The Phase 3 trial is designed to determine Flurizan's ability to alter the course of cognitive decline and behavioral change in patients with Alzheimer's disease. The trial will be conducted in approximately 750 patients with mild to moderate Alzheimer's disease, at approximately 100 centers in the United States. The Phase 3 study is a double blind, placebo-controlled trial, with randomization of patients at enrollment into one of three arms. Patients will be given 400mg or 800mg of Flurizan twice daily or placebo twice daily for the duration of the 12-month study period. The co-lead investigators for this trial are Robert C. Green, M.D., M.P.H., Associate Professor of Neurogenetics, Boston University School of Medicine, and Lon Schneider, M.D., Professor of Psychiatry, Neurology and Gerontology, Keck School of Medicine, University of Southern California.

"There is a critical need for drugs that modify the underlying disease mechanism and progression of Alzheimer's disease," said Dr. Schneider. "MPC- 7869 has the potential to do this with its effect on reducing amyloid beta levels. We hope to confirm this in a large, well-controlled clinical trial."

The primary efficacy endpoints for the trial will be the change in cognitive function, as measured by the ADAS-cog test, and the change in activities of daily living.

"Flurizan is an exciting drug candidate due to its potential to change the rate of decline in Alzheimer's disease patients," said Adrian Hobden, Ph.D., President of Myriad Pharmaceuticals, Inc. "We are pleased to take the opportunity to accelerate Flurizan's development timeline by initiating this Phase 3 trial."

Flurizan is currently being studied in a Phase 2 clinical study in approximately 210 patients with mild to moderate Alzheimer's disease. All patients have now been on drug for more than 9 months. The trial's Data Safety Monitoring Board has reviewed safety data from the trial each calendar quarterly and has determined that the trial should proceed without change. This Phase 2 trial is expected to conclude its clinical study period in March of 2005.

Flurizan has been shown to modulate gamma-secretase and selectively lower levels of Amyloid beta 42, a toxic peptide that is believed to be a chief culprit in the cause of Alzheimer's disease. In transgenic mouse studies, Flurizan has demonstrated the ability to reduce brain amyloid levels and prevent memory loss. Flurizan was selected during preclinical testing to avoid cyclooxygenase inhibition and its related side effects.

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