[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: [email protected]. 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