[Federal Register Volume 74, Number 12 (Wednesday, January 21, 2009)]
[Notices]
[Pages 3619-3620]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: E9-978]


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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.

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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.

Mice With a Conditional LoxP-Flanked Glucosylceramide Synthase Allele 
Controlling Glycosphingolipid Synthesis

    Description of Technology: Glycosphingolipids are organizational 
building blocks of plasma membranes that participate in key cellular

[[Page 3620]]

functions, such as signaling and cell-to-cell interactions. 
Glucosylceramide synthase--encoded by the Ugcg gene--controls the first 
committed step in the major pathway of glycosphingolipid synthesis. 
Global disruption of the Ugcg gene in mice is lethal during 
gastrulation. The inventors have established a Ugcg allele flanked by 
loxP sites (floxed). When cre recombinase was expressed in the nervous 
system under control of the nestin promoter, the floxed gene underwent 
recombination, resulting in a substantial reduction of Ugcg expression 
and of glycosphingolipid ganglio-series levels. The mice deficient in 
Ugcg expression in the nervous system show a striking loss of Purkinje 
cells and abnormal neurologic sphingo-lipid behavior.
    The Research Tools available are mice with a floxed Ugcg allele 
that can be deleted in a conditional manner. These mice carrying floxed 
Ugcg alleles will be useful for delineating the functional roles of 
glycosphingolipid synthesis in the nervous system and in other 
physiologic systems.

Applications

    <bullet> Study of the functional roles of glycosphingolipid 
synthesis in the nervous system and other physiologic systems.
    <bullet> The floxed Ugcg allele will facilitate analysis of the 
function of glycosphingolipids in development, physiology, and in 
diseases such as diabetes and cancer.
    Development Status: Ready to Use.
    Inventors: Richard L. Proia (NIDDK).
    Publication: T Yamashita, ML Allende, DN Kalkofen, N Werth, K 
Sandhoff, RL Proia. Conditional LoxP-flanked glucosylceramide synthase 
allele controlling glycosphingolipid synthesis. Genesis 2005 
Dec;43(4):175-180.
    Patent Status: HHS Reference No. E-320-2007/0--Research Material. 
Patent protection is not being pursued for this technology.
    Licensing Status: Available for licensing under a Biological 
Materials license agreement.
    Licensing Contact: Suryanarayana (Sury) Vepa, PhD, J.D.; 301-435-
5020; <a href="/cdn-cgi/l/email-protection#abddcedbcad8ebc6cac2c785c5c2c385ccc4dd"><span class="__cf_email__" data-cfemail="7c0a190c1d0f3c111d151052121514521b130a">[email protected]</span></a>.
    Collaborative Research Opportunity: The NIDDK Genetics of 
Development and Disease Branch is seeking statements of capability or 
interest from parties interested in collaborative research to further 
develop, evaluate, or commercialize the sphingolipid metabolism in 
physiology and disease. Please contact Dr. Proia at <a href="/cdn-cgi/l/email-protection#90e0e2fff9f1d0fef9f8bef7ffe6"><span class="__cf_email__" data-cfemail="bbcbc9d4d2dafbd5d2d395dcd4cd">[email protected]</span></a> for 
more information.

Mutant Nuclear Orphan Receptor for Drug Metabolism Assays

    Description of Technology: The constitutively active nuclear orphan 
receptor (CAR) activates transcription of genes encoding various drug-
metabolizing enzymes, such as cytochrome P450, in response to drug 
exposure. While the direct activation of CAR in response to various 
drugs has been observed in vivo, CAR is always active in cell-based 
transfection assays, even in the absence of activating drugs. This 
constitutive activity of CAR makes it difficult to perform accurate in 
vitro assays to measure drug metabolism.
    The NIH has obtained patent protection for modified CAR proteins 
that can be directly activated by drugs in vitro. This technology may 
potentially be used in the development of more efficient and cost-
effective cell-based drug metabolism assays.
    Applications: Development of improved in vitro assays to measure 
drug metabolism.
    Inventors: Masahiko Negishi et al. (NIEHS).

Publications

    1. T Sueyoshi, T Kawamoto, I Zelko, P Honkakoski, M Negishi. The 
repressed nuclear receptor CAR responds to phenobarbital in activating 
the human CYP2B6 gene. J Biol Chem. 1999 Mar 5;274(10):6043-6046.
    2. T Kawamoto, S Kakizaki, K Yoshinari, M Negishi. Estrogen 
activation of the nuclear orphan receptor CAR (constitutive active 
receptor) in induction of the mouse Cyp2b10 gene. Mol Endocrinol. 2000 
Nov;14(11):1897-1905.
    Patent Status: U.S. Patent No. 7,365,160 issued 29 Apr 2008 (HHS 
Reference No. E-034-2002/0-US-03).
    Licensing Status: Available for exclusive and non-exclusive 
licensing.
    Licensing Contact: Tara L. Kirby, PhD; 301-435-4426; 
<a href="/cdn-cgi/l/email-protection#d7a3b6a5b6bc97bab6bebbf9b9bebff9b0b8a1"><span class="__cf_email__" data-cfemail="c1b5a0b3a0aa81aca0a8adefafa8a9efa6aeb7">[email protected]</span></a>.

    Dated: January 8, 2009.
Richard U. Rodriguez,
Director, Division of Technology Development and Transfer, Office of 
Technology Transfer, National Institutes of Health.
[FR Doc. E9-978 Filed 1-16-09; 8:45 am]
BILLING CODE 4140-01-P


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