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New Compound Boosts Effectiveness of Malaria Drugs


Scientists might have developed a new weapon in the fight against malaria - a compound that when used in combination with existing drugs boost their effectiveness against the tropical illness.

For years, the drugs chloroquine and quinine have been front line treatments for malaria, a mosquito-borne illness that causes between 1.5 and 2 million deaths each year. According to the World Health Organization, more than 90 percent of deaths occured in Sub-Sahara Africa, mostly among children.

Malaria occurs when a person is bitten by a mosquito that carries the parasite. But the malaria parasite has become resistant to chloroquine and quinine. And newer drugs, including artemisinin, are becoming less effective.

Jane Kelly, a senior researcher at the U.S. Veterans Affairs Medical Center in Portland, Oregon, who led the research, says that in many areas it is difficult to monitor how people take anti-malaria drugs because of poor health care systems.

"Like in Africa, for instance, because the health infrastructure is not the same as in this country [i.e., the United States], so you would just go to a clinic and maybe you would get some medicines and then you go home [and] you take one for a day, and then you come back," she said.

Malaria parasites cause disease by invading red blood cells where they feed on an oxygen-carrying protein called hemoglobin. Anti-malaria drugs work by keeping the parasite from neutralizing a toxic byproduct of digestion.

But Kelly says the parasite gains the upper hand when anti-malarial drugs are taken sporadically. She says the parasite expels the drugs, causing resistance to medications.

Kelly and her colleagues have developed a compound that appears to block the ability of the parasite to expel anti-malarial drugs.

She says the compound readily cured drug-resistant malaria in laboratory mice. The compound seems to boost the effectiveness of several drugs that fight malaria, including chloroquine and artemisin. But Kelly says researchers still not entirely sure why the compound works.

"Some of it is because that our drug will go in and then it will bind [to] that component [protein] that's trying to spit out all the other drugs," continued Kelly. "And in this way, that protein is occupied so it will not spit out the other drugs anymore."

Kelly says more animal testing is necessary before human trials can begin.

A paper describing the scientists' work is published this week in the journal Nature.

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