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A new century of Alzheimer's disease research

but cannot be superimposed on each other), it does not inhibit COX enzymes. The result was, finally, encouraging -- r-flurbiprofen inhibited AB42 production both in cells and in the brains of mice.

As it happened, the biotech firm Myriad Genetics was testing r-flurbiprofen to treat prostate cancer, because the agent had shown it could reduce the size of tumors in mice studies. Armed with additional data that r-flurbiprofen decreased AB levels in an Alzheimer’s mouse model and improved the cognitive deficits found in that model, Drs. Golde and Koo personally approached the drug company to encourage them to test r-flurbiprofen in Alzheimer’s disease.

Myriad Genetics agreed, and in 2006 the company reported results from a phase II clinical trial enrolling 207 patients with mild Alzheimer’s. The study found that r-flurbiprofen produced functional and cognitive improvements, ranging from 34 percent to 48 percent, in patients who took the highest dose, 1,600 milligrams a day. “And it was remarkably safe,” says Dr. Golde. “It was much better tolerated in humans than it was in mice.” There was also evidence that the drug not only improved symptoms but may have actually slowed the course of disease, he says. Current drugs offered to Alzheimer’s patients only relieve symptoms.

Based on these findings, Myriad Genetics launched a 1,600-participant phase III clinical trial in the summer of 2006, describing it as the largest placebo-controlled study ever to be undertaken of an investigational medicine in patients with Alzheimer’s. Patients will use r-flurbiprofen (known now as Flurizan) for 18 months.

Dr. Golde, who is not involved in this trial, suspects that r-flurbiprofen will show some benefit, but that newer, designer AB42-lowering agents might be better. “A more potent drug would likely be more effective, but it will take a long time to develop such a second-generation drug,” he says. “The beauty of r-flurbiprofen is that it can be on the
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