[Federal Register Volume 72, Number 138 (Thursday, July 19, 2007)]
[Notices]
[Pages 39632-39633]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: E7-13955]


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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 Genetically Deficient in the Chemoattractant Receptor FPR (Formyl 
Peptide Receptor)

    Description of Invention: The present research tool is a knockout 
mouse model (FPR-/-) that lacks the high affinity N-
formylpeptide receptor (FPR), created by targeted gene disruption.
    N-formylpeptides derive from bacterial and mitochondrial proteins, 
and bind to specific receptors on mammalian phagocytes. Since binding 
induces chemotaxis and activation of phagocytes in vitro, it has been 
postulated that N-formylpeptide receptor signaling in vivo may be 
important in antibacterial host defense, although direct proof has been 
lacking. The inventors have found that FPR-/- mice have no 
obvious developmental defects and do not develop spontaneous infection 
when derived in specific pathogen-free conditions. This suggests that, 
under these conditions, FPR is dispensable. However, when challenged 
with L. monocytogenes, FPR-deficient mice have accelerated mortality 
and increased bacterial burden in liver and spleen early after 
infection, which suggests a role for FPR in host defense, specifically 
through regulation of innate immunity.
    Applications and Modality: New mouse model to study antibacterial 
host defense.
    Market: Research tool useful for innate immunity studies.
    Development Status: The technology is a research tool.
    Inventors: Philip Murphy and Ji-Liang Gao (NIAID).
    Patent Status: HHS Reference No. E-258-2007/0--Research Tool.
    Publication: JL Gao, EJ Lee, PM Murphy. Impaired antibacterial host 
defense in mice lacking the N-formylpeptide receptor. J Exp Med. 1999 
Feb 15;189(4):657-662.
    Licensing Status: This technology is not patented. The mouse model 
will be transferred through a Biological Materials License.
    Licensing Contact: Peter J. Soukas, J.D.; 301/435-4646; 
[email protected].
    Collaborative Research Opportunity: The Laboratory of Molecular 
Immunology, NIAID, is seeking statements of capability or interest from 
parties interested in collaborative research to further develop, 
evaluate, or commercialize FPR knockout mice. Please contact Philip 
Murphy, M.D. at Tel: 301-496-8616 and/or [email protected] for more 
information.

Steroid Derivatives as Inhibitors of Human Tyrosyl-DNA 
Phosphodiesterase (Tdp1)

    Description of Technology: Tyrosyl-DNA phosphodiesterase (Tdp1) is 
an enzyme that repairs topoisomerase I (Top1)-mediated DNA damage 
induced by chemotherapeutic agents and ubiquitous DNA lesions that 
interfere with transcription. The current technology are steroid 
derivatives that human inhibit Tdp1.
    Currently, there are various types of Top1 inhibitors used in 
chemotherapy, e.g., camptothecin. However, Tdp1 inhibitors are expected 
to be effective in combination therapy with Top1 inhibitors for the 
treatment of cancers. Combining Tdp1 inhibitors with Top1 inhibitors 
would allow Tdp1 to potentiate the antiproliferative activity of Top1 
inhibitors. In addition to Tdp1's effect on Top1, Tdp1 inhibitors can 
also exhibit antitumor activity independently, as tumors are shown to

[[Page 39633]]

have excess free radicals, and Tdp1 repairs DNA damage by oxygen 
radicals.
    Applications and Modality: It is anticipated that Tdp1 inhibitors 
in association with Top1 inhibitors can have selective activity toward 
tumor tissues. Tdp1 inhibitors may exhibit antitumor activity by 
themselves because tumors have excess free radicals.
    Market: 600,000 deaths from cancer related diseases were estimated 
in 2006. In 2006, cancer drug sales were estimated to be $25 billion.
    Development Status: The technology is currently in the pre-clinical 
stage of development.
    Inventors: Yves Pommier et al. (NCI).
    Relevant Publication: A manuscript directly related to the above 
technology will be available as soon as it is accepted for publication.
    Patent Status: U.S. Provisional Application No. 60/921,980 filed 05 
Apr 2007 (HHS Reference No. E-130-2007/0-US-01).
    Licensing Status: Available for exclusive and non-exclusive 
licensing.
    Licensing Contact: Adaku Nwachukwu, J.D.; 301/435-5560; 
[email protected].
    Collaborative Research Opportunity: The Center for Cancer Research, 
National Cancer Institute, Laboratory of Molecular Pharmacology is 
seeking statements of capability or interest from parties interested in 
collaborative research to further develop, evaluate, or commercialize 
inhibitors of Tyrosyl-DNA phosphodiesterase (Tdp1). Please contact John 
D. Hewes, Ph.D. at 301-435-3121 or [email protected] for more 
information.

    Dated: July 9, 2007.
Steven M. Ferguson,
Director, Division of Technology Development and Transfer, Office of 
Technology Transfer, National Institutes of Health.
[FR Doc. E7-13955 Filed 7-18-07; 8:45 am]
BILLING CODE 4140-01-P