when drugs like dihydroartemisinin, piperaquine and chloroquine are available, too often the parasites are resistant, leaving the patient to his or her own natural defenses.

Phil Low is out to change that. Low, the Ralph C. Corley Distinguished Professor of Chemistry and the director of the Purdue Institute for Drug Discovery, has identified an enzyme that, when turned off, keeps anything from coming in or out of the red blood cell, and when turned on, causes the membrane to fall apart. The malaria parasite, he’s discovered, turns on the enzyme in order to promote the membrane fragmentation that will release all of its progeny from the red blood cell, thereby enabling them to infect other red cells. 

Low, in collaboration with Dr. Franco Turrini from Italy, has harnessed this vulnerability, creating an inhibitor of the enzyme that blocks the release of the parasite’s offspring from the red blood cell, ultimately killing the parasite within its host. He and Turrini are now collaborating with Dr. Huynh Dinh Chien at the University of Hue in Vietnam, to test the drug on patients in Vietnam.

So far, they are seeing promising results. If further testing bears out, the drug will next be tried in combination with other malarial drugs.

“We are very excited about the potential efficacy of our drug because it targets a red blood cell enzyme and not a parasite enzyme, so we anticipate that the parasite will be unable to develop resistance,” Low says.

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