Government-Owned Inventions; Availability for Licensing, 15711-15712 [2010-6966]
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Federal Register / Vol. 75, No. 60 / Tuesday, March 30, 2010 / Notices
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[FR Doc. 2010–7042 Filed 3–29–10; 8:45 am]
BILLING CODE 4184–01–P
DEPARTMENT OF HEALTH AND
HUMAN SERVICES
jlentini on DSKJ8SOYB1PROD with NOTICES
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.
VerDate Nov<24>2008
16:22 Mar 29, 2010
Jkt 220001
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.
Zscan4, a Therapeutic Target for
Cancer, Regenerative Medicine and
Aging
Description of Invention: This
technology has broad potential for the
development of therapeutics for cancer,
diseases of aging, and regenerative
medicine, and targets Zscan4, a gene
that regulates telomere length and
genomic stability in embryonic stem
(ES) cells.
The ability to maintain genomic
stability in ES cells and other stem cells
is critical for the development of stem
cell-based therapies; genomic stability
and telomere length are also active areas
of cancer and aging research. NIA
investigators have discovered that the
Zscan4 gene regulates telomere length
and genomic stability in ES cells, and
plays an essential role in early
embryonic development; this activity is
independent of telomerase activity. The
investigators have shown that ablation
of Zscan4 results in shortened telomere
length and deterioration of the
karyotype of ES cells, and that Zscan4
overexpression increases telomere
length.
This technology discloses methods for
increasing genome stability or
increasing telomere length in an ES cell,
PO 00000
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Fmt 4703
Sfmt 4703
and methods of treating a subject in
need of ES cell therapy. Also disclosed
are methods of promoting blastocyst
outgrowth of embryonic stem cells, as
well as Zscan4 expression vectors and
methods of identifying stem cells
expressing Zscan4.
Applications
• Development of therapeutics for
cancer treatment, aging, and
regenerative medicine.
• Development of assisted
reproduction technologies.
• Studies of early embryonic
development.
Development Status: In vitro and in
vivo studies have been performed.
Inventors: Minoru S. H. Ko et al.
(NIA).
Publications
1. M Zalzman et al. Zscan4 regulates
telomere elongation and genomic
stability in ES cells. Nature 2010 Mar
24; advance online publication, doi
10.1038/nature08882.
2. G Falco et al. Zscan4: A novel gene
expressed exclusively in late 2-cell
embryos and embryonic stem cells. Dev
Biol. 2007 Jul 15;307(2):539–550.
[PubMed: 17553482.]
Patent Status
HHS Reference No. E–088–2007/0—
• PCT Application No. PCT/US2008/
058261 filed 26 Mar 2008.
• US Application No. 12/529,004
filed 27 Aug 2009.
• Foreign counterparts in Europe,
Australia, Canada, and Japan
HHS Reference No. E–172–2009/0—
• U.S. Provisional Application No.
61/275,983 filed 04 Sep 2009.
Licensing Status: Available for
licensing.
Licensing Contact: Tara Kirby, PhD;
301–435–4426; tarak@mail.nih.gov.
Collaborative Research Opportunity:
The National Institute on Aging,
Laboratory of Genetics, is seeking
statements of capability or interest from
parties interested in collaborative
research to further develop, evaluate, or
commercialize this technology. Please
contact Nicole Guyton, PhD at 301–435–
E:\FR\FM\30MRN1.SGM
30MRN1
15712
Federal Register / Vol. 75, No. 60 / Tuesday, March 30, 2010 / Notices
3101 or darakn@mail.nih.gov for more
information.
mFPR2 Transgenic and Knockout
Mouse Models for Alzheimer’s and
Other Inflammatory Diseases
Description of Invention: Human
Formyl Peptide-Like Receptor 1
(hFPLR1) has been implicated in host
defense for disease processes including
Alzheimer’s disease, infection, and
other inflammatory diseases. hFPLR1
and its mouse homologue Formyl
Peptide Receptor 2 (mFPR2) are
G-protein coupled receptors that are
expressed at high levels on phagocytic
leukocytes, mediating leukocyte
chemotaxis and activation in response
to a number of pathogen- and hostderived peptides. Activation of hFPRL1/
mFPR2 by lipoxin A4 may play a role
in preventing and resolving
inflammation. Also, hFPRL1/mFPR2 has
been shown to mediate the chemotactic
activity of amyloid beta 1-42, a key
pathogenic peptide in Alzheimer’s
disease.
Available for licensing are mice
expressing the mFPR2 transgene on
either the FVB or C58BL background, as
well as mFPR2 knockout mice on the
C57BL background. These mice are
anticipated to be highly useful in the
study of a wide variety of inflammatory,
infectious, immunologic and
neurodegenerative diseases.
jlentini on DSKJ8SOYB1PROD with NOTICES
Applications
• Drug development model for
Alzheimer’s disease and other
inflammatory diseases.
• Tool to probe the role of hFPRL1/
mFPR2 in host responses in a variety of
disease processes, including
inflammatory, infectious, immunologic,
and neurodegenerative disease.
Inventors: Ji Ming Wang et al. (NCI)
Publications
1. K Chen, Y Le, Y Liu, W Gong, G
Ying, J Huang, T Yoshimura, L
Tessarollo, JM Wang. Cutting Edge: A
Critical Role for the G Protein-Coupled
Receptor mFPR2 in Airway
Inflammation and Immune Responses. J
Immunol. 2010 Mar 3. Epub ahead of
print. [PubMed: 20200280.]
2. K Chen, P Iribarren, J Hu, J Chen,
W Gong, EH Cho, S Lockett, NM
Dunlop, and JM Wang. Activation of
Toll-like receptor 2 on microglia
promotes cell uptake of Alzheimer
disease-associated amyloid beta peptide.
J Biol Chem. 2006 Feb 10;281(6):3651–
3659. [PubMed: 16339765.]
3. H Yazawa, ZX Yu, Takeda, Y Le, W
Gong, VJ Ferrans, JJ Oppenheim, CC Li,
and JM Wang. Beta amyloid peptide
(Abeta42) is internalized via the G-
VerDate Nov<24>2008
16:22 Mar 29, 2010
Jkt 220001
protein-coupled receptor FPRL1 and
forms fibrillar aggregates in
macrophages. FASEB J. 2001
Nov;15(13):2454–2462. [PubMed:
11689470.]
4. YH Cui, Y Le, W Gong, P Proost,
J Van Damme, WJ Murphy, and JM
Wang. Bacterial lipopolysaccharide
selectively up-regulates the function of
the chemotactic peptide receptor formyl
peptide receptor 2 in murine microglial
cells. J Immunol. 2002 Jan 1;168(1):434–
442. [PubMed: 11751990.]
Patent Status: HHS Reference No.
E–303–2006/0—Research Tool. Patent
protection is not being pursued for this
technology.
Licensing Status: This technology is
available as a research tool under a
Biological Materials License.
Licensing Contact: Tara Kirby, PhD;
301–435–4426; tarak@mail.nih.gov.
Collaborative Research Opportunity:
The National Cancer Institute—
Frederick, Laboratory of Molecular
Immunoregulation, is seeking
statements of capability or interest from
parties interested in collaborative
research to further develop, evaluate, or
commercialize mFPR2 Transgenic and
Knockout Mouse Models for
Alzheimer’s and Other Inflammatory
Diseases. Please contact John D. Hewes,
PhD at 301–435–3121 or
hewesj@mail.nih.gov for more
information.
Dated: March 23, 2010.
Richard U. Rodriguez,
Director, Division of Technology Development
and Transfer, Office of Technology Transfer,
National Institutes of Health.
[FR Doc. 2010–6966 Filed 3–29–10; 8:45 am]
BILLING CODE 4140–01–P
DEPARTMENT OF HEALTH AND
HUMAN SERVICES
National Institutes of Health
National Institute of Allergy and
Infectious Diseases; Notice of Closed
Meeting
Pursuant to section 10(d) of the
Federal Advisory Committee Act, as
amended (5 U.S.C. App.), notice is
hereby given of the following meeting.
The meeting 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
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would constitute a clearly unwarranted
invasion of personal privacy.
Name of Committee: National Institute of
Allergy and Infectious Diseases Special
Emphasis Panel; Ancillary Studies in
Immunomodulation Clinical Trials.
Date: April 22, 2010.
Time: 11:30 a.m. to 4:30 p.m.
Agenda: To review and evaluate grant
applications.
Place: National Institutes of Health, 6700B
Rockledge Drive, Bethesda, MD 20817.
(Telephone Conference Call)
Contact Person: Paul A. Amstad, PhD,
Scientific Review Officer, Scientific Review
Program, Division of Extramural Activities,
NIAID/NIH/DHHS, 6700B Rockledge Drive,
MSC 7616, Bethesda, MD 20892–7616, 301–
402–7098, pamstad@niaid.nih.gov.
(Catalogue of Federal Domestic Assistance
Program Nos. 93.855, Allergy, Immunology,
and Transplantation Research; 93.856,
Microbiology and Infectious Diseases
Research, National Institutes of Health, HHS)
Dated: March 24, 2010.
Jennifer Spaeth,
Director, Office of Federal Advisory
Committee Policy.
[FR Doc. 2010–7089 Filed 3–29–10; 8:45 am]
BILLING CODE 4140–01–P
DEPARTMENT OF HEALTH AND
HUMAN SERVICES
National Institutes of Health
National Institute of Allergy and
Infectious Diseases; Notice of Meeting
Pursuant to section 10(a) of the
Federal Advisory Committee Act, as
amended (5 U.S.C. App.), notice is
hereby given of a meeting of the AIDS
Research Advisory Committee, NIAID.
The meeting will be open to the
public, with attendance limited to space
available. Individuals who plan to
attend and need special assistance, such
as sign language interpretation or other
reasonable accommodations, should
notify the Contact Person listed below
in advance of the meeting.
Name of Committee: AIDS Research
Advisory Committee, NIAID, AIDS Vaccine
Research Subcommittee.
Date: May 25–26, 2010.
Time: 8:30 a.m. to 5 p.m.
Agenda: To discuss follow-up studies to
the recent RV144 vaccine efficacy trial, and
to discuss the use of the nonhuman primate
model in AIDS vaccine research.
Place: Bethesda North Marriott Hotel &
Conference Center, 5701 Marinelli Road,
Bethesda, MD 20852.
Contact Person: James A. Bradac, PhD,
Program Official, Preclinical Research and
Development Branch, Division of AIDS,
Room 5116, National Institutes of Health/
NIAID, 6700B Rockledge Drive, Bethesda,
MD 20892–7628. 301–435–3754.
jbradac@mail.nih.gov.
E:\FR\FM\30MRN1.SGM
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]]>Agencies
[Federal Register Volume 75, Number 60 (Tuesday, March 30, 2010)]
[Notices]
[Pages 15711-15712]
From the Federal Register Online via the Government Printing Office [www.gpo.gov]
[FR Doc No: 2010-6966]
-----------------------------------------------------------------------
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.
Zscan4, a Therapeutic Target for Cancer, Regenerative Medicine and
Aging
Description of Invention: This technology has broad potential for
the development of therapeutics for cancer, diseases of aging, and
regenerative medicine, and targets Zscan4, a gene that regulates
telomere length and genomic stability in embryonic stem (ES) cells.
The ability to maintain genomic stability in ES cells and other
stem cells is critical for the development of stem cell-based
therapies; genomic stability and telomere length are also active areas
of cancer and aging research. NIA investigators have discovered that
the Zscan4 gene regulates telomere length and genomic stability in ES
cells, and plays an essential role in early embryonic development; this
activity is independent of telomerase activity. The investigators have
shown that ablation of Zscan4 results in shortened telomere length and
deterioration of the karyotype of ES cells, and that Zscan4
overexpression increases telomere length.
This technology discloses methods for increasing genome stability
or increasing telomere length in an ES cell, and methods of treating a
subject in need of ES cell therapy. Also disclosed are methods of
promoting blastocyst outgrowth of embryonic stem cells, as well as
Zscan4 expression vectors and methods of identifying stem cells
expressing Zscan4.
Applications
Development of therapeutics for cancer treatment, aging,
and regenerative medicine.
Development of assisted reproduction technologies.
Studies of early embryonic development.
Development Status: In vitro and in vivo studies have been
performed.
Inventors: Minoru S. H. Ko et al. (NIA).
Publications
1. M Zalzman et al. Zscan4 regulates telomere elongation and
genomic stability in ES cells. Nature 2010 Mar 24; advance online
publication, doi 10.1038/nature08882.
2. G Falco et al. Zscan4: A novel gene expressed exclusively in
late 2-cell embryos and embryonic stem cells. Dev Biol. 2007 Jul
15;307(2):539-550. [PubMed: 17553482.]
Patent Status
HHS Reference No. E-088-2007/0--
PCT Application No. PCT/US2008/058261 filed 26 Mar 2008.
US Application No. 12/529,004 filed 27 Aug 2009.
Foreign counterparts in Europe, Australia, Canada, and
Japan
HHS Reference No. E-172-2009/0--
U.S. Provisional Application No. 61/275,983 filed 04 Sep
2009.
Licensing Status: Available for licensing.
Licensing Contact: Tara Kirby, PhD; 301-435-4426;
tarak@mail.nih.gov.
Collaborative Research Opportunity: The National Institute on
Aging, Laboratory of Genetics, is seeking statements of capability or
interest from parties interested in collaborative research to further
develop, evaluate, or commercialize this technology. Please contact
Nicole Guyton, PhD at 301-435-
[[Page 15712]]
3101 or darakn@mail.nih.gov for more information.
mFPR2 Transgenic and Knockout Mouse Models for Alzheimer's and Other
Inflammatory Diseases
Description of Invention: Human Formyl Peptide-Like Receptor 1
(hFPLR1) has been implicated in host defense for disease processes
including Alzheimer's disease, infection, and other inflammatory
diseases. hFPLR1 and its mouse homologue Formyl Peptide Receptor 2
(mFPR2) are G-protein coupled receptors that are expressed at high
levels on phagocytic leukocytes, mediating leukocyte chemotaxis and
activation in response to a number of pathogen- and host-derived
peptides. Activation of hFPRL1/mFPR2 by lipoxin A4 may play a role in
preventing and resolving inflammation. Also, hFPRL1/mFPR2 has been
shown to mediate the chemotactic activity of amyloid beta 1-42, a key
pathogenic peptide in Alzheimer's disease.
Available for licensing are mice expressing the mFPR2 transgene on
either the FVB or C58BL background, as well as mFPR2 knockout mice on
the C57BL background. These mice are anticipated to be highly useful in
the study of a wide variety of inflammatory, infectious, immunologic
and neurodegenerative diseases.
Applications
Drug development model for Alzheimer's disease and other
inflammatory diseases.
Tool to probe the role of hFPRL1/mFPR2 in host responses
in a variety of disease processes, including inflammatory, infectious,
immunologic, and neurodegenerative disease.
Inventors: Ji Ming Wang et al. (NCI)
Publications
1. K Chen, Y Le, Y Liu, W Gong, G Ying, J Huang, T Yoshimura, L
Tessarollo, JM Wang. Cutting Edge: A Critical Role for the G Protein-
Coupled Receptor mFPR2 in Airway Inflammation and Immune Responses. J
Immunol. 2010 Mar 3. Epub ahead of print. [PubMed: 20200280.]
2. K Chen, P Iribarren, J Hu, J Chen, W Gong, EH Cho, S Lockett, NM
Dunlop, and JM Wang. Activation of Toll-like receptor 2 on microglia
promotes cell uptake of Alzheimer disease-associated amyloid beta
peptide. J Biol Chem. 2006 Feb 10;281(6):3651-3659. [PubMed: 16339765.]
3. H Yazawa, ZX Yu, Takeda, Y Le, W Gong, VJ Ferrans, JJ Oppenheim,
CC Li, and JM Wang. Beta amyloid peptide (Abeta42) is internalized via
the G-protein-coupled receptor FPRL1 and forms fibrillar aggregates in
macrophages. FASEB J. 2001 Nov;15(13):2454-2462. [PubMed: 11689470.]
4. YH Cui, Y Le, W Gong, P Proost, J Van Damme, WJ Murphy, and JM
Wang. Bacterial lipopolysaccharide selectively up-regulates the
function of the chemotactic peptide receptor formyl peptide receptor 2
in murine microglial cells. J Immunol. 2002 Jan 1;168(1):434-442.
[PubMed: 11751990.]
Patent Status: HHS Reference No. E-303-2006/0--Research Tool.
Patent protection is not being pursued for this technology.
Licensing Status: This technology is available as a research tool
under a Biological Materials License.
Licensing Contact: Tara Kirby, PhD; 301-435-4426;
tarak@mail.nih.gov.
Collaborative Research Opportunity: The National Cancer Institute--
Frederick, Laboratory of Molecular Immunoregulation, is seeking
statements of capability or interest from parties interested in
collaborative research to further develop, evaluate, or commercialize
mFPR2 Transgenic and Knockout Mouse Models for Alzheimer's and Other
Inflammatory Diseases. Please contact John D. Hewes, PhD at 301-435-
3121 or hewesj@mail.nih.gov for more information.
Dated: March 23, 2010.
Richard U. Rodriguez,
Director, Division of Technology Development and Transfer, Office of
Technology Transfer, National Institutes of Health.
[FR Doc. 2010-6966 Filed 3-29-10; 8:45 am]
BILLING CODE 4140-01-P
