31446 Federal Register / Vol. 74, No. 125 / Wednesday, July 1, 2009 / Notices 

Type of respondents Survey instrument Number of 

respondents 

Frequency of 

responses 

Average time 

per response 

(minutes/hour) 

Annual burden 

hours 

Smoking Cessation ‘‘Quitline’’ Clients 1,2

Reactive Service Clients ............................ Smoking Cessation ‘‘Intake’’ 

Questions 

4,641 1 5/60 386.75 

Demographic Questions 1,300 1 2/60 43.33 

Proactive Callback Service Clients 3 .......... Follow-Up 928 4 1/60 61.87 

LiveHelp Clients 4

Demographic questions 7,014 1 2/60 233.80 

Total .................................................... .................................................. 97,883 ........................ ........................ 2524.00 

1Approximately 36% of telephone and quitline clients will be sampled for the demographic questions, and 100% of telephone clients will be 

sampled for the customer service questions. Estimates based on 77.5% response rate. 2 100% of smoking cessation clients will be asked the smoking intake questions. Estimates for quitline callers answering demographic questions are based on 77.8% response rate. 3 100% of smoking cessation clients participating in the proactive callback service (about 20% of all smoking callers) will be asked the smoking 

follow-up question (at up to 4 callbacks). 4Approximately 50% of LiveHelp clients will be sampled for the demographic questions. 

The annualized cost to the 

respondents is estimated at $48,752. 

There are no Capital Costs, Operating 

Costs, and/or Maintenance Costs to 

report. 

Request for Comments: Written 

comments and/or suggestions from the 

public and affected agencies should 

address one or more of the following 

points: (1) Evaluate whether the 

proposed collection of information is 

necessary for the proper performance of 

the function of the agency, including 

whether the information will have 

practical utility; (2) Evaluate the 

accuracy of the agency’s estimate of the 

burden of the proposed collection of 

information, including the validity of 

the methodology and assumptions used; 

(3) Enhance the quality, utility, and 

clarity of the information to be 

collected; and (4) Minimize the burden 

of the collection of information on those 

who are to respond, including the use 

of appropriate automated, electronic, 

mechanical, or other technological 

collection techniques or other forms of 

information technology. 

Direct Comments to OMB: Written 

comments and/or suggestions regarding 

the item(s) contained in this notice, 

especially regarding the estimated 

public burden and associated response 

time, should be directed to the 

Attention: NIH Desk Officer, Office of 

Management and Budget, at 

OIRA_submission@omb.eop.gov or by 

fax to 202–395–6974. To request more 

information on the proposed project or 

to obtain a copy of the data collection 

plans and instruments, contact Mary 

Anne Bright, Office of Public 

Information and Resource Management, 

Office of Communications and 

Education, National Cancer Institute, 

6116 Executive Blvd., Room 3049, MSC 

8322, Bethesda, MD 20892–8322 or call 

the non-toll-free number 301–594–9048 

or e-mail your request, including your 

address, to: brightma@mail.nih.gov. 

Comments Due Date: Comments 

regarding this information collection are 

best assured of having their full effect if 

received within 30 days of the date of 

this publication. 

Dated: June 23, 2009. 

Vivian Horovitch-Kelley, 

NCI Project Clearance Liaison, National 

Institutes of Health. 

[FR Doc. E9–15583 Filed 6–30–09; 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. 

New Inhibitors of Polo-like Kinase 1 

(PLK1) as Anti-Cancer Agents 

Description of Technology: Tumor 

formation is the result of uncontrolled 

cellular growth and invasion. Polo-like 

kinase 1 (PLK1) is a regulator of cell 

growth whose overexpression has been 

associated with several types of cancer 

(e.g., breast cancer, prostate cancer, 

ovarian cancer, non-small cell lung 

carcinoma). It has been shown that 

inhibition of PLK1 causes cell death 

(apoptosis) in tumor cells but not 

normal cells. This suggested that 

inhibiting PLK1 could be an effective 

treatment for cancer patients without 

causing unwanted side-effects. 

PLK1 contains a unique protein 

domain known as the polo box domain 

(PBD), which is essential for its 

function. One strategy for inhibiting 

PLK1 involves preventing the PBD 

domain from interacting with PLK1 

substrates. A synthetic peptide with the 

ability to selectively bind to the PBD 

was recently identified. Using this 

peptide as a platform, NIH inventors 

have designed peptide mimetics that 

interact with the PBD with greater 

affinity than the wild-type peptide. By 

inhibiting PLK1 and selectively 

inducing apoptosis in cancer cells, these 

mimetics could serve as potential anticancer therapies. 

Applications: 

• New anti-cancer therapies that 

specifically target PLK1 

• Platform for the development of 

further improved PLK1 inhibitors 

Advantages: 

Federal Register / Vol. 74, No. 125 / Wednesday, July 1, 2009 / Notices 31447 

• The peptide mimetics have an 

increased affinity for the polo box 

domain of PLK1 compared to the wildtype peptide, making them superior as 

inhibitors of PLK1. 

• The peptide mimetics provide 

greater metabolic stability and potential 

effectiveness over synthetic peptides 

prepared using coded amino acids. 

• Inhibiting PLK1 provides an 

opportunity for successful treatment of 

cancer with fewer side effects because 

only tumor cells are killed. 

Development Status: Preclinical stage 

of development 

Inventors: Terrence R. Burke Jr. et al. 

(NCI) 

Patent Status: US Provisional 

Application No. 61/178,593 (HHS 

Reference No. E–181–2009/0–US–01) 

For more information, see: 

1. F Liu et al. SAR by oximecontaining peptide libraries: application 

to Tsg101 ligand optimization. 

Chembiochem. 2008 Aug 11;9(12):2000– 

2004. 

2. F Liu et al. Protected 

aminooxyprolines for expedited library 

synthesis: Application to Tsg101- 

directed proline-oxime containing 

peptides. Bioorg Med Chem Lett. 2008 

Feb 1;18(3):1096–1101. 

3. PCT Application WO 2004/046317, 

‘‘Crystal structure of human Polo-like 

kinase Plk1, Polo Box domain-binding 

phosphopeptide core sequences, and 

their therapeutic uses for cancer.’’ 

Licensing Status: Available for 

licensing. 

Licensing Contact: David A. 

Lambertson, PhD; 301–435–4632; 

lambertsond@mail.nih.gov. 

Increasing the Effectiveness of Cancer 

Treatment: T Cell Receptors Designed 

To Release Interleukin-12 Specifically 

at Cancer Sites 

Description of Technology: Many 

conventional chemotherapy drugs 

currently utilized to treat cancer also 

yield harsh side effects in patients. In 

addition, many patients do not respond 

to generalized chemotherapy and 

radiation treatments for cancer. There is 

an urgent need to develop new 

therapeutic strategies combining fewer 

side-effects and more specific antitumor activity in individual patients. 

Adoptive immunotherapy is a 

promising new approach to cancer 

treatment that engineers an individual’s 

innate and adaptive immune system to 

fight against specific diseases, including 

cancer. 

T cell receptors (TCRs) are proteins 

that recognize antigens in the context of 

infected or transformed cells and 

activate T cells to mediate an immune 

response and destroy abnormal cells. 

TCRs consist of two domains, one 

variable domain that recognizes the 

antigen and one constant region that 

helps the TCR anchor to the membrane 

and transmit recognition signals by 

interacting with other proteins. When a 

TCR is stimulated by an antigen, such 

as a tumor antigen, some signaling 

pathways activated in the cell lead to 

the production of cytokines, which 

mediate the immune response. 

Scientists at the National Institutes of 

Health (NIH) have developed T cells 

genetically engineered to express the 

human interleukin 12 (IL–12) cytokine 

only in the tumor environment. 

Specifically, these T cells have been 

designed to express a human IL–12 gene 

under the control of the nuclear factor 

of activated T cells (NFAT) promoter. 

When the TCR on these T cells 

recognizes a tumor antigen, IL–12 

expression is induced through 

activation of the NFAT promoter. Thus, 

IL–12 is only released at the cancer site 

and only after the activation of the T 

cell. This technology makes it possible 

to control the expression of IL–12 to 

enhance T cell cytolytic activity while 

also reducing or eliminating the IL–12 

toxicity observed with other IL–12 

related therapies. Infusing these IL–12 

expressing T cells into patients via 

adoptive immunotherapy could prove to 

be powerful new tools for attacking 

tumors. 

Applications: 

• Immunotherapeutics to treat and/or 

prevent the recurrence of a variety of 

human cancers by adoptively 

transferring the gene-modified T cells 

into patients. 

• A drug component of a combination 

immunotherapy regimen aimed at 

targeting the specific tumor-associated 

antigens expressed by cancer cells 

within individual patients. 

Advantages: The combination of 

enhanced T cell activity with reduced 

IL–12 toxicity: IL–12 has shown 

remarkable properties as an anti-tumor 

agent, but its clinical development has 

been hindered by its toxicity. This 

current technology delivers IL–12 only 

when and where it is needed—at the 

tumor site. 

Development Status: Clinical trials 

utilizing this technology are currently in 

the planning stage. 

Market: Cancer continues to be a 

medical and financial burden on US 

public health. According to US 

estimates, cancer is the second leading 

cause of death with over 565,000 deaths 

reported in 2008 and almost 1.5 million 

new cases were reported (excluding 

some skin cancers) in 2008. In 2007, the 

NIH estimated that the overall cost of 

cancer was $219.2 billion dollars and 

$89 billion went to direct medical costs. 

Despite our increasing knowledge of 

oncology and cancer treatment methods, 

the fight against cancer will continue to 

benefit from the development of new 

therapeutics aimed at treating 

individual patients. 

Inventors: Richard A. Morgan et al. 

(NCI) 

Publications: 

1. L Zhang et al. Improving adoptive 

T cell therapy using NFAT driven 

human single chain IL–12 expression 

vector. 2009 American Society of Gene 

Therapy, abstract submitted. 

2. B Heemskerk et al. Adoptive cell 

therapy for patients with melanoma, 

using tumor-infiltrating lymphocytes 

genetically engineered to secrete 

interleukin-2. Hum Gene Ther. 2008 

May;19(5):496–510. 

3. RA Morgan et al. Cancer regression 

in patients after transfer of genetically 

engineered lymphocytes. Science 2006 

Oct 6;314(5796):126–129. 

Patent Status: U.S. Provisional 

Application No. 61/174,046 filed 30 Apr 

2009 (HHS Reference No. E–170–2009/ 

0–US–01) 

Licensing Status: Available for 

licensing. 

Licensing Contact: Samuel E. Bish, 

Ph.D.; 301–435–5282; bishse@mail. 

nih.gov. 

Collaborative Research Opportunity: 

The National Cancer Institute, Surgery 

Branch, is seeking statements of 

capability or interest from parties 

interested in collaborative research to 

further develop, evaluate, or 

commercialize adoptive 

immunotherapies or the development of 

cancer therapeutics based on the use of 

T cell receptors. Please contact John D. 

Hewes, PhD at 301–435–3121 or 

hewesj@mail.nih.gov for more 

information. 

A Novel System for Producing 

Infectious Hepatitis C Virus (HCV) 

Virions and Development of a Novel 

Reporter System for Studying HCV 

Entry 

Description of Technology: HCV has 

infected an estimated 3% of the world 

population in whom viral infection 

persists for more than two third of the 

cases, often resulting in life-threatening 

complications. The standard of care 

(pegylated interferon alpha-2 plus 

ribavirin) is efficient in only 50% of 

treated patients, costly and has 

numerous side effects. In addition, viral 

resistance to newly developed drugs— 

targeting viral protease or RNA 

polymerase—has been described, but no 

vaccine is yet available. The difficulty 

in developing HCV vaccines is largely 

due to the broad sequence-diversity 

31448 Federal Register / Vol. 74, No. 125 / Wednesday, July 1, 2009 / Notices 

displayed by HCV, the frequent 

occurrence of viral mutations within 

immunogenic epitopes in vivo, and the 

lack of proper standard/definition for 

viral neutralization. 

One alternative strategy in HCVvaccine or drug development comprises 

measuring viral entry, the first step in 

viral infection. Such measurements are 

limited by the available screening 

systems, in that, HCV pseudo-typed 

retroviral particles have a different 

envelope conformation and contain 

foreign components that are likely to 

interfere with the measured HCV entry. 

Moreover, HCV lab strain requires 

intensive replication for its in vitro 

production, resulting in numerous 

mutations that impede development of 

convenient screening tools. 

The inventors have developed a 

system for generating infectious HCV 

particles and HCV-like particles (HCV– 

LP) suitable for a qualitative single-cycle 

entry assay, completely independent of 

HCV replication. To adapt this system 

as a single assay to study HCV–LP entry, 

HCV non-structural genes were replaced 

with a heterologous gene that upon 

viral-entry triggers firefly luciferase and 

EGFP expressions in target as well as 

non-permissive cells. The pretreatment 

of HCV-replication permissive HuH–7.5 

cells with siRNA targeting HCV 

candidate receptors inhibited viral 

entry. These new systems enable 

production of authentic HCV infectious 

particles as well as HCV–LPs suitable 

for single-cycle entry assays adaptable 

to high throughput screening. 

Applications: 

• Screening a library expressed in 

non-permissive cells for identifying new 

HCV candidate receptor(s) or entry 

molecule(s). 

• Testing drugs or compounds 

inhibiting HCV particle entry or viral 

genome uncoating, or neutralizing 

antibodies in target cells. 

• Testing drugs or compounds that 

inhibit virus assembly, maturation and/ 

or egress, or genome packaging, in 

producer cells. 

• Incorporating a ‘tag’ in the genome 

of various HCV genotypes to more 

conveniently study virus spreading and 

dissemination in an organ, tissue and/or 

small animal model. 

• Enhancing immune response in 

patients: one way to trigger high level 

anti-HCV immunity is by isolating 

antigen-presenting cells from patients 

and incubating them with HCV particles 

produced with this system using 

replication-defective viral genome (with 

or without an immunogenic tag and/or 

in combination with other viral 

epitopes) and eventually re-inject their 

primed cells to the patients. 

Advantages: 

• These systems do not use pseudotyped HCV particles, i.e. no foreign 

proteins present in the virus particles. 

• Particle production in the 

producing cells is independent of HCV 

RNA replication, hence avoids the 

occurrence of adaptive mutations that 

could be detrimental for virus particle’s 

infectivity or could alter tags or 

nucleotide sequences incorporated in 

the viral genome. 

• These systems are not specifically 

dedicated to HCV of a particular 

genotype, i.e. they can be used to 

generate HCV particles of various 

genotypes without requiring the use of 

chimeras. 

Development Status: 

• Proof of concept. 

• Preliminary tools and techniques 

for screening strategies. 

Inventors: Bertrand Saunier, Miriam 

Triyatni, Edward A. Berger (all NIAID) 

Patent Status: U.S. Provisional 

Application No. 61/195,088 filed 03 Oct 

2008 (HHS Reference No. E–005–2009/ 

0–US–01) 

Licensing Status: Available for 

licensing. 

Licensing Contact: RC Tang JD, LLM; 

301–435–5031; tangrc@mail.nih.gov. 

Collaborative Research Opportunity: 

The NIAID OTD is seeking statements of 

capability or interest from parties 

interested in collaborative research to 

further develop, evaluate, or 

commercialize a novel system for 

producing infectious HCV virions and 

developing a reporter system for 

studying HCV entry. Please contact 

Michael Piziali at 301–496–2644 for 

more information. 

Recombinant Virus-Like Particle (VLP) 

and DNA Vaccines for Chikungunya 

Virus (CHIKV) and Other Alphaviruses 

Description of Technology: Available 

for licensing and commercial 

development are compositions and 

methods of use as vaccines of virus-like 

particles (VLPs) expressing one or more 

Alphavirus capsid and envelope 

proteins, and in particular Chikungunya 

virus (CHIKV) core and envelope 

proteins. The invention also describes 

DNA, viral or other gene-based vector 

and VLP vaccines, methods of making 

and methods of their use in inducing 

immunity, for example to CHIKV 

infection. 

Alphaviruses are RNA-containing 

viruses that cause a wide variety of 

mosquito-transmitted diseases, 

including equine encephalitis. CHIKV, 

an Alphavirus in the family 

Togaviridae, was first isolated in 

Tanzania in 1952 and is transmitted to 

humans by mosquitoes. The disease 

caused by CHIKV resembles infection by 

dengue virus, characterized by rash, 

high fever, and severe, sometimes 

persistent arthritis. By 2007, an 

estimated 1.4–6.5 million people in 

India, Southeast Asia, Africa and 

Europe had been infected. Vaccines or 

anti-viral therapies against CHIKV are 

not available, raising concerns about its 

continued evolution and spread in 

humans. There has been limited success 

to date in developing a safe and 

effective CHIKV vaccine. A live CHIKV 

vaccine candidate caused transient 

arthralagia in volunteers. Other efforts 

to develop a CHIKV vaccine include a 

live attenuated vaccine, a formalinkilled vaccine, a Venezuelan equine 

encephalitis/CHIKV chimeric live 

attenuated vaccine and a consensusbased DNA vaccine, but development of 

a safe and effective CHIKV vaccine will 

require additional evaluation in 

humans. 

This invention provides CHIKV 

vaccines based on plasmid expression 

vectors encoding structural proteins of 

the virus, which gave rise to VLPs in 

transfected cells and also served as DNA 

vaccines. The VLPs consisted of the 

core, E1 and E2 proteins and were 

similar in buoyant density and 

morphology to replication-competent 

virus. To evaluate the potency and 

specificity of neutralizing antibodies, 

pseudotyped lentiviral vectors bearing 

the CHIKV glycoproteins E1/E2 were 

developed that showed pH-dependent 

entry and antibody inhibition similar to 

CHIKV. Mice were immunized with 

VLPs (West African strain, 37997) or 

with DNA vaccines encoding viral gene 

products from 37997 as well as the 

latest outbreak strain, OPY–1. 

Immunization with VLPs elicited high 

titer neutralizing antibodies against 

homologous and heterologous strain 

envelope at >100 fold higher titers than 

DNA vaccines. These vaccines also 

induced CD4 and CD8 T-cell responses 

by analysis with intracellular cytokine 

staining (ICS). These VLP vaccines are 

likely to confer protection against 

emerging CHIKV outbreaks and 

represent a strategy that could be 

applied to other pathogenic viruses to 

prevent their infection and spread. 

Applications: 

• Development of vaccines against 

CHIKV 

• Development of vaccines against 

other Alphavirus 

Advantages: 

• Immunization of mice with VLPs 

plus adjuvant results in neutralizing 

antibodies against both homologous and 

heterologous strains with titers at least 

two orders of magnitude greater than 

immunization with a DNA vaccine. 

Federal Register / Vol. 74, No. 125 / Wednesday, July 1, 2009 / Notices 31449 

• VLPs induce innate immunity 

responses as well as CD8 T-cell 

responses. 

• VLPs closely resemble mature 

virions but they do not contain viral 

genomic material. Therefore, VLPs are 

non-replicative in nature, which make 

them safe for administration in the form 

of immunogenic compositions in 

vaccines. 

Development Status: This technology 

is in the pre-clinical stage of 

development. 

Inventors: Gary J. Nabel and Wataru 

Akahata (NIAID) 

Patent Status: U.S. Provisional 

Application No. 61/201,118 filed 05 Dec 

2008, entitled ‘‘Virus Like Particle 

Compositions and Methods of Use’’ 

(HHS Reference No. E–004–2009/0–US– 

01) 

Licensing Status: Available for 

licensing. 

Licensing Contact: Cristina 

Thalhammer-Reyero, PhD, MBA; 301– 

435–4507; thalhamc@mail.nih.gov. 

Inflammatory Genes and MicroRNA–21 

as Biomarkers for Colon Cancer 

Prognosis 

Description of Technology: Colon 

adenocarcinoma is the leading cause of 

cancer mortality world-wide and 

accounts for approximately 50,000 

deaths annually in the United States. 

Adjuvant therapies improve survival for 

stage III colon cancer patients; however, 

it remains controversial if stage II 

patients should be given these therapies. 

Some stage II patients will benefit from 

therapy (such as patients with 

undetectable micro-metastases where 

surgery will not be curative); but 

therapy for others will harm quality of 

life with little therapeutic benefit (such 

as patients where surgery removed all 

cancerous tissue and therefore do not 

need additional therapy). Thus, there is 

a need for biomarkers capable of 

accurately identifying high risk, stage II 

patients that are suitable for therapeutic 

intervention. 

The investigators have identified an 

inflammatory gene and microRNA 

biomarker portfolio that can predict 

aggressive colon cancer, colon cancer 

patient survival, and patients that are 

candidates for adjuvant therapy. These 

biomarkers provide clinicians with a 

powerful tool to diagnose colon cancer 

patients and chose effective treatment 

methods. 

Applications: 

• Method to predict aggressive form 

of colon cancer, especially in stage II 

cancer patients 

• Method to determine appropriate 

colon cancer patients for adjuvant 

therapy 

• Diagnostic arrays 

Advantages: 

• Rapid, easy to use arrays to 

accurately predict colon cancer and 

patients suitable for adjuvant therapy 

• Method to stratify colon cancer 

patients for adjuvant therapy to 

minimize negative side effects 

• Method to identify stage II patients 

that are likely to have undetectable 

micro-metastases 

Development Status: The technology 

is currently in the pre-clinical stage of 

development. 

Market: 

• Global cancer market is worth more 

than eight percent of total global 

pharmaceutical sales 

• Cancer industry is predicted to 

expand to $85.3 billion by 2010 

Inventors: Curtis C. Harris and Aaron 

J. Schetter (NCI) 

Relevant Publication: AJ Schetter et 

al. MicroRNA expression profiles 

associated with prognosis and 

therapeutic outcome in colon 

adenocarcinoma. JAMA. 2008 Jan 

30;299(4):425–436. 

Patent Status: U.S. Provisional 

Application No. 61/194,340 filed 25 Sep 

2008 (HHS Reference No. E–314–2008/ 

0–US–01) 

Licensing Status: Available for 

licensing. 

Licensing Contact: Jennifer Wong; 

301–435–4633; wongje@mail.nih.gov. 

Collaborative Research Opportunity: 

The NCI Laboratory of Human 

Carcinogenesis is seeking statements of 

capability or interest from parties 

interested in collaborative research to 

further develop, evaluate, or 

commercialize cancer biomarkers and 

therapeutic targets. Please contact 

Curtis_Harris@nih.gov for more 

information. 

Differentiation of Human Embryonic 

Stem Cells Into Dopaminergic Nerve 

Cells 

Description of Technology: The 

invention described here is a novel 

method of differentiating human 

embryonic stem cells (hESCs) into 

dopaminergic nerve cells, which is 

preferable to the currently available 

dopaminergic differentiation 

techniques. 

This invention potentially provides a 

source of sufficient dopaminergic cells 

not only for the clinical transplantation 

of dopaminergic tissue but also for in 

vitro studies of human cells useful for 

pharmaceutical screens related to 

neurodegenerative disorders and 

substance abuse. 

Neurodegenerative disorders 

encompass a range of debilitating 

conditions including Parkinson’s 

disease, Alzheimer’s disease, and 

Huntington’s disease. The primary 

cause of cognitive dysfunction for these 

three disorders has been directly linked 

to neuron degeneration, usually in 

specific areas of the brain. 

Transplantation of fetal dopaminergic 

neurons in affected areas of the brain in 

late stage Parkinson’s disease has 

demonstrated clinical utility in human 

patients. However, fetal transplantation 

therapy generally requires human tissue 

from at least 3–5 embryos to obtain a 

clinically reliable improvement in the 

patient, thus demonstrating a need for a 

larger and more reliable source of 

dopaminergic cells. HESCs are a 

promising alternative source of cells 

because they can grow in culture 

indefinitely and have the ability to 

differentiate into a variety of cell types. 

One of the most efficient methods for 

conversion of hESCs to dopaminergic 

neurons requires the presence of mouse 

stromal cells which have an undefined 

dopaminergic inducing activity. 

However, the major disadvantage of this 

method is the exposure of hESC to 

mouse cells, which hinders any 

downstream clinical application due to 

possible transfer of animal cells and 

pathogens. This invention has unveiled 

the molecular nature of the activity of 

the mouse cells and established an 

efficient alternative approach for 

dopamine neuron generation, which is 

more suitable for clinical application. 

This innovative approach potentially 

provides a large and reliable source of 

dopaminergic cells sufficient for 

clinically relevant transplantation of 

dopaminergic tissue as well as in vitro 

pharmacologic studies of human 

dopaminergic cells. 

Applications: 

• Human dopaminergic cell source 

for neuronal transplantation, with 

potential clinical application to 

Parkinson’s disease and possibly other 

neurodegenerative disorders. 

• Human dopaminergic cell source 

for in vitro models for pharmaceutical 

screens relevant to neurodegenerative 

disorders and substance abuse. 

Market: Parkinson’s disease, the 

second most common neurological 

disorder, affects approximately 4.1 

million people worldwide. In 2006, 

global sales of Parkinson’s disease 

therapeutics were $3.1 billion, with 

sales expected to exceed $4.6 billion by 

2012. 

Development Status: Early stage. 

Inventors: William Freed and Tandis 

Vazin (NIDA). 

Publication: In preparation. 

Patent Status: U.S. Provisional 

Application No. 61/199,652 filed 18 

31450 Federal Register / Vol. 74, No. 125 / Wednesday, July 1, 2009 / Notices 

Nov 2008 (HHS Reference No. E–176– 

2008/0–US–01). 

Licensing Status: Available for 

licensing. 

Licensing Contact: Norbert Pontzer, 

J.D., PhD; 301–435–5502; 

pontzern@mail.nih.gov. 

Collaborative Research Opportunity: 

The National Institute on Drug Abuse, 

Development and Plasticity Section, is 

seeking statements of capability or 

interest from parties interested in 

collaborative research to further 

develop, evaluate, or commercialize this 

technology. Please contact Vio Conley, 

M.S. at 301–496–0477 or 

conleyv@mail.nih.gov for more 

information. 

Dated: June 22, 2009. 

Richard U. Rodriguez, 

Director, Division of Technology Development 

and Transfer, Office of Technology Transfer, 

National Institutes of Health. 

[FR Doc. E9–15578 Filed 6–30–09; 8:45 am] 

BILLING CODE 4140–01–P 

DEPARTMENT OF HEALTH AND 

HUMAN SERVICES 

National Institutes of Health 

Center for Scientific Review; Amended 

Notice of Meeting 

Notice is hereby given of a change in 

the meeting of the Center for Scientific 

Review Special Emphasis Panel, July 20, 

2009, 8 a.m. to July 21, 2009, 7:30 p.m., 

Hyatt Regency Bethesda, One Bethesda 

Metro Center, 7400 Wisconsin Avenue, 

Bethesda, MD 20814 which was 

published in the Federal Register on 

June 15, 2009, 74 FR 28260–28262. 

The meeting will be held at the 

Doubletree Hotel Washington, 1515 

Rhode Island Avenue, NW., 

Washington, DC 20005. The meeting 

dates and time remain the same. The 

meeting is closed to the public. 

Dated: June 22, 2009. 

Anna Snouffer, 

Deputy Director, Office of Federal Advisory 

Committee Policy. 

[FR Doc. E9–15580 Filed 6–30–09; 8:45 am] 

BILLING CODE 4140–01–M 

DEPARTMENT OF HEALTH AND 

HUMAN SERVICES 

National Institutes of Health 

Center for Scientific Review; Amended 

Notice of Meeting 

Notice is hereby given of a change in 

the meeting of the Center for Scientific 

Review Special Emphasis Panel, July 20, 

2009, 8 a.m. to July 21, 2009, 4 p.m., 

DoubleTree Hotel Bethesda, 8120 

Wisconsin Avenue, Bethesda, MD, 

20814 which was published in the 

Federal Register on June 22, 2009, 74 

FR 29500–29502. 

The meeting will be held at the Hyatt 

Regency Bethesda, One Bethesda Metro 

Center, 7400 Wisconsin Avenue, 

Bethesda, MD 20814. The meeting date 

and time remain the same. The meeting 

is closed to the public. 

Dated: June 22, 2009. 

Anna Snouffer, 

Deputy Director, Office of Federal Advisory 

Committee Policy. 

[FR Doc. E9–15582 Filed 6–30–09; 8:45 am] 

BILLING CODE 4140–01–M 

DEPARTMENT OF HEALTH AND 

HUMAN SERVICES 

National Institutes of Health 

Center for Scientific Review; Amended 

Notice of Meeting 

Notice is hereby given of a change in 

the meeting of the Center for Scientific 

Review Special Emphasis Panel, July 20, 

2009, 8 a.m. to July 21, 2009, 6 p.m., 

Ritz Carlton Hotel, 1150 22nd Street, 

NW., Washington, DC, 20037 which was 

published in the Federal Register on 

June 15, 2009, 74 FR 28260–28262. 

The meeting will be held at the 

Embassy Suites at the Chevy Chase 

Pavilion, 4300 Military Road, NW., 

Washington, DC 20015. The meeting 

dates and time remain the same. The 

meeting is closed to the public. 

Dated: June 22, 2009. 

Anna Snouffer, 

Deputy Director, Office of Federal Advisory 

Committee Policy. 

[FR Doc. E9–15588 Filed 6–30–09; 8:45 am] 

BILLING CODE 4140–01–M 

DEPARTMENT OF HEALTH AND 

HUMAN SERVICES 

National Institutes of Health 

National Eye Institute; Notice of Closed 

Meetings 

Pursuant to section 10(d) of the 

Federal Advisory Committee Act, as 

amended (5 U.S.C. App.), notice is 

hereby given of the following meetings. 

The meetings will be closed to the 

public in accordance with the 

provisions set forth in sections 

552b(c)(4) and 552b(c)(6), Title 5 U.S.C., 

as amended. The grant applications and 

the discussions could disclose 

confidential trade secrets or commercial 

property such as patentable material, 

and personal information concerning 

individuals associated with the grant 

applications, the disclosure of which 

would constitute a clearly unwarranted 

invasion of personal privacy. 

Name of Committee: National Eye Institute 

Special Emphasis Panel; NEI Research 

Project Grant, Cooperative Agreement and 

Competitive Supplement Applications. 

Date: August 3, 2009. 

Time: 8:30 a.m. to 5 p.m. 

Agenda: To review and evaluate grant 

applications. 

Place: Embassy Suites at the Chevy Chase 

Pavilion, 4300 Military Road, NW., 

Washington, DC 20015. 

Contact Person: Anne E. Schaffner, PhD, 

Scientific Review Officer, Division of 

Extramural Research, National Eye Institute, 

5635 Fishers Lane, Suite 1300, MSC 9300, 

Bethesda, MD 20892–9300, (301) 451–2020, 

aes@nei.nih.gov. 

Name of Committee: National Eye Institute 

Special Emphasis Panel NEI Translational 

Research Program on Therapy for Visual 

Disorders. 

Date: August 4, 2009. 

Time: 8:30 a.m. to 2 p.m. 

Agenda: To review and evaluate grant 

applications. 

Place: Embassy Suites at the Chevy Chase 

Pavilion, 4300 Military Road, NW., 

Washington, DC 20015. 

Contact Person: Anne E. Schaffner, PhD, 

Scientific Review Officer, Division of 

Extramural Research, National Eye Institute, 

5635 Fishers Lane, Suite 1300, MSC 9300, 

Bethesda, Md 20892–9300, (301) 451–2020, 

aes@nei.nih.gov. 

(Catalogue of Federal Domestic Assistance 

Program Nos. 93.867, Vision Research, 

National Institutes of Health, HHS) 

Dated: June 25, 2009. 

Anna Snouffer, 

Deputy Director, Office of Federal Advisory 

Committee Policy. 

[FR Doc. E9–15592 Filed 6–30–09; 8:45 am] 

BILLING CODE 4140–01–M 

DEPARTMENT OF HEALTH AND 

HUMAN SERVICES 

National Institutes of Health 

National Institute of Diabetes and 

Digestive and Kidney Diseases; Notice 

of Closed Meeting 

Pursuant to section 10(d) of the 

Federal Advisory Committee Act, as 

amended (5 U.S.C. App.), notice is 

hereby given of the following meeting. 

The meeting will be closed to the 

public in accordance with the 

provisions set forth in sections 

552b(c)(4) and 552b(c)(6), Title 5 U.S.C., 

as amended. The grant applications and 

the discussions could disclose 

confidential trade secrets or commercial 

property such as patentable material, 

and personal information concerning