63840 Federal Register / Vol. 75, No. 200 / Monday, October 18, 2010 / Notices 

management activities, for both CDC 

and the Agency for Toxic Substances 

and Disease Registry. 

Dated: October 8, 2010. 

Elaine L. Baker, 

Director, Management Analysis and Services 

Office, Centers for Disease Control and 

Prevention. 

[FR Doc. 2010–26114 Filed 10–15–10; 8:45 am] 

BILLING CODE 4163–18–P 

DEPARTMENT OF HEALTH AND 

HUMAN SERVICES 

National Institutes of Health 

Government-Owned Inventions; 

Availability for Licensing 

AGENCY: National Institutes of Health, 

Public Health Service, 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. 

Prevention and Treatment of Herpes 

Virus Infection by Inhibition of the 

JMJD2 Family of Histone Demethylases 

Description of Invention: Investigators 

at the NIH have discovered a potential 

means for preventing or treating a 

herpes virus infection by inhibiting the 

activity of the host cell’s histone 

demethylases. When herpesviruses 

enter a cell, they are inactivated by 

cellular defense mechanisms that wrap 

the viral genome in repressive 

chromatin structures. In order for viral 

replication to progress, the host’s own 

histone demethylases are recruited to 

the viral genome to reverse this 

repression. In a preceding invention, the 

laboratory disclosed that viral 

replication and reactivation can be 

significantly reduced through inhibition 

of the histone demethylase LSD1 using 

Mono-Amino Oxidase Inhibitors 

(MAOIs); drugs that are in clinical use. 

The current invention further discloses 

that inhibition of a second set of histone 

demethylases (JMJD2 family) using a 

specific JMJD2 inhibitor, 

dimethyloxaloylglycine (DMOG), also 

results in significant repression of 

herpes viral replication. 

Either alone or in combination, small 

molecule inhibition of LSD1 and the 

JMJD2 family present novel approaches 

for preventing herpes virus infection 

and halting viral reactivation that can 

lead to a disease that ranges from mild 

core sores to herpesvirus keratitis and 

life-threatening encephalitis. 

Additionally, chromatin-mediated 

repression of viral genomes and the 

requirement to de-repress these 

genomes for productive infection 

appears to be general to herpesviruses. 

Therefore, this treatment could also be 

applicable to chicken pox, shingles, 

CMV disease, mononucleosis, and 

Kaposi’s sarcoma. 

Applications: Prevention or treatment 

of infection by herpes simplex virus and 

other diseases caused by herpesviruses 

(i.e. Epstein-Barr virus, 

cytomegalovirus, varicella zoster, and 

Kaposi’s sarcoma-associated 

herpesvirus). 

Advantage: Inhibition of histone 

demethylases provides an alternative 

pathway for repressing herpes virus 

infection as compared to purine analog 

antivirals. While purine analogs are the 

most widely prescribed treatment for 

herpes infection, drug resistance is 

prevalent. Additionally, inhibition of 

histone demethylases results in no 

expression of viral gene products; in 

contrast to DNA replication inhibitors. 

Development Status: 

• Early-stage development 

• Pre-clinical data available for mice 

• Further pre-clinical and clinical 

development is needed 

Market: 

• Genital herpes can result from 

infection with either HSV type 2 or type 

1, mainly by HSV type 2 in the U.S., 

which typically causes more recurrent 

and severe manifestations of the disease. 

• According to the Centers for Disease 

Control and Prevention, nationwide, 

16.2%, or about one out of six, people 

14 to 49 years of age have genital HSV– 

2 infection. 

• HSV keratitis is the most frequent 

cause of corneal blindness in the United 

States. 

Inventors: Thomas Kristie et al. 

(NIAID) 

Publications: None related to this 

invention available at this time. 

Patent Status: U.S. Provisional 

Application No. 61/366,563 filed 22 Jul 

2010 (HHS Reference No. E–184–2010/ 

0–US–01). 

Related Technologies: ‘‘Use of MonoAmine Oxidase Inhibitors to Prevent 

Herpes Virus Infections and 

Reactivation from Latency’’—HHS 

Reference No. E–275–2008/2–PCT–02. 

Licensing Status: Available for 

licensing. 

Licensing Contacts: 

• Eric W. Odom, PhD; 301–435–5009; 

odome@mail.nih.gov. 

• Susan O. Ano, PhD; 301–435–5515; 

anos@mail.nih.gov. 

Collaborative Research Opportunity: 

The NIAID Laboratory of Viral Diseases 

is seeking statements of capability or 

interest from parties interested in 

collaborative research to further 

develop, evaluate, or commercialize 

prevention and treatment of viral 

diseases. Please contact Thomas Kristie, 

PhD at 301.496.3854 or 

tkristie@niaid.nih.gov for more 

information. 

Treatment of Inflammatory Bowel 

Disease (IBD) Using IL–13 Modulators 

and Inhibitors 

Description of Invention: Ulcerative 

colitis (UC), a chronic inflammatory 

disease of the colorectum, affects 

approximately 400,000 people in the 

United States. The cause of UC is not 

known, although an abnormal 

immunological response to bacterial 

antigens in the gut microflora is thought 

to be involved. Available for licensing 

are broad claims covering (1) treatments 

preventing the inflammatory response of 

colitis by modulating IL–13 and Natural 

Killer T cell (NKT) activity and (2) 

methods for screening for therapeutic 

compounds effective for colitis. NIH 

scientists and their collaborators have 

used a mouse model of experimental 

colitis (oxazolone colitis, OC) to show 

that IL–13, a Th2 cytokine, is a 

significant pathologic factor in OC and 

that neutralizing IL–13 in these animals 

effectively prevents colitis. 

Inflammation in this mouse model has 

also been shown to be effectively 

blocked by neutralizing IL–13 or by 

inhibiting the activation of NK–T cells 

through CD1. 

Oxazolone colitis (OC) is a colitis 

induced by intrarectal administration of 

a relatively low dose of the haptenating 

agent oxazolone subsequent to skin 

sensitization with oxazolone. A highly 

reproducible and chronic colonic 

inflammation is obtained that is 

histologically similar to human 

ulcerative colitis. Studies show that 

NKT cells, rather than conventional 

CD4+T cells, mediate oxazolone colitis, 

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Federal Register / Vol. 75, No. 200 / Monday, October 18, 2010 / Notices 63841 

are the source of IL–13, and are 

activated by CD1 expressing intestinal 

epithelial cells. Tissue removed from 

UC patients were also shown to contain 

increased numbers of nonclassical NKT 

cells that produce markedly increased 

amounts of IL–13. In addition, these 

NKT cells are cytotoxic for epithelial 

cells, supporting the concept that 

epithelial damage is a key factor in UC. 

Applications: Development of IL–13 

and CD1 based therapeutics to treat or 

prevent ulcerative colitis. 

Development Status: Small animal 

model studies. 

Inventors: Warren Strober, Ivan Fuss, 

Frank Heller, Richard Blumberg 

(NIAID). 

Related Publications: 

1. IJ Fuss et al. Nonclassical CD1drestricted NK T cells that produce IL–13 

characterize an atypical Th2 response in 

ulcerative colitis. J Clin Invest. 2004 

May;113(10):1490–1497. [PubMed: 

15146247]. 

2. F Heller et al. Oxazolone colitis, a 

Th2 colitis model resembling ulcerative 

colitis, is mediated by IL–13-producing 

NK–T cells. Immunity 2002 

Nov;17(5):629–638. [PubMed: 

12433369]. 

Patent Status: 

• U.S. Patent No. 7,666,411 issued 23 

Feb 2010 (HHS Reference No. E–131– 

2002/0–US–02). 

• U.S. Patent Application No. 12/ 

709,029 filed 19 Feb 2010 (HHS 

Reference No. E–131–2002/0–US–10). 

• International patent/patent 

application filings. 

Related Technologies: Related IBD 

technologies also available for licensing 

include IL–13 mutant and chimeric 

molecules (HHS Reference No. E–003– 

2005/0) and NF-kappa B decoy 

oligonucleotides (HHS Reference No. 

E–108–2005/0). 

Licensing Status: Available for 

licensing. 

Licensing Contact: Sury Vepa, PhD, 

J.D.; 301–435–5020; 

vepas@mail.nih.gov. 

Dated: October 12, 2010. 

Richard U. Rodriguez, 

Director, Division of Technology Development 

and Transfer, Office of Technology Transfer, 

National Institutes of Health. 

[FR Doc. 2010–26153 Filed 10–15–10; 8:45 am] 

BILLING CODE 4140–01–P 

DEPARTMENT OF HEALTH AND 

HUMAN SERVICES 

National Institutes of Health 

Government-Owned Inventions; 

Availability for Licensing 

AGENCY: National Institutes of Health, 

Public Health Service, 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 Anti-Mouse CXCL9 (Mig) 

Monoclonal Antibodies 

Description of Invention: This 

technology describes monoclonal 

antibodies against mouse chemokine 

(C–X–C motif) ligand 9 (CXCL9), also 

known as Monokine induced by gamma 

interferon (Mig). CXCL9 is a secreted 

protein that functions to attract white 

cells and increased expression of CXCL9 

has been linked to several diseases. The 

inventors at the NIH generated over 100 

anti-mouse CXCL9 antibodies from a 

CLXL9/Mig knockout mouse and further 

characterized several antibodies to show 

neutralization of CXCL9. As such, these 

antibodies could be used to measure 

concentrations of mouse CLXL9 in 

laboratory samples and block the 

activity of CXCL9 in injected mice. 

These antibodies are suitable for ELISA 

and Western blot. The antibodies have 

not been tested in flow cytometry or 

immunohistochemistry, but may also be 

useful for these applications. 

Applications 

• ELISA assays for detection and 

measurement of CXCL9. 

• Neutralization of CXCL9 activity in 

mouse models and in vitro assays to 

study the role of CXCL9 in immune 

response and disease. 

Advantages: Can be used in mice 

without eliciting endogenous antibodies 

reacting against the injected antiCXCL9. 

Development Status: The technology 

is currently in the pre-clinical stage of 

development. 

Inventors: Joshua M. Farber and 

Hongwei H. Zhang (NIAID). 

Patent Status: HHS Reference No. 

E–198–2009/0—Research Tool. Patent 

protection is not being pursued for this 

technology. 

Licensing Status 

Available for licensing. 

Licensing Contact: Whitney A. 

Hastings; 301–451–7337; 

hastingw@mail.nih.gov. 

Signal-to-Noise Enhancement in 

Imaging Applications Using a TimeSeries of Images 

Description of Invention: The 

invention offered for licensing relates to 

the field of imaging and specifically to 

the field of medical imaging. The 

apparatus and method of the invention 

provide for noise reduction in imaging 

applications that use a time-series of 

images. In one embodiment of the 

invention, a time-series of images is 

acquired using a same imaging protocol 

of the same subject area, but the images 

are spaced in time by one or more time 

intervals (e.g., 1, 2, 3 * * * seconds 

apart). A sub-region is projected across 

all of the images to perform a localized 

analysis (corresponding X–Y pixels or 

X–Y–Z voxels are analyzed across all 

images) that identifies temporal 

components within each sub-region. 

Subsequently, within the sub-regions, 

only those temporal components are 

selected whose amplitude is above a 

predetermined amplitude threshold. 

The images are then reconstructed using 

the sub-regions with reduced 

components. A maximal-intensityprojection (MIP) is applied in the 

temporal domain (tMIP) in order to 

obtain a single image with reduced 

noise (this can be done either at the subregion level or at the reconstructed 

image level). The technology can be 

applied to a broad spectrum of medical 

imaging technologies such as MRI, XRay, CT and others. 

Applications: Medical imaging and 

diagnostics applied to MRI, X-Ray, CT 

scans or other imaging modalities 

including PET, SPECT, ultrasound or 

optical. 

Advantages: Enhancing signal-tonoise of medical imaging techniques. 

Development Status 

• Proof of concept has been 

demonstrated. Data is available. 

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