Federal Register / Vol. 77, No. 79 / Tuesday, April 24, 2012 / Notices 24497 

provide an addendum to the fourth 

quarter report to describe estimates used 

in deriving any expenditures reported in 

any category. 

Respondents: TANF Agencies. 

ANNUAL BURDEN ESTIMATES 

Instrument Number of 

respondents 

Number of 

responses per 

respondent 

Average 

burden hours 

per response 

Total burden 

hours 

ACF–196 .......................................................................................................... 51 4 8 1,632 

Estimated Total Annual Burden 

Hours: 1,632. 

Additional Information: Copies of the 

proposed collection may be obtained by 

writing to the Administration for 

Children and Families, Office of 

Planning, Research and Evaluation, 370 

L’Enfant Promenade, SW., Washington, 

DC 20447, Attn: ACF Reports Clearance 

Officer. All requests should be 

identified by the title of the information 

collection. Email address: 

infocollection@acf.hhs.gov. 

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make a decision concerning the 

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and 60 days after publication of this 

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within 30 days of publication. Written 

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Attn: Desk Officer for the 

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Robert Sargis, 

Reports Clearance Officer. 

[FR Doc. 2012–9759 Filed 4–23–12; 8:45 am] 

BILLING CODE 4184–01–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. 

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. 

Small-Molecule Modulators of Lipid 

Storage for Treatment of Obesity, 

Atherosclerosis, Metabolic Syndrome 

and Lipid Storage Diseases 

Description of Technology: Lipid 

droplets are key organelles involved in 

lipid homeostasis. In normal 

physiology, these droplets are formed in 

response to elevated fatty acid levels, 

and are broken down when needed for 

energy production. Imbalances in lipid 

homeostasis trigger compensatory 

alterations in metabolism that can lead 

to diseases such as obesity, 

atherosclerosis, and metabolic 

syndrome. There are also a number of 

inherited lipid storage diseases that 

result in harmful buildup of various 

lipids, such as Gaucher disease, Fabry 

disease, and others. Reducing the 

accumulation of lipid droplets is a 

promising potential strategy for 

treatment of such disorders. 

This technology describes three novel 

structural classes of small-molecule 

compounds that significantly reduce the 

accumulation of lipid droplets. These 

compounds hold promise for the 

treatment of diseases associated with 

aberrant lipid deposition. 

Potential Commercial Applications: 

• Treatment of inherited metabolic 

diseases such as Gaucher disease, Fabry 

disease, and Tay Sachs disease. 

• Treatment of obesity and metabolic 

disease. 

• Treatment of atherosclerosis. 

Competitive Advantages: Modulation 

of lipid droplet accumulation is a novel 

mechanism for treatment of lipid storage 

diseases. 

Development Stage: 

• Early-stage 

• In vitro data available 

Inventors: Matthew Boxer et al. 

(NCATS). 

Intellectual Property: HHS Reference 

No. E–277–2011/0—U.S. Provisional 

Patent Application No. 61/562,894 filed 

22 Nov 2011. 

Licensing Contact: Tara L. Kirby, 

Ph.D.; 301–435–4426; 

tarak@mail.nih.gov. 

A Broadly Neutralizing Human AntiHIV Monoclonal Antibody (10E8) 

Capable of Neutralizing Most HIV–1 

Strains 

Description of Technology: This 

Human Anti-HIV Monoclonal Antibody 

(10E8) has great potential to provide 

passive protection from infection, as a 

therapeutic vaccine, or as a tool for the 

development of vaccine immunogens. 

10E8 is one of the most potent HIVneutralizing antibodies isolated thus far 

and it can potently neutralize up to 98% 

of genetically diverse HIV–1 strains. 

10E8 is specific to the membraneproximal external region (MPER) of the 

HIV envelope protein, GP41. It is 

anticipated that 10E8 could be used in 

combination with another human antiHIV–1 monoclonal antibody to provide 

an antibody response that neutralizes 

nearly all strains of HIV–1. 

Additionally, 10E8 is a useful tool for 

the design of vaccine immunogens that 

can elicit an adaptive immune response 

to produces 10E8 like antibodies. This 

technology also includes monoclonal 

antibodies from the same germ line as 

10E8. 

Potential Commercial Applications: 

• Passive protection to prevent HIV 

infection 

• Passive protection to prevent motherto-infant HIV transmission 

• Topical microbicide to prevent HIV 

infection 

• Gene-based vectors for anti-gp41 

antibody expression 

• Therapeutic for the elimination of 

HIV infected cells that are actively 

producing virus 

Competitive Advantages: 

mstockstill on DSK4VPTVN1PROD with NOTICES

24498 Federal Register / Vol. 77, No. 79 / Tuesday, April 24, 2012 / Notices 

• One of the most potent Human 

broadly-neutralizing anti HIV 

antibodies isolated to date 

• Broad reactivity and high affinity to 

most HIV–1 strains 

• Activity is highly complementary to 

existing broadly neutralizing 

antibodies, such as CD4 binding site 

antibodies 

• Capable of neutralizing all HIV–1 

strains, if used in combination with 

another anti-HIV monoclonal 

antibody 

Development Stage: 

• Pre-clinical 

• In vitro data available 

• In vivo data available (animal) 

Publication: In press. 

Intellectual Property: HHS Reference 

No. E–253–2011/0—US Provisional 

Application No. 61/556,660 filed 07 

Nov 2011. 

Related Technologies: 

• HHS Reference No. E–123–2005/1— 

PCT Application No. PCT/US2006/ 

005613 filed 17 Feb 2006 

• HHS Reference No. E–291–2008/0— 

US Application No. 13/057,414 filed 

03 Feb 2011 

Licensing Contact: Cristina 

Thalhammer-Reyero, Ph.D., MBA; 301– 

435–4507; thalhamc@mail.nih.gov. 

Collaborative Research Opportunity: 

The National Institute of Allergy and 

Infectious Diseases is seeking statements 

of capability or interest from parties 

interested in collaborative research to 

further develop, evaluate or 

commercialize vaccine immunogens 

capable of eliciting a 10E8-like adaptive 

immune response. For collaboration 

opportunities, please contact Bill 

Ronnenberg at 301–451–3522 or 

wronnenberg@niaid.nih.gov. 

Cytochromes P450 CYP2J and CYP2C 

Polyclonal Antibodies and 

Recombinant Proteins 

Description of Technology: The 

National Institutes of Health announces 

polyclonal antibodies against mouse 

cytochrome P450s CYP2J and CYP2C. 

Cytochrome P450s catalyze the 

metabolism of a wide range of 

exogenous compounds, including drugs, 

industrial chemicals, environmental 

pollutants, and carcinogens. The 2C 

family of cytochrome P450 metabolizes 

an extensive number of drugs which 

include tolbutamide, S-Warfarin, 

mephenytoin, diazepam and taxol. 

Many of the P450 enzymes are also 

active in the NADPH-dependent 

oxidation of arachidonic acid to various 

eicosanoids found in several species. 

The 2J family is expressed at high levels 

in the heart and has been shown to 

metabolize both arachidonic acid and 

linoleic acid. The CYP2J and CYP2C 

subfamily members have a wide tissue 

distribution and may be useful as model 

systems for studies of cardiovascular 

disease, drug metabolism and toxicity. 

Recombinant proteins of mouse 

cytochrome P450s CYP2C and CYP2J 

have also been expressed and can be 

used as controls in immunoblotting, as 

well as for metabolism studies. 

Potential Commercial Applications: 

• These antibodies can be used to 

study the expression of the P450s in 

various tissues by 

immunohistochemistry and 

immunoblotting. 

• The recombinant proteins can be 

used as controls in immunoblotting as 

well as for metabolism studies. 

Competitive Advantages: The CYP2J 

and CYP2C subfamily members have a 

wide tissue distribution and may be 

useful as model systems for studies of 

cardiovascular disease, drug metabolism 

and toxicity. 

Development Stage: In vitro data 

available. 

Inventors: Darryl C. Zeldin (NIEHS) et 

al. 

Publications: Manuscripts in 

preparation. 

Intellectual Property: HHS Reference 

No. E–153–2011/0—Research Material. 

Patent protection has not been pursued 

for this technology. 

Licensing Contact: Fatima Sayyid, 

M.H.P.M.; 301–435–4521; 

Fatima.Sayyid@nih.hhs.gov. 

Collaborative Research Opportunity: 

The NIEHS is seeking statements of 

capability or interest from parties 

interested in collaborative research to 

further develop, evaluate or 

commercialize antibodies against mouse 

cytochrome P450s CYP2J and CYP2C. 

For collaboration opportunities, please 

contact Elizabeth M. Denholm, Ph.D. at 

denholme@niehs.nih.gov. 

Monoclonal Antibodies Targeting 

Human DNA Polymerase beta, a DNA 

Repair Enzyme 

Description of Technology: Available 

for licensing are monoclonal antibodies 

targeting human DNA polymerase beta 

(Pol B). Pol B is a constitutively 

expressed ‘‘housekeeping’’ enzyme that 

plays a role in base excision repair 

(BER), a cellular defense mechanism 

that repairs DNA base damage and loss. 

Aberrant Pol B expression is associated 

with genomic instability indicating that 

Pol B is required for DNA maintenance, 

replication and recombination. 

These antibodies can be utilized to 

elucidate BER’s mechanism of action 

and Pol B’s structure and function. 

Moreover, the antibodies can be used to 

detect Pol B in samples with a variety 

of techniques including 

immunoblotting, ELISA, 

immunoprecipitation, and 

immunohistochemistry. 

Potential Commercial Applications: 

• Research tool to elucidate the 

mechanism of base excision repair 

• Research reagents 

Competitive Advantages: Can be 

utilized in a variety of applications to 

study Pol B. 

Development Stage: 

• Early-stage 

• In vitro data available 

Inventors: Samuel Wilson and 

Rajendra Prasad (NIEHS). 

Publications: 

1. Srivastava DK, et al. Phorbol ester 

abrogates up-regulation of DNA 

polymerase beta by DNA-alkylating 

agents in Chinese hamster ovary 

cells. J Biol Chem. 1995 Jul 

7;270(27):16402–8. [PMID 7608211] 

2. Singhal R, et al. DNA polymerase beta 

conducts the gap-filling step in 

uracil-initiated base excision repair 

in a bovine testis nuclear extract. J 

Biol Chem. 1995 Jan 13;270(2):949– 

57. [PMID 7822335] 

3. Prasad R, et al. Specific interaction of 

DNA polymerase beta and DNA 

ligase I in a multiprotein base 

excision repair complex from 

bovine testis. J Biol Chem. 1996 Jul 

5;271(27):16000–7. [PMID 8663274] 

4. Piersen C, et al. Evidence for an imino 

intermediate in the DNA 

polymerase beta deoxyribose 

phosphate excision reaction. J Biol 

Chem. 1996 Jul 26;271(30):17811–5. 

[PMID 8663612] 

5. Sobol R, et al. Regulated overexpression of DNA polymerase beta 

mediates early onset cataract in 

mice. DNA Repair (Amst). 2003 

May 13;2(5):609–22. [PMID 

12713817] 

6. Poltoratsky V, et al. Down-regulation 

of DNA polymerase beta 

accompanies somatic 

hypermutation in human BL2 cell 

lines. DNA Repair (Amst). 2007 Feb 

4;6(2):244–53. [PMID 17127106] 

Intellectual Property: HHS Reference 

No. E–036–2008/0—Research Tool. 

Patent protection is not being pursued 

for this technology. 

Licensing Contact: Jennifer Wong; 

301–435–4633; wongje@mail.nih.gov. 

Collaborative Research Opportunity: 

The NIEHS is seeking statements of 

capability or interest from parties 

interested in collaborative research to 

further develop, evaluate or 

commercialize these monoclonal 

antibodies. For collaboration 

mstockstill on DSK4VPTVN1PROD with NOTICES

Federal Register / Vol. 77, No. 79 / Tuesday, April 24, 2012 / Notices 24499 

opportunities, please contact Elizabeth 

M. Denholm, Ph.D. at 

denholme@niehs.nih.gov. 

Treatment of Acute and Chronic 

Neurological Disorders Using GLP–1, 

Exendin-4 and Analogs 

Description of Technology: Glucagonlike peptide-1 (GLP–1) and related 

peptides, including exendin-4 and 

liraglutide, are incretin mimetics that 

enhance glucose-dependent insulin 

secretion following food ingestion as a 

regulator of glucose homeostasis. 

Exendin-4 and liraglutide are used 

clinically in the safe and effective 

treatment of type 2 diabetes to enhance 

insulin secretion and maintain a 

euglycemic state. These actions are 

primarily mediated at the level of the 

GLP–1 receptor in the pancreas; 

however, these compounds are known 

to enter the brain where the GLP–1 

receptor also is expressed. 

Researchers at the NIH have 

discovered the novel use of GLP–1 and 

exendin-4 analogs in the treatment of 

acute and chronic neurological 

disorders and neurodegenerative 

diseases. Studies conducted in 

extensive cell culture and in mouse 

models using these analogs have 

demonstrated significant neurotrophic 

and neuroprotective actions in models 

of several disorders, including 

Alzheimer’s disease, Parkinson’s 

disease, Huntington’s disease, ALS, 

stroke, head trauma and peripheral 

neuropathy. These studies have now 

been extensively published and 

independently validated by other 

scientific groups. Furthermore, clinical 

studies are ongoing to evaluate the use 

of GLP–1 receptor agonists for the 

treatment of early Alzheimer’s disease, 

Parkinson’s disease and diabetic 

neuropathy by several groups within the 

US and Europe. 

Potential Commercial Applications: 

Therapeutics for: 

• Neurodegenerative diseases— 

Alzheimer’s, Huntington’s, 

Parkinson’s, ALS 

• Stroke 

• Head trauma (traumatic brain injury) 

• Peripheral neuropathies 

Competitive Advantages: 

• Compounds reduce neuronal cell 

death, amyloid deposition and 

neuroinflammation while promoting 

neurogenesis. 

• Compounds in this class have 

already been shown to be safe and 

effective for other indications. 

• Extensive in vitro and animal data 

are available, and clinical studies are 

ongoing. 

• There are extensive publications in 

the literature, both from the inventors 

and independent groups. 

Development Stage: 

• Pre-clinical 

• Clinical 

• In vitro data available 

• In vivo data available (animal) 

• In vivo data available (human) 

Inventors: Nigel Greig, Harold 

Halloway, Maire Doyle, Josephine Egan 

(all of NIA). 

Publications: 

1. Li Y, et al. Exendin-4 ameliorates 

motor neuron degeneration in 

cellular and animal models of 

amyotrophic lateral sclerosis. PLoS 

One. 2012;7(2):e32008. [PMID 

22384126] 

2. Li Y, et al. Enhancing the GLP–1 

receptor signaling pathway leads to 

proliferation and neuroprotection in 

human neuroblastoma cells. J 

Neurochem. 2010 Jun;113(6):1621– 

1631. [PMID 20374430] 

3. Li Y, et al. GLP–1 receptor 

stimulation reduces amyloid-beta 

peptide accumulation and 

cytotoxicity in cellular and animal 

models of Alzheimer’s disease. J 

Alzheimers Dis. 2010;19(4):1205– 

1219. [PMID 20308787] 

4. Li Y, et al. GLP–1 receptor 

stimulation preserves primary 

cortical and dopaminergic neurons 

in cellular and rodent models of 

stroke and Parkinsonism. Proc Natl 

Acad Sci USA. 2009 Jan 

27;106(4):1285–1290. [PMID 

19164583] 

5. Martin B, et al. Exendin-4 improves 

glycemic control, ameliorates brain 

and pancreatic pathologies and 

extends survival in a mouse model 

of Huntington’s disease. Diabetes. 

2009 Feb;58(2):318–328. 

[PMID:18984744] 

6. Perry T, et al. Evidence of GLP–1- 

mediated neuroprotection in an 

animal model of pyridoxineinduced peripheral sensory 

neuropathy. Exp Neurol. 2007 

Feb;203(2):293–301. [PMID 

17125767] 

7. Perry T, Greig NH. Enhancing central 

nervous system endogenous GLP–1 

receptor pathways for intervention 

in Alzheimer’s disease. Curr 

Alzheimers Res. 2005 Jul;2(3):377– 

385. [PMID 15974903] 

8. Greig NH, et al. New therapeutic 

strategies and drug candidates for 

neurodegenerative diseases: p53 

and TNF-alpha inhibitors, and 

GLP–1 receptor agonists. Ann NY 

Acad Sci. 2004 Dec;1035:290–315. 

[PMID 15681814] 

9. Perry TA, Greig NH. A new 

Alzheimer’s disease interventive 

strategy: GLP–1. Curr Drug Targets. 

2004 Aug;5(6):565–571. [PMID 

15270203] 

Listing of additional related 

publications available upon request. 

Intellectual Property: HHS Reference 

No. E–049–2001/0— 

• U.S. Patent 7,576,050 issued 18 Aug 

2009 

• U.S. Patent Application No. 12/ 

317,042 filed 18 Dec 2008 

• Foreign counterparts in Australia, 

Canada, Europe, India, and Japan 

Licensing Contact: Tara L. Kirby, 

Ph.D.; 301–435–4426; 

tarak@mail.nih.gov. 

Collaborative Research Opportunity: 

The National Institute on Aging, Drug 

Design and Development Section, is 

seeking statements of capability or 

interest from parties interested in 

collaborative research to further 

develop, evaluate or commercialize this 

technology. For collaboration 

opportunities, please contact Vio Conley 

at conleyv@mail.nih.gov. 

Dated: April 18, 2012. 

Richard U. Rodriguez, 

Director, Division of Technology Development 

and Transfer, Office of Technology Transfer, 

National Institutes of Health. 

[FR Doc. 2012–9776 Filed 4–23–12; 8:45 am] 

BILLING CODE 4140–01–P 

DEPARTMENT OF HEALTH AND 

HUMAN SERVICES 

National Institutes of Health 

Government-Owned Inventions; 

Availability for Licensing: Mouse 

Models 

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. 

FOR FURTHER INFORMATION CONTACT: 

Licensing information for the 

technologies 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– 

mstockstill on DSK4VPTVN1PROD with NOTICES