Skip to Content


Government-Owned Inventions; Availability for Licensing

Document Details

Information about this document as published in the Federal Register.

Published Document

This document has been published in the Federal Register. Use the PDF linked in the document sidebar for the official electronic format.

Start Preamble


National Institutes of Health, Public Health Service, HHS.




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.


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;

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 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 Start Printed Page 39633have 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;

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 for more information.

Start Signature

Dated: July 9, 2007.

Steven M. Ferguson,

Director, Division of Technology Development and Transfer, Office of Technology Transfer, National Institutes of Health.

End Signature End Preamble

[FR Doc. E7-13955 Filed 7-18-07; 8:45 am]