[Federal Register: June 20, 2007 (Volume 72, Number 118)]
[Notices]
[Page 34024-34025]
From the Federal Register Online via GPO Access [wais.access.gpo.gov]
[DOCID:fr20jn07-108]
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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.
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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.
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.
Patent Status:
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;
soukasp@mail.nih.gov
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 hewesj@mail.nih.gov 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
[[Page 34025]]
approaches 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.
Patent Status:
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;
soukasp@mail.nih.gov.
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,
pmm@nih.gov) or Edward Berger (301-402-2481, edward_berger@nih.gov)
for more information.
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