Technology Listings

Nicotinamide Adenine Dinucleotide (NAD) for the Treatment of Cardiac Arrhythmia


Treatment of cardiac arrhythmias, pain, and seizures from the administration of nicotinamide adenine dinucleotide (NAD).

Key Benefits
  • Therapeutic approach involving the oxidized and reduced forms of NAD, a biological coenzyme.
  • Potential treatment for heart failure, cardiac arrhythmias, pain, and seizures.
Technical Summary

Cardiac arrhythmia is a condition in which the electrical activity of the heart is irregular or abnormal. Some arrhythmias are life-threatening and can cause cardiac arrest and sudden death. Others cause aggravating symptoms, such as palpitations. Voltage-gated sodium channels are pore-forming membrane proteins responsible for the initiation and propagation of action potentials in excitable membranes in nerve, skeletal muscle and heart cells. The controlled gating of sodium channels in response to membrane depolarization is necessary for normal electrical signaling and establishing of intracellular communication. Interventions that modulate sodium current have potent physiological effects. Mutations in the human SCN5A gene, which encodes a subunit of the cardiac sodium channel, cause the long QT syndrome and idiopathic ventricular fibrillation. In addition, Brugada syndrome, a disease that leads to an increased risk for lethal arrhythmias, has been associated with SCN5A mutations that cause decreased sodium current.

This invention involves the use of nicotinamide adenine dinucleotide, the coenzyme involved in metabolic redox reactions, in a novel therapeutic strategy to modulate sodium channel current, thereby reducing the risk of developing arrhythmias as well as treating pain and seizures. Research studies have shown that the oxidized form of nicotinamide adenine dinucleotide (NAD+) increases sodium channel current and sodium channel levels while NADPH, the reduced form, lowers sodium channel current and sodium channel levels. Administration of NAD+ increases the current necessary for proper heart function, thereby reducing the risk of heart failure and ventricular fibrillation. Administration of NADPH alleviates conditions associated with high sodium channel current including pain, seizures and other cardiac arrhythmias.

Developmental Stage & Potential Market
  • Proof-of-principle studies have been conducted in vivo demonstrating NAD+ prevents tachycardia in a murine model of Brugada syndrome.
  • In the US, nearly 38,000 deaths result from cardiac arrhythmias each year.
  • Medicare reimbursements for the treatment of cardiac arrhythmias exceed $2.5 billion annually.
Patent Information
App Type Country Serial No. Patent No. File Date Issued Date Expire Date Patent Status
Utility (parent) United States 12/289,005 8,003,324 10/17/2008 8/23/2011 2/10/2029 Issued
Tech ID: 07145
Published: 4/29/2009

Justin Burns
Assistant Director, Licensing
Emory University

Samuel Dudley