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Government-Owned Inventions; Availability for Licensing

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National Institutes of Health, Public Health Service, DHHS.




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.


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.

A Peptide That Elicits Neutralizing Antibodies Targeting the HIV Co-Receptor CCR5

Drs. Hana Golding and Surender Khurana (FDA)

U.S. Provisional Application filed 09 Apr 2004 (DHHS Reference No. E-150-2004/0-US-01)

Licensing Contact: Sally Hu; 301/435-5606;

This invention identifies a peptide sequence that closely mimics the conformational epitope in CCR5, recognized by the HIV neutralizing monoclonal antibody targeting the co-receptor, by using a random peptide phage display library. This peptide upon immunization of rabbits generated antibodies that bind to the HIV-1 co-receptor CCR5 resulting in blocking HIV transmission to target cells, including peripheral blood lymphocytes from human and monkeys. Thus, such antibodies could be directly used for preventing mother to child HIV transmission, for therapy of HIV-1 infected individuals, and may also have particular value when used in combination treatments with other antiviral therapies directed at viral targets, such as protease and reverse transcriptase. The peptide sequence can be used for potential vaccine development. This peptide can also be used for screening of human antibody phage display libraries to isolate human monoclonal with HIV entry-blocking potential. In addition, the peptide and antibodies recognizing it can be used as research tools for increasing the understanding of the mechanisms by which HIV, CCR5 and the HIV receptor, CD4, interact, and in general to understand mechanisms of HIV infectivity.

Inhibition of HIV Replication in Resting CD4+ Lymphocytes by Murr1

Gary J. Nabel et al. (NIAID)

U.S. Provisional Application No. 60/523,683 filed 21 Nov 2003 (DHHS Reference No. E-042-2004/0-US-01)

Licensing Contact: Susan Ano; 301/435-5515;

This technology describes the inhibition of HIV-1 growth in resting CD4+ T cells by Murr1, a highly conserved protein. This finding therefore could be used to prolong the asymptomatic phase of HIV infection. HIV-1 infects both proliferative and quiescent CD4+ T cells, although the virus replicates poorly in the latter. It has been demonstrated that Murr1 restricts HIV-1 replication by inhibiting basal and cytokine nuclear factor (NF)-κB activity. Short interfering RNAs (siRNAs) experiments that used specific Murr1 siRNAs resulted in lower levels of IκB-A and higher NF-κB activity and HIV-1 replication. These results allude to the potential for a more effective HIV therapeutic that uses Murr1 to regulate viral replication. A Murr1 anti-viral drug that can block viral replication in quiescent lymphocytes and latent cells with provirus might increase the number of patients that remain in the HIV-1 asymptomatic phase and thus lower the number that progress to the AIDS state.

This technology is further described in Ganesh et al., Nature (18/25 December 2003), 426(6968): 853-857.

Mechanisms for Improving the Breadth of the Immune Response to Diverse Strains and Clades of HIV

Gary J. Nabel et al. (NIAID)

U.S. Provisional Application No. 60/503,509 filed 15 Sep 2003 (DHHS Reference No. E-335-2003/0-US-01)

Licensing Contact: Susan Ano; 301/435-5515;

This technology describes a multiclade Env vaccine candidate that elicited neutralizing antibodies to a diverse group of primary HIV-1 isolates as compared to antibodies generated from immunization with single clade vaccines. The immunogens of the vaccine included V3 loops from clades A, B, and C and had the cleavage site, fusion peptide, and interhelical regions deleted. Competition studies suggested that the neutralization activity is directed toward shared, conserved epitopes other than the V3 loop. Also described in this technology are immunogens involving deletion of the V3 loop that generated more potent neutralizing antibodies, suggesting that the highly conserved subregions within V3 may be relevant targets to elicit neutralizing antibody responses and increase the immunogenicity of HIV/AIDS vaccines. Such selective deletions in the V3 loop are effective in combination with deletions of other V loops. Immunogens with deletions of the V regions in general (V1—V4), including combinations of deletion immunogens, were also shown to elicit potent neutralizing antibodies. Previous studies of the cell-mediated immune response in mice using the multiclade vaccines of this current technology have shown that they induce Env-specific CD4 and CD8 immune response to Start Printed Page 32595multiple clades. Thus, this technology offers promise in developing a globally effective HIV/AIDS vaccine, which must induce both cellular and humoral immunity to multiple strains from the various clades.

This work is described, in part, in Z. Yang et al., J. Virol. (April 2004) 78(8): 4029-4036.

Methods for Inhibiting Proinflammatory Cytokine Expression Using Ghrelin

Drs. Vishwa D. Dixit, Dennis D. Taub, Eric Schaffer and Dzung Nguyen (NIA)

U.S. Provisional Patent Application filed 11 May 2004 (DHHS Reference No. E-016-2004/0-US-01)

Licensing Contact: Sally Hu; 301/435-5606;

Ghrelin, a recently described endogenous ligand for growth hormone secretagogue receptors (GHS-R), is produced from stomach serving as a potent circulating orexigen controlling energy expenditure, adiposity and GH secretion. We have discovered that ghrelin exerts anti-inflammatory effects by inhibiting the secretion of both acute and chronic cytokines including IL-1, IL-6, TNF-α, IFN-γ, IL-12 p40, , chemokines, and CSFs in vitro in human cells as well as in vivo in mouse model of sepsis and inflammation. We also found that ghrelin directly controls human growth hormone and insulin growth factor expression by human immune cells. This invention is useful for treatment of various inflammatory disorders including inflammatory bowel disease, Crohn's disease, rheumatoid arthritis, multiple sclerosis, atherosclerosis, endotoxemia and graft-versus-host disease.

Stem Cell Factor (SCF) Stimulates Neural Stem Cell Migration to Sites of Brain and Spinal Cord Injury

Howard A. Fine et al. (NCI)

U.S. Provisional Application No. 60/525,760 filed 26 Nov 2003 (DHHS Reference No. E-035-2004/0-US-01) and U.S. Provisional Application filed 19 Apr 2004 (DHHS Reference No. E-035-2004/1-US-01)

Licensing Contact: Fatima Sayyid; 301/435-4521;

Endogenous neural stem/progenitor cells (NSPCs) have recently been recognized to hold the promise for therapeutics to combat neurodegenerative diseases, such as Parkinson's and Alzheimer's disease. Endogenous NSPCs have been shown to generate new functional neurons to replace the nerve cells that have been injured, lost, or destroyed in the diseases and recover brain functions. Such therapy, however, is limited due to lack of methods to mobilize endogenous NSPCs to the site of injury.

The present invention relates to methods for recruiting large numbers of NSPC to the specific site of neurological injury through local injection of recombinant or genetic vector-derived Stem Cell Factor (SCF). The inventors have identified that SCF secreted by nerve cells in the site of injury leads to migration of endogenous NSPCs to the site of injury and their proliferation to form neurons. The inventors have shown that local injection of recombinant SCF at the site of brain or spinal cord injury induces increased migration of NSPCs to the site of injury. Therefore, this invention could have significant commercial application in the development of therapeutic interventions including cell-based therapies for neurodegenerative diseases.

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Dated: June 4, 2004.

Steven M. Ferguson,

Director, Division of Technology Development and Transfer, Office of Technology Transfer, National Institutes of Health.

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[FR Doc. 04-13100 Filed 6-9-04; 8:45 am]