[Federal Register Volume 71, Number 156 (Monday, August 14, 2006)]
[Notices]
[Pages 46492-46493]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: E6-13191]


-----------------------------------------------------------------------

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.

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; [email protected]
    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 
[email protected] 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