[Federal Register Volume 80, Number 85 (Monday, May 4, 2015)]
[Notices]
[Pages 25307-25308]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 2015-10275]


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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, HHS.

[[Page 25308]]


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. 209 and 37 CFR part 404 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.

FOR FURTHER INFORMATION CONTACT: 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.

SUPPLEMENTARY INFORMATION: Technology descriptions follow.

Novel Furoquinolinediones as Inhibitors of TDP2 and Their Potential Use 
to Treat Cancer

    Description of Technology: The invention relates to novel 
Furoquinolinediones derivatives and their ability to inhibit the enzyme 
tyrosyl-DNA phosphodiesterase 2 (TDP2), and therefore to serve as anti-
cancer agents. Furthermore, these compounds can be used in combination 
with topoisomerase II (Top2) inhibitors, such as etoposide or 
doxorubicin, to more effectively kill cancer cells in a synergistic 
fashion.
    Pharmaceutical compositions containing these novel 
Furoquinolinediones and methods of treatment comprising administering 
of such compositions are disclosed in the invention.
    Potential Commercial Applications: Furoquinolinediones derivatives 
can potentially be utilized for cancer treatment either as stand alone 
or in combination with other drugs such as Top2 inhibitors.
    Competitive Advantages: Combination therapies based on the 
association of a TDP2 and a Top2 inhibitor because of their synergistic 
effect should allow the decrease of the effective dosage. Their 
therapeutic benefit should be observed at non-toxic concentrations for 
normal cells as it has already been demonstrated for PARP inhibitors in 
BRCA-deficient tumors.
    Development Stage: In vitro data available
    Inventors: Christophe R. Marchand, Likun An, Yves G. Pommier (all 
of NCI)
    Intellectual Property: HHS Reference No. E-275-2014/0--US 
Provisional Application No. 62/100,968 filed January 8, 2015
    Licensing Contact: Kevin Chang, Ph.D.; 301-435-5018; 
[email protected]

Transgenic Mouse Model of Human Open Angle Glaucoma

    Description of Technology: Glaucoma is a group of chronic 
neurodegenerative disorders, which is characterized by progressive loss 
of retinal ganglion cells (RGC) and results in irreversible damage to 
optic nerve and thereby loss of vision. Primary open angle glaucoma 
(POAG) is the most common form of glaucoma; mutations in MYOC gene are 
the most common genetically defined cause of POAG. As such, MYOC 
transgenic mouse models are very useful to study MYOC-associated 
glaucoma and to develop therapies to treat these diseases.
    The NIH inventors generated a new MYOC mouse model carrying a 
mutant human MYOC (Y437H) gene. The Y437H mutation is associated with a 
severe form of glaucoma among the identified MYOC mutations.
    Potential Commercial Applications:
     Research tools
     Drug development for glaucoma
    Competitive Advantages: The new transgenic mouse model carries a 
mutation associated with a severe form of glaucoma in humans.
    Development Stage: Prototype.
    Inventors: Stanislav Tomarev (NEI), Yu Zhou (former NEI), Oleg 
Grinchuk (former NEI).
    Publications:

    1. Zhou Y, et al. Transgenic mice expressing the Tyr437His 
mutant of human myocilin protein develop glaucoma. Invest Ophthalmol 
Vis Sci. 2008 May;49(5):1932-9. [PMID 18436825]
    2. Joe MK, Tomarev SI. Expression of myocilin mutants sensitizes 
cells to oxidative stress-induced apoptosis: implication for 
glaucoma pathogenesis. Am J Pathol. 2010 Jun;176(6):2880-90. [PMID 
20382707]
    3. Chou TH, et al. Transgenic mice expressing mutated Tyr437His 
human myocilin develop progressive loss ofretinal ganglion cell 
electrical responsiveness and axonopathy with normal IOP. Invest 
Ophthalmol Vis Sci. 2014 Aug 14;55(9):5602-9. [PMID 25125600]

    Intellectual Property: HHS Reference No. E-091-2015/0--Research 
Tool. Patent protection is not being pursued for this technology.
    Licensing Contact: Tedd Fenn; 424-297-0336; [email protected].

    Dated: April 27, 2015.
Richard U. Rodriguez,
Acting Director, Office of Technology Transfer, National Institutes of 
Health.
[FR Doc. 2015-10275 Filed 5-1-15; 8:45 am]
 BILLING CODE 4140-01-P