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Medivation Presents New Data on Dimebon's Novel Mechanism of Action
Date:12/9/2008

SAN FRANCISCO, Dec. 9 /PRNewswire-FirstCall/ -- Medivation, Inc. (Nasdaq: MDVN) presented new data that provide additional evidence that Dimebon, its lead product candidate in development to treat Alzheimer's and Huntington's diseases, potentially operates via a novel mitochondrial mechanism of action. In preclinical studies, Dimebon was shown to impact two key aspects of brain cell function: it promoted neurite outgrowth and it preserved mitochondrial function after brain cells were challenged with beta amyloid, a toxic substance often associated with Alzheimer's disease and the loss of brain cells.

"In experiments in which brain cells were exposed to different toxins, including beta amyloid, Dimebon was shown to stabilize mitochondrial function, a vital element of neuron function and survival," said Andrew Protter, Ph.D., vice president, preclinical development for Medivation. "These findings suggest that Dimebon may have benefits on slowing the progression of Alzheimer's disease by preserving mitochondrial function. This potential novel mechanism may help explain the clinical benefits seen to date in Alzheimer's patients treated with Dimebon."

Dr. Protter presented the new data in an oral presentation, entitled "Dimebon Induces Neurite Outgrowth and Stabilization in the Setting of Cell Stress," at Cold Spring Harbor Laboratory's "Neurodegenerative Diseases: Biology & Therapeutics" meeting.

Mitochondria and Cell Function

Mitochondria generate energy for cells and play important roles in mediating cell function and survival. Improved mitochondrial function has been correlated with increased synapse formation. Autopsy studies of brains from patients with Alzheimer's disease suggest that mitochondrial damage and synapse dysfunction are early cellular events in Alzheimer's disease develo
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SOURCE Medivation, Inc.
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