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Video: UCB Launches Vimpat(R) in the U.S. for Add-On Treatment of Epilepsy in Adults
Date:5/26/2009

oom or hospital setting. These formulations are bioequivalent, meaning doses do not need to be adjusted when converting from IV to oral. The IV formulation of Vimpat(R) does not require dilution prior to administration.

Vimpat(R) was approved by the U.S. Food and Drug Administration in October 2008 for the adjunctive treatment of partial onset seizures in patients with epilepsy age 17 and over. Vimpat(R) has been designated as a Schedule V controlled substance by U.S. regulators.

In August 2008, the European Commission approved Vimpat(R) for the adjunctive treatment of partial onset seizures with or without secondary generalization in patients with epilepsy age 16 and over. Vimpat(R) is available in Germany, the U.K., Greece, Austria, Denmark, Sweden, and Netherlands, with other European countries to follow.

Vimpat(R) offers new way of targeting pathways involved in seizure onset

Preclinical studies indicate that Vimpat(R) has a novel mechanism of action, although the precise mechanism by which Vimpat(R) exerts its antiepileptic effect in humans is not yet clear.

In preclinical studies, the mechanism of action for Vimpat(R) has been shown to involve the modulation of sodium channel activity in the nervous system. Sodium channels play a crucial role in regulating the activity of the nervous system to help nerve cells communicate. Sometimes sodium channels are abnormally overactive and nerve cells become too excited, which may produce a seizure. The mechanism of action for Vimpat(R) is thought to reduce this sodium channel over-activity by enhancing the longer lasting inactive state of the channel, a different action compared with current sodium channel blocking drugs. This action then regulates the activity of over-excited nerve cells, which may contribute to the control of seizures.

Preclinical studies also suggest that Vimpat(R) binds to the collapsin response mediat
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