Method of Treating or Preventing Oxidative Stress-related Diseases (stroke and neurodegenerative diseases, wound healing and car
Posted Jun 30 2007 5:00pm
Description of Invention: Reactive oxygen species (ROS) and reactive nitrogen species (RNS) produce oxidative stress to DNA, lipids and proteins thus causing cellular and tissue damage. A number of diseases are associated with oxidative stress including Alzheimer's disease, ischemic stroke, heart disease, cancer, hepatitis, and autoimmune disease. Uric acid is a natural antioxidant effective in reducing ROS and research has shown that uric acid contributes approximately two-thirds of all free radical scavenging capacity in plasma. Because uric oxide is too insoluble to be used as a therapeutic agent, scientists at the NIH developed uric acid analogs with improved anti-oxidative and solubility properties for use as free radical scavengers or antioxidants. These analogs increased survival of PC12 and hippocampal neurons after challenge by Fe, MPP and Glutamate. When administered to a mouse model of focal ischemic stroke, these compounds protect neuronal cells from ROS and reduce brain damage and ameliorate neurological deficits. Other studies show a single application of these analogs on skin lacerations in mice decreased the time for wound repair. Available for licensing are methods of treating ischemic stroke and wound healing, and for the prevention or treatment of other oxidative stress-related diseases, such as epilepsy, Parkinson's disease and dementia.
Applications: Novel uric acid analogs for use as antioxidants to help reduce the risk of stroke, neurological diseases and assisting with wound repair.
Collaborative Research Opportunity: The National Institute on Aging, Laboratory of Neurosciences is seeking statements of capability or interest from parties interested in collaborative research to further develop, evaluate, or commercialize the described uric acid analogue technology in the treatment of neurodegenerative diseases, wound healing and cardiovascular disease. Please contact John D. Hewes, Ph.D. at 301-435-3121 or email@example.com for more information.
Portfolios: Internal Medicine Internal Medicine - Therapeutics Central Nervous System Central Nervous System - Therapeutics
For Additional Information Please Contact: Norbert Pontzer Ph.D., J.D. NIH Office of Technology Transfer 6011 Executive Blvd. Suite 325
Room 23, Rockville, MD 20852 United States Email: firstname.lastname@example.org Phone: 301-435-5502 Fax: 301-402-0220