Drug Candidate Shows Promise for Alzheimer's

A study has found that a new drug candidate, MPC-7869 (R-flurbiprofen), reduces levels of Abeta42 in vitro and in an animal model more effectively than any other compound tested. The results were published in the August 2003 issue of the Journal of Clinical Investigation.

Abeta42 is the primary constituent of the senile plaques that accumulate in the brains of patients with Alzheimer's disease and is thought to be the key initiator of the disease since it has the tendency to cause neuronal damage and initiate amyloid deposits in the brain. The study demonstrated that only a select minority of nonsteroidal anti-inflammatory drugs (NSAIDS) lower levels of the Abeta42 peptide, and among those few compounds, R-flurbiprofen was shown to be most effective by selectively targeting gamma-sectretase without inhibiting its essential biologic functions.

"We have long known that the use of NSAIDS is associated with a reduced risk of Alzheimer's disease,” noted Adrian Hobden, Ph.D., president of Myriad Pharmaceuticals, Inc., (Salt Lake City, UT, USA), which is developing the drug.

The company is conducting a Phase II human clinical trial in Alzheimer's disease that will assess the efficacy of R-flurbiprofen in reducing the cognitive decline in Alzheimer's patients. Researchers from the Mayo Clinic, (Jacksonville, FL, USA) and the University of California, San Diego (CA, USA) also took part in the study, led by Jason Erikson, Ph.D., of the Mayo Clinic.




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