[Federal Register: August 14, 2006 (Volume 71, Number 156)]
[Notices]
[Page 46492-46493]
From the Federal Register Online via GPO Access [wais.access.gpo.gov]
[DOCID:fr14au06-64]
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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.
Amyloid Beta Is a Ligand for FPR Class Receptors
Description of Technology: Alzheimer's disease is the most
important dementing illness in the United States because of its high
prevalence. Five to ten percent of the United States population 65
years and older are afflicted with the disease. In 1990 there were
approximately 4 million individuals with Alzheimer's, and this number
is expected to reach 14 million by the year 2050. It is the fourth
leading cause of death for adults, resulting in more than 100,000
deaths annually. Amyloid beta has been identified as playing an
important role in the neurodegeneration of Alzheimer's disease.
However, the mechanism by which this occurred was unknown, but has been
postulated to be either direct or indirect through an induction of
inflammatory responses.
The NIH announces the identification of the 7-transmembrane, G-
protein-coupled receptor, FPRL-1, in the cellular uptake and fibrillar
aggregation of amyloid [beta][beta](A[beta][beta]) peptides. The
A[beta][beta] peptides use the FPRL-1 receptor to attract and activate
human monocytes and mouse microglial cells (publications referenced
below), and have been identified as a principal component of the
amyloid plaques associated with Alzheimer's disease. In addition, the
known anti-inflammatory drug, Colchicine, has been shown to inhibit the
FPRL1 activation by amyloid [beta][beta]** and the internalization of
FPRL1/amyloid beta complexes.
Inventors: Ji Ming Wang et al. (NCI).
Publications:
1. Y Le, W Gong, L Tiffany, A Tumanov, S Nedospasov, W Shen, NM
Dunlop, J-L Gao, PM Murphy, JJ Oppenheim, and JM Wang, ``Amyloid
(beta)42 activates a G-protein-coupled chemoattractant receptor, FPR-
like-1,'' J. Neuroscience 2001 Jan 15; 21(2):RC123.
2. HL Tiffany, MC Lavigne, YH Cui, JM Wang, TL Leto, JL Gao, and PM
Murphy, ``Amyloid-beta induces chemotaxis and oxidant stress by acting
at formylpeptide receptor 2, a G protein-coupled receptor expressed in
phagocytes and brain,'' J Biol Chem. 2001 Jun 29;276(26):23645-52.
3. YH Cui, Y Le, W Gong, P Proost, J Van Damme, WJ Murphy, and JM
Wang, ``Bacterial lipopolysaccharide selectively up-regulates the
function of the chemotactic peptide receptor formyl peptide receptor 2
in murine microglial cells,'' J Immunol. 2002 Jan 1;168(1):434-42.
4. H Yazawa., Z-X Yu, K Takeda, Y Le, W Gong, VJ Ferrans, JJ
Oppenheim, CC Li, and JM Wang, ``Beta amyloid peptide (Ab42) is
internalized via the G-protein coupled receptor FPRL1 and forms
fibrillar aggregates in macrophages,'' FASEB J. 2001 Nov; 15(13):2454-
2642.
5. P Iribarren, K Chen, J Hu, G Gong, EH Cho, S Lockett, B
Uranchimeg, and JM Wang, ``CpG-containing oligodeoxynucleotide promotes
microglial the up-take of amyloid beta 1-42 by up-regulating the
expression of the G-protein coupled receptor mFPR2,''.FASEB J. 2005
Dec;19(14):2032-4.
6. K Chen, P Iribarren, J Hu, J Chen, G Gong, EH Cho, S Lockett, NM
Dunlop, and JM Wang, ``Activation of Toll-like receptor 2 on microglia
promotes cell uptake of Alzheimer disease-associated amyloid beta
peptide,'' J Biol Chem. 2006 Feb 10;281(6):3651-9.
Patent Status: U.S. Patent Application No. 10/831,524 filed 23 Apr
2004 (HHS Reference No. E-336-01/0-US-02), claiming priority to 26 Oct
2001.
Licensing Status: Available for non-exclusive or exclusive
licensing.
Licensing Contact: 301/496-7057; nihott@mail.nih.gov
Collaborative Research Opportunity: The National Cancer Institute,
Laboratory of Molecular Immunoregulation, is seeking statements of
capability or interest from parties interested in collaborative
research to further develop, evaluate, or commercialized siRNA delivery
development. Please contact Diana Bialozor at 301/846-5465 or
bialozod@mail.nih.gov for more information.
[[Page 46493]]
Dated: August 1, 2006.
Steven M. Ferguson,
Director, Division of Technology Development and Transfer, Office of
Technology Transfer, National Institutes of Health.
[FR Doc. E6-13191 Filed 8-11-06; 8:45 am]
BILLING CODE 4140-01-P