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Government-Owned Inventions; Availability for Licensing

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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.

Methods for Enhancing Beta Cell Function in Diabetes

Description of Technology: Diabetes results when beta cell performance is compromised through loss of cells or by reduced cell function. Anti-diabetic drugs that stimulate insulin production, such as sulfonylureas and meglitinides, have limited efficacy when beta cell responsiveness is deficient. There exists a critical need, therefore, for new diagnostics and therapeutics that focus on beta cell responsiveness in diabetes.

This technology describes methods for improving pancreatic endocrine function and delaying the onset of diabetes by enhancing beta cell function using ligands and/or regulators of Notch receptors. These methods are directed not only to mature beta cells, but to immature beta cells and to beta cells formed from differentiation of stem cells. This technology also describes isolated pancreatic progenitor cells, and offers an effective method for identifying and isolating these cells using Notch receptor markers.

Applications: (1) Treatment for diabetes that enhances beta cell function or replaces lost beta cells; (2) Isolation and expansion of pancreatic progenitor cells for diabetes therapy; (3) Diagnostic test to monitor beta cell function

Market: (1) Over 20 million people suffer from diabetes in the United States, and approximately 170 million people are affected worldwide. (2) There are an estimated 6.2 million undiagnosed cases of diabetes in the United States.

Development Status: Pre-clinical data are available.

Inventors: Josephine M. Egan, et al. (NIA).

Patent Status: U.S. Provisional Application No. 60/590,281 filed 22 Jul 2004 (HHS Reference No. E-262-2003/0-US-01); PCT Application No. PCT/US2005/026207 filed 22 Jul 2005, which published as WO 2006/023209 on 02 Mar 2006 (HHS Reference No. E-262-2003/0-PCT-02).

Licensing Status: Available for exclusive or non-exclusive licensing.

Licensing Contact: Tara L. Kirby, Ph.D.; 301/435-4426; tarak@mail.nih.gov.

A Nurr1-Knockout Mouse Model for Parkinson's Disease and Stem Cell Differentiation

Description of Technology: The researchers have generated Nurr1-knockout mice via genomic locus inactivation using homologous recombination.

Transcription factor Nurr1 is an obligatory factor for neurotransmitter dopamine biosynthesis in ventral midbrain. From a neurological and clinical perspective, it suggests an entirely new mechanism for dopamine depletion in a region where dopamine is known to be involved in Parkinson's disease. Activation of Nurr1 may be therapeutically useful for Parkinson's disease patients; therefore, the mice would be useful in Parkinson's disease research.

Additionally, Nurr1 has been shown to be critical for development of midbrain dopaminergic neurons, and thus may contribute to stem cell-based therapies for neurological disorders. Nurr1 is also important for osteoblast differentiation, suggesting a general role in stem cell differentiation and growth.

Applications: (1) Research and drug testing for Parkinson's disease and other neurological disorders; (2) Stem cell research relating to neurological and other disorders and bone formation.

Inventor: Dr. Vera Nikodem (NIDDK).

Relevant Publication: SO Castillo, JS Baffi, M Palkovits, DS Goldstein, IJ Kopin, J Witta, MA Magnuson, VM Nikodem. Dopamine biosynthesis is selectively abolished in substantia nigra/ventral tegmental area but not in hypothalamic neurons in mice with targeted disruption of the Nurr1 gene. Mol Cell Neurosci. 1998 May, 11(1-2):36-46.

Related Publications:

1. MK Lee, H Choi, M Gil, VM Nikodem. Regulation of osteoblast differentiation by Nurr1 in MC3T3-E1 cell line and mouse calvarial osteoblasts. J Cell Biochem. 2006 June 1 [Epub ahead of print, doi:10.1002/jcb.20990].

2. J Jankovic, S Chen, WD Le. The role of Nurr1 in the development of dopaminergic neurons and Parkinson's disease. Prog Neurobiol. 2005 Sep-Oct, 77(1-2):128-138. Epub 2005 Oct 21, doi:10.1016/j.pneurobio.2005.09.001.Start Printed Page 52806

Patent Status: HHS Reference No. E-024-1999/0—Research Tool.

Licensing Status: This technology is available under a Biological Materials License.

Licensing Contact: Tara L. Kirby, Ph.D.; 301/435-4426; tarak@mail.nih.gov.

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Dated: August 31, 2006.

Steven M. Ferguson,

Director, Division of Technology Development and Transfer,Office of Technology Transfer, National Institutes of Health.

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[FR Doc. E6-14832 Filed 9-6-06; 8:45 am]

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