Federal Register / Vol. 69, No. 243 / Monday, December 20, 2004 / Notices 75993

invention proposes a method to increase 

GM–CSF levels in a treated subject, and 

this increase is achieved by inhibiting 

the degradation of GM–CSF messenger 

RNA (mRNA). Tristetraprolin (TTP) is 

one member of a family of cys-cys-cyshis (CCCH) zinc finger proteins, and it 

is a factor that binds to and causes the 

instability of GM–CSF mRNA. Methods 

are provided for the development of 

screening assays for molecules that 

inhibit the binding of TTP and its 

related proteins to GM–CSF mRNA, or 

otherwise inhibit the effect of TTP to 

promote breakdown of the mRNA, 

leading in turn to increased mRNA 

stability and enhanced production of 

GM–CSF. Compounds identified by 

such screens, and their derivatives, 

could be useful in treating 

granulocytopenia from whatever cause. 

Additional information about this 

technology may be found in the 

following research articles: 

Carballo, E, Lai, WS and Blackshear, 

PJ. Evidence that tristetraprolin (TTP) is 

a physiological regulator of granulocytemacrophage colony-stimulating factor 

(GM–CSF) mRNA deadenylation and 

stability. 2000; Blood 95:1891–1899. 

Lai, WS, Carballo, E, Thorn, JM, 

Kennington, EA and Blackshear, PJ. 

Interactions of CCCH zinc finger 

proteins with mRNA. 1. Binding of 

tristetraprolin-related zinc finger 

proteins to AU-rich elements and 

destabilization of mRNA. 2000; J. Biol. 

Chem., 275:17827–19837. 

In addition to licensing, the 

technology is available for further 

development through collaborative 

research with the inventors via a 

Cooperative Research and Development 

Agreement (CRADA).

Dated: December 13, 2004. 

Steven M. Ferguson, 

Director, Division of Technology Development 

and Transfer, Office of Technology Transfer, 

National Institutes of Health.

[FR Doc. 04–27782 Filed 12–17–04; 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, DHHS.

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. 

The Use of Rabbits With Defined 

Immunoglobulin Light Chain Genes 

(Ckappa b Allotypes) To Optimize 

Production of Chimeric and Humanized 

Monoclonal Antibodies for 

Therapeutic, Imaging and Diagnostic 

Applications 

Rose G. Mage, Cornelius Alexander 

(NIAID). 

DHHS Reference No. E–332–2004/0—

Research Tool. 

Licensing Contact: Pradeep Ghosh; (301) 

435–5282; ghoshpr@mail.nih.gov.

Biological materials are important 

research tools that can be used for 

diagnostic as well as therapeutic 

purposes. Antibodies have become 

viable drugs in the market today and 

there is a general market need for 

systems that may facilitate production 

of efficient and effective antibodies. In 

recent years, monoclonal antibodies 

have gained significant importance in 

their use, both as diagnostics and 

therapeutics, to intervene and combat 

diseases such as cancer, cardiovascular 

diseases, and infections. The present 

invention relates to the discovery of 

rabbits, genetically defined as b9, as the 

biological vehicle for the isolation of 

chimeric phage displaying Fab with 

human constant regions and rabbit 

immunoglobulin heavy and light chain 

variable regions for the development of 

diagnostic antibodies and humanized 

monoclonal therapeutic antibodies of 

high affinity and specificity (Popkov et 

al., J. Molec. Biol. 325: 325–335, 2003; 

Popkov et al. J. Immunol. Methods 288: 

149–164, 2004). Recently, many 

effective antibodies have been 

developed as a result of the integration 

of antibody libraries with phage display 

technology. The rabbit model described 

in this invention may be used for 

production of antibodies that may cross 

react with both human and mouse 

antigens. Rabbit monoclonal antibodies 

that react with both human and mouse 

antigens are of particular relevance for 

the preclinical evaluation of therapeutic 

antibodies in mouse models of human 

diseases. Therefore, this invention has a 

broad commercial potential in its use as 

a source for producing monoclonal 

antibodies for therapeutic interventions 

in infectious, autoimmune and 

neurological diseases, nerve damage and 

cancer. 

Methods for Diagnosis of 

Atherosclerosis 

Paul Hwang et al. (NHLBI). 

U.S. Provisional Application No. 60/

607,031 filed 03 Sep 2004 (DHHS 

Reference No. E–276–2004/0–US–01). 

Licensing Contact: Fatima Sayyid; 301/

435–4521; sayyidf@mail.nih.gov.

In industrialized countries coronary 

heart disease and stroke due to 

atherosclerosis are the leading causes of 

morbidity and mortality. Coronary heart 

disease is the single largest cause of 

death in the U.S.A. and will cost 

approximately $133.2 billion according 

to the 2004 American Heart Association 

statistics update. 

The identification of more sensitive 

and specific markers of atherosclerosis 

that are non-invasive and cost-effective 

may have profound impacts on public 

health. One such strategy involves the 

detection of marker genes or their 

products in blood or serum. Such 

markers may help identify high-risk 

patients with subclinical atherosclerosis 

who may benefit from intensive primary 

prevention or they may help determine 

the activity of established disease for 

monitoring response to treatment, 

resulting in more targeted secondary 

prevention.

The present invention relates to 

methods for detecting atherosclerosis 

using highly reactive biomarkers (FOS 

and/or DUSP1) expressed in blood cells 

or released into serum. Because these 

markers are also involved in 

pathogenesis, they may serve as 

potential targets for drug discovery and 

for intervention to modify disease 

progression. 

An Improved Method To Separate and 

Expand Antigen-Specific T Cells 

Jonming Li and John Barrett (NHLBI). 

U.S. Provisional Application No. 60/

606,197 filed 31 Aug 2004 (DHHS 

Reference No. E–246–2004/0–US–01). 

Licensing Contact: Fatima Sayyid; (301) 

435–4521; sayyidf@mail.nih.gov.

Stem cell transplants can be used to 

treat patients with leukemia or other 

disorders. Transplanted donor T cells 

(lymphocytes) exert strong alloimmune 

75994 Federal Register / Vol. 69, No. 243 / Monday, December 20, 2004 / Notices 

graft versus leukemia and other antitumor effects however they can also 

cause potentially lethal graft versus host 

disease (GVHD), requiring posttransplant immunosuppression. Such 

immunosuppression may place patients 

at a greater risk of contracting 

potentially fatal cytomegalovirus 

infection further reducing their capacity 

to be cured of their malignant disease. 

The transfer of T lymphocytes specific 

for leukemia cells or micro-organism 

antigens can be useful since therapeutic 

immune effects would be enhanced 

while GVHD reactions would not be 

induced. Currently available methods 

for isolating and expanding antigenspecific T cells including selection 

using HLA tetramers, magnetic beads 

binding to activation markers or 

laborious limiting dilution techniques 

are unreliable, poorly reproducible, 

expensive and impede clinical progress. 

The present invention relates to 

methods for selecting and expanding 

antigen specific T-cells that recognize a 

pre selected target antigen, to purified 

populations of antigen-specific T cells 

that recognize a pre selected target 

antigen and to therapeutic uses of 

antigen-specific T cells that recognize a 

pre selected target antigen. Potential 

applications include treatment of 

cytomegalovirus, Epstein-Barr virus and 

adenovirus reactivation following stem 

cell transplantation or organ 

transplantation, prevention and 

treatment of leukemic relapse after 

transplantation or chemotherapy using 

autologous expanded T cells, and 

selective depletion of alloreactive T 

cells from transplants which may 

produce GVHD. 

Novel Compounds for Selectively 

Inactivating Pain Pathways 

Peter Blumberg, Jeewoo Lee (NCI). 

U.S. Provisional Application No. 60/

558,003 filed 26 Mar 2004 (DHHS 

Reference No. E–141–2004/0–US–01). 

Licensing Contact: Norbert Pontzer; 301/

435–5502; pontzern@mail.nih.gov.

Available for licensing are 

compositions and methods for the longterm control of pain and other 

pathological conditions caused by the 

over-activity of pain pathways. Neurons 

in the dorsal root, trigeminal and 

nodose ganglia project unmyelinated Cfibers and Ad-fibers that transmit pain 

and temperature sensation between the 

periphery and spinal cord. Along with 

acute and chronic pain, over activation 

of those pathways leads to neurogenic 

and neuropathic inflammation leading 

to such conditions as post-herpetic 

neuralgia, diabetic neuropathy, cystitis, 

and reflex sympathetic dystrophy 

among many others. 

These neurons are activated both 

centrally and peripherally by a 

relatively non-selective cation channel 

initially identified as site of action of 

capsaicin, the pungent ingredient in 

chili peppers. That channel is now 

called VR1 or TRPV1 and is found in 

high concentration only on C and Ad

neurons. These inventors previously 

discovered and patented resiniferatoxin 

(RTX), an ultrapotent agonist of the VR1 

receptor. RTX desensitizes C and Adfibers when applied peripherally and 

may selectively ablate those neurons 

when applied centrally without causing 

substantial pain from activation of the 

neurons. RTX type compounds thus 

provide a method of controlling pain 

other conditions caused by C and Adfiber activity. The present invention 

provides new RTX analogues that may 

have an improved therapeutic index and 

metabolic profile.

Dated: December 9, 2004. 

Steven M. Ferguson, 

Director, Division of Technology Development 

and Transfer, Office of Technology Transfer, 

National Institutes of Health.

[FR Doc. 04–27783 Filed 12–17–04; 8:45 am] 

BILLING CODE 4140–01–P

DEPARTMENT OF HEALTH AND 

HUMAN SERVICES 

National Institutes of Health 

National Human Genome Research 

Institute; Notice of Closed Meeting 

Pursuant to section 10(d) of the 

Federal Advisory Committee Act, as 

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

individuals associated with the grant 

applications, the disclosure of which 

would constitute a clearly unwarranted 

invasion of personal privacy.

Name of Committee: National Human 

Genome Research Institute Special Emphasis 

Panel. 

Date: December 16–17, 2004. 

Time: December 16, 2004, 7 p.m. to 10 p.m. 

Agenda: To review and evaluate grant 

applications. 

Place: Stanford University, Stanford 

Terrace Inn, 531 Stanford Avenue, Palo Alto, 

CA 94306. 

Time: December 17, 2004, 8 a.m. to 5 p.m. 

Agenda: To review and evaluate grant 

applications. 

Place: Stanford University, Stanford 

Terrace Inn, 531 Stanford Avenue, Palo Alto, 

CA 94306. 

Contact Person: Ken D. Nakamura, PHD, 

Scientific Review Administrator, Office of 

Scientific Review, National Human Genome 

Research Institute, National Institutes of 

Health, Bethesda, MD 20892, (301) 402–0838. 

This notice is being published less than 15 

days prior to the meeting due to the timing 

limitations imposed by the review and 

funding cycle.

(Catalogue of Federal Domstic Assistance 

Program Nos. 93.172, Human Genome 

Research, National Institutes of Health, HHS) 

Dated: December 14, 2004. 

Anna P. Snouffer, 

Acting Director, Office of Federal Advisory 

Committee Policy.

[FR Doc. 04–27779 Filed 12–17–04; 8:45 am] 

BILLING CODE 4140–01–M

DEPARTMENT OF HEALTH AND 

HUMAN SERVICES 

National Institutes of Health 

National Institute on Drug Abuse; 

Notice of Meeting 

Pursuant to section 10(d) of the 

Federal Advisory Committee Act, as 

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

is hereby given of a meeting of the 

National Advisory Council on Drug 

Abuse. 

The meeting will be open to the 

public as indicated below, 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. 

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 

individuals associated with the grant 

applications, the disclosure of which 

would constitute a clearly unwarranted 

invasion of personal privacy.

Name of Committee: National Advisory 

Council on Drug Abuse. 

Date: February 15–16, 2005. 

Closed: February 15, 2005, 2 p.m. to 4 p.m. 

Agenda: To review and evaluate grant 

applications. 

Place: National Institutes of Health, 

Neuroscience Center, 6001 Executive 

Boulevard, Rockville, MD 20852. 

Open: February 16, 2005, 9 a.m. to 4 p.m.