[Federal Register Volume 75, Number 60 (Tuesday, March 30, 2010)]
[Notices]
[Pages 15711-15712]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 2010-6966]


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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.

Zscan4, a Therapeutic Target for Cancer, Regenerative Medicine and 
Aging

    Description of Invention: This technology has broad potential for 
the development of therapeutics for cancer, diseases of aging, and 
regenerative medicine, and targets Zscan4, a gene that regulates 
telomere length and genomic stability in embryonic stem (ES) cells.
    The ability to maintain genomic stability in ES cells and other 
stem cells is critical for the development of stem cell-based 
therapies; genomic stability and telomere length are also active areas 
of cancer and aging research. NIA investigators have discovered that 
the Zscan4 gene regulates telomere length and genomic stability in ES 
cells, and plays an essential role in early embryonic development; this 
activity is independent of telomerase activity. The investigators have 
shown that ablation of Zscan4 results in shortened telomere length and 
deterioration of the karyotype of ES cells, and that Zscan4 
overexpression increases telomere length.
    This technology discloses methods for increasing genome stability 
or increasing telomere length in an ES cell, and methods of treating a 
subject in need of ES cell therapy. Also disclosed are methods of 
promoting blastocyst outgrowth of embryonic stem cells, as well as 
Zscan4 expression vectors and methods of identifying stem cells 
expressing Zscan4.

Applications

     Development of therapeutics for cancer treatment, aging, 
and regenerative medicine.
     Development of assisted reproduction technologies.
     Studies of early embryonic development.
    Development Status: In vitro and in vivo studies have been 
performed.
    Inventors: Minoru S. H. Ko et al. (NIA).

Publications

    1. M Zalzman et al. Zscan4 regulates telomere elongation and 
genomic stability in ES cells. Nature 2010 Mar 24; advance online 
publication, doi 10.1038/nature08882.
    2. G Falco et al. Zscan4: A novel gene expressed exclusively in 
late 2-cell embryos and embryonic stem cells. Dev Biol. 2007 Jul 
15;307(2):539-550. [PubMed: 17553482.]

Patent Status

    HHS Reference No. E-088-2007/0--
     PCT Application No. PCT/US2008/058261 filed 26 Mar 2008.
     US Application No. 12/529,004 filed 27 Aug 2009.
     Foreign counterparts in Europe, Australia, Canada, and 
Japan
    HHS Reference No. E-172-2009/0--
     U.S. Provisional Application No. 61/275,983 filed 04 Sep 
2009.
    Licensing Status: Available for licensing.
    Licensing Contact: Tara Kirby, PhD; 301-435-4426; 
[email protected].
    Collaborative Research Opportunity: The National Institute on 
Aging, Laboratory of Genetics, is seeking statements of capability or 
interest from parties interested in collaborative research to further 
develop, evaluate, or commercialize this technology. Please contact 
Nicole Guyton, PhD at 301-435-

[[Page 15712]]

3101 or [email protected] for more information.

mFPR2 Transgenic and Knockout Mouse Models for Alzheimer's and Other 
Inflammatory Diseases

    Description of Invention: Human Formyl Peptide-Like Receptor 1 
(hFPLR1) has been implicated in host defense for disease processes 
including Alzheimer's disease, infection, and other inflammatory 
diseases. hFPLR1 and its mouse homologue Formyl Peptide Receptor 2 
(mFPR2) are G-protein coupled receptors that are expressed at high 
levels on phagocytic leukocytes, mediating leukocyte chemotaxis and 
activation in response to a number of pathogen- and host-derived 
peptides. Activation of hFPRL1/mFPR2 by lipoxin A4 may play a role in 
preventing and resolving inflammation. Also, hFPRL1/mFPR2 has been 
shown to mediate the chemotactic activity of amyloid beta 1-42, a key 
pathogenic peptide in Alzheimer's disease.
    Available for licensing are mice expressing the mFPR2 transgene on 
either the FVB or C58BL background, as well as mFPR2 knockout mice on 
the C57BL background. These mice are anticipated to be highly useful in 
the study of a wide variety of inflammatory, infectious, immunologic 
and neurodegenerative diseases.

Applications

     Drug development model for Alzheimer's disease and other 
inflammatory diseases.
     Tool to probe the role of hFPRL1/mFPR2 in host responses 
in a variety of disease processes, including inflammatory, infectious, 
immunologic, and neurodegenerative disease.
    Inventors: Ji Ming Wang et al. (NCI)

Publications

    1. K Chen, Y Le, Y Liu, W Gong, G Ying, J Huang, T Yoshimura, L 
Tessarollo, JM Wang. Cutting Edge: A Critical Role for the G Protein-
Coupled Receptor mFPR2 in Airway Inflammation and Immune Responses. J 
Immunol. 2010 Mar 3. Epub ahead of print. [PubMed: 20200280.]
    2. K Chen, P Iribarren, J Hu, J Chen, W 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):3651-3659. [PubMed: 16339765.]
    3. H Yazawa, ZX Yu, Takeda, Y Le, W Gong, VJ Ferrans, JJ Oppenheim, 
CC Li, and JM Wang. Beta amyloid peptide (Abeta42) is internalized via 
the G-protein-coupled receptor FPRL1 and forms fibrillar aggregates in 
macrophages. FASEB J. 2001 Nov;15(13):2454-2462. [PubMed: 11689470.]
    4. 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):434-442. 
[PubMed: 11751990.]
    Patent Status: HHS Reference No. E-303-2006/0--Research Tool. 
Patent protection is not being pursued for this technology.
    Licensing Status: This technology is available as a research tool 
under a Biological Materials License.
    Licensing Contact: Tara Kirby, PhD; 301-435-4426; 
[email protected].
    Collaborative Research Opportunity: The National Cancer Institute--
Frederick, Laboratory of Molecular Immunoregulation, is seeking 
statements of capability or interest from parties interested in 
collaborative research to further develop, evaluate, or commercialize 
mFPR2 Transgenic and Knockout Mouse Models for Alzheimer's and Other 
Inflammatory Diseases. Please contact John D. Hewes, PhD at 301-435-
3121 or [email protected] for more information.

    Dated: March 23, 2010.
Richard U. Rodriguez,
Director, Division of Technology Development and Transfer, Office of 
Technology Transfer, National Institutes of Health.
[FR Doc. 2010-6966 Filed 3-29-10; 8:45 am]
BILLING CODE 4140-01-P