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Schering says its drug subdues AIDS virus

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Bloomberg News / February 4, 2008

NEW YORK - Schering-Plough Corp.'s new AIDS drug, designed to block the virus from entering human cells, suppressed infections in patients who don't respond to older medicines, according to research presented yesterday.

A combination of drugs including Schering-Plough's vicriviroc held back the virus better than the combination of older medicines alone, the study sponsored by the Kenilworth, N.J.-based company found. The findings were presented yesterday at the Conference on Retroviruses and Opportunistic Infections in Boston.

Vicriviroc may become the second medicine after Pfizer Inc.'s Selzentry in a new family of drugs that work by blocking the CCR5 receptor, a chemical doorway the virus uses to enter human cells. The drugs promise to give doctors a new weapon against resistant forms of the human immunodeficiency virus that causes AIDS.

"This is a potent oral CCR5 antagonist that has significant potential for treatment of HIV," said Barry Zingman, professor of infectious disease at Montefiore Medical Center in Bronx, N.Y., during a presentation at the meeting.

Vicriviroc, like Pfizer's drug, works by altering the shape of a protein on the surface of healthy human cells, making it impossible for HIV to get a good enough grip to enter. Before Selzentry won US approval in August 2007, the only so-called entry inhibitor available was Fuzeon

Fuzeon, made by Roche Holding AG and Trimeris Inc., is an injectable therapy. Vicriviroc and Selzentry are pills.

In a 48-week study, 56 percent of patients on a 30 milligram dose of vicriviroc combined with older drugs had the virus reduced to undetectable levels, compared with 14 percent taking only the older medicines. Also, 52 percent of patients on 20 milligrams of vicriviroc combined with other drugs had the virus lowered to undetectable levels in the blood.

HIV has proven to be a formidable foe for drug designers because of its ability to mutate, develop new strains, and change its shape to force its way into human cells. The virus's attack begins when it attaches itself to a cell surface molecule, called a receptor, and uses one of its proteins to force its way into the cell.

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