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Columbia Missourian

MU researcher advancing potential HIV prevention drug

By Matthew Reinig
November 13, 2009 | 12:01 a.m. CST

COLUMBIA — An HIV treatment drug has the potential to be up to 60,000 times more powerful than any other used, in part because of the work of MU researcher Stefan Sarafianos. 

Sarafianos, assistant professor of microbiology and immunology at MU, worked with researchers in Japan, as well as researchers from the University of Pittsburgh and the National Institutes of Health, to develop a compound known as EFdA, an HIV inhibitor that blocks viral replication.

"There are more than 20 drugs for the treatment of the virus, but there are none for the prevention. Not a single approved microbicide," Sarafianos said Thursday as he darted through the corridors of the School of Medicine.

Sarafianos was headed to Bryant Auditorium to receive the 2009 Dorsett L. Spurgeon, MD Distinguished Medical Research Award for his work. Roughly 100 students and medical professionals attended the ceremony.

He also gave a presentation on EFdA, demonstrating what potential the HIV inhibitor has in two primary categories. One is that the compound can block viral replication, lending itself as a potential therapeutic for individuals harboring multi-resistant HIV. Another is the potential to be a microbicide, or a product that could reduce HIV infections.

That, Sarafianos said, is what excites him most.

"Hopefully it will be picked up by a company and it will be developed as a microbicide and it will be cheap and accessible to many people not only in this country but also where it's needed most," he said. "I want to make a huge difference."

He said trying to patent the drug has been a challenge.

"Even though it's a fantastic compound, I think the big challenge now is companies are reluctant to go into new compounds," he said.

Some commercial preventative agents with which the HIV inhibitor could be marketed include vaginal gels, tablets and condoms.

EFdA prohibits HIV from replicating, Sarafianos said, by binding to reverse transcriptase — the enzyme that causes HIV to replicate — and blocking it.

"We have found that EFdA works with a very different mechanism," he said.

Sarafianos is optimistic about the patent process. "I think it's taking it's course," he said. "And it's getting there."