National Institutes of Health, Public Health Service, HHS.
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.
Vibrio Cholerae O139 Conjugate Vaccines
Description of Technology: Cholera remains an important public health problem. Epidemic cholera is caused by two Vibrio cholerae serotypes O1 and O139. The disease is spread through contaminated water. According to information reported to the World Health Organization in 1999, nearly 8,500 people died and another 223,000 were sickened with cholera worldwide. This invention is a polysaccharide-protein conjugate vaccine to prevent and treat infection by Vibrio cholerae O139 comprising the capsular polysaccharide (CPS) of V. cholerae O139 conjugated through a dicarboxylic acid dihydrazide linker to a mutant diphtheria toxin carrier. In addition to the conjugation methods, also claimed in the invention are methods of immunization against V. cholerae O139 using the conjugates of the invention. The inventors have shown that the conjugates of the invention elicited in mice high levels of serum antibodies to CPS, a surface antigen of Vibrio cholerae O139, that have vibriocidal activity. Clinical trials of the two most immunogenic conjugates have been planned by the inventors. The conjugate vaccine is aimed for long lasting immunity, especially in young children, and can be administered in concurrent with routine vaccines.
Inventors: Shousun Szu, Zuzana Kossaczka, John Robbins (NICHD).
Related Publication: Z Kossaczka et al. Vibrio cholerae O139 conjugate vaccines: synthesis and immunogenicity of V. cholerae O139 capsular polysaccharide conjugates with recombinant diphtheria toxin mutant in mice. Infect Immun. 2000 Sep;68(9):5037-5043.
PCT Application No. PCT/US00/24119 filed 01 Sep 2000, which published as WO 02/20059 on 14 Mar 2002 (HHS Reference No. E-274-2000/0-PCT-01)
U.S. Patent Application No. 10/363,618 filed 01 Sep 2000 (HHS Reference No. E-274-2000/0-US-02)
U.S. Patent Application No. 11/695,735 filed 03 Apr 2007 (HHS Reference No. E-274-2000/0-US-03)
Licensing Status: Available for exclusive or non-exclusive licensing.
Licensing Contact: Peter A. Soukas, J.D.; 301/435-4646; firstname.lastname@example.org
Collaborative Research Opportunity: The NICHD/LDMI is seeking statements of capability or interest from parties interested in collaborative research to further develop, evaluate, or commercialize Vibrio cholera O139 or O1 conjugate vaccines. Please contact John D. Hewes, Ph.D. at 301-435-3121 or email@example.com for more information.
CC Chemokine Receptor 5 DNA, New Animal Models and Therapeutic Agents for HIV Infection
Description of Technology: Chemokine receptors are expressed by many cells, including lymphoid cells, and function to mediate cell trafficking and localization. CC chemokine receptor 5 (CCR5) is a seven-transmembrane, G protein-coupled receptor (GPCR) which regulates trafficking and effector functions of memory/effector T-lymphocytes, macrophages, and immature dendritic cells. Chemokine binding to CCR5 leads to cellular activation through pertussis toxin-sensitive heterotrimeric G proteins as well as G protein-independent signalling pathways. Like many other GPCRs, CCR5 is regulated by agonist-dependent processes which involve G protein coupled receptor kinase (GRK)-dependent phosphorylation, beta-arrestin-mediated desensitization and internalization.
Human CCR5 also functions as the main coreceptor for the fusion and entry of many strains of human immunodeficiency virus (HIV-1, HIV-2). HIV-1 transmission almost invariably involves such CCR5-specific variants (designated R5); individuals lacking functional CCR5 (by virtue of homozygosity for a defective CCR5 allele) are almost completely resistant to HIV-1 infection. Specific blocking of CCR5 (e.g. with chemokine ligands, anti-CCR5 antibodies, CCR5-blocking low MW inhibitors, etc.) inhibits entry/infection of target cells by R5 HIV strains. Cells expressing CCR5 and CD4 are useful for screening for agents that inhibit HIV by binding to CCR5. Such agents represent potential new Start Printed Page 34025approaches to block HIV transmission and to treat infected people. A small animal expressing both human CCR5 along with human CD4 supports entry of HIV into target cells, a necessary hurdle that must be overcome for development of a small animal model (e.g. transgenic mouse, rat, rabbit, mink) to study HIV infection and its inhibition.
The invention embodies the CCR5 genetic sequence, cell lines and transgenic animals, the cells of which coexpress human CD4 and CCR5, and which may represent valuable tools for the study of HIV infection and for screening anti-HIV agents. The invention also embodies anti-CCR5 agents that block HIV env-mediated membrane fusion associated with HIV entry into human CD4-positive target cells or between HIV-infected cells and uninfected human CD4-positive target cells.
Inventors: Christophe Combadiere, Yu Feng, Ghalib Alkahatib, Edward A. Berger, Philip M. Murphy, Christopher C. Broder, Paul E. Kennedy (NIAID).
Publication: This technology was reported in Alkhatib et al., “CC CKR5: a RANTES, MIP-1alpha, MIP-1beta receptor as a fusion cofactor for macrophage-tropic HIV-1,” Science 1996 Jun 28;272(5270):1955-1958.
U.S. Provisional Application No. 60/018,508 filed 28 May 1996 (HHS Reference No. E-090-1996/0-US-01)
U.S. Patent Application No. 08/864,458 filed 28 May 1997 (HHS Reference No. E-090-1996/0-US-04)
U.S. Patent No. 7,151,087 issued 19 Dec 2006 (HHS Reference No. E-090-1996/0-US-06)
U.S. Patent Application No. 10/439,845 filed 15 May 2003 (HHS Reference No. E-090-1996/0-US-05)
U.S. Patent Application No. 10/846,185 filed 14 May 2004 (HHS Reference No. E-090-1996/0-US-07)
U.S. Patent Application No. 11/594,375 filed 07 Nov 2006 (HHS Reference No. E-090-1996/0-US-08)
PCT Application No. PCT/US97/09586 filed 28 May 1997 (HHS Reference No. E-090-1996/0-PCT-02)
European Patent Application No. 97929777.7 filed 28 May 1997 (HHS Reference No. E-090-1996/0-EP-03)
Licensing Status: The technology is available for exclusive or nonexclusive licensing.
Licensing Contact: Peter Soukas; 301/435-4646; firstname.lastname@example.org.
Collaborative Research Opportunity: The NIAID Laboratory of Molecular Immunology and Laboratory of Viral Diseases are seeking statements of capability or interest from parties interested in collaborative research to further develop, evaluate, or commercialize CCR5-related products. Please contact Philip Murphy (301-496-8616, email@example.com) or Edward Berger (301-402-2481, firstname.lastname@example.org) for more information.Start Signature
Dated: June 11, 2007.
Steven M. Ferguson,
Director,Division of Technology Development and Transfer,Office of Technology Transfer,National Institutes of Health.
[FR Doc. E7-11854 Filed 6-19-07; 8:45 am]
BILLING CODE 4140-01-P