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Therapeutic Application of Fatty Acid Amide Hydrolase Inhibitors

Posted Jun 30 2008 5:00pm

Description of Invention:
The enzyme fatty acid amide hydrolase (FAAH) is responsible for the degradation of the lipid anandamide. This is a cannabinoid naturally secreted from both the brain and body. Cannabinoid receptors mediate blood pressure, pain sensation, hunger and anxiety among other actions. Drugs inhibiting FAAH increase cannabinoid receptor activity in a manner distinct from cannabinoid agonists to treat hypertension, relieve pain or have other therapeutic effect with lessened side effects.

Applications:
  • Treat hypertension and accompanying cardiac hypertrophy
  • reatment of anxiety
  • Treatment of glaucoma
  • As a pain reliever or sleep aid


Development Status:
Pre-clinical data available

Inventors:
George Kunos (NIAAA)


Patent Status:
HHS, Reference No. E-211-2006/0
US, Application No. 12/755,227 filed 06 Apr 2010


Relevant Publication:
  1. Bátkai S, Pacher P, Osei-Hyiaman D, Radaeva S, Liu J, Harvey-White J, Offertáler L, Mackie K, Rudd MA, Bukoski RD, Kunos G. Endocannabinoids acting at cannabinoid-1 receptors regulate cardiovascular function in hypertension. Circulation. 2004 Oct 5;110(14):1996-2002. [ PubMed abs ]


Licensing Status:
Available for licensing.

Collaborative Research Opportunity:
The NIAAA Laboratory of Physiologic Studies is seeking statements of capability or interest from parties interested in collaborative research to further develop, evaluate, or commercialize fatty acid amide hydrolase inhibitors. Please contact Peter B. Silverman ( psilverm@mail.nih.gov ) for more information.


Portfolios:
Internal Medicine
Internal Medicine - Therapeutics
Central Nervous System
Central Nervous System - Therapeutics
Ophthalmology
Ophthalmology - 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: pontzern@mail.nih.gov
Phone: 301-435-5502
Fax: 301-402-0220


Ref No: 1766

Updated: 07/2008

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