[Federal Register Volume 76, Number 131 (Friday, July 8, 2011)]
[Notices]
[Pages 40383-40384]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 2011-17227]
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DEPARTMENT OF HEALTH AND HUMAN SERVICES
National Institutes of Health
Government-Owned Inventions; Availability for Licensing
AGENCY: Public Health Service, National Institutes of Health, HHS.
ACTION: Notice.
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SUMMARY: The inventions listed below are owned by an agency 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.
Mouse Model and Derived Cells That Hypersecrete Leukemia Inhibitory
Factor (LIF)
Description of Technology: Embryonic stem cells (ESCs) are
pluripotent cells that can be cultured indefinitely, and maintain their
capability to differentiate into all cell lineages. To maintain these
cells as well as various types of related induced stem cells and
progenitor cells in culture, Mouse Embryonic Fibroblasts (MEFs) are
routinely used as feeder cells, largely to serve as a source of
Leukemia Inhibitory Factor (LIF). ESCs can also be cultured without
feeders if the medium is supplemented with recombinant LIF and other
factors. However, these methods of culturing ESCs suffer from certain
drawbacks, such as limited proliferation capacity and variability of
primary MEFs. Therefore, finding improved conditions that maintain ESC
pluripotency is an area of great interest.
Scientists at NIEHS have now developed a knock-in (KI) mouse model
in which LIF is overproduced from its endogenous locus because of
increased stability of its mRNA. MEFs and presumably other cells
derived from the homozygous mice hypersecrete LIF protein; lesser
degrees of overexpression would be expected from heterozygous mice.
These mice can be used to study LIF function, including how LIF
contributes to various physiological and pathological states. Cells
derived from these mice can be used to culture ESCs, as well as other
progenitor cells. Cells or genetic material derived from these mice can
also be used as sources of LIF for isolation and purification.
Applications
Maintenance of ESCs and progenitor cells.
In vivo, cellular and cell-free sources of LIF.
Sources of LIF for isolation and purification.
Studies of LIF function in mice, such as contribution of
LIF to tumor growth.
Inventors: Dr. Perry Blackshear (NIEHS), et al.
[[Page 40384]]
Patent Status: HHS Reference No. E-175-2011/0 --Research Tool.
Patent protection is not being pursued for this technology.
Licensing Status: Available for licensing under a Biological
Materials License Agreement.
Licensing Contact: Betty B. Tong, PhD; 301-594-6565;
[email protected].
Collaborative Research Opportunity: The NIEHS Laboratory of Signal
Transduction is seeking statements of capability or interest from
parties interested in collaborative research to further develop,
evaluate, or commercialize these mice or other strains derived from
them, or cells or other reagents derived from them. Please contact Dr.
Elizabeth Denholm ([email protected]) in the NIEHS Office of
Technology Transfer, or the Inventor Dr. Perry Blackshear
([email protected]) for more information.
Inhibitors of Human Apurinic/Apyrimidinic Endonuclease 1 (APE1), an
Anticancer Drug Target
Description of Technology: APE1 is the primary mammalian enzyme
responsible for the removal of abasic (AP sites) in DNA and functions
as part of the base excision DNA repair pathway (BER). BER is
instrumental in the repair of DNA damage caused by DNA alkylating
agents (e.g. many cancer chemotherapeutics). APE1 has been shown to be
overexpressed in cancer cells. It has been postulated that APE1 would
be an attractive target in anti-cancer treatment paradigms; preclinical
and clinical data confirm that APE1 is a valid anticancer drug target.
To date, only one APE1 small molecule inhibitor has progressed to
clinical trials (methoxyamine hydrochloride), and this compound
inhibits a wide range of repair processes, which could result in
undesired side-effects. The NIH inventors now report the discovery of a
novel APE1 small molecule inhibitor, which exhibits potent in vitro
activity, potentiates the cytotoxicity of DNA damaging agents
(alkylators methylmethane sulfonate and Temozolomide), results in the
accumulation of AP sites, and has favorable pharmacokinetic properties.
The inventors plan to carry out further studies in mouse tumor
xenograft models.
Applications: Cancer therapeutics as single agent as well as in
combination therapy.
Development Status: In vivo pharmacokinetics data on lead compounds
available.
Inventors: David J. Maloney, et al. (NHGRI).
Publication: Manuscript submitted.
Patent Status: U.S. Provisional Patent Application No. 61/480,145
filed April 28, 2011 (HHS Reference No. E-094-2011/0-US-01).
Licensing Status: Available for licensing.
Licensing Contact: Betty B. Tong, PhD; 301-594-6565;
[email protected].
Collaborative Research Opportunity: The NIH Center for
Translational Therapeutics, NHGRI is seeking statements of capability
or interest from parties interested in collaborative research to
further develop, evaluate, or commercialize the above technology.
Please contact Lili Portilla, Acting Director of Technology Transfer
and Partnerships, NCTT at [email protected] for more information.
Dated: July 1, 2011.
Richard U. Rodriguez,
Director, Division of Technology Development and Transfer, Office of
Technology Transfer, National Institutes of Health.
[FR Doc. 2011-17227 Filed 7-7-11; 8:45 am]
BILLING CODE 4140-01-P