Published data on ranolazine’s mechanism suggests that during ischemic episodes excess sodium can flow into cardiac cells through sodium channels. This excess sodium can trigger a subsequent overload of calcium that can lead to problems with proper contraction and relaxation of the heart. Late sodium current inhibition has been shown to improve mechanical and electrical dysfunctions of cardiac cells under these circumstances.
Ranexa is currently indicated for the treatment of chronic angina in patients who have not achieved an adequate response with other antianginal drugs, and should be used in combination with amlodipine, beta-blockers or nitrates.
Louis Lange, chairman and CEO of CV Therapeutics, said: “We believe it is important for physicians to have as much information as possible on the mechanism of action for Ranexa and we are very pleased that the FDA has worked with us to add this new language to the approved product labeling.”