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Methods and Compositions for Antagonizing Septic Shock

Description of Invention:
Septic shock is an often fatal type of vasodilatory shock that may accompany microbial infections. Septic shock has therefore been an increasing problem in recent years because of the increasing number of individuals who are immunocompromised. Recent studies have indicated that the hypotension associated with hemorrhagic shock (Wagner et al., Nature 1997; 390:518-521) or septic shock (Varga et al., FASEB J. 1998; 12:1035-1044) may be mediated by macrophage-derived endogenous cannabinoids such as anandamide, acting at vascular cannabinoid receptors. In an earlier study (PNAS, 1999; 96:14136) the NIH inventor(s) presented several lines of evidence indicating the vasodilator effect of anandamide is mediated by a receptor distinct from the two known cannabinoid receptors, CB1 and CB2. In particular, anandamide-induced vasodilation persists in mice deficient in both CB1 and CB2 receptors. They postulated that a yet unidentified cannabinoid receptor was responsible for the observed effect. The invention described and claimed in the pending patent application provides compounds acting as agonists and antagonists at the newly described cannabinoid receptor and methods for reversing pathological vasodilation of blood vessels observed during conditions such as septic shock.

Inventors:
George Kunos (NIAAA)

Patent Status:
DHHS Reference No. E-321-2001/0 --
U.S. Provisional Application No. 60/312,674 filed 15 Aug 2001
International Application No. PCT/US02/26050 filed 14 Aug 2002, which published as WO 03/015700 on 27 Feb 2003
U.S. Patent Application No. 10/486,810 filed 13 Feb 2004

Portfolios:
Internal Medicine
Infectious Diseases

Internal Medicine-Diagnostics-Cardiology-In Vivo
Infectious Diseases -Therapeutics
Internal Medicine-Diagnostics

For Additional Information Please Contact:
Norbert J. Pontzer PhD JD
NIH Office of Technology Transfer
6011 Executive Blvd, Suite 325
Rockville, MD 20852-3804
Phone: (301) 435-5502
Email: pontzern@mail.nih.gov
Fax: (301) 402-0220


Web Ref: 631

Updated: 8/02

 

 
 
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