Government-Owned Inventions; Availability for Licensing, 34022-34024 [E7-11830]
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34022
Federal Register / Vol. 72, No. 118 / Wednesday, June 20, 2007 / Notices
aimed at developing control strategies
such as vaccines and therapeutic drugs.
Inventors: Gael M. Belliot, Kim Y.
Green, Stanislav V. Sosnovtsev (NIAID)
Patent Status: HHS Reference No. E–
212–2003/0—Research Material
Licensing Status: The cDNA clone for
norovirus strain MD145–12 is available
for licensing via a biological material
license (BML).
Licensing Contact: Peter A. Soukas,
J.D.; 301/435–4646;
soukasp@mail.nih.gov.
Collaborative Research Opportunity:
The Laboratory of Infectious Diseases,
NIAID, NIH, is seeking statements of
capability or interest from parties
interested in collaborative research to
further develop, evaluate, or
commercialize reagents derived from a
cDNA clone of the genome of a
predominant human norovirus strain,
Genogroup II.4. Please contact Kim Y.
Green at kgreen@niaid.nih.gov for more
information.
rwilkins on PROD1PC63 with NOTICES
Construction of an Infectious FullLength cDNA Clone of the Porcine
Enteric Calicivirus RNA Genome
Description of Technology: Porcine
enteric calicivirus (PEC) is a member of
the genus Sapovirus in the family
Caliciviridae. This virus causes
diarrheal illness in pigs. In addition,
PEC serves as an important model for
the study of enteric caliciviruses that
cause diarrhea and that cannot be grown
in cell culture (including the
noroviruses represented by Norwalk
virus and the sapoviruses represented
by Sapporo virus). The development of
an infectious cDNA clone is important
because it enables the use of ‘‘reverse
genetics’’ to engineer mutations of
interest into the genome of PEC and to
study their effects. In addition, it allows
the introduction of foreign coding
sequences into the genome of PEC that
could be useful for vaccine development
in swine and possibly humans. This
discovery has both basic research
applications such as mapping mutations
involved in tissue culture adaptation,
tissue tropism, and virulence as well as
practical applications such as providing
a genetic backbone for the development
of chimeric vaccine viruses.
Inventors: Kyeong-Ok Chang (NIAID),
Stanislav V. Sosnovtsev (NIAID), Gael
M. Belliot (NIAID), Kim Y. Green
(NIAID), et al.
Publication: The materials are further
described in KO Chang et al., ‘‘Cellculture propagation of porcine enteric
calicivirus mediated by intestinal
contents is dependent on the cyclic
AMP signaling pathway,’’ Virology.
2002 Dec 20;304(2):302–310.
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Patent Status: HHS Reference No. E–
214–2003/0—Research Material.
Licensing Status: The materials
embodied in this invention are available
nonexclusively through a biological
materials license.
Licensing Contact: Peter A. Soukas,
J.D.; 301/435–4646;
soukasp@mail.nih.gov
Collaborative Research Opportunity:
The Laboratory of Infectious Diseases,
NIAID, NIH, is seeking statements of
capability or interest from parties
interested in collaborative research to
further develop, evaluate, or
commercialize reagents derived from an
infectious cDNA copy of the genome of
porcine enteric calicivirus. Please
contact Kim Y. Green at
kgreen@niaid.nih.gov for more
information.
Enzymatically-Active RNA-Dependent
RNA Polymerase From a Human
Norovirus (Calicivirus)
Description of Technology: The
noroviruses (formerly known as
‘‘Norwalk-like viruses’’) are associated
with gastroenteritis outbreaks, affecting
large numbers of individuals each year.
Emerging data are supporting their
increasing recognition as important
agents of diarrhea-related morbidity and
mortality. The frequency with which
noroviruses are associated with
gastroenteritis as ‘‘food and water-borne
pathogens’’ has led to the inclusion of
caliciviruses as Category B Bioterrorism
Agents/Diseases. Because the
noroviruses cannot be propagated by
any means in the laboratory, an
important strategy in their study is the
development of molecular biology-based
tools and replication systems. This
invention reports the isolation of the
first recombinant, enzymatically-active
proteinase and RNA dependent RNA
polymerase (RdRp) complex for a
human norovirus. This enzyme should
facilitate studies aimed at developing
therapeutic drugs for norovirus disease.
Inventors: Gael M. Belliot, Stanislav
V. Sosnovtsev, Kyeong-Ok Chang, Kim
Y. Green (NIAID).
Publication: The materials are further
described in L Wei et al., ‘‘Proteinasepolymerase precursor as the active form
of feline calicivirus RNA-dependent
RNA polymerase,’’ J. Virol. 2001
Feb;75(3):1211–1219.
Patent Status: HHS Reference No. E–
283–2003/0—Research Material.
Licensing Status: The materials
embodied in this invention are available
nonexclusively through a biological
materials license.
Licensing Contact: Peter A. Soukas,
J.D.; 301/435–4646;
soukasp@mail.nih.gov.
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Collaborative Research Opportunity:
The Laboratory of Infectious Diseases,
NIAID, NIH, is seeking statements of
capability or interest from parties
interested in collaborative research to
further develop, evaluate, or
commercialize an active human
norovirus proteinase-polymerase
enzyme. Please contact Kim Y. Green at
kgreen@niaid.nih.gov for more
information.
Dated: June 8, 2007.
Steven M. Ferguson,
Director,Division of Technology Development
and Transfer,Office of Technology
Transfer,National Institutes of Health.
[FR Doc. E7–11826 Filed 6–19–07; 8:45 am]
BILLING CODE 4140–01–P
DEPARTMENT OF HEALTH AND
HUMAN SERVICES
National Institutes of Health
Government-Owned Inventions;
Availability for Licensing
National Institutes of Health,
Public Health Service, HHS.
ACTION: Notice.
AGENCY:
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.
Methods for Prevention and Treatment
of Polyomavirus Infection or
Reactivation
Description of Technology: Available
for licensing and commercial
development are methods of using two
MAP kinase kinase (MEK) inhibitors,
PD98059 and U0126, in the prevention
and treatment of polyomavirus
infection. Decrease in viral protein
expression upon treatment with the
MEK inhibitors has been demonstrated
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rwilkins on PROD1PC63 with NOTICES
Federal Register / Vol. 72, No. 118 / Wednesday, June 20, 2007 / Notices
for two polyomavirus species, JC virus
(JCV) and BK virus (BKV). It is believed
that these MEK inhibitors may also be
effective against other polyomavirus
species in which TGF-b expression is
elevated.
JCV is responsible for the
demyelination of the central nervous
system which is observed in cases of
progressive multifocal
leukoencephalopathy (PML). PML is
most frequently seen in patients with
HIV/AIDS, but is also a contributing
factor in fatalities in patients with
leukemia, lymphoma, and connective
tissue diseases, in addition to
individuals receiving
immunosuppressive therapy for
autoimmune disorders or prevention of
transplant rejection.
BKV is associated with deadly clinical
syndromes such as viruria and viremia,
utreteral ulceration and stenosis, and
hemorrhagic cystitis. BKV also causes
polyomavirus-associated nephrophathy
in 1–10% of all renal transplant
recipients.
Currently, no effective antiviral agents
are available to treat these opportunistic
infections. In all observed cases,
activation of either JCV and BKV in
immunosuppressed patients has
resulted in fatality.
Applications: Treatment and
prevention of polyomavirus infection in
immunocompromised patients.
Development Status: In vitro data is
currently available and inventors are
actively developing the technology.
Inventors: Veersamy Ravichandran
and Eugene Major (NINDS).
Publication: V Ravichandran, PN
Jensen, EO Major. MEK1/2 inhibitors
block basal and TGF-b1 stimulated JC
virus multiplication. J Virol. 2007 Apr 4;
Epub ahead of print, doi:10.1128/
JVI.02658–06.
Patent Status: U.S. Provisional
Application No. 60/908,950 filed 29 Mar
2007 (HHS Reference No. E–101–2007/
0–US–01).
Licensing Status: Available for
licensing.
Licensing Contact: Cristina
Thalhammer-Reyero, Ph.D., M.B.A.;
301/435–4507; thalhamc@mail.nih.gov.
Collaborative Research Opportunity:
The National Institute of Neurological
Disorders and Stroke is seeking
statements of capability or interest from
parties interested in collaborative
research to further develop, evaluate, or
commercialize treatment and prevention
of polyomavirus infections in
immunocompromised patients. Please
contact Melissa Maderia, Ph.D. at
maderiam@mail.nih.gov for more
information.
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18:25 Jun 19, 2007
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Monoclonal Antibodies That Bind or
Neutralize Hepatitis B Virus
Description of Technology: Hepatitis
B virus (HBV) chronically infects over
300 million people worldwide. Many of
them will die of chronic hepatitis or
hepatocellular carcinoma. The present
technology relates to the isolation and
characterization of a novel neutralizing
chimpanzee monoclonal antibody to
HBV. The antibody was identified
through a combinatorial antibody
library constructed from bone marrow
cells of a chimpanzee experimentally
infected with HBV. The selected
monoclonal antibody has been shown to
react equally well with wild-type HBV
and the most common neutralization
escape mutant variants. Therefore, this
monoclonal antibody with high affinity
and broad reactivity may have distinct
advantages over other approaches to
immunoprophylaxis and
immunotherapy of chronic HBV
infection, as most of the monoclonal
antibodies currently in use are not
sufficiently and broadly reactive to
prevent the emergence of neutralization
escape mutants of HBV. This technology
describes such antibodies, fragments of
such antibodies retaining hepatitis B
virus-binding ability, fully human or
humanized antibodies retaining
hepatitis B virus-binding ability, and
pharmaceutical compositions including
such antibodies. This invention further
describes isolated nucleic acids
encoding the antibodies and host cells
transformed with nucleic acids. In
addition, this invention provides
methods of employing these antibodies
and nucleic acids in the in vitro and in
vivo diagnosis, prevention and therapy
of HBV diseases.
Inventors: Suzanne U. Emerson
(NIAID), Robert H. Purcell (NIAID), et
al.
Patent Status: U.S. Provisional
Application No. 60/644,309 filed 14 Jan
2005 (HHS Reference No. E–144–2004/
0–US–01); PCT Application No. PCT/
US2006/001336 filed 13 Jan 2006,
which published as WO 2006/076640
on 20 Jul 2006 (HHS Reference No. E–
144–2004/0–PCT–02)
Licensing Contact: Chekesha S.
Clingman, Ph.D.; 301/435–5018;
clingmac@mail.nih.gov.
Endotracheal Tube Using Unique Leak
Hole To Lower Dead Space
Description of Technology: Through
injury or diseases, human or animal
lungs may become too weak to sustain
a sufficient flow of oxygen to the body
and to remove adequate amounts of
expired carbon dioxide. The present
invention is a tracheal tube ventilation
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34023
apparatus which efficiently rids patients
of expired gases and promotes healthier
breathing. This is accomplished by
creating one or more leak holes in the
wall of the endotracheal tube above the
larynx, such as in the back of the mouth
(i.e., oropharynx), so that expired gases
can leak out of the endotracheal tube.
The described apparatus is a two stage
tube where the first stage has a smaller
diameter such that it fits within the
confined area of the lower trachea and
the second stage has a larger diameter,
which fits properly within the larger
diameter of the patient’s pharynx. The
endotracheal tube is preferably wire
reinforced and ultra-thin walled so as to
reduce airway resistance. The invention
substantially reduces endotracheal dead
space and is expected to benefit those
patients with both early and late stage
acute respiratory failure, and reduce or
obviate the need for mechanical
pulmonary ventilation in many patients.
Applications: Tracheal tube
ventilation; Efficiently rid patient of
expired gases and thereby promote
healthier breathing.
Development Status: System is well
developed and operational.
Inventor: Theodor Kolobow (NHLBI).
Patent Status: U.S. Patent No.
7,107,991 issued 19 Sep 2006 (HHS
Reference No. E–269–2001/0–US–01);
PCT Application No. PCT/US02/29319
filed 16 Sep 2002 (HHS Reference No.
E–269–2001/0–PCT–02); Canadian
National Stage Filing, Application No.
2463538, filed 16 Sep 2002 (HHS
Reference No. E–269–2001/0–CA–03);
European National Stage Filing,
Application No. 02773398.9, filed 28
Mar 2004 (HHS Reference No. E–269–
2001/0–EP–04).
Licensing Status: Available for nonexclusive or exclusive licensing.
Licensing Contact: Michael A.
Shmilovich, Esq.; 301/435–5019;
shmilovm@mail.nih.gov.
Collaborative Research Opportunity:
The NHLBI/Pulmonary Critical Care
Medicine Branch (PCCMB) is seeking
statements of capability or interest from
parties interested in collaborative
research to further develop, evaluate, or
commercialize innovative endotracheal
tube technology. Please contact
Marianne Lynch at 301–594–4094 or
lynchm@nhlbi.nih.gov for more
information.
Increased Protein Expression Vector for
Vaccine Applications
Description of Technology: An
expression vector with a unique
promoter that results in higher level of
protein expression than vectors
currently in use is available for
licensing from the NIH. The elevated
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34024
Federal Register / Vol. 72, No. 118 / Wednesday, June 20, 2007 / Notices
levels of expression are achieved
through use of a specific promoter,
known as CMV/R, in which the Human
T-Lymphotrophic Virus (HTLV–1) Long
Terminal Repeat (LTR) R–U5 region is
substituted for a portion of the intron
downstream of the CMV immediate
early region 1 enhancer (Barouch et al.,
2005). Sequences of 95% or better
homology to CMV/R can be used as
well. CMV/R vectors are currently being
used in a number of clinical trials,
including vaccines against West Nile
Virus, Ebola virus, and HIV and
achieving promising results. The related
HIV vaccine technology is available for
licensing, as is the Ebola DNA vaccine
technology (non-exclusive licensing
only). The CMV/R vector can be used
for any DNA vaccine or for the
production of recombinant proteins in
high yields.
Applications: Vector for DNA
vaccines; High yield expression of
recombinant proteins.
Inventors: Gary Nabel and Zhi-yong
Yang (NIAID).
Patent Status: U.S. Patent No.
7,094,598 issued 22 Aug 2006 [HHS
Reference No. E–241–2001/1–US–01
(CMV/R)], applications pending in EP,
JP, CA, and AU; U.S. Patent Application
No. 10/491,121 filed 23 Aug 2004 [HHS
Reference No. E–241–2001/0–US–07
(Ebola DNA vaccine)], applications
pending in EP, JP, CA, and AU; U.S.
Patent Application No. 11/632,522 filed
16 Jan 2007 [HHS Reference No. E–267–
2004/1–US–08 (HIV DNA vaccine)].
Licensing Status: Available for nonexclusive licensing.
Licensing Contact: Susan Ano, Ph.D.;
301/435–5515; anos@mail.nih.gov.
Dated: June 11, 2007.
Steven M. Ferguson,
Director, Division of Technology Development
and Transfer, Office of Technology Transfer,
National Institutes of Health.
[FR Doc. E7–11830 Filed 6–19–07; 8:45 am]
BILLING CODE 4140–01–P
DEPARTMENT OF HEALTH AND
HUMAN SERVICES
National Institutes of Health
Government-Owned Inventions;
Availability for Licensing
National Institutes of Health,
Public Health Service, HHS.
ACTION: Notice.
rwilkins on PROD1PC63 with NOTICES
AGENCY:
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
VerDate Aug<31>2005
18:25 Jun 19, 2007
Jkt 211001
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 polysaccharideprotein 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
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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 Tlymphocytes, macrophages, and
immature dendritic cells. Chemokine
binding to CCR5 leads to cellular
activation through pertussis toxinsensitive heterotrimeric G proteins as
well as G protein-independent
signalling pathways. Like many other
GPCRs, CCR5 is regulated by agonistdependent processes which involve G
protein coupled receptor kinase (GRK)dependent phosphorylation, betaarrestin-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
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Agencies
[Federal Register Volume 72, Number 118 (Wednesday, June 20, 2007)]
[Notices]
[Pages 34022-34024]
From the Federal Register Online via the Government Printing Office [www.gpo.gov]
[FR Doc No: E7-11830]
-----------------------------------------------------------------------
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.
Methods for Prevention and Treatment of Polyomavirus Infection or
Reactivation
Description of Technology: Available for licensing and commercial
development are methods of using two MAP kinase kinase (MEK)
inhibitors, PD98059 and U0126, in the prevention and treatment of
polyomavirus infection. Decrease in viral protein expression upon
treatment with the MEK inhibitors has been demonstrated
[[Page 34023]]
for two polyomavirus species, JC virus (JCV) and BK virus (BKV). It is
believed that these MEK inhibitors may also be effective against other
polyomavirus species in which TGF-[beta] expression is elevated.
JCV is responsible for the demyelination of the central nervous
system which is observed in cases of progressive multifocal
leukoencephalopathy (PML). PML is most frequently seen in patients with
HIV/AIDS, but is also a contributing factor in fatalities in patients
with leukemia, lymphoma, and connective tissue diseases, in addition to
individuals receiving immunosuppressive therapy for autoimmune
disorders or prevention of transplant rejection.
BKV is associated with deadly clinical syndromes such as viruria
and viremia, utreteral ulceration and stenosis, and hemorrhagic
cystitis. BKV also causes polyomavirus-associated nephrophathy in 1-10%
of all renal transplant recipients.
Currently, no effective antiviral agents are available to treat
these opportunistic infections. In all observed cases, activation of
either JCV and BKV in immunosuppressed patients has resulted in
fatality.
Applications: Treatment and prevention of polyomavirus infection in
immunocompromised patients.
Development Status: In vitro data is currently available and
inventors are actively developing the technology.
Inventors: Veersamy Ravichandran and Eugene Major (NINDS).
Publication: V Ravichandran, PN Jensen, EO Major. MEK1/2 inhibitors
block basal and TGF-[beta]1 stimulated JC virus
multiplication. J Virol. 2007 Apr 4; Epub ahead of print, doi:10.1128/
JVI.02658-06.
Patent Status: U.S. Provisional Application No. 60/908,950 filed 29
Mar 2007 (HHS Reference No. E-101-2007/0-US-01).
Licensing Status: Available for licensing.
Licensing Contact: Cristina Thalhammer-Reyero, Ph.D., M.B.A.; 301/
435-4507; thalhamc@mail.nih.gov.
Collaborative Research Opportunity: The National Institute of
Neurological Disorders and Stroke is seeking statements of capability
or interest from parties interested in collaborative research to
further develop, evaluate, or commercialize treatment and prevention of
polyomavirus infections in immunocompromised patients. Please contact
Melissa Maderia, Ph.D. at maderiam@mail.nih.gov for more information.
Monoclonal Antibodies That Bind or Neutralize Hepatitis B Virus
Description of Technology: Hepatitis B virus (HBV) chronically
infects over 300 million people worldwide. Many of them will die of
chronic hepatitis or hepatocellular carcinoma. The present technology
relates to the isolation and characterization of a novel neutralizing
chimpanzee monoclonal antibody to HBV. The antibody was identified
through a combinatorial antibody library constructed from bone marrow
cells of a chimpanzee experimentally infected with HBV. The selected
monoclonal antibody has been shown to react equally well with wild-type
HBV and the most common neutralization escape mutant variants.
Therefore, this monoclonal antibody with high affinity and broad
reactivity may have distinct advantages over other approaches to
immunoprophylaxis and immunotherapy of chronic HBV infection, as most
of the monoclonal antibodies currently in use are not sufficiently and
broadly reactive to prevent the emergence of neutralization escape
mutants of HBV. This technology describes such antibodies, fragments of
such antibodies retaining hepatitis B virus-binding ability, fully
human or humanized antibodies retaining hepatitis B virus-binding
ability, and pharmaceutical compositions including such antibodies.
This invention further describes isolated nucleic acids encoding the
antibodies and host cells transformed with nucleic acids. In addition,
this invention provides methods of employing these antibodies and
nucleic acids in the in vitro and in vivo diagnosis, prevention and
therapy of HBV diseases.
Inventors: Suzanne U. Emerson (NIAID), Robert H. Purcell (NIAID),
et al.
Patent Status: U.S. Provisional Application No. 60/644,309 filed 14
Jan 2005 (HHS Reference No. E-144-2004/0-US-01); PCT Application No.
PCT/US2006/001336 filed 13 Jan 2006, which published as WO 2006/076640
on 20 Jul 2006 (HHS Reference No. E-144-2004/0-PCT-02)
Licensing Contact: Chekesha S. Clingman, Ph.D.; 301/435-5018;
clingmac@mail.nih.gov.
Endotracheal Tube Using Unique Leak Hole To Lower Dead Space
Description of Technology: Through injury or diseases, human or
animal lungs may become too weak to sustain a sufficient flow of oxygen
to the body and to remove adequate amounts of expired carbon dioxide.
The present invention is a tracheal tube ventilation apparatus which
efficiently rids patients of expired gases and promotes healthier
breathing. This is accomplished by creating one or more leak holes in
the wall of the endotracheal tube above the larynx, such as in the back
of the mouth (i.e., oropharynx), so that expired gases can leak out of
the endotracheal tube. The described apparatus is a two stage tube
where the first stage has a smaller diameter such that it fits within
the confined area of the lower trachea and the second stage has a
larger diameter, which fits properly within the larger diameter of the
patient's pharynx. The endotracheal tube is preferably wire reinforced
and ultra-thin walled so as to reduce airway resistance. The invention
substantially reduces endotracheal dead space and is expected to
benefit those patients with both early and late stage acute respiratory
failure, and reduce or obviate the need for mechanical pulmonary
ventilation in many patients.
Applications: Tracheal tube ventilation; Efficiently rid patient of
expired gases and thereby promote healthier breathing.
Development Status: System is well developed and operational.
Inventor: Theodor Kolobow (NHLBI).
Patent Status: U.S. Patent No. 7,107,991 issued 19 Sep 2006 (HHS
Reference No. E-269-2001/0-US-01); PCT Application No. PCT/US02/29319
filed 16 Sep 2002 (HHS Reference No. E-269-2001/0-PCT-02); Canadian
National Stage Filing, Application No. 2463538, filed 16 Sep 2002 (HHS
Reference No. E-269-2001/0-CA-03); European National Stage Filing,
Application No. 02773398.9, filed 28 Mar 2004 (HHS Reference No. E-269-
2001/0-EP-04).
Licensing Status: Available for non-exclusive or exclusive
licensing.
Licensing Contact: Michael A. Shmilovich, Esq.; 301/435-5019;
shmilovm@mail.nih.gov.
Collaborative Research Opportunity: The NHLBI/Pulmonary Critical
Care Medicine Branch (PCCMB) is seeking statements of capability or
interest from parties interested in collaborative research to further
develop, evaluate, or commercialize innovative endotracheal tube
technology. Please contact Marianne Lynch at 301-594-4094 or
lynchm@nhlbi.nih.gov for more information.
Increased Protein Expression Vector for Vaccine Applications
Description of Technology: An expression vector with a unique
promoter that results in higher level of protein expression than
vectors currently in use is available for licensing from the NIH. The
elevated
[[Page 34024]]
levels of expression are achieved through use of a specific promoter,
known as CMV/R, in which the Human T-Lymphotrophic Virus (HTLV-1) Long
Terminal Repeat (LTR) R-U5 region is substituted for a portion of the
intron downstream of the CMV immediate early region 1 enhancer (Barouch
et al., 2005). Sequences of 95% or better homology to CMV/R can be used
as well. CMV/R vectors are currently being used in a number of clinical
trials, including vaccines against West Nile Virus, Ebola virus, and
HIV and achieving promising results. The related HIV vaccine technology
is available for licensing, as is the Ebola DNA vaccine technology
(non-exclusive licensing only). The CMV/R vector can be used for any
DNA vaccine or for the production of recombinant proteins in high
yields.
Applications: Vector for DNA vaccines; High yield expression of
recombinant proteins.
Inventors: Gary Nabel and Zhi-yong Yang (NIAID).
Patent Status: U.S. Patent No. 7,094,598 issued 22 Aug 2006 [HHS
Reference No. E-241-2001/1-US-01 (CMV/R)], applications pending in EP,
JP, CA, and AU; U.S. Patent Application No. 10/491,121 filed 23 Aug
2004 [HHS Reference No. E-241-2001/0-US-07 (Ebola DNA vaccine)],
applications pending in EP, JP, CA, and AU; U.S. Patent Application No.
11/632,522 filed 16 Jan 2007 [HHS Reference No. E-267-2004/1-US-08 (HIV
DNA vaccine)].
Licensing Status: Available for non-exclusive licensing.
Licensing Contact: Susan Ano, Ph.D.; 301/435-5515;
anos@mail.nih.gov.
Dated: June 11, 2007.
Steven M. Ferguson,
Director, Division of Technology Development and Transfer, Office of
Technology Transfer, National Institutes of Health.
[FR Doc. E7-11830 Filed 6-19-07; 8:45 am]
BILLING CODE 4140-01-P