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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.

Human Sweet and Umami Taste Receptor Variants

Dennis Drayna and Un-Kyung Kim (NIDCD)

U.S. Provisional Application No. 60/671,173 filed 13 Apr 2005 (HHS Reference No. E-099-2005/0-US-01)

Licensing Contact: Susan Carson; 301/435-5020; carsonsu@mail.nih.gov

The complexity of taste discrimination (salty, sour, sweet, umami and bitter) varies between human individuals and populations. Sweet and umami (the taste of glutamate) tastes play a major role in the perception of calorically-rich and essential nutrients and there are well-documented differences in individual perception of sweet and umami flavorings, many of which appear to be genetic in origin. Studies of individuals within and between populations that vary in any of the taste receptors should be of direct interest to the multi-billion dollar food and flavoring industry as the characterization of such variants could be used to aid in the development of a variety of taste improvements in foods and orally administered medications. NIH researchers previously characterized bitter taste receptor variants in world wide populations [Human Mutation 26, 199-204; HHS Ref. No. E-222-2003/0] and have now extended their studies to the sweet and umami receptors in global populations.

The group of Dr. Dennis Drayna at NIDCD have now discovered novel coding sequence polymorphisms in the human TAS1R genes. These genes encode dimeric receptors that sense sweet taste (as TAS1R2+TAS1R3) and the taste of umami (as TAS1R1+TAS1R3). To achieve maximum genetic diversity, TAS1R receptors from a panel of 30 Europeans, 20 East Asian, 10 Native Americans, 8 South Asians and 20 sub-Saharan Africans were sequenced. Approximately 60% of the identified SNPs caused an amino acid substitution in the encoded receptor protein. This variation may account for individual preferences in sweet and umami tastes in foods and could be of use in the understanding and control of dietary preferences that lead to obesity and diabetes.

These novel variants and methods of use are available for licensing and should be of particular use to those using sensorial analysis in the food and flavoring industry where the use of taster panels in the development of flavors and flavor enhancers for different foods is key to the development of new food products and taste masking compounds. The ability, for example, to genetically match taster individuals employed by industry with the target consumer populations can both guide improved formulations and marketing decisions as well as reducing the total sample size in the testing of new products in this highly competitive industry.

The Human Taste Receptor Haplotype patent portfolio is also available for licensing and includes: HHS Ref No. E-169-2001/0-PCT-02, Phenylthiocarbamide Taste Receptor, International Publication No. WO 2003/008627, PCT filed 19 July 2002 and global IP and HHS Ref. No 222-2003/1: Variants of Human Taste Receptor Genes, International Publication No. WO 2005/007891, PCT filed 18 June 2004 and global IP.

In addition to licensing, the technology is available for further development through collaborative research opportunities with the inventors.

Genes for Niemann-Pick Type C Disease

Eugene D. Carstea (NINDS) et al.

U.S. Patent No. 6,426,198 issued 30 Jul 2002 (HHS Reference No. E-122-1997/0-US-03) Start Printed Page 8863

U.S. Patent Application No. 10/208,731 filed 29 Jul 2002, allowed (HHS Reference No. E-122-1997/0-US-04)

Licensing Contact: Marlene Astor; 301/435-4426; shinnm@mail.nih.gov

Niemann-Pick disease is a class of inherited lipid storage diseases. Niemann-Pick Type C disease is an autosomal recessive neurovisceral lipid storage disorder which leads to systemic and neurological abnormalities including ataxia, seizures, and loss of speech. Patients with the disease typically die as children. The biochemical hallmark of Niemann-Pick Type C cells is the abnormal accumulation of unesterified cholesterol in lysosomes, which results in the delayed homeostatic regulation of both uptake and esterification of low density lipoprotein (LDL) cholesterol. Niemann-Pick Type C is characterized by phenotypic variability. The disease appears at random in families that have no history of the disorder, making diagnosis problematic. This invention provides the human gene for Niemann-Pick Type C disease and the nucleic acid sequences corresponding to the human gene for Niemann-Pick Type C disease. Also provided is the mouse homolog of the human gene. The invention could lead to improved diagnosis and the design of therapies for the disease and improved means of detection of carriers of the gene. In addition, this invention may contribute to the understanding and development of treatments for atherosclerosis, a more common disorder associated with cholesterol buildup that involves the accumulation of fatty tissue inside arteries that blocks blood flow, leading to heart disease and stroke. The invention may also lead to additional discoveries concerning how cholesterol is processed in the body.

This invention is described, in part, in: S.K. Loftus et al., “Murine model of Niemann-Pick C disease: Mutation in a cholesterol homeostasis gene,” Science 277(5323):232-235, 1997; S.K. Loftus et al., “Rescue of neurodegeneration in Niemann Pick-C mice by a prion-promoter driven Npc1 cDNA transgene,” Human Molec. Genet. 11(24):3107-14, 2002.

The NHGRI Genetic Disease Research Branch is seeking statements of capability or interest from parties interested in collaborative research to further develop, evaluate or commercialize Niemann-Pick Type C disease diagnostics and therapies as well as potential applications of the Niemann-Pick Type C gene related to atherosclerosis and cholesterol processing. Please contact Claire T. Driscoll for more information (telephone: 301/594-2235; e-mail: cdriscol@mail.nih.gov).

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Dated: February 10, 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. E6-2363 Filed 2-17-06; 8:45 am]

BILLING CODE 4140-01-P