[Federal Register: July 3, 2008 (Volume 73, Number 129)] [Notices] [Page 38228-38230] From the Federal Register Online via GPO Access [wais.access.gpo.gov] [DOCID:fr03jy08-72] ----------------------------------------------------------------------- DEPARTMENT OF HEALTH AND HUMAN SERVICES National Institutes of Health Government-Owned Inventions; Availability for Licensing AGENCY: National Institutes of Health, Public Health Service, HHS. ACTION: Notice. ----------------------------------------------------------------------- SUMMARY: The inventions listed below are owned by an agency of the U.S. Government and are available for licensing in the U.S. in accordance with 35 U.S.C. 207 to achieve expeditious commercialization of results of federally-funded research and development. Foreign patent applications are filed on selected inventions to extend market coverage for companies and may also be available for licensing. ADDRESSES: Licensing information and copies of the U.S. patent applications listed below may be obtained by writing to the indicated licensing contact at the Office of Technology Transfer, National Institutes of Health, 6011 Executive Boulevard, Suite 325, Rockville, Maryland 20852-3804; telephone: 301/496-7057; fax: 301/402-0220. A signed Confidential Disclosure Agreement will be required to receive copies of the patent applications. [[Page 38229]] Tendon Stem Cells Description of Technology: Tendon injuries due to trauma and overuse are common clinical problems that result in significant pain and loss of mobility. Tendon injuries are slow to heal and the healed tendon rarely matches the original in mechanical strength and structural integrity. Due to a limited understanding of basic tendon biology, development of new treatment options for injured tendons has posed significant challenges. This invention relates to a cell based therapy. Specifically, it relates to the isolation and enrichment of stem cells from adult tendons, known as tendon stem progenitor cells, that can form tendon structures and are capable of integrating into bones to form enthesis- like structures. Two extra-cellular matrix proteoglycans, biglycan and fibromodulin, further assist in the maintenance and multiplication of these tendon stem cells. Applications: Treatment of damaged tendons that are slow to repair after injury. May remedy other pathological conditions that are caused by ectopic calcification such as ectopic calcification that occurs around artificial heart valves or that develops in the rare inherited disease, Fibrodysplasia Ossificans Progressiva (FOP). Development Status: Early stage. Inventors: Marian Young et al. (NIDCR). Patent Status: U.S. Provisional Application No. 60/934,606 filed 14 Jun 2007 (HHS Reference No: E-233-2007/0-US-01). Licensing Status: Available for licensing. Licensing Contact: Fatima Sayyid, M.H.P.M.; 301-435-4521; Fatima.Sayyid@nih.hhs.gov. Collaborative Research Opportunity: The NIDCR, Molecular Biology of Bones and Teeth Section is seeking statements of capability or interest from parties interested in collaborative research to further develop, evaluate, or commercialize the use of tendon stem cells. Please contact Marian Young at 301-496-8860 or myoung@dir.nidcr.nih.gov. A2 Adenosine Receptor Agonists Description of Technology: Four adenosine receptor subtypes exist, namely A1, A2A, A2B and A3, each with different functions, tissue distributions and ligand coupling abilities. While activation of A2B AR can induce angiogenesis, reduce vascular permeabilization, increase production of the anti-inflammatory cytokine IL-10, increase chloride secretion in epithelial cells or increase release of inflammatory mediators from human and canine mast cells, there still remains a need for A2B receptor agonists for clinical use. Recognizing that an unmet medical need exists, the inventors synthesized an assortment of adenosine derivatives with the goal of preparing highly potent and selective A2B receptor agonists. They identified a compound as a full agonist at the A2A and A2B adenosine receptors, capable of reducing infarct size in rabbit hearts induced by 30 minutes of ischemia. As activation of A2A and A2B receptors induces a cardioprotective effect and this compound activates both A2A and A2B receptors, this compound may be beneficial for protecting against myocardial ischemia/reperfusion injury. Available for licensing and commercial development are compositions and methods of use of A2 adenosine receptor (AR) agonists for treating conditions modulated by A2A and A2B ARs including myocardial ischemia, reperfusion injury, cystic fibrosis, erectile dysfunction, inflammation, restenosis and septic shock. Applications: Potential treatment for heart attacks. Potential treatment of septic shock, cystic fibrosis and erectile dysfunction. Potential treatment for medical conditions that would benefit from changes in vascular tone. Market: Heart disease is the number one cause of death in the United States, and the most frequent cause of hospital admission for patients over 65 years of age. Development Status: Early-stage of development. Inventors: Kenneth A. Jacobson et al. (NIDDK). Patent Status: U.S. Provisional Application No. 60/947,066 filed 29 Jun 2007 (HHS Reference No. E-218-2007/0-US-01). U.S. Provisional Application No. 60/950,250 filed 17 Jul 2007 (HHS Reference No. E-218-2007/1-US-01). Licensing Status: Available for licensing. Licensing Contact: Charlene A. Sydnor, PhD.; 301-435-4689; sydnorc@mail.nih.gov. Collaborative Research Opportunity: The NIDDK Laboratory of Bioorganic Chemistry is seeking statements of capability or interest from parties interested in collaborative research to further develop, evaluate, or commercialize A2A and A2B adenosine receptor agonists. Please contact Rochelle S. Blaustein at 301-451-3636 or Rochelle.Blaustein@nih.gov for more information. Therapeutic Application of Fatty Acid Amide Hydrolase Inhibitors Description of Technology: 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. Treatment of anxiety. Treatment of glaucoma. As a pain reliever or sleep aid. Market: It is estimated that nearly a third of U.S. adults have high blood pressure. Despite the lack of symptoms, treatment is imperative. People with untreated high blood pressure have an increased chance of developing stroke, heart attack, heart failure or kidney failure. The forecast of the world hypertension market is that it will grow to nearly $30 billion per year by 2010. Development Status: Pre-clinical data available. Inventors: George Kunos (NIAAA) et al. Publication: B[aacute]tkai S, Pacher P, Osei-Hyiaman D, Radaeva S, Liu J, Harvey-White J, Offert[aacute]ler 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. Patent Status: U.S. Provisional Application No. 60/998,661 filed 12 Dec 2007 (HHS Reference No. E-211-2006/0-US-01). Licensing Status: Available for exclusive or non-exclusive licensing. Licensing Contact: Norbert Pontzer, J.D., PhD.; 301-435-5502; pontzern@mail.nih.gov. 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. [[Page 38230]] Dated: June 27, 2008. Richard U. Rodriguez, Director, Division of Technology Development and Transfer, Office of Technology Transfer, National Institutes of Health. [FR Doc. E8-15178 Filed 7-2-08; 8:45 am] BILLING CODE 4140-01-P
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