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Ranolazine Shortens QT Interval and Improves Cardiac Relaxation in Study of Patients With Genetic Sodium Channel Disorder
Date:3/31/2008

- Clinical evidence for unique Ranexa(R) mechanism of action -

CHICAGO, March 31 /PRNewswire-FirstCall/ -- CV Therapeutics, Inc. (Nasdaq: CVTX) announced today that ranolazine significantly (p<0.001) shortened the QT interval of patients with a hereditary form of long QT syndrome called LQT3, which is caused by a genetic mutation in the late sodium channel and can be associated with heart rhythm problems, including sudden death. Ranolazine also shortened cardiac relaxation time in the study.

The data were presented today at the American College of Cardiology 57th Annual Scientific Session in Chicago by Arthur Moss, MD, professor of medicine (cardiology) and director of the heart research follow-up program at the University of Rochester Medical School.

"Since individuals with LQT3 syndrome have a defect in the specific sodium channel where ranolazine has its activity, it makes sense that we are seeing ranolazine shorten the QT interval and improve cardiac relaxation in these patients," Moss said.

Five patients with LQT3 syndrome were prospectively investigated during an eight hour intravenous infusion of ranolazine, with ECG and ECHO evaluation before, during and after ranolazine administration.

In December 2007, the U.S. Food and Drug Administration approved new language for the product labeling for Ranexa(R) (ranolazine extended-release tablets) which describes the ability of ranolazine to inhibit the late sodium current at therapeutic levels.

Published data on ranolazine's mechanism of action suggests that during ischemic episodes excess sodium can flow into cardiac cells through sodium channels. This excess sodium can lead to calcium overload, which in turn can lead to impaired relaxation of
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SOURCE CV Therapeutics, Inc.
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