MS Drug Shows Promise to Treat Heart Condition

Gilenya shown to reverse ventricular hypertrophy in lab study

/ Author:  / Reviewed by: Joseph V. Madia, MD

(RxWiki News) A multiple sclerosis drug may work double duty. It has been shown in a lab study to prevent and even reverse one of the leading causes of heart attack.

Gilenya (fingolimod), which was recently approved by the U.S. Food and Drug Administration to treat MS, also appears to reverse symptoms of ventricular hypertrophy in mice, a potentially fatal heart disorder.

"Discuss treatments for ventricular hypertrophy with your cardiologist."

Dr. Xin Wang, a study co-author and a lecturer in molecular cardiology at the University of Manchester, noted that his team's research had previously identified the effect of Pak1, an enzyme molecule that naturally occurs in human bodies, in preventing tissue damage by reduced blood flow to the heart.

The latest study used mice with a genetic modification to the Pak1 gene to show how the enzyme prevents and reverses signs of ventricular hypertrophy when stimulated with Gilenya.

Ventricular hypertrophy can result in an abnormal heart rhythm, heart failure and cardiac arrest. It is caused by sustained pressure on the heart from stress or disease, such as hypertension, valvular heart disease or heart attack.

"In recent years, escalating costs, risks, and uncertainty associated with drug development for treating cardiovascular diseases have posed daunting challenges to the pharmaceutical industry. Our discovery opens up fresh avenues for developing a new class of drug for treating several fatal heart conditions," said Dr. Ming Lei, a study leader from the University of Manchester.

"The novel effect of this existing drug means that we have the potential to accelerate the availability of a new therapy for patients with these heart conditions."

The pre-clinical study, funded by the British Heart Foundation and the Medical Research Council, was recently published in American Heart Association journal Circulation.

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Last Updated:
February 14, 2012