Government-Owned Inventions; Availability for Licensing, 36816-36817 [06-5868]
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36816
Federal Register / Vol. 71, No. 124 / Wednesday, June 28, 2006 / Notices
Patent Status: U.S. Provisional Patent
Application filed 07 Apr 2006 (HHS
Reference No. E–336–2005/0–US–01).
Licensing Status: This technology is
available for licensing under an
exclusive or non-exclusive patent
license.
Licensing Contact: Michelle A.
Booden, PhD; 301/451–7337;
boodenm@mail.nih.gov.
Collaborative Research Opportunity:
The NCI Center for Cancer Research
Nanobiology Program is seeking
statements of capability or interest from
parties interested in collaborative
research to further develop, evaluate, or
commercialize monoclonal antibodies to
treat human diseases. Please contact
Melissa Maderia at
maderiam@mail.nih.gov or by phone at
(301) 846–5465 for more information.
jlentini on PROD1PC65 with NOTICES
Immortal Human Prostate Epithelial
Cell Cultures as a Prostate Cancer
Model
Description of Technology: The
National Institutes of Health has
multiple immortalized, malignant,
human, adult prostate epithelial cell
lines available for license. They are
useful as models in epithelial cell
oncogenesis studies and in the diagnosis
and treatment of prostate cancer.
The cell lines were generated from
primary adenocarcinomas of the
prostate. Long-term cultures were
established by immortalizing cells with
human papillomavirus (HPV)
transforming proteins. The cultures
were characterized and single-cell
clones with unique genetic
characteristics were selected based on
allelic loss of heterozygosity (LOH).
Tissue-matched normal cell lines are
available also, useful for the appropriate
controls.
The invention also encompasses
polyclonal and monoclonal antibodies
directed to the cell lines, which may be
useful as immunotherapeutics.
Applications: (1) Screening tool to
identify novel genes unique to or
overexpressed in prostate cancer; (2)
Raising of prostate cancer-reactive
antibodies, useful as
immunotherapeutics or diagnostics; (3)
Screen for compounds that kill tumor
cells and represent potential therapeutic
agents; (4) Identification of prostate
cancer antigens to develop recombinant
prostate cancer vaccines.
Inventors: Susan L. Topalian, W.
Marston Linehan, Robert K. Bright,
Cathy D. Vocke (NCI).
Publication: R.K. Bright, et al.,
‘‘Generation and genetic
characterization of immortal human
prostate epithelial cell lines derived
VerDate Aug<31>2005
16:52 Jun 27, 2006
Jkt 208001
from primary cancer specimens,’’
Cancer Res. 1997 Mar 5;57(5):995–1002.
Patent Status: U.S. Patent 6,982,168
issued on 07 May 2003 (HHS Reference
No. E–053–1996/0–US–03).
Licensing Status: Available for nonexclusive internal use and biological
material license.
Licensing Contact: Michelle A.
Booden, PhD; 301/451–7337;
boodenm@mail.nih.gov.
Collaborative Research Opportunity:
The NCI Center for Cancer Research,
Surgery Branch, is seeking statements of
capability or interest from parties
interested in collaborative research to
further develop, evaluate, or
commercialize this technology. Please
contact Brian W. Bailey, PhD, at 301/
451–2158 or bbailey@mail.nih.gov for
more information.
Dated: June 21, 2006.
David R. Sadowski,
Acting Director, Division of Technology
Development and Transfer, Office of
Technology Transfer, National Institutes of
Health.
[FR Doc. 06–5867 Filed 6–27–06; 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.
AGENCY:
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.
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.
ADDRESSES:
PO 00000
Frm 00064
Fmt 4703
Sfmt 4703
Treatment of Inflammatory Bowel
Disease (IBD) Using NF–KB Decoy
Polynucleotides
Warren Strober (NIAID), Ivan Fuss
(NIAID), Atsushi Kitani (NIAID), and
Stefan Fichtner-Feigl (NIAID)
U.S. Patent Application No. 11/125,919
filed 10 May 2005 (HHS Reference
No. E–108–2005/0–US–01); PCT
International Application filed 10
May 2006 (HHS Reference No. E–108–
2005/0–PCT–02)
Licensing Contact: Susan Carson, D.
Phil; 301/435–5020;
carsonsu@mail.nih.gov.
Inflammatory Bowel Diseases (IBDs;
Crohn’s disease and ulcerative colitis)
are chronic inflammatory disorders
affecting almost 1 million people in the
developed world at an estimated annual
cost of one billion dollars in lost work
days. Current treatments include
corticosteroids, 5-aminosalicylates and
immunomodulators but novel and more
effective therapies without adverse side
effects continue to be needed. NIH
researchers have previously shown that
a variety of immunomodulators
affecting the Th1 and Th2 T cell
responses which underlie Inflammatory
Bowel Diseases can be used to treat IBD
disease models and have now extended
this work by inhibiting NF–KB
transcriptional activity in a variety of
animal models using decoy
oligodeoxynucleotides (decoy ODNs).
Dr. Strober and colleagues at the
National Institute of Allergy and
Infectious Diseases (NIAID) have shown
that intrarectal (i.r.) or intraperitoneal
(i.p.) administration of decoy ODNs
encapsulated in a viral envelope (HVJ–
E) prevented and treated a model of
acute trinitrobenzene sulfonic acidinduced (TNBS-induced) colitis, a
model for Crohn’s disease, as assessed
by clinical course and the effect on Th1
cytokine production. NF–KB decoy
ODNs were also shown to be an
effective treatment of a model of chronic
TNBS-colitis, inhibiting both the
production of IL–23/Il–17 and the
development of fibrosis that
characterizes this model. Treatment of
TNBS-induced inflammation by i.r.
administration of NF–KB decoy ODNs
did not inhibit NF–KB in extraintestinal
organs and resulted in CD4+ T cell
apoptosis, suggesting that such
treatment is highly focused and durable.
Additionally, NF–KB decoy ODNs also
prevented and treated oxazolone-colitis,
a mouse model for ulcerative colitis,
and thus affected a Th2-mediated
inflammatory process. In each case,
decoy administration led to
inflammation clearing effects,
suggesting a therapeutic potency
E:\FR\FM\28JNN1.SGM
28JNN1
Federal Register / Vol. 71, No. 124 / Wednesday, June 28, 2006 / Notices
jlentini on PROD1PC65 with NOTICES
applicable to human IBD [J. Clin. Invest.
(2005) 115, 3057–3071].
Available for licensing are methods
for treating or preventing the
inflammatory response of IBDs by
intrarectally or intraperitoneally
administering a therapeutic effective
amount of NF–KB decoy ODN. Claims
are directed to treatment of Th1 and Th2
inflammatory response and these
studies suggest that NF–KB decoy ODNs
targeting the consensus NF–KB binding
site and encapsulated in a viral
envelope represent an effective
approach for the treatment of IBDs.
Related IBD technologies available for
licensing also include IL–13 modulators
and inhibitors (HHS Reference No. E–
131–2002/0–PCT–02, WO 2004/001655,
filed 14 June 2002) and IL–13 mutant
and chimeric molecules (HHS Reference
No. E–003–2005/0–US–01, U.S.
Provisional Patent Application No. 60/
671,624 filed 15 April 2005).
In addition to licensing, the
technology is available for further
development through collaborative
research opportunities with the
inventors.
Treatment and Prevention of
Inflammatory Bowel Disease (IBD)
using Mutant and Chimeric IL–13
Molecules
Warren Strober (NIAID), Ivan Fuss
(NIAID), Peter Mannon (NIAID), Jan
Preiss (NIAID), Raj Puri (FDA), Koji
Kawakami (FDA), Stefan FichtnerFeigl (NIAID), and Atsushi Kitani
(NIAID)
U.S. Provisional Patent Application No.
60/671,624 filed 15 April 2005 (HHS
Reference No. E–003–2005/ 0-US–01);
PCT International Application filed
14 April 2006 (HHS Reference No. E–
003–2005/0–PCT–02)
Licensing Contact: Susan Carson, D.
Phil; 301/435–5020;
carsonsu@mail.nih.gov.
Ulcerative colitis (UC) is a chronic
inflammatory disease of the colorectum
and affects approximately 400,000
people in the United States. The cause
of UC is not known, although an
abnormal immunological response to
bacterial antigens in the gut microflora
is thought to be involved. Present
treatments for UC include antiinflammatory therapy using
aminosalicylates or corticosteroids, as
well as immunomodulators and diet.
However, 25–40% of ulcerative colitis
patients must eventually have their
colons removed due to massive
bleeding, severe illness, rupture of the
colon, risk of cancer or due to side
effects of corticosteroids and novel
treatments are still actively being
sought. NIH scientists and their
VerDate Aug<31>2005
16:52 Jun 27, 2006
Jkt 208001
collaborators have used a mouse model
of experimental colitis (oxazolone
colitis, OC) to show that IL–13, a Th2
cytokine, is a significant pathologic
factor in OC and that neutralizing IL–13
in these animals effectively prevents
colitis [Immunity (2002) 17, 629–638].
OC is a colitis induced by intrarectal
administration of a relatively low dose
of the haptenating agent oxazolone
subsequent to skin sensitization with
oxazolone. A highly reproducible and
chronic colonic inflammation is
obtained that is histologically similar to
human ulcerative colitis. Studies show
that Natural Killer T (NKT) cells, rather
than conventional CD4+T cells, mediate
oxazolone colitis and are the source of
IL–13 as well as being activated by CD1expressing intestinal epithelial cells.
Tissue removed from ulcerative colitis
patients were also shown to contain
increased numbers of nonclassical NKT
cells that produce markedly increased
amounts of IL–13 and that in keeping
with epithelial damage being a key
factor in UC, these NKT cells are
cytotoxic for epithelial cells [J. Clin.
Invest. (2004) 113, 1490–1497]. Building
on their previous work, scientists at
NIAID and FDA have shown that an Il13 chimeric fusion protein linked to an
effector molecule was able to prevent
colitis in a mouse model of ulcerative
colitis.
Available for licensing are methods
for treating or preventing the
inflammatory response of IBD by
inhibiting the binding of IL–13 to IL–13
receptors on NKT cells. Additionally,
these mutant and chimeric Il-13
molecules are able to block the chronic
inflammatory response that results in
fibrosis as seen in Crohn’s disease.
Preventing the inflammatory response of
colitis by either modulating or blocking
IL–13 and NKT cell activity continues to
be an effective therapeutic approach in
animal models of colitis with
implications for the treatment of human
ulcerative colitis and for the treatment
of fibrosis associated with Crohn’s
disease.
Related IBD technologies available for
licensing also include IL–13 modulators
and inhibitors (HHS Reference No. E–
131–2002/0–PCT–02, WO 2004/001655,
filed 14 June 2002) and NF-kappa B
decoy oligonucleotides [HHS Reference
No. E–108–2005/0–US–01, U.S. Patent
Application No. 11/125,919, filed 10
May 2005; J. Clin. Invest. (2005) 115,
3057–3071].
In addition to licensing, the
technology is available for further
development through collaborative
research opportunities with the
inventors.
PO 00000
Frm 00065
Fmt 4703
Sfmt 4703
36817
Dated: June 21, 2006.
David R. Sadowski,
Acting Director, Division of Technology
Development and Transfer, Office of
Technology Transfer, National Institutes of
Health.
[FR Doc. 06–5868 Filed 6–27–06; 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 Special Emphasis Panel,
CTSA Center Grants #1.
Date: July 11–12, 2006.
Time: 8 a.m. to 5 p.m.
Agenda: To review and evaluate grant
applications.
Place: Double Tree Rockville, 1750
Rockville Pike, Rockville, MD 20852.
Contact Person: Sheryl K. Brining, PhD,
Scientific Review Administrator, Director,
Office of Review, NCRR, National Institutes
of Health, 6701 Democracy Boulevard, 1
Democracy Plaza, Room 1074, MSC 4874,
Bethesda, MD 20892–4874. (301) 435–0811.
sb44k@nih.gov.
This notice is being published less than 15
days prior to the meeting due to the timing
limitations imposed by the review and
funding cycle.
Name of Committee: National Center for
Research Resources Special Emphasis Panel,
CTSA Center Grants #2.
Date: July 20–21, 2006.
Time: 8 a.m. to 5 p.m.
Agenda: To review and evaluate grant
applications.
Place: Double Tree Rockville, 1750
Rockville Pike, Rockville, MD 20852.
Contact Person: Guo Zhang, PhD, Scientific
Review Administrator, National Center for
Research Resources/OR, National Institutes
of Health, 6701 Democracy Boulevard, 1
Democracy Plaza, Room 1064, Bethesda, MD
20892–4874. (301) 435–0812.
zhanggu@nih.gov.
E:\FR\FM\28JNN1.SGM
28JNN1
]]>Agencies
[Federal Register Volume 71, Number 124 (Wednesday, June 28, 2006)]
[Notices]
[Pages 36816-36817]
From the Federal Register Online via the Government Printing Office [www.gpo.gov]
[FR Doc No: 06-5868]
-----------------------------------------------------------------------
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.
Treatment of Inflammatory Bowel Disease (IBD) Using NF-KB Decoy
Polynucleotides
Warren Strober (NIAID), Ivan Fuss (NIAID), Atsushi Kitani (NIAID), and
Stefan Fichtner-Feigl (NIAID)
U.S. Patent Application No. 11/125,919 filed 10 May 2005 (HHS Reference
No. E-108-2005/0-US-01); PCT International Application filed 10 May
2006 (HHS Reference No. E-108-2005/0-PCT-02)
Licensing Contact: Susan Carson, D. Phil; 301/435-5020;
carsonsu@mail.nih.gov.
Inflammatory Bowel Diseases (IBDs; Crohn's disease and ulcerative
colitis) are chronic inflammatory disorders affecting almost 1 million
people in the developed world at an estimated annual cost of one
billion dollars in lost work days. Current treatments include
corticosteroids, 5-aminosalicylates and immunomodulators but novel and
more effective therapies without adverse side effects continue to be
needed. NIH researchers have previously shown that a variety of
immunomodulators affecting the Th1 and Th2 T cell responses which
underlie Inflammatory Bowel Diseases can be used to treat IBD disease
models and have now extended this work by inhibiting NF-KB
transcriptional activity in a variety of animal models using decoy
oligodeoxynucleotides (decoy ODNs).
Dr. Strober and colleagues at the National Institute of Allergy and
Infectious Diseases (NIAID) have shown that intrarectal (i.r.) or
intraperitoneal (i.p.) administration of decoy ODNs encapsulated in a
viral envelope (HVJ-E) prevented and treated a model of acute
trinitrobenzene sulfonic acid-induced (TNBS-induced) colitis, a model
for Crohn's disease, as assessed by clinical course and the effect on
Th1 cytokine production. NF-KB decoy ODNs were also shown to be an
effective treatment of a model of chronic TNBS-colitis, inhibiting both
the production of IL-23/Il-17 and the development of fibrosis that
characterizes this model. Treatment of TNBS-induced inflammation by
i.r. administration of NF-KB decoy ODNs did not inhibit NF-KB in
extraintestinal organs and resulted in CD4+ T cell apoptosis,
suggesting that such treatment is highly focused and durable.
Additionally, NF-KB decoy ODNs also prevented and treated oxazolone-
colitis, a mouse model for ulcerative colitis, and thus affected a Th2-
mediated inflammatory process. In each case, decoy administration led
to inflammation clearing effects, suggesting a therapeutic potency
[[Page 36817]]
applicable to human IBD [J. Clin. Invest. (2005) 115, 3057-3071].
Available for licensing are methods for treating or preventing the
inflammatory response of IBDs by intrarectally or intraperitoneally
administering a therapeutic effective amount of NF-KB decoy ODN. Claims
are directed to treatment of Th1 and Th2 inflammatory response and
these studies suggest that NF-KB decoy ODNs targeting the consensus NF-
KB binding site and encapsulated in a viral envelope represent an
effective approach for the treatment of IBDs.
Related IBD technologies available for licensing also include IL-13
modulators and inhibitors (HHS Reference No. E-131-2002/0-PCT-02, WO
2004/001655, filed 14 June 2002) and IL-13 mutant and chimeric
molecules (HHS Reference No. E-003-2005/0-US-01, U.S. Provisional
Patent Application No. 60/671,624 filed 15 April 2005).
In addition to licensing, the technology is available for further
development through collaborative research opportunities with the
inventors.
Treatment and Prevention of Inflammatory Bowel Disease (IBD) using
Mutant and Chimeric IL-13 Molecules
Warren Strober (NIAID), Ivan Fuss (NIAID), Peter Mannon (NIAID), Jan
Preiss (NIAID), Raj Puri (FDA), Koji Kawakami (FDA), Stefan Fichtner-
Feigl (NIAID), and Atsushi Kitani (NIAID)
U.S. Provisional Patent Application No. 60/671,624 filed 15 April 2005
(HHS Reference No. E-003-2005/ 0-US-01); PCT International Application
filed 14 April 2006 (HHS Reference No. E-003-2005/0-PCT-02)
Licensing Contact: Susan Carson, D. Phil; 301/435-5020;
carsonsu@mail.nih.gov.
Ulcerative colitis (UC) is a chronic inflammatory disease of the
colorectum and affects approximately 400,000 people in the United
States. The cause of UC is not known, although an abnormal
immunological response to bacterial antigens in the gut microflora is
thought to be involved. Present treatments for UC include anti-
inflammatory therapy using aminosalicylates or corticosteroids, as well
as immunomodulators and diet. However, 25-40% of ulcerative colitis
patients must eventually have their colons removed due to massive
bleeding, severe illness, rupture of the colon, risk of cancer or due
to side effects of corticosteroids and novel treatments are still
actively being sought. NIH scientists and their collaborators have used
a mouse model of experimental colitis (oxazolone colitis, OC) to show
that IL-13, a Th2 cytokine, is a significant pathologic factor in OC
and that neutralizing IL-13 in these animals effectively prevents
colitis [Immunity (2002) 17, 629-638].
OC is a colitis induced by intrarectal administration of a
relatively low dose of the haptenating agent oxazolone subsequent to
skin sensitization with oxazolone. A highly reproducible and chronic
colonic inflammation is obtained that is histologically similar to
human ulcerative colitis. Studies show that Natural Killer T (NKT)
cells, rather than conventional CD4+T cells, mediate oxazolone colitis
and are the source of IL-13 as well as being activated by CD1-
expressing intestinal epithelial cells. Tissue removed from ulcerative
colitis patients were also shown to contain increased numbers of
nonclassical NKT cells that produce markedly increased amounts of IL-13
and that in keeping with epithelial damage being a key factor in UC,
these NKT cells are cytotoxic for epithelial cells [J. Clin. Invest.
(2004) 113, 1490-1497]. Building on their previous work, scientists at
NIAID and FDA have shown that an Il-13 chimeric fusion protein linked
to an effector molecule was able to prevent colitis in a mouse model of
ulcerative colitis.
Available for licensing are methods for treating or preventing the
inflammatory response of IBD by inhibiting the binding of IL-13 to IL-
13 receptors on NKT cells. Additionally, these mutant and chimeric Il-
13 molecules are able to block the chronic inflammatory response that
results in fibrosis as seen in Crohn's disease. Preventing the
inflammatory response of colitis by either modulating or blocking IL-13
and NKT cell activity continues to be an effective therapeutic approach
in animal models of colitis with implications for the treatment of
human ulcerative colitis and for the treatment of fibrosis associated
with Crohn's disease.
Related IBD technologies available for licensing also include IL-13
modulators and inhibitors (HHS Reference No. E-131-2002/0-PCT-02, WO
2004/001655, filed 14 June 2002) and NF-kappa B decoy oligonucleotides
[HHS Reference No. E-108-2005/0-US-01, U.S. Patent Application No. 11/
125,919, filed 10 May 2005; J. Clin. Invest. (2005) 115, 3057-3071].
In addition to licensing, the technology is available for further
development through collaborative research opportunities with the
inventors.
Dated: June 21, 2006.
David R. Sadowski,
Acting Director, Division of Technology Development and Transfer,
Office of Technology Transfer, National Institutes of Health.
[FR Doc. 06-5868 Filed 6-27-06; 8:45 am]
BILLING CODE 4140-01-P
