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Notice

Government-Owned Inventions; Availability for Licensing

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AGENCY:

National Institutes of Health, Public Health Service, DHHS.

ACTION:

Notice.

SUMMARY:

The inventions listed below are owned by agencies 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.

Combined Inhibition of Phosphodiesterase-4 (PDE-4) and Phosphodiesterase-3 (PDF-3) as a Therapy for Th1 Mediated Autoimmune Diseases

Dr. Bibiana Bielekova et al. (NINDS)

DHHS Reference No. E-077-00/0, filed Dec 22 2000

Licensing Contact: Marlene Shinn; 301/496-7056 ext. 285; e-mail: shinnm@od.nih.gov

Hyperactive Th1-mediated immune responses are thought to be involved in the pathogenesis of many autoimmune diseases, including rheumatoid arthritis, diabetes, inflammatory bowel disease, vitiligo, and multiple sclerosis among others. Immune cells are known to produce primarily two classes of phosphodiesterases (PDE), the PDE4 and the PDE3 classes. Inhibitors of these PDEs have been shown to down-regulate the expression or production of Th1 cytokines and have either no effect or augment the production of Th2 cytokines, therefore making them good candidates for the treatment of Th1-mediated autoimmune diseases.

The NIH announces a new technology wherein PDE-4 and PDE-3 inhibitors are used in combination and a synergistic enhancement of therapeutic activity is achieved. This results in a more potent immunomodulatory effect on the immune cells and could lead to the administration of lower dose rate of the inhibitors. This new form of treatment will alleviate side effects through the use of a lower dose rate for each and will make for a more effective therapy.

Determination of AM-Binding Proteins and the Association of Adrenomedullin (AM) Therewith

F. Cuttitta et al. (NCI)

DHHS Reference No. E-256-99/1 filed, Sep 08 2000 (Note: This invention is related to E-206-95/3, filed Aug 18 1996, the disclosure of which is incorporated herein.)

Licensing Contact: Matthew Kiser; 301/496-7056 ext. 224; e-mail: kiserm@od.nih.gov

The present invention provides methods for the isolation, identification, and purification of adrenomedullin (AM)-binding proteins. Methods for utilizing the purified AM-binding proteins, or functional portions thereof, to diagnose, treat, and monitor AM-related diseases are described. A second aspect of this technology discloses the identification and isolation of a novel complex between AM and a specific AM-binding protein 1 (AMBP-1), designated factor H (fH). The identification of small molecule Start Printed Page 29156antagonist, which down-regulate the function of AM, factor H, and the AM/fH complex has been achieved. Collectively, the invention provides methods for treating conditions such as cancer or diabetes, via antibodies and small molecule antagonists.

Adrenomedullin (AM) is expressed in human cancer cell lines of diverse origin and functions as a universal autocrine growth factor, driving neoplastic proliferation. Experimental models for use in identifying the role of AM in pancreatic physiology have been validated and are available for licensing. The interesting observations show that AM inhibits insulin secretion in a dose-dependent manner. Further experiments have shown that a neutralizing antibody up-regulates insulin release at least five-fold, an effect that is reversed with the addition of synthetic AM.

Novel Inhibitors of p53 for Treatment of Neurodegenerative Disorders, Myocardial Infarction and Other Tissue Insults

Nigel H. Greig, et al. (NIA)

Serial No. 60/216,388, filed July 6, 2000 Licensing Contact: Norbert Pontzer; 301/496-7736, ext. 284; e-mail: pontzern@nih.gov

The tumor suppressor protein p53 is a key modulator of stress responses, and activation of p53 precedes apoptosis (programmed cell death) in many cell types. Conditions that stress tissue, such as deposition of amyloid b-peptide, may thus cause tissue degeneration through activation or up-regulation of p53. This invention provides novel inhibitors of p53 and methods of using these inhibitors for the prevention or treatment of the stress related tissue degeneration observed in Alzheimer's disease, myocardial infarction and stroke. In vitro and ex vivo studies demonstrated that p53 inhibition protected nerve cells from toxic insults that otherwise induced programmed cell death. In a rat model of stroke, p53 inhibition produced a 50% reduction in stroke volume.

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Dated: May 17, 2001.

Jack Spiegel,

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

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[FR Doc. 01-13346 Filed 5-25-01; 8:45 am]

BILLING CODE 4140-01-P