Prospective Grant of an Exclusive License: Development and Commercialization of Therapeutic Products for Rheumatoid Arthritis (RA), 26413-26414 [E7-8889]
Download as PDF
<![CDATA[
Federal Register / Vol. 72, No. 89 / Wednesday, May 9, 2007 / Notices
Dated: May 2, 2007.
Judith Spaeth,
Director, Office of Federal Advisory
Committee Policy.
[FR Doc. 07–2299 Filed 5–8–07; 8:45 am]
BILLING CODE 4140–01–M
DEPARTMENT OF HEALTH AND
HUMAN SERVICES
National Institutes of Health
Prospective Grant of Exclusive
License: Use of Licensee’s proprietary
delivery formulation containing
synthetic peptides of the CEA antigen
(or modifications, derivatives,
fragments, or immunogenic epitopes
thereof) as claimed in the Licensed
Patent Rights, alone or in combination
with at least one other synthetic
peptide for use in the prevention and/
or treatment of adenocarcinomas in
humans. For the avoidance of doubt,
said delivery formulation specifically
excludes all poxviruses, eukaryotic
expression vectors, and recombinant
yeast
National Institutes of Health,
Public Health Service, HHS.
ACTION: Notice.
sroberts on PROD1PC70 with NOTICES
AGENCY:
SUMMARY: This is notice, in accordance
with 35 U.S.C. 209(c)(1) and 37 CFR
Part 404.7(a)(1)(i), that the National
Institutes of Health, Department of
Health and Human Services, is
contemplating the grant of an exclusive
patent license to practice the inventions
embodied in U.S. Patent 6,756,038 and
PCT Application Serial No. PCT/US98/
19794 and foreign equivalents thereof,
entitled ‘‘Agonist and Antagonist
Peptides of Carcinoembryonic Antigen
(CEA)’’ (E–099–1996/0), to Immatics
Biotechnologies, GmbH, which is
located in Tuebingen, Germany. The
patent rights in these inventions have
been assigned to the United States of
America.
The prospective exclusive license
territory may be worldwide and the
field of use may be limited to the use
of Licensee’s proprietary delivery
formulation containing synthetic
peptides of the CEA antigen (or
modifications, derivatives, fragments, or
immunogenic epitopes thereof) as
claimed in the Licensed Patent Rights,
alone or in combination with at least
one other synthetic peptide for use in
the prevention and/or treatment of
adenocarcinomas in humans. For the
avoidance of doubt, said delivery
formulation specifically excludes all
poxviruses, eukaryotic expression
vectors, and recombinant yeast.
VerDate Aug<31>2005
18:12 May 08, 2007
Jkt 211001
Only written comments and/or
applications for a license which are
received by the NIH Office of
Technology Transfer on or before July 9,
2007 will be considered.
ADDRESSES: Requests for copies of the
patent application, inquiries, comments,
and other materials relating to the
contemplated exclusive license should
be directed to: Michelle A. Booden,
PhD., Technology Licensing Specialist,
Office of Technology Transfer, National
Institutes of Health, 6011 Executive
Boulevard, Suite 325, Rockville, MD
20852–3804; Telephone: (301) 451–
7337; Facsimile: (301) 402–0220; E-mail:
boodenm@mail.nih.gov.
SUPPLEMENTARY INFORMATION: The
technology describes the composition
and use of nucleic acid sequences that
encode agonist and one antagonist
peptide variants of the human
carcinoembryonic antigen (CEA)
peptide, including but not limited to
CAP–1. CEA is an antigen, which is
expressed on the surface of various
types of cancer cells. It is capable of
stimulating a specific cytolytic T cell
response, as is CAP–1, which is a highly
immunogenic epitope of CEA.
Therefore, CAP–1 agonists which are
capable of eliciting a CEA-specific
cytolytic T cell response, such as those
identified by the inventors, may
represent potential immunogens for use
as therapeutic agents or vaccines against
various cancers, and possibly also for
use against autoimmune diseases. In
fact, at least one of the agonist peptides
appears to be more immunogenic than
the native CAP–1 peptide. CAP–1
antagonists which are capable of
reducing or eliminating this T cell
response, such as the antagonist peptide
variant identified by the inventors, may
represent potential agents for use
against autoimmune responses to CEA
or to agonist peptide variants thereof.
The prospective exclusive license will
be royalty bearing and will comply with
the terms and conditions of 35 U.S.C.
209 and 37 CFR Part 404.7. The
prospective exclusive license may be
granted unless within sixty (60) days
from the date of this published notice,
the NIH receives written evidence and
argument that establishes that the grant
of the license would not be consistent
with the requirements of 35 U.S.C. 209
and 37 CFR Part 404.7.
Applications for a license in the field
of use filed in response to this notice
will be treated as objections to the grant
of the contemplated exclusive license.
Comments and objections submitted to
this notice will not be made available
for public inspection and, to the extent
permitted by law, will not be released
DATES:
PO 00000
Frm 00081
Fmt 4703
Sfmt 4703
26413
under the Freedom of Information Act,
5 U.S.C. 552.
Dated: May 1, 2007.
Steven M. Ferguson,
Director, Division of Technology Development
and Transfer, Office of Technology Transfer,
National Institutes of Health.
[FR Doc. E7–8888 Filed 5–8–07; 8:45 am]
BILLING CODE 4140–01–P
DEPARTMENT OF HEALTH AND
HUMAN SERVICES
National Institutes of Health
Prospective Grant of an Exclusive
License: Development and
Commercialization of Therapeutic
Products for Rheumatoid Arthritis (RA)
National Institutes of Health,
Public Health Service, HHS.
ACTION: Notice.
AGENCY:
SUMMARY: This notice, in accordance
with 35 U.S.C. § 209(c)(1) and 37 CFR
Part 404.7(a)(1)(i), announces that the
Department of Health and Human
Services is contemplating the grant of an
exclusive license to practice the
inventions embodied in PCT
Application No. PCT/US01/04125, filed
February 9, 2001, entitled
‘‘Identification of a Novel Domain in the
Tumor Necrosis Factor Receptor Family
that Mediates Pre-ligand Receptor
Assembly and Function’’ [E–095–2000/
0–PCT–02]; U.S. Patent No. 7,148,061,
issued December 12, 2006, entitled
‘‘Identification of Novel Domain in the
Tumor Necrosis Factor Receptor Family
that Mediates Pre-ligand Receptor
Assembly and Function’’ [E–095–2000/
0–US–03]; U.S. Patent Application No.
11/637,272, filed December 12, 2006,
entitled ‘‘Identification of Novel Domain
in the Tumor Necrosis Factor Receptor
Family that Mediates Pre-ligand
Receptor Assembly and Function’’ [E–
095–2000/0–US–08]; PCT Application
No. PCT/US06/24909, filed June 26,
2006, entitled ‘‘A Potential Novel
Therapeutic Protein Molecule of
Inflammatory Arthritis Targeting the
Pre-ligand Assembly Domain (PLAD) of
Tumor Necrosis Factor Receptor Type
1’’ [E–095–2000/4–PCT–01]; European
Patent Application No. 01910476.9,
filed February 9, 2001, entitled
‘‘Identification of Novel Domain in the
Tumor Necrosis Factor Receptor Family
that Mediates Pre-ligand Receptor
Assembly and Function’’ [E–095–2000/
0–EP–06]; Australian Patent Application
No. 2001238076, filed on February 9,
2001, entitled ‘‘Identification of Novel
Domain in the Tumor Necrosis Factor
Receptor Family that Mediates Pre-
E:\FR\FM\09MYN1.SGM
09MYN1
sroberts on PROD1PC70 with NOTICES
26414
Federal Register / Vol. 72, No. 89 / Wednesday, May 9, 2007 / Notices
ligand Receptor Assembly and
Function’’ [E–095–2000/0–AU–04];
Australian Patent Application No.
2006203490, filed on August 11, 2006,
entitled ‘‘Identification of Novel Domain
in the Tumor Necrosis Factor Receptor
Family that Mediates Pre-ligand
Receptor Assembly and Function’’ [E–
095–2000/0–AU–07]; and Canadian
Patent Application No. 2399388, filed
February 9, 2001, entitled
‘‘Identification of Novel Domain in the
Tumor Necrosis Factor Receptor Family
that Mediates Pre-ligand Receptor
Assembly and Function’’ [E–095–2000/
0–CA–05] to Welson Pharmaceuticals,
Inc.
The prospective exclusive license
territory may be worldwide and the
field of use may be limited to
therapeutic applications for rheumatoid
arthritis (RA) using Welson’s
proprietary platform.
DATES: Only written comments and/or
license applications which are received
by the National Institutes of Health on
or before July 9, 2007 will be
considered.
ADDRESSES: Requests for copies of the
patent and/or patent applications,
inquiries, comments and other materials
relating to the contemplated exclusive
license should be directed to: Mojdeh
Bahar, J.D., M.A., Technology Licensing
Specialist, Office of Technology
Transfer, National Institutes of Health,
6011 Executive Boulevard, Suite 325,
Rockville, MD 20852–3804. Telephone:
(301) 435–2950; Facsimile: (301) 402–
0220; E-mail: baharm@od.nih.gov.
SUPPLEMENTARY INFORMATION: The
invention relates to methods and
compositions that are useful for novel
treatment of arthritis and other
autoimmune diseases. This technology
discloses the identification of a
functional domain, Pre-ligand Assembly
Domain (PLAD), an essential part in
signaling involving receptors of the
Tumor Necrosis Factor superfamily and
its use in ameliorating rheumatoid
arthritis (RA). PLAD is essential for
signaling involving TFNR including
TNFR–1 (p60), TNFR–2 (p80), Fas,
TRAIL–R, LTR, CD40, CD30, CD27,
HVEM, OX40 and DR4 and can be
isolated as functional polypeptides
which can be useful in inhibiting the
first step in TNFR mediated signaling,
ligand-independent assembly of
members of the TNFR superfamily. The
ability to inhibit TNFR signaling
suggests that these PLAD polypeptides
may be useful in development of new
therapeutic molecules or as therapeutic
molecules themselves used for
modulation of immune responses,
apoptosis, and inflammation. The
VerDate Aug<31>2005
18:12 May 08, 2007
Jkt 211001
inventors have discovered compounds
that interfere with PLAD and can block
the effects of TNF-alpha.
The prospective exclusive license will
be royalty-bearing and will comply with
the terms and conditions of 35 U.S.C.
209 and 37 CFR part 404.7. The
prospective exclusive license may be
granted unless within sixty (60) days
from the date of this published notice,
the NIH receives written evidence and
argument that establish that the grant of
the license would not be consistent with
the requirements of 35 U.S.C. 209 and
37 CFR part 404.7.
Applications for a license in the field
of use filed in response to this notice
will be treated as objections to the grant
of the contemplated exclusive license.
Comments and objections submitted to
this notice will not be made available
for public inspection and, to the extent
permitted by law, will not be released
under the Freedom of Information Act,
5 U.S.C. 552.
Dated: April 30, 2007.
Steven M. Ferguson,
Director, Division of Technology Development
and Transfer,Office of Technology
Transfer,National Institutes of Health.
[FR Doc. E7–8889 Filed 5–8–07; 8:45 am]
BILLING CODE 4140–01–P
DEPARTMENT OF HEALTH AND
HUMAN SERVICES
National Institutes of Health
Prospective Grant of Exclusive
License: Treatment of Inflammatory
Bowel Disease (IBD) Using IL–13
Modulators and Inhibitors
National Institutes of Health,
Public Health Service, HHS.
ACTION: Notice.
AGENCY:
SUMMARY: This is notice, in accordance
with 35 U.S.C. 209(c) (1) and 37 CFR
404.7(a)(1)(i), that the National
Institutes of Health (NIH), Department
of Health and Human Services (HHS), is
contemplating the grant of an exclusive
license to practice the invention
embodied in:
PCT patent application PCT/US2002/
018790 filed 14 June 2002, entitled:
‘‘Methods of Treating and Preventing Colitis
involving IL–13 and NK–T Cells’’ [HHS
Reference Number: E–131–2002/0-PCT–01],
to
Wyeth Pharmaceuticals, based in
Madison, New Jersey. The field of use
may be limited to the use of IL–13
modulators or NK–T cell modulators
(such as antibodies) for the treatment or
prevention of Inflammatory Bowel
Disease, including ulcerative colitis and
PO 00000
Frm 00082
Fmt 4703
Sfmt 4703
Crohn’s disease. The United States of
America is an assignee of the patent
rights in these inventions.
DATES: Only written comments and/or
application for a license, which are
received by the NIH Office of
Technology Transfer on or before July 9,
2007 will be considered.
ADDRESSES: Requests for a copy of the
patent application, inquiries, comments
and other materials relating to the
contemplated license should be directed
to: Susan Carson, D.Phil., Office of
Technology Transfer, National Institutes
of Health, 6011 Executive Boulevard,
Suite 325, Rockville, MD 20852–3804;
E-mail: carsonsu@od.nih.gov;
Telephone: (301) 435–5020; Facsimile:
(301) 402–0220.
SUPPLEMENTARY INFORMATION: 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 by the mucosal
T cells responsive 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 NKT cells rather than conventional
CD4+T cells mediate oxazolone colitis
and that NKT cells are the source of IL–
13, and are activated by CD1 expressing
intestinal epithelial cells. Tissue
removed from UC patients was 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. Investigation (2004) 113,
E:\FR\FM\09MYN1.SGM
09MYN1
]]>Agencies
[Federal Register Volume 72, Number 89 (Wednesday, May 9, 2007)]
[Notices]
[Pages 26413-26414]
From the Federal Register Online via the Government Printing Office [www.gpo.gov]
[FR Doc No: E7-8889]
-----------------------------------------------------------------------
DEPARTMENT OF HEALTH AND HUMAN SERVICES
National Institutes of Health
Prospective Grant of an Exclusive License: Development and
Commercialization of Therapeutic Products for Rheumatoid Arthritis (RA)
AGENCY: National Institutes of Health, Public Health Service, HHS.
ACTION: Notice.
-----------------------------------------------------------------------
SUMMARY: This notice, in accordance with 35 U.S.C. Sec. 209(c)(1) and
37 CFR Part 404.7(a)(1)(i), announces that the Department of Health and
Human Services is contemplating the grant of an exclusive license to
practice the inventions embodied in PCT Application No. PCT/US01/04125,
filed February 9, 2001, entitled ``Identification of a Novel Domain in
the Tumor Necrosis Factor Receptor Family that Mediates Pre-ligand
Receptor Assembly and Function'' [E-095-2000/0-PCT-02]; U.S. Patent No.
7,148,061, issued December 12, 2006, entitled ``Identification of Novel
Domain in the Tumor Necrosis Factor Receptor Family that Mediates Pre-
ligand Receptor Assembly and Function'' [E-095-2000/0-US-03]; U.S.
Patent Application No. 11/637,272, filed December 12, 2006, entitled
``Identification of Novel Domain in the Tumor Necrosis Factor Receptor
Family that Mediates Pre-ligand Receptor Assembly and Function'' [E-
095-2000/0-US-08]; PCT Application No. PCT/US06/24909, filed June 26,
2006, entitled ``A Potential Novel Therapeutic Protein Molecule of
Inflammatory Arthritis Targeting the Pre-ligand Assembly Domain (PLAD)
of Tumor Necrosis Factor Receptor Type 1'' [E-095-2000/4-PCT-01];
European Patent Application No. 01910476.9, filed February 9, 2001,
entitled ``Identification of Novel Domain in the Tumor Necrosis Factor
Receptor Family that Mediates Pre-ligand Receptor Assembly and
Function'' [E-095-2000/0-EP-06]; Australian Patent Application No.
2001238076, filed on February 9, 2001, entitled ``Identification of
Novel Domain in the Tumor Necrosis Factor Receptor Family that Mediates
Pre-
[[Page 26414]]
ligand Receptor Assembly and Function'' [E-095-2000/0-AU-04];
Australian Patent Application No. 2006203490, filed on August 11, 2006,
entitled ``Identification of Novel Domain in the Tumor Necrosis Factor
Receptor Family that Mediates Pre-ligand Receptor Assembly and
Function'' [E-095-2000/0-AU-07]; and Canadian Patent Application No.
2399388, filed February 9, 2001, entitled ``Identification of Novel
Domain in the Tumor Necrosis Factor Receptor Family that Mediates Pre-
ligand Receptor Assembly and Function'' [E-095-2000/0-CA-05] to Welson
Pharmaceuticals, Inc.
The prospective exclusive license territory may be worldwide and
the field of use may be limited to therapeutic applications for
rheumatoid arthritis (RA) using Welson's proprietary platform.
DATES: Only written comments and/or license applications which are
received by the National Institutes of Health on or before July 9, 2007
will be considered.
ADDRESSES: Requests for copies of the patent and/or patent
applications, inquiries, comments and other materials relating to the
contemplated exclusive license should be directed to: Mojdeh Bahar,
J.D., M.A., Technology Licensing Specialist, Office of Technology
Transfer, National Institutes of Health, 6011 Executive Boulevard,
Suite 325, Rockville, MD 20852-3804. Telephone: (301) 435-2950;
Facsimile: (301) 402-0220; E-mail: baharm@od.nih.gov.
SUPPLEMENTARY INFORMATION: The invention relates to methods and
compositions that are useful for novel treatment of arthritis and other
autoimmune diseases. This technology discloses the identification of a
functional domain, Pre-ligand Assembly Domain (PLAD), an essential part
in signaling involving receptors of the Tumor Necrosis Factor
superfamily and its use in ameliorating rheumatoid arthritis (RA). PLAD
is essential for signaling involving TFNR including TNFR-1 (p60), TNFR-
2 (p80), Fas, TRAIL-R, LTR, CD40, CD30, CD27, HVEM, OX40 and DR4 and
can be isolated as functional polypeptides which can be useful in
inhibiting the first step in TNFR mediated signaling, ligand-
independent assembly of members of the TNFR superfamily. The ability to
inhibit TNFR signaling suggests that these PLAD polypeptides may be
useful in development of new therapeutic molecules or as therapeutic
molecules themselves used for modulation of immune responses,
apoptosis, and inflammation. The inventors have discovered compounds
that interfere with PLAD and can block the effects of TNF-alpha.
The prospective exclusive license will be royalty-bearing and will
comply with the terms and conditions of 35 U.S.C. 209 and 37 CFR part
404.7. The prospective exclusive license may be granted unless within
sixty (60) days from the date of this published notice, the NIH
receives written evidence and argument that establish that the grant of
the license would not be consistent with the requirements of 35 U.S.C.
209 and 37 CFR part 404.7.
Applications for a license in the field of use filed in response to
this notice will be treated as objections to the grant of the
contemplated exclusive license. Comments and objections submitted to
this notice will not be made available for public inspection and, to
the extent permitted by law, will not be released under the Freedom of
Information Act, 5 U.S.C. 552.
Dated: April 30, 2007.
Steven M. Ferguson,
Director, Division of Technology Development and Transfer,Office of
Technology Transfer,National Institutes of Health.
[FR Doc. E7-8889 Filed 5-8-07; 8:45 am]
BILLING CODE 4140-01-P
