[Federal Register Volume 64, Number 55 (Tuesday, March 23, 1999)]
[Notices]
[Pages 14000-14001]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 99-6952]
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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 contacting Charles
Maynard, J.D., M.P.H., at the Office of Technology Transfer, National
Institutes of Health, 6011 Executive Boulevard, Suite 325, Rockville,
Maryland 20852-3804; telephone: 301/496-7057 ext. 243; fax: 301/402-
0220; e-mail: cm251n@nih.gov. A signed Confidential Disclosure
Agreement will be required to receive copies of the patent
applications.
Novel Adipose Seven Transmembrane Domain Protein
C Montrose-Rafizadeh (NIA), C-F Yang
DHHS Reference No. E-213-97/1 filed June 19, 1998
This technology relates to the discovery and isolation of a novel
cDNA clone from mouse adipocytes. This invention comprises the
identification and isolation of receptors from extra-pancreatic
tissues. More specifically, this invention has identified and isolated
a novel cDNA clone from mouse adipocytes that appears to be involved in
glucose tolerance/intolerance. Clone A contains seven transmembrane
domains, designated I through VII. Experiments in human, rat and mice
tissues indicates that clone A may be a critical component in the
glucose intolerance associated with aging and diabetes. This invention
further provides vectors such as plasmids comprising a DNA molecule
encoding clone A, adapted for expression in a bacterial cell, a yeast
cell, an insect cell or a mammalian cell which additionally comprises
the regulatory elements necessary for the expression of the DNA in the
bacterial, yeast, insect or mammalian cells operatively linked to the
DNA encoding clone A to permit expression thereof.
Methods and Compositions for Reducing Ischemic Injury of the Heart
by Administering Adenosine A3 and Adenosine
A1 Receptor Agonists
KA Jacobson, BT Liang (NIDDK
DHHS Reference No. E-006-98/0 filed May 9, 1997
This technology relates to methods of administering compounds to
protect the heart from ischemic injury. In particular, this invention
provides agonists which selectively activate adenosine A3
and A1 receptors simultaneously, thereby enhancing the
protective effects of preconditioning and rendering the myocardium more
resistant to ischemia. This invention involves administration of
specific A1 and A3 agonists during ischemic
attacks, or at risk for ischemic damage. The agonists of the invention
may be delivered prior to a surgical procedure, and may also be
administered to a patient to prevent or reduce the severity of ischemic
damage during surgery. Additionally, the A3/A1
agonists may be administered following surgical procedures to reduce
the risk of post-surgical ischemic complications. The A3 and
A1 agonists may be administered to patients with agina,
which may be chronic and stable, unstable or due to post-myocardial
infarction.
Methods and Compositions for Protecting Against Cardiac Ischemia by
Administering Adenosine A2a Receptor Antagonists
KA Jacobson, BT Liang (NIDDK)
Serial No. 08/813,787 filed March 7, 1997
This technology relates to methods of administering compounds to
protect the heart from ischemic injury. In particular, this invention
provides antagonists, which selectively inhibit activation of
A2a receptors thereby enhancing the protective effects of
preconditioning and rendering the heart more resistant to ischemia.
This invention involves administration of a specific A2a
antagonist to patients
[[Page 14001]]
during ischemic attacks, or at risk for ischemic damage. The
antagonists of this invention may be delivered prior to a surgical
procedure. They may also be administered to a patient to prevent or
reduce the severity of ischemic damage during surgery. Additionally,
the A2a antagonists may be administered following surgical
procedures to reduce the risk of post-surgical ischemic complications.
The A2a antagonists may be administered to patients with
angina, which may be chronic and stable, unstable or due to post-
myocardial infarction.
Treatment of Stroke and Neurodegeneration
DK Von Lubitz, KA Jacobson (NIDDK)
DHHS Reference No. E-023-96/0 filed April 10, 1996
This technology relates to a method of using certain adenosine
amine congeners in the prevention and treatment of brain damage caused
by ischemia, hypoxia, and anoxia. The present invention provides a
method of treating ischemic, hypoxic, or anoxic brain damage in an
animal, particularly a human, comprising administering to an animal
recently afflicted with ischemic, hypoxic, or anoxic brain damage, or
an animal in imminent danger of suffering ischemic brain damage, a
therapeutic does of adenosine or structural analogues of ADAC.
The present invention is predicated on the surprising discovery
that ADAC is effective for post-ischemic neuropreservation in the brain
at concentrations at least 10-fold lower than other A1 adenosine
receptor selective agonists previously studied. At these doses,
cardiovascular side effects are not observed in experimental animals.
Method of Treating Ischemic, Hypoxic, and Anoxic Brain Damage
DK Von Lubitz, KA Jacobson (NIDDK)
DHHS Reference No. E-023-96/1 filed May 9, 1996
This technology relates to a method of using certain adenosine
amine congeners in the prevention and treatment of brain damage caused
by ischemia, hypoxia, and anoxia. The present invention provides a
method of treating ischemic, hypoxic, or anoxic brain damage in an
animal, particularly a human, comprising administering to an animal
recently afflicted with ischemic, hypoxic, or anoxic brain damage, or
an animal in imminent danger of suffering ischemic brain damage, a
therapeutic dose of adenosine or structural analogues of ADAC.
The present invention is predicated on the surprising discovery
that ADAC is effective for post-ischemic neuropreservation in the brain
at concentrations at least 10-fold lower than other A1 adenosine
receptor selective agonists previously studied. At these doses,
cardivascular side effects are not observed in experimental animals.
Dated: March 15, 1999.
Jack Spiegel,
Director, Division of Technology Development and Transfer, Office of
Technology Transfer.
[FR Doc. 99-6952 Filed 3-22-99; 8:45 am]
BILLING CODE 4140-01-M
