[Federal Register: May 29, 2001 (Volume 66, Number 103)]
[Notices]
[Page 29155-29156]
From the Federal Register Online via GPO Access [wais.access.gpo.gov]
[DOCID:fr29my01-89]
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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:
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
[[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: 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.
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