26404 Federal Register / Vol. 72, No. 89 / Wednesday, May 9, 2007 / Notices 

Aug 2006 (HHS Ref. No. E–110–2004/0–

US–06). 

Licensing Status: Available for 

exclusive and non-exclusive licensing. 

Licensing Contact: Adaku 

Nwachukwu, J.D.; 301/435–5560; 

madua@mail.nih.gov. 

Leu574 of HIF–1alpha as a Molecular 

Basis for Therapeutic Application 

Description of Technology: The 

hypoxia-inducible factor 1 (HIF–1) is a 

transcription factor that plays a pivotal 

role in cellular adaptation to oxygen 

availability. HIF–1alpha protein is a 

subunit of HIF–1. Although the gene for 

HIF–1alpha is constitutively expressed, 

it is an extremely short-lived protein 

under normoxic conditions and is 

targeted for destruction via the 

proteosome pathway by an E3 ubiquitin 

ligase involving the VHL protein. 

The invention relates to the discovery 

that mutations or deletions of Leu574 

result in a more stable and more active 

form of HIF–1alpha. Therefore, the 

invention relates to methods and 

compositions for modulating oxygen 

homeostasis for therapeutic application. 

In one aspect, the inventors contemplate 

the use of a more stable form of HIF–

1alpha protein for therapeutic 

angiogenesis purposes such as may be 

useful in ischemic vascular disease. In 

another aspect, the inventors 

contemplate the use of this particular 

site in a screen for targeted drugs that 

modulates HIF–1alpha activity. The 

inventors also suggest that Leu574 could 

be used for developing drugs targeted to 

HIF hydroxylase binding, thereby 

altering HIF–1alpha stability. 

Inventor: L. Eric Huang (NCI). 

Patent Status: U.S. Patent No. 

7,193,053 issued 20 Mar 2007 (HHS 

Reference No. E–281–2002/0–US–02). 

Licensing Status: This technology is 

available for licensing on an exclusive 

or a non-exclusive basis. 

Licensing Contact: Jesse S. Kindra, 

J.D.; 301/435–5559; 

kindraj@mail.nih.gov. 

Dated: April 30, 3007. 

Steven M. Ferguson, 

Director, Division of Technology Development 

and Transfer,Office of Technology Transfer, 

National Institutes of Health. 

[FR Doc. E7–8893 Filed 5–8–07; 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 Compounds and Methods for the 

Treatment of Spinal Muscular Atrophy 

and Other Diseases 

Description of Technology: Spinal 

muscular atrophy (SMA) is caused by 

mutations in the SMN1 gene that result 

in reduced expression of the survival 

motor neuron (SMN) protein and a loss 

of spinal motor neurons. An SMN2 gene 

paralog that differs from SMN by a 

single base pair has inadequate 

expression of SMN to support motor 

neuron survival. Alternative splicing 

caused by the single base substitution in 

the SMN2 gene results in a slightly 

truncated and highly unstable SMN 

protein. Drugs that allow translational 

read through of the stop codons 

introduced by the alternative splice 

event have been shown to stabilize the 

mutant protein, resulting in increased 

levels of SMN. 

A chemical library screen identified 

indoprofen, a nonsteroidal antiinflammatory drug, as an inducer of 

SMN expression in cultured cells. 

However, indoprofen cannot enter the 

brain in satisfactory amounts, has a 

relatively low level of activity and can 

cause substantial side-effects in part due 

to its cyclooxygenase inhibitory activity. 

NIH inventors designed indoprofen 

derivatives without cyclooxygenase 

activity that can enter the CNS and 

increase expression of a SMN protein 

from the SMN2 gene with increased 

potency and efficacy. The mechanism of 

action of these indoprofen analogs 

appears to be translational readthrough 

of stop codons introduced by the 

alternative SMN2 splicing event. In 

addition to treating SMA, novel drugs 

that allow read through of stop codons 

could potentially treat many other 

diseases caused by such mutations such 

as cystic fibrosis and muscular 

dystrophy. 

Available for licensing are 

compounds and methods useful for the 

treatment of spinal muscular atrophy by 

increasing SMN expression and 

increasing the expression from any 

nucleic acid that encodes a translational 

stop codon. 

Applications: Efficacious treatment 

for SMA, utilizing indoprofen analogs 

that increase SMN protein expression; 

Treatment of any genetic disease caused 

by premature termination of protein 

translation. 

Market: SMA is a rare genetic disease 

that affects approximately 1 in 6,000 

live births, and is the leading genetic 

cause of death in infants and toddlers. 

The projected market size for SMA is 

between $250 million and $750 million. 

Development Status: Clinical 

candidate selection scheduled for June 

2007. 

Inventors: Jill Heemskerk (NINDS), et 

al. 

Publication: MR Lunn, DE Root, AM 

Martino, SP Flaherty, BP Kelley, DD 

Coovert, AH Burghes, NT Man, GE 

Morris, J Zhou, EJ Androphy, CJ 

Sumner, BR Stockwell. Indoprofen 

upregulates the survival motor neuron 

protein through a cyclooxygenaseindependent mechanism. Chem. Biol. 

2004 Nov;11(11):1489–1493. 

Patent Status: U.S. Provisional 

Application No. 60/783,292 filed 17 Mar 

2006 (HHS Reference No. E–133–2006/ 

0-US–01); PCT Application No. PCT/ 

2007/006772 filed 16 Mar 2007 (HHS 

Reference No. E–133–2006/1–PCT–01) 

Licensing Availability: Available for 

exclusive and non-exclusive licensing. 

Licensing Contact: Norbert Pontzer, 

J.D., Ph.D.; 301/435–5502; 

pontzern@mail.nih.gov. 

STAMP, a Novel Cofactor and Possible 

Steroid Sparing Agent, Modulates 

Steroid-Induced Induction or 

Repression of Steroid Receptors 

Description of Technology: Steroid 

hormones such as androgens, 

glucocorticoids, and estrogens are used 

in the treatments of many diseases. 

They act to regulate many physiological 

responses by binding to steroid 


sroberts on PROD1PC70 with NOTICES
Federal Register / Vol. 72, No. 89 / Wednesday, May 9, 2007 / Notices 26405 

receptors. However, because steroid 

receptors are expressed in many tissues, 

efforts to therapeutically modify the 

effects of steroid hormones on a specific 

tissue or on a specific receptor of the 

steroid receptor family often cause 

undesirable effects in other tissues or on 

other receptors. STAMP (SRC–1 and 

TIF–2 Associated Modulatory Protein), a 

novel protein that acts to lower the 

concentration of steroid hormone 

needed to induce (or repress) selected 

target genes by regulating steroid 

receptor synthesis, offers an novel 

approach for reducing the severity of 

unwanted side-effects, thereby 

increasing the ability to use steroid 

hormone therapies. 

Applications 

1. Diseases requiring chronic steroid 

treatment such as rheumatoid arthritis, 

psoriatic arthritis, asthma, inflammatory 

and auto-immune diseases; 

2. Diseases characterized by excess or 

deficiency of glucocorticoids such as 

obesity, diabetes, hypertension, 

Cushing’s Syndrome, Parkinson’s 

Disease, Addison’s Disease; 

3. Diseases in which glucocorticoidresponsive gene expression is deranged, 

so deranging carbohydrate, protein or 

lipid metabolism; 

4. Cancers responsive to androgen or 

estrogen, such as breast cancer or 

prostate cancer; 

5. Therapeutic applications related to 

male or female hormone replacement, 

symptoms related to menopause, birth 

control, menstrual cycle/amenorrhea, 

fertility or endometriosis. 

Advantages 

1. STAMP reduces the severity of 

unwanted side-effects of steroid 

hormone therapies; 

2. STAMP modulates the gene 

induction properties of androgen and 

progesterone receptors; 

3. STAMP modulates both induction 

and repression properties of 

glucocorticoid receptors; 

4. STAMP is inactive toward alpha 

and beta estrogen receptors, thyroid 

receptor beta, PPAR gamma 2, retinoid 

receptor alpha or RXR alpha; 

5. The siRNAs could be useful as 

therapeutics. 

Market: The protein, STAMP, offers a 

novel approach for reducing the severity 

of unwanted side-effects of steroid 

hormone therapies. Therefore, STAMP 

would be helpful in the treatment of 

diseases requiring chronic steroid 

treatments, those characterized by 

excess or deficiency of glucocorticoid 

response, therapies related to male or 

female hormone replacement or cancers 

responsive to androgen or estrogen. 

Development Status 

1. STAMP, a protein which is a novel 

nuclear receptor cofactor, has been 

identified; 

2. STAMP siRNAs have been shown 

to change the dose response curve of 

endogenous glucocorticoid receptor 

induced genes; 

3. A STAMP antibody has been 

prepared. 

Further Research & Development 

Required 

1. Further in-vivo studies into the role 

of STAMP in glucocorticoid receptormediated repression; 

2. Further study into the activity of 

STAMP in androgen receptor-mediated 

responses; 

3. Investigation into the mechanism of 

action of STAMP; 

4. Development of STAMP knockout 

mouse. 

Inventors: Drs. S. Stoney Simons Jr 

(NIDDK) and Yuanzheng He (NIDDK) 

Publication: Y He and SS Simons Jr. 

STAMP: A Novel Predicted Factor 

Assisting TIF2 Actions in 

Glucocorticoid Receptor-mediated 

Induction and Repression. Mol Cell 

Biol. 2007 Feb;27(4);1467–1485. 

Patent Status: PCT International No. 

PCT/US2005/006393 filed 25 Feb 2005 

(priority date 26 Feb 2004), which 

published as WO 2005/082935 on 09 

Sep 2005, entitled ‘‘A Novel Cofactor 

that Modulates Steroid Receptor 

Activities’’; National Stage U.S., Europe, 

Canada, Australia (HHS Reference No. 

E–056–2004/0). 

Related Technologies: HHS Reference 

No. E–015–2000/0, ‘‘Antiprogestins 

with Partial Agonist Activity.’’ Global IP 

pending: US, Europe, Australia, Canada, 

Japan. 

Licensing Status: Available for 

exclusive and non-exclusive licensing. 

Licensing Contact: Dr. Susan Carson; 

301/435–5020; carsonsu@mail.nih.gov. 

Collaborative Research Opportunity: 

The National Institute of Diabetes, 

Digestive and Kidney Diseases, 

Laboratory of Molecular and Cellular 

Biology is seeking statements of 

capability or interest from parties 

interested in collaborative research to 

further develop, evaluate or 

commercialize this technology. Please 

contact Dr. Stoney Simons, Chief, 

Steroid Hormones Section (NIDDK) at 

steroids@helix.nih.gov; Tel: 301–4960–

6796 for more information. 

TMC1, a Deafness-Related Gene 

Description of Technology: Hearing 

loss is a common communication 

disorder affecting nearly 1 in 1,000 

children in the United States alone, and 

nearly 50% of adults by the age of 

eighty. Hearing loss can be caused by 

environmental and disease-related 

factors; however, hearing loss due to 

genetic factors accounts for 

approximately 50% of cases. 

The NIH announces the isolation of 

two novel genes involved in hearing; 

TMC1, short for transmembrane 

channel-like gene 1. The inventors have 

discovered that dominant and recessive 

mutations in TMC1 underlie two forms 

of hereditary deafness, known as 

DFNA36 and DFNB7/11. TMC1 encodes 

a protein required for normal function 

of the mammalian hair cell, which plays 

a critical role within the hearing 

pathway that detects sound in the inner 

ear. 

The invention discloses TMC1 

nucleic acids, vectors, and cells. Also 

disclosed are methods of detecting 

hearing loss, or a predisposition to 

hearing loss, due to a mutation in 

TMC1, as well as methods for 

identifying agents that interact with the 

TMC1 gene in a cell. Nucleic acids and 

methods of use for TMC2, a gene closely 

related to TMC1, are also disclosed. 

Applications: Development of a 

genetic diagnostic test for hearing loss; 

Development of pharmaceuticals to treat 

hearing loss. 

Market: Hearing loss with a genetic 

component accounts for 50% of all 

cases of hearing loss. 

Development Status: Early stage. 

Inventors: Andrew J. Griffith et al. 

(NIDCD). 

Publication: K Kurima et al. Dominant 

and recessive deafness caused by 

mutations of a novel gene, TMC1, 

required for cochlear hair-cell function. 

Nat Genet. 2002 Mar;30(3):277–284. 

Patent Status 

1. HHS Reference No. E–168–2001/0: 

a. U.S. Provisional Application No. 

60/323,275 filed 19 Sep 2001. 

b. PCT Application No. PCT/US02/ 

29614 filed 19 Sep 2002, which 

published as WO 03/025140 on 27 Mar 

2003. 

c. U.S. Patent No. 7,192,705 issued 20 

Mar 2007. 

d. U.S. Patent Application No. 11/ 

615,250 filed 22 Dec 2006. 

e. Foreign counterparts in Australia, 

Canada, Europe, and Japan. 

2. HHS Reference No. E–168–2001/1: 

a. U.S. Patent No. 7,116,433 issued 23 

Jan 2007. 

b. Foreign counterparts in Australia 

and Canada. 

Licensing Status: Available for nonexclusive licensing. 

Licensing Contact: Tara L. Kirby, 

Ph.D.; 301/435–4426; 

tarak@mail.nih.gov. 


sroberts on PROD1PC70 with NOTICES
26406 Federal Register / Vol. 72, No. 89 / Wednesday, May 9, 2007 / Notices 

Collaborative Research Opportunity: 

The NIDCD Otolaryngology Branch is 

seeking statements of capability or 

interest from parties interested in 

collaborative research to further 

develop, evaluate, or commercialize this 

technology as well as collaborate on 

further pre-clinical and clinical studies 

with the TMC2 gene mutations. Please 

contact Ms. Marianne Lynch at 301–

402–5579 or via e-mail at 

lynchm@nhlbi.nih.gov for more 

information. 

Dated: April 30, 2007. 

Steven M. Ferguson, 

Director, Division of Technology Development 

and Transfer, Office of Technology Transfer, 

National Institutes of Health. 

[FR Doc. E7–8894 Filed 5–8–07; 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. 

Influenza Vaccines and Antiviral 

Agents 

Description of Technology: The 

subject invention offers candidate DNA 

vaccines to target H5N1, H1N1, H3N2 

and other subtypes of influenza. These 

candidates are designed primarily to 

elicit neutralizing antibodies. The 

candidate vaccines express 

hemagglutinin (H/HA) or neuramidase 

(N/NA) protein that has been codon 

optimized and/or modified at the 

protease cleavage site. The modified 

genes could be used in DNA vaccines, 

in viral vectors, recombinant proteins/ 

particles or combination. The studies 

use proprietary expression systems that 

increase protein expression relative to 

commonly used alternatives. This 

invention potentially provides a vaccine 

strategy for controlling influenza 

epidemics, including avian flu, should 

it cross over to humans; the 1918 strain 

of flu; and seasonal flu strains. In 

addition, this invention is designed to 

lead to a combination vaccine to 

provide a broadly protective vaccine. 

The incorporation of specific cleavage 

site types to facilitate preparation of 

pseudotypes from a variety of strains is 

an important aspect of this invention. 

In addition, HA pseudotyped 

lentiviral vectors are being tested to 

screen for neutralizing abs in patients 

and to screen for diagnostic and 

therapeutic monoclonal abs. 

Applications and Advantages: 

Influenza vaccine for pandemic or 

epidemic application; Potential for 

combination vaccine for broad 

protection, removing need for seasonal 

strain monitoring; DNA vaccines are 

easy to produce and store; No risk of 

reversion to pathogenic strain as with 

live-attenuated virus vaccines. 

Development Status Highlights: Phase 

I clinical trials planned for select 

candidates; DNA vaccine encoding 1918 

influenza virus HA protein protects 

mice against lethal viral challenge; 

Codon optimized for expression in 

human cells. 

Inventors: Gary J. Nabel (VRC/NIAID), 

Wing-pui Kong (VRC/NIAID), Zhi-yong 

Yang (VRC, NIAID), et al. 

Publication: Certain aspects of this 

technology were published in WP Kong 

et al. Protective immunity to lethal 

challenge of the 1918 pandemic 

influenza virus by vaccination. Proc 

Natl Acad Sci USA. 2006 Oct 

24;103(43):15987–15991. Epub 2006 Oct 

16, doi: 10.1073/pnas.0607564103. 

Patent Status: U.S. Provisional 

Application No. 60/774,923 filed 16 Feb 

2006 (HHS Reference No. E–116–2006/ 

0–US–01) and PCT Application No. 

PCT/US2007/004506 filed 16 Feb 2007 

(influenza) (HHS Reference No. E–116–

2006/1–PCT–01); U.S. Patent No. 

7,094,598 issued 22 Aug 2006 (CMV/R) 

(HHS Reference No. E–241–2001/1–US–

01) and associated foreign rights. 

Licensing Status: Available for 

exclusive or non-exclusive licensing. 

Licensing Contact: Susan Ano, Ph.D.; 

301/435–5515; anos@mail.nih.gov. 

Enhanced, Targeted Delivery for DNA 

Vaccines 

Description of Technology: Available 

for licensing from the NIH is a fusion 

protein for enhanced gene delivery. 

Exemplary proteins for achieving this 

improvement comprise an adenovirus 

serotype 5 fiber, penton base and core 

protein V fused to the DNA binding 

domain of HMG. In vitro studies have 

shown the effectiveness of the chimeric 

protein-DNA vaccine co-administration 

by an increase in uptake of ten to twenty 

fold. In particular, the plasmid with the 

chimeric core protein V was delivered 

efficiently to dendritic cells (DC) as well 

as 293T cells. The utilization of this 

chimeric protein could further enhance 

the immune response elicited by DNA 

vaccines. 

Potential Applications: Improved 

DNA vaccine delivery and uptake. 

Inventors: Gary J. Nabel and Wataru 

Akahata (VRC/NIAID). 

Patent Status: U.S. Provisional 

Application No. 60/737,896 filed 18 

Nov 2005 (HHS Reference No. E–043–

2006/0–US–01); U.S. Provisional 

Application No. 60/795,529 filed 26 Apr 

2006 (HHS Reference No. E–043–2006/ 

1–US–01); PCT Application No. PCT/ 

US2006/044525 filed 20 Nov 2006 (HHS 

Reference No. E–043–2006/3–PCT–01) 

Licensing Status: Available for nonexclusive or exclusive licensing. 

Licensing Contact: Susan Ano, Ph.D.; 

301/435–5515; anos@mail.nih.gov. 

Dated: April 30, 2007. 

Steven M. Ferguson, 

Director, Division of Technology Development 

and Transfer, Office of Technology Transfer, 

National Institutes of Health. 

[FR Doc. E7–8895 Filed 5–8–07; 8:45 am] 

BILLING CODE 4140–01–P 

DEPARTMENT OF HEALTH AND 

HUMAN SERVICES 

National Institutes of Health 

National Cancer Institute; Notice of 

Meeting 

Pursuant to section 10(a) of the 

Federal Advisory Committee Act, as 

amended (5 U.S.C. Appendix 2), notice 

is hereby given of a meeting of the 

National Cancer Institute Director’s 

Consumer Liaison Group. 

The meeting will be open to the 

public, with attendance limited to space 

available. Individuals who plan to 

attend and need special assistance, such 

as sign language interpretation or other 

reasonable accommodations, should 

notify the Contact Person listed below 

in advance of the meeting. 


sroberts on PROD1PC70 with NOTICES