Skip to Content

Notice

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

AGENCY:

National Institutes of Health, Public Health Service, DHHS.

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.

Proteomic Profiles Associated With Aging

Dr. Shari M. Ling (NIA).

DHHS Reference No. E-354-2004/1—Research Tool.

Licensing Contact: Marlene Shinn-Astor; 301/435-4426; shinnm@mail.nih.gov.

This invention relates to proteomic profiles associated with normal aging. Biological markers (Biomarkers) that characterize the state of “normal aging” could provide a useful comparison for biomarkers of age-associated diseases (cardiovascular, cancer, arthritis). The profiles could then be used to develop markers linked with other diseases.

The proteins identified could either be included in elisa or multiplex assays, or incorporated into a protein-based chip. These products would be of utility to characterize research subjects for clinical trials. Specific proteins or groups of proteins could be used as potential therapeutic targets to prevent or attenuate disease development or help to improve the normal aging process.

In addition to licensing, the technology is available for further development through collaborative research opportunities with the inventors.

AlphaB-Crystallin/HSPBE Gene Knockout Mouse

Dr. Eric F. Wawrousek, et al. (NEI).

DHHS Reference No. E-135-2001/0—Research Tool.

Licensing Contact: Marlene Shinn-Astor; (301) 435-4426; shinnm@mail.nih.gov.

The alpha crystallins and other members of the small heat shock family of proteins, have been shown to be very important proteins for preventing the irreversible destruction of other proteins. AlphaA is mostly restricted to the ocular lens, while alphaB is present in almost all cells of the body with the highest levels in ocular lens, heart, and skeletal muscle. The NIH has created lines of mice, which lack the alphaB-crystallin gene (and unintentionally, its neighboring gene HSPB2). These mouse lines could be used to study functions of these proteins in the eye, skeletal muscle, heart, and any other tissue or organ.

In addition to licensing, the technology is available for further development through collaborative research opportunities with the inventors.

Three Myelin Basic Protein-Specific T Cell Clones, TL2A6, TL5F6, and TL5G7 That Are Restricted by Multiple Sclerosis-Associated HLA-DR Molecules and Recognize the Immunodominant Myelin Basic Protein (MBP) Peptide MBP (83-99)

Dr. Roland Martin, et al. (NINDS).

DHHS Reference No. E-277-1999/0—Research Tool.

Licensing Contact: Marlene Shinn-Astor; (301) 435-4426; shinnm@mail.nih.gov.

Autoreactive T cell clones such as TL3A6 and TL5F6 that recognize an autoantigen, which is potentially relevant for an autoimmune disease, for example, multiple sclerosis (MS), offer the potential to examine the disease pathogenesis and develop new treatments. Such treatments aim at disrupting or interfering with the specific interaction between autoreactive T cells, antigen presenting cells and antigenic peptide. Current treatments have immunomodulatory effects and side effects. These T cell lines will be useful for developing novel treatment approaches for multiple sclerosis. The T cell lines can be used to test treatments that block or interfere with surface receptors of these cells.

Mouse Model for Myasthenia Gravis

Dr. Michael J. Lenardo et al. (NIAID).

DHHS Reference No. E-188-1999/0—Research Tool.Start Printed Page 33911

Licensing Contact: Marlene Shinn-Astor; (301) 435-4426; shinnm@mail.nih.gov.

Myasthenia gravis is a disease that causes muscle weakness and paralysis due to an autoimmune process that attacks the muscle. So far no mouse model has been available which has limited investigation of the disease and the development of better treatments or a cure. Our inventors have created a transgenic mouse strain that manifests immunological reactivity that underlines myasthenia gravis.

Use of Transgenic Mice To Assess the Systemic Effects of Tissue Inhibitor of Metalloproteinases-1 (TIMP) on Tumor Progression, Liver Fibrosis, Rheumatoid Arthritis, Wound Healing, and Angiogenesis

Dr. Unnur P. Thorgeirsson, et al. (NCI).

DHHS Reference No. E-273-1998/0—Research Tool.

Licensing Contact: Marlene Shinn-Astor; (301) 435-4426; shinnm@mail.nih.gov.

NIH researchers have produced transgenic mice over expressing human tissue inhibitor of metalloproteinases-1 (hTIMP) in the liver under the control of an albumin promoter. These mice produce large amounts of hTIMP-1 for extended periods of time, resulting in high levels of biologically active inhibitor released into the systemic circulation. In considering that the sustained high levels of circulating hTIMP-1 do not appear to affect the general health of these mice, this model can be used to study the protective effects of TIMP-1 on diseases, which involve extensive proteolytic matrix degradation and tissue remodeling. Examples of such diseases include malignant tumors, liver fibrosis, wound healing, rheumatoid arthritis, and a variety of angioproliferative diseases.

Start Signature

Dated: June 3, 2005.

Steven M. Ferguson,

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

End Signature End Preamble

[FR Doc. 05-11577 Filed 6-9-05; 8:45 am]

BILLING CODE 4140-01-P