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

pment and progression. Similarly, mitochondrial dysfunction has been linked in the published literature to the progression of Huntington's disease.

Preclinical Study Results

As synapse formation is dependent on mitochondrial function and synapse loss is a major characteristic observed in the brain tissue of individuals with Alzheimer's disease, researchers evaluated the effects of Dimebon on neurite outgrowth, an important aspect of synapse formation.

Results of the study showed that Dimebon induced a statistically significant increase in neurite outgrowth from cortical, hippocampal and spinal cord neurons. Dimebon's potent effect on neurite outgrowth was seen at low concentrations and was comparable to that achieved with maximally effective concentrations of a potent growth factor (Brain Derived Neurotrophic Factor). Study results also showed that Dimebon reduced mitochondrial impairment in the setting of cellular stress. Specifically, Dimebon treatment mitigated mitochondrial impairment induced by beta amyloid.

Dimebon's effect on improving mitochondrial dysfunction has been confirmed previously in the independent laboratory of Maria Ankarcrona, Ph.D., associate professor at the Karolinska Institutet in Sweden. Additional data about Dimebon's potential novel mechanism of action were presented in November at the Society for Neuroscience's "Neuroscience 2008" conference in Washington, D.C.

Preclinical data also have been presented that suggest that Dimebon works through a different mechanism of action than other drugs that focus on targets implicated in cognition and memory loss, such as cholinesterase inhibition. In these experiments, Dimebon was shown to be a weak cholinesterase inhibitor, and additional data from binding assays showed that Dimebon did not have strong affinity to other standard targets. This suggests that Dimebon's potential novel mitochondri
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SOURCE Medivation, Inc.
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