[Federal Register Volume 76, Number 131 (Friday, July 8, 2011)]
[Pages 40383-40384]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 2011-17227]



National Institutes of Health

Government-Owned Inventions; Availability for Licensing

AGENCY: Public Health Service, National Institutes of Health, HHS.

ACTION: Notice.


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.


     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 
    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]