[Federal Register Volume 66, Number 103 (Tuesday, May 29, 2001)]
[Notices]
[Pages 29155-29156]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 01-13346]


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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, DHHS.

ACTION: Notice.

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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: 
<a href="/cdn-cgi/l/email-protection#e19289888f8f8ca18e85cf8f8889cf868e97"><span class="__cf_email__" data-cfemail="582b303136363518373c76363130763f372e">[email protected]</span></a>

    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: 
<a href="/cdn-cgi/l/email-protection#c2a9abb1a7b0af82ada6ecacabaaeca5adb4"><span class="__cf_email__" data-cfemail="7d16140e180f103d121953131415531a120b">[email protected]</span></a>

    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

[[Page 29156]]

antagonist, 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: <a href="/cdn-cgi/l/email-protection#deaeb1b0aaa4bbacb09eb0b7b6f0b9b1a8"><span class="__cf_email__" data-cfemail="90e0fffee4eaf5e2fed0fef9f8bef7ffe6">[email protected]</span></a>

    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.

    Dated: May 17, 2001.
Jack Spiegel,
Director, Division of Technology Development and Transfer, Office of 
Technology Transfer, National Institutes of Health.
[FR Doc. 01-13346 Filed 5-25-01; 8:45 am]
BILLING CODE 4140-01-P


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