Government-Owned Inventions; Availability for Licensing, 21633-21636 [E8-8620]
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Federal Register / Vol. 73, No. 78 / Tuesday, April 22, 2008 / Notices
Teresa.Watkins@fda.hhs.gov, or FDA
Advisory Committee Information Line,
1–800–741–8138 (301–443–0572) in
Washington, DC area), codes
3014512529 and 3014512535. Please
call the Information Line for up-to-date
information on this meeting.
SUPPLEMENTARY INFORMATION: In the
Federal Register of March 27, 2008,
FDA announced that a meeting of the
Anesthetic and Life Support Drugs
Advisory Committee and the Drug
Safety and Risk Management Advisory
Committee would be held on May 5 and
6, 2008.
On page 16314, in the third column,
the introductory paragraph of the
document is amended to read as
follows:
This notice announces a forthcoming
meeting of a public advisory committee
of the Food and Drug Administration
(FDA). At least one portion of the
meeting will be closed to the public.
On page 16315, the second column of
the document is amended to add a
portion entitled ‘‘Closed Committee
Deliberations’’ to read as follows:
Closed Committee Deliberations: On
May 5, 2008, from 8 a.m. to 9:15 a.m.,
the meeting will be closed to permit
discussion and review of trade secret
and/or confidential commercial
information (5 U.S.C. 552b(c)(4)).
During this session, the committee will
discuss the details of a proprietary
research report and protocol addressing
characteristics of different formulations.
This notice is issued under the
Federal Advisory Committee Act (5
U.S.C. app. 2) and 21 CFR part 14,
relating to the advisory committees.
Dated: April 16, 2008.
Randall W. Lutter,
Deputy Commissioner for Policy.
[FR Doc. E8–8683 Filed 4–21–08; 8:45 am]
BILLING CODE 4160–01–S
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.
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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
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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.
Platform for the High Throughput
Screening of Single Nucleotide
Polymorphisms and Small Insertions
and Deletions
Description of Technology: Available
for licensing and commercial
development is an oligoarray-based
process for gene-specific single
nucleotide polymorphism (SNP)
genotyping based on comparative
hybridization. This process can detect,
even in heterozygous conditions, known
and potentially flag unknown variants
(point mutations, base insertion or
deletion) along the complete sequence
of a given gene while drastically cutting
the time and costs compared to highthroughput direct sequencing without
affecting sensitivity and specificity. The
accuracy and efficiency of the invention
was validated based on the BRCA–1
breast and ovarian cancer predisposing
gene. This process can easily be custom
designed to include within the same
platform a relatively large number of
genes relevant to a specific clinical
condition and it is particularly useful
for the screening of long genomic region
with relatively infrequent but clinically
relevant variants.
More specifically, the invention is
made reliable by the development of
two tailored algorithms: the first
automatically designs the complete data
set of gene-specific probes starting from
the genomic sequence according to the
user specification (size of the probes,
relative position, etc.); and the other is
based on an algorithm that flags gene
variants in the test sample. This allows
detecting unknown variants in the
region in which only the reference
hybridizes to the probes. These features
drastically reduce the amount of
sequencing (the gold standard for SNP
detection) to small regions in which a
discrepancy between test signal and
reference signal is found. Moreover,
there is no limit, other than the physical
area of the slide, to the number of
probes that can be added to the array
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and the number of genes that can be
queried simultaneously. Thus, a
repertoire of considerable size can be
scanned in a single test for each sample
with sensitivity and specificity
comparable to direct sequencing.
Applications: The immediate clinical
applications of this platform is a
remarkable improvement of genetic
testing by increasing the number of
target genes that can be screened in a
short time, at a minimal cost using an
automated simplified analysis, such as
the sequencing-grade screening for
BRCA–1 variants and the detection of
mutations in cancerous tissues. The
method can be also applied to other
human genes (coding and non-coding
sequences), and other sequences from
animals, bacterial and viruses.
Development Status: Method fully
developed and validated.
Inventors: Ena Wang (CC), Alessandro
Monaco (CC), Francesco M Marincola
(CC), et al.
Patent Status: U.S. Provisional
Application No. 61/068,182 filed 05 Mar
2008 (HHS Reference No. E–082–2008/
0–US–01).
Licensing Status: Available for nonexclusive or exclusive licensing.
Licensing Contact: Cristina
Thalhammer-Reyero, Ph.D., M.B.A.;
301–435–4507; thalhamc@mail.nih.gov.
Generation of Wild-Type Dengue
Viruses for Use in Rhesus Monkey
Infection Studies
Description of Technology: Dengue
virus is a positive-sense RNA virus
belonging to the Flavivirus genus of the
family Flaviviridae. Dengue virus is
widely distributed throughout the
tropical and semitropical regions of the
world and is transmitted to humans by
mosquito vectors. Dengue virus is a
leading cause of hospitalization and
death in children in at least eight
tropical Asian countries. There are four
serotypes of dengue virus (DEN–1,
DEN–2, DEN–3, and DEN–4) that
annually cause an estimated 50–100
million cases of dengue fever and
500,000 cases of the more severe form
of dengue virus infection known as
dengue hemorrhagic fever/dengue shock
syndrome (DHF/DSS). This latter
disease is seen predominately in
children and adults experiencing a
second dengue virus infection with a
serotype different than that of their first
dengue virus infection and in primary
infection of infants who still have
circulating dengue-specific maternal
antibody. A vaccine is needed to lessen
the disease burden caused by dengue
virus, but none is licensed.
Because of the association of more
severe disease with secondary dengue
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virus infection, a successful vaccine
must induce immunity to all four
serotypes. Immunity is primarily
mediated by neutralizing antibody
directed against the envelope (E)
glycoprotein, a virion structural protein.
Infection with one serotype induces
long-lived homotypic immunity and a
short-lived heterotypic immunity.
Therefore, the goal of immunization is
to induce a long-lived neutralizing
antibody response against DEN–1, DEN–
2, DEN–3, and DEN–4, which can best
be achieved economically using live
attenuated virus vaccines. This is a
reasonable goal since a live attenuated
vaccine has already been developed for
the related yellow fever virus, another
mosquito-borne flavivirus present in
tropical and semitropical regions of the
world.
The evaluation of live attenuated
dengue vaccine candidates in rhesus
monkeys requires wild type control
viruses for each of the four dengue
serotypes. These control viruses are
used for comparison to the attenuated
strains and post-vaccination challenge
to assess vaccine efficacy. As such,
these viruses need to be well
characterized and sufficiently pure to
ensure that they will replicate to
consistent levels in rhesus monkeys.
Characterization generally includes
sequence analysis, titration, and
evaluation in monkeys. The following
viruses have been characterized: (1)
DEN1 WP (2) DEN1 Puerto Rico/94 (3)
DEN2 NGC prototype (4) DEN2 Tonga/
74 (5) DEN3 Sleman/78 and (6) DEN4
Dominica/81.
Application: Dengue/flavivirus
vaccine studies, dengue/flavivirus
diagnostics, dengue/flavivirus research
tools.
Development Status: Materials are
available for transfer.
Inventors: Stephen S. Whitehead and
Joseph E. Blaney, Jr. (NIAID).
Publications:
1. AP Durbin, RA Karron, W Sun, DW
Vaughn, MJ Reynolds, JR Perreault, B
Thumar, R Men, C-J Lai, WR Elkins, RM
Chanock, BR Murphy, SS Whitehead. A
live attenuated dengue virus type 4
vaccine candidate with a 30 nucleotide
deletion in the 3′ untranslated region is
highly attenuated and immunogenic in
humans. Am J Trop Med Hyg. 2001
Nov;65(5):405–413.
2. SS Whitehead, B Falgout, KA
Hanley, JE Blaney Jr., L Markoff, BR
Murphy. A live, attenuated dengue virus
type 1 vaccine candidate with a 30nucleotide deletion in the 3′
untranslated region is highly attenuated
and immunogenic in monkeys. J Virol.
2003 Jan;77(2):1653–1657.
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3. SS Whitehead, KA Hanley, JE
Blaney Jr., LE Gilmore, WR Elkins, BR
Murphy. Substitution of the structural
genes of dengue virus type 4 with those
of type 2 results in chimeric vaccine
candidates which are attenuated for
mosquitoes, mice, and rhesus monkeys.
Vaccine 2003 Oct 1;21(27–30):4307–
4316.
4. JE Blaney Jr., CT Hanson, KA
Hanley, BR Murphy, SS Whitehead.
Vaccine candidates derived from a
novel infectious cDNA clone of an
American genotype dengue virus type 2.
BMC Infect Dis. 2004 Oct 4;4:39.
5. JE Blaney Jr., CT Hanson, CY
Firestone, KA Hanley, BR Murphy, SS
Whitehead. Genetically modified, live
attenuated dengue virus type 3 vaccine
candidates. Am J Trop Med Hyg. 2004
Dec;71(6):811–821.
6. JE Blaney Jr., JM Matro, BR
Murphy, SS Whitehead. Recombinant,
live-attenuated tetravalent dengue virus
vaccine formulations induce a balanced,
broad, and protective neutralizing
antibody response against each of the
four serotypes in rhesus monkeys. J
Virol. 2005 May;79(9):5516–5528.
7. JE Blaney Jr., NS Sathe, CT Hanson,
CY Firestone, BR Murphy, SS
Whitehead. Vaccine candidates for
dengue virus type 1 (DEN1) generated
by replacement of the structural genes of
rDEN4 and rDEN4Delta30 with those of
DEN1. Virol J. 2007 Feb 28;4:23.
Patent Status: HHS Reference No. E–
042–2008/0—Research Tool. Patent
protection is not being sought for this
technology.
Licensing Status: Available for
nonexclusive biological materials
licensing only.
Licensing Contact: Peter A. Soukas,
J.D.; 301–435–4646;
soukasp@mail.nih.gov.
A Rapid Ultrasensitive Assay for
Detecting Prions in Samples Based on
the Seeded Polymerization of
Recombinant Normal Prion Protein
(rPrP-sen)
Description of Technology: Prion
diseases are infectious
neurodegenerative diseases of great
public concern. Humans may be
infected by eating infected animals
(primarily hoofed animals or ungulates).
Blood transfusions have also been
documented as a cause of human cases
of prion infection. Prion diseases
include: Creutzfeldt-Jakob disease (CJD)
(humans); variant Creutzfeldt-Jakob
disease (vCJD) (humans); Scrapie
(sheep); Bovine Spongiform
Encephalopathy (BSE) (cattle); and
Chronic Wasting Disease (deer, elk and
moose). Currently available rapid tests
for infectious prions, which are
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routinely used to monitor slaughtered
animals, are not sensitive enough to
detect prion infections in samples from
live animals or humans and must be
performed post-mortem. Additionally,
these tests cannot be used to detect
subinfectious concentrations of
infectious prions in humans or animals.
An ultrasensitive assay for infectious
prions, the protein-misfolding cyclic
amplification assay (PMCA), is available
for testing live animals or humans;
however, this test is expensive because
it is difficult to perform, relies on the
use of brain homogenates, and can take
2–3 weeks to perform.
This technology enables the rapid
detection of extremely low, sub-lethal,
concentrations of prions. This assay,
like PMCA, is based on the prioninduced polymerization of normal prion
protein (PrP-sen). However, this assay,
unlike PMCA uses recombinant normal
prion protein (rPrP-sen) rather than
normal prion protein derived from brain
homogenate. The use of rPrP-sen
provides major advantages over PMCA.
rPrP-sen provides a relatively
inexpensive, abundant, and
concentrated source of pure PrP-sen as
a substrate for the PMCA prion
amplification reaction. This permits the
detection of PrP-res in 2–3 hours and
the ultrasensitive detection of PrP-res in
2 to 3 days. Moreover, relative to PrPsen in brain tissue, rPrP-sen is much
easier to mutate and chemically modify
to facilitate detection of prion-induced
PMCA amplification products in
potentially high-throughput formats. In
its current embodiment, the
ultrasensitive assay has been used to
consistently detect (by western blot)
around 50 ag of hamster PrP-Sc (0.003
lethal dose) in cerebral spinal fluid and
brain tissue within 2 to 3 days.
Applications:
A diagnostic assay for detecting prion
diseases early.
An assay for monitoring the
progression of prion disease and the
effectiveness of treatments.
A veterinary assay for detecting PrPres in live animals and assessing the
extent of prion disease in live herds.
An assay for the detection of prion in
commercial products (e.g.,
biotechnological or agricultural), blood
and blood products, transplantation
tissues, medical devices, and
environmental samples.
Market:
Currently, there is a need for a rapid,
ultrasensitive, veterinary test for prion
diseases in live animals used for human
consumption and a need for assessing
the extent of prion infection in live
herds.
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Currently, there is a need for a human
diagnostic assay to detect prion disease
early when treatment is most effective
and a need for monitoring the
effectiveness of treatments for prion
diseases.
Currently, there is a need for a rapid,
ultrasensitive test for prions in
commercial products (e.g.,
biotechnological or agricultural), blood
and blood products, transplantation
tissues, medical devices, and
environmental samples in which prion
contamination might be a concern.
Inventors: Ryuichiro Atarashi, Roger
A. Moore, Suzette A. Priola, and Byron
W. Caughey (NIAID).
Related Publication: R Atarashi et al.
Ultrasensitive detection of scrapie prion
protein using seeded conversion of
recombinant prion protein. Nat Methods
2007 Aug;4(8):645–650.
Patent Status: U.S. Provisional
Application No.60/961,364 filed 20 Jul
2007 (HHS Reference No. E–109–2007/
0-US–01).
Licensing Status: Available for
exclusive and non-exclusive licensing.
Licensing Contact: RC Tang, J.D.,
LL.M.; 301–435–5031;
tangrc@mail.nih.gov.
Collaborative Research Opportunity:
The NIAID Laboratory of Persistent
Viral Diseases, TSE/Prion Biochemistry
Section, is seeking statements of
capability or interest from parties
interested in collaborative research to
further develop, evaluate, or
commercialize this technology. Please
contact Byron Caughey, Ph.D. at (406)
363–9264 or bcaughey@niaid.nih.gov for
more information.
Identification of a Cell-Surface CoReceptor That Mediates the Uptake and
Immunostimulatory Activity of ‘‘D’’
Type CpG Oligonucleotides
Description of Technology:
Unmethylated CpG motifs are present at
high frequency in bacterial DNA. They
provide a danger signal to the
mammalian immune system that
triggers a protective immune response
characterized by the production of Th1
and proinflammatory cytokines and
chemokines. Although the recognition
of CpG DNA by B cells and
plasmacytoid dendritic cells is mediated
by TLR 9, these cell types differ in their
ability to bind and respond to
structurally distinct classes of CpG
oligonucleotides. The inventors’ work
established that CXCL16, a membranebound scavenger receptor, influences
the uptake, subcellular localization, and
cytokine profile induced by D
oligonucleotides.
Knowing that CXCL16 can be used to
selectively internalize ODN could be
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useful for (1) Improving the activity of
D type ODN, (2) improving recognition
(and side effects) of other types of ODNs
by deleting regions that interact with
CXCL16 (3) potentially improving the
targeting of any drug or biologic to
CXCL16 expressing cells, (4) targeting
antisense ODNs to immune cells or
preventing side effects from antisense
therapy, and also applications to (5)
DNA vaccines and other agents that
require targeting to CXCL16 expressing
cells such as dendritic cells and
monocytes.
This application claims methods of
inducing an immune response that
include administering agents that
increase the activity and/or expression
of CXCL16 and a D ODN. The
application also claims methods of
decreasing an immune response to a
CpG ODN, including administering
agents that decrease the activity and/or
expression of CXCL16. Compositions
including one or more D type ODNs and
an agent that modulates the activity
and/or expression of CXCL16 are also
claimed.
Application: Vaccine adjuvants,
production of vaccines,
immunotherapeutics.
Developmental Status: Preclinical
studies have been performed;
oligonucleotides have been synthesized.
Inventors: Dennis Klinman (FDA/
CBER; NCI), Ihsan Gursel (FDA/CBER),
Mayda Gursel (FDA/CBER).
Publication: M Gursel et al. CXCL16
influences the nature and specificity of
CpG-induced immune activation. J
Immunol. 2006 Aug 1;177(3):1575–
1580.
Patent Status: U.S. Provisional
Application No. 60/713,547 filed 31
Aug 2005 (HHS Reference No. E–036–
2005/0–US–01); PCT Application No.
PCT/US2006/033774 filed 28 Aug 2006
(HHS Reference Number E–036–2005/0–
PCT–02); U.S. Patent Application No.
12/065,085 filed 27 Feb 2008 (HHS
Reference Number E–036–2005/0–US–
03).
Licensing Status: Available for
exclusive or nonexclusive licensing.
Licensing Contact: Peter A. Soukas,
J.D.; 301–435–4646;
soukasp@mail.nih.gov.
Collaborative Research Opportunity:
The National Cancer Institute,
Laboratory of Experimental
Immunology, Immune Modulation
Group, is seeking statements of
capability or interest from parties
interested in collaborative research to
further develop, evaluate, or
commercialize this technology. Please
contact John D. Hewes, Ph.D. at 301–
435–3121 or hewesj@mail.nih.gov for
more information.
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Use of Suppressive Oligonucleotides To
Treat Uveitis
Description of Technology: Uveitis is
a major cause of visual loss in
industrialized nations. Uveitis refers to
an intraocular inflammation of the uveal
tract, namely, the iris, choroids, and
ciliary body. Uveitis is responsible for
about ten percent (10%) of the legal
blindness in the United States.
Complications associated with uveitis
include posterior synechia, cataracts,
glaucoma and retinal edema.
Suppressive CpG
oligodeoxynucleotides (ODNs) are
ODNs capable of reducing an immune
response, such as inflammation.
Suppressive ODNs are DNA molecules
of at least eight nucleotides in length,
where the ODN forms a G-tetrad, and
has a circular dichroism value greater
than 2.9. In a suppressive ODN, the
number of guanosines is at least two.
This application claims compositions
and methods for the treatment of
uveitis. Specifically, the application
claims use of suppressive CpG ODNs to
treat uveitis. The compositions and
methods of the application can be used
for the treatment of anterior, posterior
and diffuse uveitis.
Application: Vaccine adjuvants,
production of vaccines,
immunotherapeutics.
Developmental Status: Preclinical
studies have been performed;
oligonucleotides have been synthesized.
Inventors: Dennis Klinman (FDA/
CBER; NCI), Igal Gery (NEI), Chiaki
Fujimoto (NEI).
Patent Status: U.S. Provisional
Application No. 60/569,276 filed 06
May 2004 (HHS Reference No. E–152–
2004/0–US–01); PCT Application No.
PCT/US2005/015761 filed 05 May 2005,
which published as WO 2005/11539 on
09 Dec 2006 (HHS Reference No. E–
152–2004/0–PCT–02); U.S. Patent
Application No. 11/579,518 filed 03
Nov 2006 (HHS Reference Number E–
152–2004/0–US–03); International
filings in Australia, Canada, China,
Europe, India, Japan, Mexico.
Licensing Status: Available for
exclusive or nonexclusive licensing.
Licensing Contact: Peter A. Soukas,
J.D.; 301–435–4646;
soukasp@mail.nih.gov.
Collaborative Research Opportunity:
The National Cancer Institute,
Laboratory of Experimental
Immunology, Immune Modulation
Group, is seeking statements of
capability or interest from parties
interested in collaborative research to
further develop, evaluate, or
commercialize this technology. Please
contact John D. Hewes, Ph.D. at 301–
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435–3121 or hewesj@mail.nih.gov for
more information.
DEPARTMENT OF HEALTH AND
HUMAN SERVICES
Mapping Internal and Bulk Motion of
an Object With Phase Labeling in
Magnetic Resonance Imaging
National Institutes of Health
sroberts on PROD1PC70 with NOTICES
Description of Technology: Current
MRI methods for tracking the motion of
an object over a relatively long period of
time requires the use of precisely
defined grid points that may be inexact
because of limited image resolution or
the size of the element being tracked.
Phase contrast velocity mapping
generally provides high spatial
resolution and simple data processing.
However, it is generally unsuitable for
motion tracking and prone to error. This
invention is a cutting edge Magnetic
Resonance Imaging (MRI) technique that
provides a method for mapping the
internal and bulk motion of a specimen
by labeling the phase of the specimen
magnetization with a selected spatial
function and measuring changes in the
phase of the magnetization. The special
function is selectable to provide
magnetization phase modulation
corresponding to displacements in a
selected direction such as Cartesian or
radial or azimuthal direction. This
method and associated apparatus is
capable of producing images based on
magnetization phase modulation using
data from stimulated echoes and antiechoes. This invention has important
applications in, among other areas,
cardiac functional imaging and can be
used to compute accurate strain maps of
the heart.
Inventors: Anthony H. Aletras and
Han Wen (NHLBI).
Patent Status: U.S. Patent No.
7,233,818 issued 19 Jun 2007 (HHS
Reference No. E–234–1999/3–US–06);
U.S. Patent Application No. 11/800,398
filed 03 May 2007 (HHS Reference No.
E–234–1999/3–US–08).
Licensing Status: Available for nonexclusive licensing.
Licensing Contact: Susan Ano, Ph.D.;
301–435–5515; anos@mail.nih.gov.
Dated: April 14, 2008.
David Sadowski,
Deputy Director, Division of Technology
Development and Transfer, Office of
Technology Transfer, National Institutes of
Health.
[FR Doc. E8–8620 Filed 4–21–08; 8:45 am]
BILLING CODE 4140–01–P
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Center for Scientific Review; Amended
Notice of Meeting
Notice is hereby given of a change in
the meeting of the Center for Scientific
Review Special Emphasis Panel, April
17, 2008, 3 p.m. to April 17, 2008, 5
p.m. National Institutes of Health, 6701
Rockledge Drive, Bethesda MD 20892
which was published in the Federal
Register on April 9, 2008, 73 FR 19229.
The meeting will be held April 21,
2008. The meeting time and location
remain the same. The meeting is closed
to the public.
Dated: April 14, 2008.
Jennifer Spaeth,
Director, Office of Federal Advisory
Committee Policy.
[FR Doc. E8–8452 Filed 4–21–08; 8:45 am]
BILLING CODE 4140–01–M
DEPARTMENT OF HEALTH AND
HUMAN SERVICES
National Institutes of Health
Center for Scientific Review; Notice of
Closed Meetings
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
meetings.
The meetings 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: Center for Scientific
Review Special Emphasis Panel; Multicale
Models of Physiome Conflict.
Date: May 21, 2008.
Time: 8 a.m. to 5 p.m.
Agenda: To review and evaluate grant
applications.
Place: Georgetown Suites, 1111 30th Street,
NW., Washington, DC 20007.
Contact Person: Ping Fan, PhD, Scientific
Review Administrator, Center for Scientific
Review, National Institutes of Health, 6701
Rockledge Drive, Room 5154, MSC 7840,
Bethesda, MD 20892, 301–435–1740,
fanp@csr.nih.gov.
Name of Committee: Immunology
Integrated Review Group; Transplantation,
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Tolerance, and Tumor Immunology Study
Section.
Date: May 29–30, 2008.
Time: 8 a.m. to 5 p.m.
Agenda: To review and evaluate grant
applications.
Place: Hilton Silver Spring, 8727 Colesville
Road, Silver Spring, MD 20910.
Contact Person: Cathleen L. Cooper, PhD,
Scientific Review Officer, Center for
Scientific Review, National Institutes of
Health, 6701 Rockledge Drive, Room 4208,
MSC 7812, Bethesda, MD 20892, 301–435–
3566, cooperc@csr.nih.gov.
Name of Committee: Center for Scientific
Review Special Emphasis Panel; Member
Conflict: Cell Death and Neurodegeneration.
Date: June 2, 2008.
Time: 2 p.m. to 4 p.m.
Agenda: To review and evaluate grant
applications.
Place: National Institutes of Health, 6701
Rockledge Drive, Bethesda, MD 20892,
(Telephone Conference Call).
Contact Person: Alexander Yakovlev, PhD,
Scientific Review Officer, Center for
Scientific Review, National Institutes of
Health, 6701 Rockledge Drive, Room 5206,
MSC 7846, Bethesda, MD 20892, 301–435–
1254, yakovleva@csr.nih.gov.
Name of Committee: Center for Scientific
Review Special Emphasis Panel; Chronic
Fatigue and Fibromyalgia Syndromes,
Temporomandibular Disorders.
Date: June 4, 2008.
Time: 1 p.m. to 4 p.m.
Agenda: To review and evaluate grant
applications.
Place: National Institutes of Health, 6701
Rockledge Drive, Bethesda, MD 20892,
(Telephone Conference Call).
Contact Person: J. Terrell Hoffeld, DDS,
PhD, USPHS Dental Director, Center for
Scientific Review, National Institutes of
Health, 6701 Rockledge Drive, Room 4116,
MSC 7816, Bethesda, MD 20892, 301–435–
1781, th88q@nih.gov.
Name of Committee: Endocrinology,
Metabolism, Nutrition and Reproductive
Sciences Integrated Review Group; Cellular
Aspects of Diabetes and Obesity Study
Section.
Date: June 5–6, 2008.
Time: 8 a.m. to 5 p.m.
Agenda: To review and evaluate grant
applications.
Place: San Francisco Airport Marriott, 1800
Old Bayshore Highway, Burlingame, CA
94010.
Contact Person: Ann A. Jerkins, PhD,
Scientific Review Officer, Center for
Scientific Review, National Institutes of
Health, 6701 Rockledge Drive, Room 6154,
MSC 7892, Bethesda, MD 20892, (301) 435–
4514, jerkinsa@csr.nih.gov.
Name of Committee: Health of the
Population Integrated Review Group; Nursing
Science: Children and Families Study
Section.
Date: June 5, 2008.
Time: 8 a.m. to 5 p.m.
Agenda: To review and evaluate grant
applications.
Place: Bethesda Marriott, 5151 Pooks Hill
Road, Bethesda, MD 20814.
E:\FR\FM\22APN1.SGM
22APN1
]]>Agencies
[Federal Register Volume 73, Number 78 (Tuesday, April 22, 2008)]
[Notices]
[Pages 21633-21636]
From the Federal Register Online via the Government Printing Office [www.gpo.gov]
[FR Doc No: E8-8620]
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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.
Platform for the High Throughput Screening of Single Nucleotide
Polymorphisms and Small Insertions and Deletions
Description of Technology: Available for licensing and commercial
development is an oligoarray-based process for gene-specific single
nucleotide polymorphism (SNP) genotyping based on comparative
hybridization. This process can detect, even in heterozygous
conditions, known and potentially flag unknown variants (point
mutations, base insertion or deletion) along the complete sequence of a
given gene while drastically cutting the time and costs compared to
high-throughput direct sequencing without affecting sensitivity and
specificity. The accuracy and efficiency of the invention was validated
based on the BRCA-1 breast and ovarian cancer predisposing gene. This
process can easily be custom designed to include within the same
platform a relatively large number of genes relevant to a specific
clinical condition and it is particularly useful for the screening of
long genomic region with relatively infrequent but clinically relevant
variants.
More specifically, the invention is made reliable by the
development of two tailored algorithms: the first automatically designs
the complete data set of gene-specific probes starting from the genomic
sequence according to the user specification (size of the probes,
relative position, etc.); and the other is based on an algorithm that
flags gene variants in the test sample. This allows detecting unknown
variants in the region in which only the reference hybridizes to the
probes. These features drastically reduce the amount of sequencing (the
gold standard for SNP detection) to small regions in which a
discrepancy between test signal and reference signal is found.
Moreover, there is no limit, other than the physical area of the slide,
to the number of probes that can be added to the array and the number
of genes that can be queried simultaneously. Thus, a repertoire of
considerable size can be scanned in a single test for each sample with
sensitivity and specificity comparable to direct sequencing.
Applications: The immediate clinical applications of this platform
is a remarkable improvement of genetic testing by increasing the number
of target genes that can be screened in a short time, at a minimal cost
using an automated simplified analysis, such as the sequencing-grade
screening for BRCA-1 variants and the detection of mutations in
cancerous tissues. The method can be also applied to other human genes
(coding and non-coding sequences), and other sequences from animals,
bacterial and viruses.
Development Status: Method fully developed and validated.
Inventors: Ena Wang (CC), Alessandro Monaco (CC), Francesco M
Marincola (CC), et al.
Patent Status: U.S. Provisional Application No. 61/068,182 filed 05
Mar 2008 (HHS Reference No. E-082-2008/0-US-01).
Licensing Status: Available for non-exclusive or exclusive
licensing.
Licensing Contact: Cristina Thalhammer-Reyero, Ph.D., M.B.A.; 301-
435-4507; thalhamc@mail.nih.gov.
Generation of Wild-Type Dengue Viruses for Use in Rhesus Monkey
Infection Studies
Description of Technology: Dengue virus is a positive-sense RNA
virus belonging to the Flavivirus genus of the family Flaviviridae.
Dengue virus is widely distributed throughout the tropical and
semitropical regions of the world and is transmitted to humans by
mosquito vectors. Dengue virus is a leading cause of hospitalization
and death in children in at least eight tropical Asian countries. There
are four serotypes of dengue virus (DEN-1, DEN-2, DEN-3, and DEN-4)
that annually cause an estimated 50-100 million cases of dengue fever
and 500,000 cases of the more severe form of dengue virus infection
known as dengue hemorrhagic fever/dengue shock syndrome (DHF/DSS). This
latter disease is seen predominately in children and adults
experiencing a second dengue virus infection with a serotype different
than that of their first dengue virus infection and in primary
infection of infants who still have circulating dengue-specific
maternal antibody. A vaccine is needed to lessen the disease burden
caused by dengue virus, but none is licensed.
Because of the association of more severe disease with secondary
dengue
[[Page 21634]]
virus infection, a successful vaccine must induce immunity to all four
serotypes. Immunity is primarily mediated by neutralizing antibody
directed against the envelope (E) glycoprotein, a virion structural
protein. Infection with one serotype induces long-lived homotypic
immunity and a short-lived heterotypic immunity. Therefore, the goal of
immunization is to induce a long-lived neutralizing antibody response
against DEN-1, DEN-2, DEN-3, and DEN-4, which can best be achieved
economically using live attenuated virus vaccines. This is a reasonable
goal since a live attenuated vaccine has already been developed for the
related yellow fever virus, another mosquito-borne flavivirus present
in tropical and semitropical regions of the world.
The evaluation of live attenuated dengue vaccine candidates in
rhesus monkeys requires wild type control viruses for each of the four
dengue serotypes. These control viruses are used for comparison to the
attenuated strains and post-vaccination challenge to assess vaccine
efficacy. As such, these viruses need to be well characterized and
sufficiently pure to ensure that they will replicate to consistent
levels in rhesus monkeys. Characterization generally includes sequence
analysis, titration, and evaluation in monkeys. The following viruses
have been characterized: (1) DEN1 WP (2) DEN1 Puerto Rico/94 (3) DEN2
NGC prototype (4) DEN2 Tonga/74 (5) DEN3 Sleman/78 and (6) DEN4
Dominica/81.
Application: Dengue/flavivirus vaccine studies, dengue/flavivirus
diagnostics, dengue/flavivirus research tools.
Development Status: Materials are available for transfer.
Inventors: Stephen S. Whitehead and Joseph E. Blaney, Jr. (NIAID).
Publications:
1. AP Durbin, RA Karron, W Sun, DW Vaughn, MJ Reynolds, JR
Perreault, B Thumar, R Men, C-J Lai, WR Elkins, RM Chanock, BR Murphy,
SS Whitehead. A live attenuated dengue virus type 4 vaccine candidate
with a 30 nucleotide deletion in the 3' untranslated region is highly
attenuated and immunogenic in humans. Am J Trop Med Hyg. 2001
Nov;65(5):405-413.
2. SS Whitehead, B Falgout, KA Hanley, JE Blaney Jr., L Markoff, BR
Murphy. A live, attenuated dengue virus type 1 vaccine candidate with a
30-nucleotide deletion in the 3' untranslated region is highly
attenuated and immunogenic in monkeys. J Virol. 2003 Jan;77(2):1653-
1657.
3. SS Whitehead, KA Hanley, JE Blaney Jr., LE Gilmore, WR Elkins,
BR Murphy. Substitution of the structural genes of dengue virus type 4
with those of type 2 results in chimeric vaccine candidates which are
attenuated for mosquitoes, mice, and rhesus monkeys. Vaccine 2003 Oct
1;21(27-30):4307-4316.
4. JE Blaney Jr., CT Hanson, KA Hanley, BR Murphy, SS Whitehead.
Vaccine candidates derived from a novel infectious cDNA clone of an
American genotype dengue virus type 2. BMC Infect Dis. 2004 Oct 4;4:39.
5. JE Blaney Jr., CT Hanson, CY Firestone, KA Hanley, BR Murphy, SS
Whitehead. Genetically modified, live attenuated dengue virus type 3
vaccine candidates. Am J Trop Med Hyg. 2004 Dec;71(6):811-821.
6. JE Blaney Jr., JM Matro, BR Murphy, SS Whitehead. Recombinant,
live-attenuated tetravalent dengue virus vaccine formulations induce a
balanced, broad, and protective neutralizing antibody response against
each of the four serotypes in rhesus monkeys. J Virol. 2005
May;79(9):5516-5528.
7. JE Blaney Jr., NS Sathe, CT Hanson, CY Firestone, BR Murphy, SS
Whitehead. Vaccine candidates for dengue virus type 1 (DEN1) generated
by replacement of the structural genes of rDEN4 and rDEN4Delta30 with
those of DEN1. Virol J. 2007 Feb 28;4:23.
Patent Status: HHS Reference No. E-042-2008/0--Research Tool.
Patent protection is not being sought for this technology.
Licensing Status: Available for nonexclusive biological materials
licensing only.
Licensing Contact: Peter A. Soukas, J.D.; 301-435-4646;
soukasp@mail.nih.gov.
A Rapid Ultrasensitive Assay for Detecting Prions in Samples Based on
the Seeded Polymerization of Recombinant Normal Prion Protein (rPrP-
sen)
Description of Technology: Prion diseases are infectious
neurodegenerative diseases of great public concern. Humans may be
infected by eating infected animals (primarily hoofed animals or
ungulates). Blood transfusions have also been documented as a cause of
human cases of prion infection. Prion diseases include: Creutzfeldt-
Jakob disease (CJD) (humans); variant Creutzfeldt-Jakob disease (vCJD)
(humans); Scrapie (sheep); Bovine Spongiform Encephalopathy (BSE)
(cattle); and Chronic Wasting Disease (deer, elk and moose). Currently
available rapid tests for infectious prions, which are routinely used
to monitor slaughtered animals, are not sensitive enough to detect
prion infections in samples from live animals or humans and must be
performed post-mortem. Additionally, these tests cannot be used to
detect subinfectious concentrations of infectious prions in humans or
animals. An ultrasensitive assay for infectious prions, the protein-
misfolding cyclic amplification assay (PMCA), is available for testing
live animals or humans; however, this test is expensive because it is
difficult to perform, relies on the use of brain homogenates, and can
take 2-3 weeks to perform.
This technology enables the rapid detection of extremely low, sub-
lethal, concentrations of prions. This assay, like PMCA, is based on
the prion-induced polymerization of normal prion protein (PrP-sen).
However, this assay, unlike PMCA uses recombinant normal prion protein
(rPrP-sen) rather than normal prion protein derived from brain
homogenate. The use of rPrP-sen provides major advantages over PMCA.
rPrP-sen provides a relatively inexpensive, abundant, and concentrated
source of pure PrP-sen as a substrate for the PMCA prion amplification
reaction. This permits the detection of PrP-res in 2-3 hours and the
ultrasensitive detection of PrP-res in 2 to 3 days. Moreover, relative
to PrP-sen in brain tissue, rPrP-sen is much easier to mutate and
chemically modify to facilitate detection of prion-induced PMCA
amplification products in potentially high-throughput formats. In its
current embodiment, the ultrasensitive assay has been used to
consistently detect (by western blot) around 50 ag of hamster PrP-Sc
(0.003 lethal dose) in cerebral spinal fluid and brain tissue within 2
to 3 days.
Applications:
A diagnostic assay for detecting prion diseases early.
An assay for monitoring the progression of prion disease and the
effectiveness of treatments.
A veterinary assay for detecting PrP-res in live animals and
assessing the extent of prion disease in live herds.
An assay for the detection of prion in commercial products (e.g.,
biotechnological or agricultural), blood and blood products,
transplantation tissues, medical devices, and environmental samples.
Market:
Currently, there is a need for a rapid, ultrasensitive, veterinary
test for prion diseases in live animals used for human consumption and
a need for assessing the extent of prion infection in live herds.
[[Page 21635]]
Currently, there is a need for a human diagnostic assay to detect
prion disease early when treatment is most effective and a need for
monitoring the effectiveness of treatments for prion diseases.
Currently, there is a need for a rapid, ultrasensitive test for
prions in commercial products (e.g., biotechnological or agricultural),
blood and blood products, transplantation tissues, medical devices, and
environmental samples in which prion contamination might be a concern.
Inventors: Ryuichiro Atarashi, Roger A. Moore, Suzette A. Priola,
and Byron W. Caughey (NIAID).
Related Publication: R Atarashi et al. Ultrasensitive detection of
scrapie prion protein using seeded conversion of recombinant prion
protein. Nat Methods 2007 Aug;4(8):645-650.
Patent Status: U.S. Provisional Application No.60/961,364 filed 20
Jul 2007 (HHS Reference No. E-109-2007/0-US-01).
Licensing Status: Available for exclusive and non-exclusive
licensing.
Licensing Contact: RC Tang, J.D., LL.M.; 301-435-5031;
tangrc@mail.nih.gov.
Collaborative Research Opportunity: The NIAID Laboratory of
Persistent Viral Diseases, TSE/Prion Biochemistry Section, is seeking
statements of capability or interest from parties interested in
collaborative research to further develop, evaluate, or commercialize
this technology. Please contact Byron Caughey, Ph.D. at (406) 363-9264
or bcaughey@niaid.nih.gov for more information.
Identification of a Cell-Surface Co-Receptor That Mediates the Uptake
and Immunostimulatory Activity of ``D'' Type CpG Oligonucleotides
Description of Technology: Unmethylated CpG motifs are present at
high frequency in bacterial DNA. They provide a danger signal to the
mammalian immune system that triggers a protective immune response
characterized by the production of Th1 and proinflammatory cytokines
and chemokines. Although the recognition of CpG DNA by B cells and
plasmacytoid dendritic cells is mediated by TLR 9, these cell types
differ in their ability to bind and respond to structurally distinct
classes of CpG oligonucleotides. The inventors' work established that
CXCL16, a membrane-bound scavenger receptor, influences the uptake,
subcellular localization, and cytokine profile induced by D
oligonucleotides.
Knowing that CXCL16 can be used to selectively internalize ODN
could be useful for (1) Improving the activity of D type ODN, (2)
improving recognition (and side effects) of other types of ODNs by
deleting regions that interact with CXCL16 (3) potentially improving
the targeting of any drug or biologic to CXCL16 expressing cells, (4)
targeting antisense ODNs to immune cells or preventing side effects
from antisense therapy, and also applications to (5) DNA vaccines and
other agents that require targeting to CXCL16 expressing cells such as
dendritic cells and monocytes.
This application claims methods of inducing an immune response that
include administering agents that increase the activity and/or
expression of CXCL16 and a D ODN. The application also claims methods
of decreasing an immune response to a CpG ODN, including administering
agents that decrease the activity and/or expression of CXCL16.
Compositions including one or more D type ODNs and an agent that
modulates the activity and/or expression of CXCL16 are also claimed.
Application: Vaccine adjuvants, production of vaccines,
immunotherapeutics.
Developmental Status: Preclinical studies have been performed;
oligonucleotides have been synthesized.
Inventors: Dennis Klinman (FDA/CBER; NCI), Ihsan Gursel (FDA/CBER),
Mayda Gursel (FDA/CBER).
Publication: M Gursel et al. CXCL16 influences the nature and
specificity of CpG-induced immune activation. J Immunol. 2006 Aug
1;177(3):1575-1580.
Patent Status: U.S. Provisional Application No. 60/713,547 filed 31
Aug 2005 (HHS Reference No. E-036-2005/0-US-01); PCT Application No.
PCT/US2006/033774 filed 28 Aug 2006 (HHS Reference Number E-036-2005/0-
PCT-02); U.S. Patent Application No. 12/065,085 filed 27 Feb 2008 (HHS
Reference Number E-036-2005/0-US-03).
Licensing Status: Available for exclusive or nonexclusive
licensing.
Licensing Contact: Peter A. Soukas, J.D.; 301-435-4646;
soukasp@mail.nih.gov.
Collaborative Research Opportunity: The National Cancer Institute,
Laboratory of Experimental Immunology, Immune Modulation Group, is
seeking statements of capability or interest from parties interested in
collaborative research to further develop, evaluate, or commercialize
this technology. Please contact John D. Hewes, Ph.D. at 301-435-3121 or
hewesj@mail.nih.gov for more information.
Use of Suppressive Oligonucleotides To Treat Uveitis
Description of Technology: Uveitis is a major cause of visual loss
in industrialized nations. Uveitis refers to an intraocular
inflammation of the uveal tract, namely, the iris, choroids, and
ciliary body. Uveitis is responsible for about ten percent (10%) of the
legal blindness in the United States. Complications associated with
uveitis include posterior synechia, cataracts, glaucoma and retinal
edema.
Suppressive CpG oligodeoxynucleotides (ODNs) are ODNs capable of
reducing an immune response, such as inflammation. Suppressive ODNs are
DNA molecules of at least eight nucleotides in length, where the ODN
forms a G-tetrad, and has a circular dichroism value greater than 2.9.
In a suppressive ODN, the number of guanosines is at least two.
This application claims compositions and methods for the treatment
of uveitis. Specifically, the application claims use of suppressive CpG
ODNs to treat uveitis. The compositions and methods of the application
can be used for the treatment of anterior, posterior and diffuse
uveitis.
Application: Vaccine adjuvants, production of vaccines,
immunotherapeutics.
Developmental Status: Preclinical studies have been performed;
oligonucleotides have been synthesized.
Inventors: Dennis Klinman (FDA/CBER; NCI), Igal Gery (NEI), Chiaki
Fujimoto (NEI).
Patent Status: U.S. Provisional Application No. 60/569,276 filed 06
May 2004 (HHS Reference No. E-152-2004/0-US-01); PCT Application No.
PCT/US2005/015761 filed 05 May 2005, which published as WO 2005/11539
on 09 Dec 2006 (HHS Reference No. E-152-2004/0-PCT-02); U.S. Patent
Application No. 11/579,518 filed 03 Nov 2006 (HHS Reference Number E-
152-2004/0-US-03); International filings in Australia, Canada, China,
Europe, India, Japan, Mexico.
Licensing Status: Available for exclusive or nonexclusive
licensing.
Licensing Contact: Peter A. Soukas, J.D.; 301-435-4646;
soukasp@mail.nih.gov.
Collaborative Research Opportunity: The National Cancer Institute,
Laboratory of Experimental Immunology, Immune Modulation Group, is
seeking statements of capability or interest from parties interested in
collaborative research to further develop, evaluate, or commercialize
this technology. Please contact John D. Hewes, Ph.D. at 301-
[[Page 21636]]
435-3121 or hewesj@mail.nih.gov for more information.
Mapping Internal and Bulk Motion of an Object With Phase Labeling in
Magnetic Resonance Imaging
Description of Technology: Current MRI methods for tracking the
motion of an object over a relatively long period of time requires the
use of precisely defined grid points that may be inexact because of
limited image resolution or the size of the element being tracked.
Phase contrast velocity mapping generally provides high spatial
resolution and simple data processing. However, it is generally
unsuitable for motion tracking and prone to error. This invention is a
cutting edge Magnetic Resonance Imaging (MRI) technique that provides a
method for mapping the internal and bulk motion of a specimen by
labeling the phase of the specimen magnetization with a selected
spatial function and measuring changes in the phase of the
magnetization. The special function is selectable to provide
magnetization phase modulation corresponding to displacements in a
selected direction such as Cartesian or radial or azimuthal direction.
This method and associated apparatus is capable of producing images
based on magnetization phase modulation using data from stimulated
echoes and anti-echoes. This invention has important applications in,
among other areas, cardiac functional imaging and can be used to
compute accurate strain maps of the heart.
Inventors: Anthony H. Aletras and Han Wen (NHLBI).
Patent Status: U.S. Patent No. 7,233,818 issued 19 Jun 2007 (HHS
Reference No. E-234-1999/3-US-06); U.S. Patent Application No. 11/
800,398 filed 03 May 2007 (HHS Reference No. E-234-1999/3-US-08).
Licensing Status: Available for non-exclusive licensing.
Licensing Contact: Susan Ano, Ph.D.; 301-435-5515;
anos@mail.nih.gov.
Dated: April 14, 2008.
David Sadowski,
Deputy Director, Division of Technology Development and Transfer,
Office of Technology Transfer, National Institutes of Health.
[FR Doc. E8-8620 Filed 4-21-08; 8:45 am]
BILLING CODE 4140-01-P
