Government-Owned Inventions; Availability for Licensing, 54504-54505 [E6-15294]
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54504
Federal Register / Vol. 71, No. 179 / Friday, September 15, 2006 / Notices
Dated: September 7, 2006.
Rachelle Ragland-Greene,
NCI Project Clearance Liaison, National
Institutes of Health.
[FR Doc. E6–15296 Filed 9–14–06; 8:45 am]
BILLING CODE 4101–01–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.
jlentini on PROD1PC65 with NOTICES
Human Protein Tissue Inhibitor of
Metalloproteinases-2 (TIMP–2) Derived
Anti-Angiogenic Peptides
Description of Technology: Cancer is
the second leading cause of death in
United States and it is estimated that
there will be approximately 600,000
deaths caused by cancer in 2006. A
major drawback of the existing
chemotherapies is the cytotoxic sideeffects that are associated with them.
Thus, there is a need to develop new
therapeutic approaches with reduced
side-effects.
Anti-angiogenic therapy is a recent
approach in cancer therapeutics
targeting the formation of blood vessels
that are necessary for tumor growth.
Recently, the anti-angiogenic molecule
bevacizumab (Avastin) has gained
approval from the FDA for the first-line
treatment of metastatic colon cancer in
combination with standard
chemotherapy.
VerDate Aug<31>2005
14:51 Sep 14, 2006
Jkt 208001
Human protein tissue inhibitor of
metalloproteinases-2 (TIMP–2) has been
shown to inhibit angiogenesis in vivo
independent of metalloproteinase
inhibition. This technology discloses
new peptide sequences derived from
TIMP–2. They retain their in vivo antiangiogenic property acting via the same
mechanism as TIMP–2 and some of
them have significantly higher activity
than TIMP–2. Anti-angiogenic
peptidomimetics based on this
technology can be developed for the
treatment of angiogenesis associated
diseases.
Applications:
1. Novel human TIMP–2 derived
peptide sequences.
2. Novel human TIMP–2 derived
peptide sequences with considerable
anti-angiogenic activity in vivo.
3. Human TIMP–2 derived peptides
with high anti-angiogenic activity that
can be used for the treatment of several
cancers.
4. Human TIMP–2 derived peptides
with high anti-angiogenic activity that
can be used for the treatment of several
other angiogenesis associated diseases
such as retinopathy and rheumatoid
arthritis.
Market:
1. 600,000 deaths from cancer related
diseases estimated in 2006.
2. The technology platform involving
novel anti-angiogenic cancer therapy
technology has a potential market of
more than 2 billion U.S. dollars.
3. The technology platform has
additional market in treating several
other clinical problems such as
autoimmune diseases.
Development Status: The technology
is currently in the pre-clinical stage of
development.
Inventors: William G. StetlerStevenson and Dong-Wan Seo (NCI)
(Lead Inventor Web page: https://
ccr.cancer.gov/staff/
staff.asp?profileid=5853)
Related Publications:
1. DW Seo, et al. TIMP–2 mediated
inhibition of angiogenesis: an MMPindependent mechanism. Cell 2003 Jul
25; 114(2):171–180.
2. WG Stetler-Stevenson, et al. Tissue
inhibitor of metalloproteinases-2
(TIMP–2) mRNA expression in tumor
cell lines and human tumor tissues. J
Biol Chem. 1990 Aug 15;
265(23):13933–13938.
3. WG Stetler-Stevenson and DW Seo.
TIMP–2: an endogenous inhibitor of
angiogenesis. Trends Mol Med. 2005
Mar; 11(3):97–103.
4. DW Seo, et al. Shp-1 mediates the
antiproliferative activity of tissue
inhibitor of metalloproteinase-2 in
human microvascular endothelial cells.
PO 00000
Frm 00052
Fmt 4703
Sfmt 4703
J Biol Chem. 2006 Feb 10; 281(6):3711–
3721.
5. H Chang, et al. TIMP–2 promotes
cell spreading and adhesion via
upregulation of RAP1 signaling.
Biochem. Biophys. Res. Comm. 2006 Jul
7; 345(3):1201–1206.
6. J Oh, et al. TIMP–2 upregulates
RECK expression via dephosphorylation
of paxillin tyrosine residues 31 and 118.
Oncogene 2006 Jul 13; 25(30):4230–
4234.
Patent Status: U.S. Provisional
Application No. 60/728,146 filed 18 Oct
2005, entitled ‘‘Angio-inhibitory
Peptides Derived from TIMP–2’’ (HHS
Reference No. E–186–2005/0–US–01).
Licensing Status: Available for
exclusive and non-exclusive licensing.
Licensing Contact: Thomas P. Clouse,
J.D.; 301/435–4076;
clousetp@mail.nih.gov.
Collaborative Research Opportunity:
The NCI Cell and Cancer Biology
Branch is seeking statements of
capability or interest from parties
interested in collaborative research to
further develop, evaluate, or
commercialize TIMP–2 derived antiangiogenic peptides. Please contact
Betty Tong at 301–496–0477 or
tongb@mail.nih.gov for more
information.
Novel Chemoattractant-Based Toxins
To Improve Vaccine Immune
Responses for Cancer and Infectious
Diseases
Description of Technology: Cancer is
one of the leading causes of death in
United States and it is estimated that
there will be more than half a million
deaths caused by cancer in 2006. A
major drawback of the current
chemotherapy-based therapeutics is the
cytotoxic side-effects associated with
them. Thus there is a dire need to
develop new therapeutic strategies with
fewer side-effects. Immuno-therapy has
taken a lead among the new therapeutic
approaches. Enhancing the innate
immune response of an individual has
been a key approach for the treatment
against different diseases such as cancer
and infectious diseases.
This technology involves the
generation of novel chemoattractant
toxins that deplete the T regulatory cells
(Treg) or other immunosuppressive or
hyperactivated cells locally. Treg
controls activation of immune responses
by suppressing the induction of
adaptive immune responses,
particularly T cell responses.
Immunosuppressive cells such as tumor
infiltrating macrophages or NKT and
other cells down regulate antitumor
immune responses. The chemoattractant
toxins consist of a toxin moiety fused
E:\FR\FM\15SEN1.SGM
15SEN1
jlentini on PROD1PC65 with NOTICES
Federal Register / Vol. 71, No. 179 / Friday, September 15, 2006 / Notices
with a chemokine receptor ligand,
chemokines and other chemoattractants
that enables specific targeting and
delivery to the Treg cells. This
technology is advantageous over the
more harmful antibodies and chemicals
that are currently used for the systemic
depletion of Treg cells. The current
technology can be used therapeutically
in a variety of ways. They can be used
together with vaccines to increase
efficacy of the vaccine for the treatment
of cancer, and can used to locally
deplete Treg cells or other immuno
suppressive cells to induce cytolytic cell
responses at the tumor site or to
eliminate chronic infectious diseases
such as HIV and tuberculosis.
Applications:
1. New chemoattractant based toxins
targeted towards Treg cells.
2. New chemoattractant based toxins
targeted towards immunosuppressive
NKT, and macrophages.
3. New chemoattractant based toxins
targeted towards local depletion of
hyperactivated CD4 T cells to treat
autoimmune diseases.
4. Chemoattractant based toxins
depleting Treg cells or other
immunosuppressive cells causing
enhanced vaccine immune responses.
5. Novel immunotherapy by
increasing vaccine efficacy against
cancer and infectious diseases.
Market:
1. 600,000 deaths from cancer related
diseases estimated in 2006.
2. The technology platform involving
novel chemo-attractant based toxins can
be used to improve vaccine immune
responses. The vaccine market is
believed to reach $10bn in 2006.
3. The technology platform has
additional market in treating several
other clinical problems such as
autoimmune diseases.
Development Status: The technology
is currently in the pre-clinical stage of
development.
Inventors: Arya Biragyn (NIA), Dolgor
Bataar (NIA), et al. (Lead Inventor Web
page: https://www.grc.nia.nih.gov/
branches/irp/abiragyn.htm).
Related Publications:
1. Copy of manuscript from this
technology can be provided once
accepted for publication.
2. M Coscia, A Biragyn. Cancer
immunotherapy with chemoattractant
peptides. Semin Cancer Biol 2004 Jun;
14(3):209–218.
3. R Schiavo et al. Chemokine
receptor targeting efficiently directs
antigens to MHC class I pathways and
elicits antigen-specific CD8+ T-cell
responses. Blood 2006 Jun 15; 107
(12):4597–4605. Epub 2006 Mar 2, doi
10.1182/blood–2005–08–3207.
VerDate Aug<31>2005
14:51 Sep 14, 2006
Jkt 208001
Patent Status: U.S. Provisional
Application No. 60/722,675 filed 30 Sep
2005, entitled ‘‘Methods and
Compositions for Modulating Immune
Tolerance’’ (HHS Reference No. E–027–
2005/0–US–01).
Licensing Status: Available for nonexclusive or exclusive licensing.
Licensing Contact: Thomas P. Clouse,
J.D.; 301/435–4076;
clousetp@mail.nih.gov.
Collaborative Research Opportunity:
The NIA Laboratory of Immunology is
seeking statements of capability or
interest from parties interested in
collaborative research to further
develop, evaluate, or commercialize
novel chemoattractant-based toxins.
Please contact Betty Tong at 301–496–
0477 or tongb@mail.nih.gov for more
information.
Dated: September 8, 2006.
Steven M. Ferguson,
Director, Division of Technology Development
and Transfer, Office of Technology Transfer,
National Institutes of Health.
[FR Doc. E6–15294 Filed 9–14–06; 8:45 am]
BILLING CODE 4140–01–P
DEPARTMENT OF HEALTH AND
HUMAN SERVICES
National Institutes of Health
National Center for Research
Resources; 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: National Center for
Research Resources Initial Review Group;
Clinical Research Review Committee.
Date: October 4–5, 2006.
Time: 8 a.m. to 5 p.m.
Agenda: To review and evaluate grant
applications.
Place: Residence Inn Bethesda, 7335
Wisconsin Avenue, Bethesda, MD 20814.
Contact Person: Mohan Viswanathan, PhD,
Deputy Director, National Center for
Research Resources, OR, National Institutes
of Health, 6701 Democracy Blvd., Room
1084, MSC 4874, 1 Democracy Plaza,
PO 00000
Frm 00053
Fmt 4703
Sfmt 4703
54505
Bethesda, MD 20892–4874; 301–435–0829;
mv10f@nih.gov.
Name of Committee: National Center for
Research Resources Special Emphasis Panel;
CMRC–A
Date: October 5, 2006.
Time: 9 a.m. to 10 a.m.
Agenda: To review and evaluate grant
applications.
Place: National Institutes of Health, One
Democracy Plaza, 6701 Democracy
Boulevard, Bethesda, MD 20892. (Telephone
Conference Call).
Contact Person: John R. Glowa, PhD,
Scientific Review Administrator, Office of
Review, National Center for Research
Resources, 6701 Democracy Boulevard, Room
1078—MSC 4874, Bethesda, MD 20892–4874;
301.435.0807; glowaj@mail.nih.gov.
Name of Committee: National Center for
Research Resources Initial Review Group;
Comparative Medicine Review Committee.
Date: October 10–11, 2006.
Time: 8 a.m. to 5 p.m.
Agenda: To review and evaluate grant
applications.
Place: Double Tree Rockville, 1750
Rockville Pike, Roosevelt Room, Rockville,
MD 20852.
Contact Person: John R. Glowa, PhD,
Scientific Review Administrator, Office of
Review, National Center for Research
Resources, 6701 Democracy Boulevard, Room
1078—MSC 4874; Bethesda, MD 20892–4874;
301.435.0807; glowaj@mail.nih.gov.
Name of Committee: National Center for
Research Resources Special Emphasis Panel;
GCRC and K23 SEP.
Date: October 19–20, 2006.
Time: 8 a.m. to 5 p.m.
Agenda: To review and evaluate grant
applications.
Place: Gaithersburg Hilton, 620 Perry
Parkway, Gaithersburg, MD 20877.
Contact Person: Guo Zhang, PhD, Scientific
Review Administrator, National Center for
Research Resources/OR, National Institutes
of Health, 6701 Democracy Boulevard, 1
Democracy Plaza, Rm. 1064, Bethesda, MD
20892–4874; 301–435–0812;
zhanggu@mail.nih.gov.
Name of Committee: National Center for
Research Resources Special Emphasis Panel;
RCMI Net Teleconference.
Date: October 26, 2006.
Time: 1 p.m. to 4 p.m.
Agenda: To review and evaluate grant
applications.
Place: National Institutes of Health, One
Democracy Plaza, 6701 Democracy
Boulevard, Bethesda, MD 20892; (Telephone
Conference Call).
Contact Person: Guo Zhang, PhD, Scientific
Review Administrator, Office of Review,
National Center for Research Resources,
National Institutes of Health, 6701
Democracy Boulevard, 1 Democracy Plaza,
Rm. 1064, Bethesda, MD 20892; (301) 435–
0812; zhanggu@mail.nih.gov.
(Catalogue of Federal Domestic Assistance
Program Nos. 93.306, Comparative Medicine;
93.333, Clinical Research; 93.371, Biomedical
Technology; 93.389, Research Infrastructures,
93.306, 93.333, National Institutes of Health,
HHS)
E:\FR\FM\15SEN1.SGM
15SEN1
]]>Agencies
[Federal Register Volume 71, Number 179 (Friday, September 15, 2006)]
[Notices]
[Pages 54504-54505]
From the Federal Register Online via the Government Printing Office [www.gpo.gov]
[FR Doc No: E6-15294]
-----------------------------------------------------------------------
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.
Human Protein Tissue Inhibitor of Metalloproteinases-2 (TIMP-2) Derived
Anti-Angiogenic Peptides
Description of Technology: Cancer is the second leading cause of
death in United States and it is estimated that there will be
approximately 600,000 deaths caused by cancer in 2006. A major drawback
of the existing chemotherapies is the cytotoxic side-effects that are
associated with them. Thus, there is a need to develop new therapeutic
approaches with reduced side-effects.
Anti-angiogenic therapy is a recent approach in cancer therapeutics
targeting the formation of blood vessels that are necessary for tumor
growth. Recently, the anti-angiogenic molecule bevacizumab (Avastin)
has gained approval from the FDA for the first-line treatment of
metastatic colon cancer in combination with standard chemotherapy.
Human protein tissue inhibitor of metalloproteinases-2 (TIMP-2) has
been shown to inhibit angiogenesis in vivo independent of
metalloproteinase inhibition. This technology discloses new peptide
sequences derived from TIMP-2. They retain their in vivo anti-
angiogenic property acting via the same mechanism as TIMP-2 and some of
them have significantly higher activity than TIMP-2. Anti-angiogenic
peptidomimetics based on this technology can be developed for the
treatment of angiogenesis associated diseases.
Applications:
1. Novel human TIMP-2 derived peptide sequences.
2. Novel human TIMP-2 derived peptide sequences with considerable
anti-angiogenic activity in vivo.
3. Human TIMP-2 derived peptides with high anti-angiogenic activity
that can be used for the treatment of several cancers.
4. Human TIMP-2 derived peptides with high anti-angiogenic activity
that can be used for the treatment of several other angiogenesis
associated diseases such as retinopathy and rheumatoid arthritis.
Market:
1. 600,000 deaths from cancer related diseases estimated in 2006.
2. The technology platform involving novel anti-angiogenic cancer
therapy technology has a potential market of more than 2 billion U.S.
dollars.
3. The technology platform has additional market in treating
several other clinical problems such as autoimmune diseases.
Development Status: The technology is currently in the pre-clinical
stage of development.
Inventors: William G. Stetler-Stevenson and Dong-Wan Seo (NCI)
(Lead Inventor Web page: https://ccr.cancer.gov/staff/
staff.asp?profileid=5853)
Related Publications:
1. DW Seo, et al. TIMP-2 mediated inhibition of angiogenesis: an
MMP-independent mechanism. Cell 2003 Jul 25; 114(2):171-180.
2. WG Stetler-Stevenson, et al. Tissue inhibitor of
metalloproteinases-2 (TIMP-2) mRNA expression in tumor cell lines and
human tumor tissues. J Biol Chem. 1990 Aug 15; 265(23):13933-13938.
3. WG Stetler-Stevenson and DW Seo. TIMP-2: an endogenous inhibitor
of angiogenesis. Trends Mol Med. 2005 Mar; 11(3):97-103.
4. DW Seo, et al. Shp-1 mediates the antiproliferative activity of
tissue inhibitor of metalloproteinase-2 in human microvascular
endothelial cells. J Biol Chem. 2006 Feb 10; 281(6):3711-3721.
5. H Chang, et al. TIMP-2 promotes cell spreading and adhesion via
upregulation of RAP1 signaling. Biochem. Biophys. Res. Comm. 2006 Jul
7; 345(3):1201-1206.
6. J Oh, et al. TIMP-2 upregulates RECK expression via
dephosphorylation of paxillin tyrosine residues 31 and 118. Oncogene
2006 Jul 13; 25(30):4230-4234.
Patent Status: U.S. Provisional Application No. 60/728,146 filed 18
Oct 2005, entitled ``Angio-inhibitory Peptides Derived from TIMP-2''
(HHS Reference No. E-186-2005/0-US-01).
Licensing Status: Available for exclusive and non-exclusive
licensing.
Licensing Contact: Thomas P. Clouse, J.D.; 301/435-4076;
clousetp@mail.nih.gov.
Collaborative Research Opportunity: The NCI Cell and Cancer Biology
Branch is seeking statements of capability or interest from parties
interested in collaborative research to further develop, evaluate, or
commercialize TIMP-2 derived anti-angiogenic peptides. Please contact
Betty Tong at 301-496-0477 or tongb@mail.nih.gov for more information.
Novel Chemoattractant-Based Toxins To Improve Vaccine Immune Responses
for Cancer and Infectious Diseases
Description of Technology: Cancer is one of the leading causes of
death in United States and it is estimated that there will be more than
half a million deaths caused by cancer in 2006. A major drawback of the
current chemotherapy-based therapeutics is the cytotoxic side-effects
associated with them. Thus there is a dire need to develop new
therapeutic strategies with fewer side-effects. Immuno-therapy has
taken a lead among the new therapeutic approaches. Enhancing the innate
immune response of an individual has been a key approach for the
treatment against different diseases such as cancer and infectious
diseases.
This technology involves the generation of novel chemoattractant
toxins that deplete the T regulatory cells (Treg) or other
immunosuppressive or hyperactivated cells locally. Treg controls
activation of immune responses by suppressing the induction of adaptive
immune responses, particularly T cell responses. Immunosuppressive
cells such as tumor infiltrating macrophages or NKT and other cells
down regulate antitumor immune responses. The chemoattractant toxins
consist of a toxin moiety fused
[[Page 54505]]
with a chemokine receptor ligand, chemokines and other chemoattractants
that enables specific targeting and delivery to the Treg cells. This
technology is advantageous over the more harmful antibodies and
chemicals that are currently used for the systemic depletion of Treg
cells. The current technology can be used therapeutically in a variety
of ways. They can be used together with vaccines to increase efficacy
of the vaccine for the treatment of cancer, and can used to locally
deplete Treg cells or other immuno suppressive cells to induce
cytolytic cell responses at the tumor site or to eliminate chronic
infectious diseases such as HIV and tuberculosis.
Applications:
1. New chemoattractant based toxins targeted towards Treg cells.
2. New chemoattractant based toxins targeted towards
immunosuppressive NKT, and macrophages.
3. New chemoattractant based toxins targeted towards local
depletion of hyperactivated CD4 T cells to treat autoimmune diseases.
4. Chemoattractant based toxins depleting Treg cells or other
immunosuppressive cells causing enhanced vaccine immune responses.
5. Novel immunotherapy by increasing vaccine efficacy against
cancer and infectious diseases.
Market:
1. 600,000 deaths from cancer related diseases estimated in 2006.
2. The technology platform involving novel chemo-attractant based
toxins can be used to improve vaccine immune responses. The vaccine
market is believed to reach $10bn in 2006.
3. The technology platform has additional market in treating
several other clinical problems such as autoimmune diseases.
Development Status: The technology is currently in the pre-clinical
stage of development.
Inventors: Arya Biragyn (NIA), Dolgor Bataar (NIA), et al. (Lead
Inventor Web page: https://www.grc.nia.nih.gov/branches/irp/
abiragyn.htm).
Related Publications:
1. Copy of manuscript from this technology can be provided once
accepted for publication.
2. M Coscia, A Biragyn. Cancer immunotherapy with chemoattractant
peptides. Semin Cancer Biol 2004 Jun; 14(3):209-218.
3. R Schiavo et al. Chemokine receptor targeting efficiently
directs antigens to MHC class I pathways and elicits antigen-specific
CD8+ T-cell responses. Blood 2006 Jun 15; 107 (12):4597-4605. Epub 2006
Mar 2, doi 10.1182/blood-2005-08-3207.
Patent Status: U.S. Provisional Application No. 60/722,675 filed 30
Sep 2005, entitled ``Methods and Compositions for Modulating Immune
Tolerance'' (HHS Reference No. E-027-2005/0-US-01).
Licensing Status: Available for non-exclusive or exclusive
licensing.
Licensing Contact: Thomas P. Clouse, J.D.; 301/435-4076;
clousetp@mail.nih.gov.
Collaborative Research Opportunity: The NIA Laboratory of
Immunology is seeking statements of capability or interest from parties
interested in collaborative research to further develop, evaluate, or
commercialize novel chemoattractant-based toxins. Please contact Betty
Tong at 301-496-0477 or tongb@mail.nih.gov for more information.
Dated: September 8, 2006.
Steven M. Ferguson,
Director, Division of Technology Development and Transfer, Office of
Technology Transfer, National Institutes of Health.
[FR Doc. E6-15294 Filed 9-14-06; 8:45 am]
BILLING CODE 4140-01-P
