Government-Owned Inventions; Availability for Licensing, 19299-19300 [2012-7709]
Download as PDF
<![CDATA[
Federal Register / Vol. 77, No. 62 / Friday, March 30, 2012 / Notices
resolve the disagreement with reporting
entity but was unsuccessful. The
Department can only determine whether
the report was legally required to be
filed and whether the report accurately
depicts the action taken and the
reporter’s basis for action. Additional
detail on the process of dispute
resolution and Secretarial Review
process can be found at 45 CFR 60.14
of the NPDB regulations.
RECORD SOURCE CATEGORIES:
The records contained in the system
are submitted by the following entities:
(1) Insurance companies and others who
have made payment as a result of a
malpractice action or claim, (2) State
Boards of Medical and Dental
Examiners; (3) State Licensing Boards;
(4) hospitals and other health care
entities; (5) DEA; and (6) Federal
entities which employ health
practitioners or who have authority to
sanction such practitioners covered by a
Federal program. Section 1921 of the
Social Security Act expands reporting of
actions submitted by State health care
practitioner licensing and certification
authorities (including medical and
dental boards), State entity licensing
and certification authorities, peer
review organizations and private
accreditation organizations.
SYSTEMS EXEMPTED FROM CERTAIN PROVISIONS
OF THE ACT:
The Secretary has exempted this
system from certain provisions of the
Act. In accordance with 5 U.S.C.
552(k)(2) and 45 CFR 5b.11(b)(ii)(L), this
system is exempt from subsections 5
U.S.C. 552a(c)(3), (d)(1)–(4), (e)(4)(G)
and (H), and (f).
[FR Doc. 2012–7612 Filed 3–29–12; 8:45 am]
BILLING CODE 4165–15–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:
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
mstockstill on DSK4VPTVN1PROD with NOTICES
SUMMARY:
VerDate Mar<15>2010
19:11 Mar 29, 2012
Jkt 226001
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.
MUC–1 Tumor Antigen Agonist
Epitopes for Enhancing T-cell
Responses to Human Tumors
Description of Technology: The MUC–
1 tumor associated antigen has been
shown to be overexpressed and/or
underglycosylated in a wide range of
human cancers. The C-terminus region
of MUC–1 (MUC–1C) has been shown to
be an oncogene and has been associated
with a more aggressive phenotype in
several different cancers.
Scientists at NIH have identified 7
new agonist epitopes of the MUC–1
tumor associated antigen. Compared to
their native epitope counterparts,
peptides reflecting these agonist
epitopes have been shown to enhance
the generation of human tumor cells,
which in turn have a greater ability to
kill human tumor cells endogenously
expressing the native MUC–1 epitope.
The agonist epitopes span both the
VNTR region of MUC–1 and the Cterminus region. The epitopes
encompass 2 major MHC alleles
reflecting the majority of the population.
Along with the method of use, the
technology encompasses the use of
these agonist epitopes in peptide- and
protein-based vaccines, with dendritic
cells or other antigen presenting cells, or
encoding sequences in DNA, viral,
bacterial, yeast, or other types of
vectors, or to stimulate T-cells in vitro
for adoptive immunotherapy protocols.
Potential Commercial Applications:
• As a therapeutic vaccine to enhance
patient’s immune responses to a range
of human cancers
• As a preventive vaccine for patients
with preneoplastic conditions or a high
risk of developing cancer
• As a preventive vaccine for cancers
• For in vitro stimulation of
lymphocytes for adoptive transfer
protocols for cancer
Competitive Advantages:
• The agonist epitopes have been
shown to be much more potent than
their natural counterparts in activating
human T-cells to MUC–1.
• Compared to T-cells activated with
the corresponding native epitopes, the
PO 00000
Frm 00123
Fmt 4703
Sfmt 4703
19299
T-cells activated by the agonist epitopes
lyse tumor cells to a greater extent.
• The technology can be used in a
wide range of cancer vaccine platforms
and in adoptive immunotherapy
protocols.
• The technology can be combined
with existing vaccine platforms
including those currently showing
patient benefit, as well as with other
therapeutic modalities.
Development Stage:
• Pre-clinical
• In vitro data available
Inventors: Jeffrey Schlom and KwongYok Tsang (NCI).
Intellectual Property: HHS Reference
No. E–001–2012/0—U.S. Patent
Application No. 61/582,723 filed 03 Jan
2012.
Related Technologies:
• HHS Reference No. E–154–1998/0
—PCT Application No. PCT/US98/
03693
• HHS Reference No. E–321–2003/0
—PCT Application No. PCT/US2004/
41921
Licensing Contact: Sabarni Chatterjee,
Ph.D., MBA; 301–435–5587;
chatterjeesa@mail.nih.gov.
Collaborative Research Opportunity:
The Laboratory of Tumor Immunology
and Biology, National Cancer Institute,
is seeking statements of capability or
interest from parties interested in
collaborative research to further
develop, evaluate or commercialize the
use of MUC–1 tumor antigen agonist
epitopes for the treatment or prevention
of cancer. For collaboration
opportunities, please contact John
Hewes, Ph.D. at hewesj@mail.nih.gov.
Novel Diagnostic, Prognostic and
Therapeutic Biomarker for
Hepatocellular Carcinoma
Description of Technology: Scientists
at the National Cancer Institute have
discovered that Stearol-CoA desaturase1 (SCD–1) is associated with
hepatocellular carcinoma (HCC).
Utilizing a microarray to analyze HCC
patient samples, the investigators found
SCD–1 is elevated in liver tumor tissues
and it is a marker for a highly aggressive
form of HCC, hepatic stem cell-like HCC
subtype (HpSC HCC), which retains
stem-cell features capable of cellular
plasticity and cell motility. The
investigators found SCD–1 is
significantly elevated in HpSC tumors
in comparison to less aggressive HCC
tumors and it is associated with poor
patient survival. In vitro studies
demonstrate SCD–1 inhibition and/or
addition of saturated palmitic acid
reduces HpSC HCC characteristics. In
addition to diagnostic, prognostic, and
treatment applications, this technology
E:\FR\FM\30MRN1.SGM
30MRN1
19300
Federal Register / Vol. 77, No. 62 / Friday, March 30, 2012 / Notices
may enable clinicians to effectively
stratify patients for more aggressive
cancer treatment and prioritize
candidates for liver transplantation.
Potential Commercial Applications:
• Method to diagnose HCC
• Method to prognose patient survival
• Method to stratify HCC for
appropriate treatment
• Method to treat HCC
Competitive Advantages:
• Retrospective studies performed on
human samples
• Modulation of SCD–1 reduces
HpSC HCC characteristics
Development Stage:
• Early-stage
• In vitro data available
• In vivo data available (human)
Inventors: Anuradha Budhu and Xin
W. Wang (NCI).
Intellectual Property: HHS Reference
No. E–205–2011/0—U.S. Provisional
Application No. 61/533,392 filed 12 Sep
2011.
Related Technology: HHS Reference
No. E–139–2010/0—PCT Application
No. PCT/US2011/032285 filed 13 Apr
2011.
Licensing Contact: Jennifer Wong;
301–435–4633; wongje@mail.nih.gov.
Collaborative Research Opportunity:
The National Cancer Institute is seeking
statements of capability or interest from
parties interested in collaborative
research to further develop, evaluate or
commercialize biomarkers for liver
cancer. For collaboration opportunities,
please contact John Hewes, Ph.D. at
hewesj@mail.nih.gov.
mstockstill on DSK4VPTVN1PROD with NOTICES
Potential Use of Anti-IgE in the
Treatment of Lupus Nephritis
Description of Technology: Systemic
lupus erythematosus (SLE) is a multiorgan inflammatory disease
characterized by a significant morbidity
and mortality related to both disease
evolution as well as therapeutic side
effects. At least half of SLE patients
develop lupus nephritis.
The inventors have used a Lyn -/mouse model that develops an
autoimmune disease exhibiting some
features of human SLE. Using this
model the inventors identified basophils
and self-reactive IgEs as important
components in the development of
autoantibody-mediated kidney disease.
The inventors found that depletion of
basophils or the absence of IgE causes
a considerable reduction in
autoantibody production and preserves
kidney function in the Lyn -/- mice. The
inventors’ work demonstrates that IgE
immune complexes can activate
basophils and that removal of selfreactive IgEs that form functional
circulating immune complexes prevents
VerDate Mar<15>2010
19:11 Mar 29, 2012
Jkt 226001
kidney disease. Further, the inventors
have shown that basophils are
contributors to the production of the
self-reactive antibodies that cause
lupus-like nephritis in the Lyn -/- mice.
Accordingly, reducing circulating IgE
levels or reducing basophil activation
may be of therapeutic benefit.
Potential Commercial Applications:
Further research and development of
therapeutic approach to treat lupus
nephritis.
Competitive Advantages: Current
treatment of lupus has not advanced for
many years. This finding is of
importance for its potential in
advancing treatment of the disease.
Development Stage:
• Early-stage
• Pre-clinical
Inventors: Juan Rivera and Nicolas
Charles (NIAMS).
Publications:
1. Charles N, et al. Basophils and the
T helper 2 environment can promote the
development of lupus nephritis. Nat
Med. 2010 Jun;16(6):701–707. [PMID
20512127].
2. Brightbill HD, et al. Antibodies
specific for a segment of human
membrane IgE deplete IgE-producing B
cells in humanized mice. J Clin Invest.
2010 Jun;120(6):2218–2229. [PMID
20458139].
3. Mack M, et al. Basophils and mast
cells in renal injury. Kidney Int. 2009
Dec;76(11):1142–1147. [PMID
19692999].
4. Busse W, et al. Omalizumab, antiIgE recombinant humanized monoclonal
antibody for the treatment of severe
allergic asthma. J Allergy Clin Immunol.
2001 Aug;108(2):184–90. [PMID:
11496232].
Intellectual Property: HHS Reference
No. E–216–2010/0—PCT Application
No. PCT/US2010/058077 filed 24 Nov
2010.
Licensing Contact: Jaime M. Greene;
301–435–5559;
greenejaime@mail.nih.gov.
Collaborative Research Opportunity:
The National Institute of Arthritis and
Musculoskeletal and Skin Diseases is
seeking statements of capability or
interest from parties interested in
collaborative research to further
develop, evaluate or commercialize the
technology for the use of anti-IgE in the
treatment of Lupus Nephritis. For
collaboration opportunities, please
contact Cecilia Pazman at
pazmance@mail.nih.gov.
PO 00000
Frm 00124
Fmt 4703
Sfmt 4703
Dated: March 27, 2012.
Richard U. Rodriguez,
Director, Division of Technology Development
and Transfer, Office of Technology Transfer,
National Institutes of Health.
[FR Doc. 2012–7709 Filed 3–29–12; 8:45 am]
BILLING CODE 4140–01–P
DEPARTMENT OF HOMELAND
SECURITY
[Docket No. DHS–2012–0012]
National Infrastructure Advisory
Council
National Protection and
Programs Directorate, DHS.
ACTION: Committee Management; Notice
of an open Federal Advisory Committee
meeting.
AGENCY:
The National Infrastructure
Advisory Council (NIAC) will meet on
Tuesday, April 17, 2012, 1310 N.
Courthouse Road, Suite 300, Virginia
Room, Arlington, VA 22201. The
meeting will be open to the public.
DATES: The NIAC will meet Tuesday,
April 17, 2012, from 1:30 p.m. to 4:30
p.m. The meeting may close early if the
committee has completed its business.
For additional information, please
consult the NIAC Web site,
www.dhs.gov/NIAC, or contact the NIAC
Secretariat by phone at (703) 235–2888
or by email at NIAC@dhs.gov.
ADDRESSES: 1310 N. Courthouse Road,
Suite 300, Virginia Room, Arlington, VA
22201.
While this meeting is open to the
public, participation in the NIAC
deliberations is limited to committee
members and appropriate Federal
Government officials. Discussions may
include committee members,
appropriate Federal Government
officials, and other invited persons
attending the meeting to provide
information that may be of interest to
the Council.
Immediately following the committee
member deliberation and discussion
period, there will be a limited time
period for public comment. Comments
should be limited to meeting agenda
items and previous NIAC studies. All
previous NIAC studies can be located at
www.dhs.gov/NIAC. Relevant public
comments may be submitted in writing
or presented in person for the Council
to consider. Comments should be
limited to the issues and topics
addressed by the Council. In-person
presentations will be limited to three
minutes per speaker, with no more than
30 minutes for all speakers. Parties
interested in making in-person
SUMMARY:
E:\FR\FM\30MRN1.SGM
30MRN1
]]>Agencies
[Federal Register Volume 77, Number 62 (Friday, March 30, 2012)]
[Notices]
[Pages 19299-19300]
From the Federal Register Online via the Government Printing Office [www.gpo.gov]
[FR Doc No: 2012-7709]
-----------------------------------------------------------------------
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.
MUC-1 Tumor Antigen Agonist Epitopes for Enhancing T-cell Responses to
Human Tumors
Description of Technology: The MUC-1 tumor associated antigen has
been shown to be overexpressed and/or underglycosylated in a wide range
of human cancers. The C-terminus region of MUC-1 (MUC-1C) has been
shown to be an oncogene and has been associated with a more aggressive
phenotype in several different cancers.
Scientists at NIH have identified 7 new agonist epitopes of the
MUC-1 tumor associated antigen. Compared to their native epitope
counterparts, peptides reflecting these agonist epitopes have been
shown to enhance the generation of human tumor cells, which in turn
have a greater ability to kill human tumor cells endogenously
expressing the native MUC-1 epitope. The agonist epitopes span both the
VNTR region of MUC-1 and the C-terminus region. The epitopes encompass
2 major MHC alleles reflecting the majority of the population.
Along with the method of use, the technology encompasses the use of
these agonist epitopes in peptide- and protein-based vaccines, with
dendritic cells or other antigen presenting cells, or encoding
sequences in DNA, viral, bacterial, yeast, or other types of vectors,
or to stimulate T-cells in vitro for adoptive immunotherapy protocols.
Potential Commercial Applications:
As a therapeutic vaccine to enhance patient's immune
responses to a range of human cancers
As a preventive vaccine for patients with preneoplastic
conditions or a high risk of developing cancer
As a preventive vaccine for cancers
For in vitro stimulation of lymphocytes for adoptive
transfer protocols for cancer
Competitive Advantages:
The agonist epitopes have been shown to be much more
potent than their natural counterparts in activating human T-cells to
MUC-1.
Compared to T-cells activated with the corresponding
native epitopes, the T-cells activated by the agonist epitopes lyse
tumor cells to a greater extent.
The technology can be used in a wide range of cancer
vaccine platforms and in adoptive immunotherapy protocols.
The technology can be combined with existing vaccine
platforms including those currently showing patient benefit, as well as
with other therapeutic modalities.
Development Stage:
Pre-clinical
In vitro data available
Inventors: Jeffrey Schlom and Kwong-Yok Tsang (NCI).
Intellectual Property: HHS Reference No. E-001-2012/0--U.S. Patent
Application No. 61/582,723 filed 03 Jan 2012.
Related Technologies:
HHS Reference No. E-154-1998/0 --PCT Application No. PCT/
US98/03693
HHS Reference No. E-321-2003/0 --PCT Application No. PCT/
US2004/41921
Licensing Contact: Sabarni Chatterjee, Ph.D., MBA; 301-435-5587;
chatterjeesa@mail.nih.gov.
Collaborative Research Opportunity: The Laboratory of Tumor
Immunology and Biology, National Cancer Institute, is seeking
statements of capability or interest from parties interested in
collaborative research to further develop, evaluate or commercialize
the use of MUC-1 tumor antigen agonist epitopes for the treatment or
prevention of cancer. For collaboration opportunities, please contact
John Hewes, Ph.D. at hewesj@mail.nih.gov.
Novel Diagnostic, Prognostic and Therapeutic Biomarker for
Hepatocellular Carcinoma
Description of Technology: Scientists at the National Cancer
Institute have discovered that Stearol-CoA desaturase-1 (SCD-1) is
associated with hepatocellular carcinoma (HCC). Utilizing a microarray
to analyze HCC patient samples, the investigators found SCD-1 is
elevated in liver tumor tissues and it is a marker for a highly
aggressive form of HCC, hepatic stem cell-like HCC subtype (HpSC HCC),
which retains stem-cell features capable of cellular plasticity and
cell motility. The investigators found SCD-1 is significantly elevated
in HpSC tumors in comparison to less aggressive HCC tumors and it is
associated with poor patient survival. In vitro studies demonstrate
SCD-1 inhibition and/or addition of saturated palmitic acid reduces
HpSC HCC characteristics. In addition to diagnostic, prognostic, and
treatment applications, this technology
[[Page 19300]]
may enable clinicians to effectively stratify patients for more
aggressive cancer treatment and prioritize candidates for liver
transplantation.
Potential Commercial Applications:
Method to diagnose HCC
Method to prognose patient survival
Method to stratify HCC for appropriate treatment
Method to treat HCC
Competitive Advantages:
Retrospective studies performed on human samples
Modulation of SCD-1 reduces HpSC HCC characteristics
Development Stage:
Early-stage
In vitro data available
In vivo data available (human)
Inventors: Anuradha Budhu and Xin W. Wang (NCI).
Intellectual Property: HHS Reference No. E-205-2011/0--U.S.
Provisional Application No. 61/533,392 filed 12 Sep 2011.
Related Technology: HHS Reference No. E-139-2010/0--PCT Application
No. PCT/US2011/032285 filed 13 Apr 2011.
Licensing Contact: Jennifer Wong; 301-435-4633;
wongje@mail.nih.gov.
Collaborative Research Opportunity: The National Cancer Institute
is seeking statements of capability or interest from parties interested
in collaborative research to further develop, evaluate or commercialize
biomarkers for liver cancer. For collaboration opportunities, please
contact John Hewes, Ph.D. at hewesj@mail.nih.gov.
Potential Use of Anti-IgE in the Treatment of Lupus Nephritis
Description of Technology: Systemic lupus erythematosus (SLE) is a
multi-organ inflammatory disease characterized by a significant
morbidity and mortality related to both disease evolution as well as
therapeutic side effects. At least half of SLE patients develop lupus
nephritis.
The inventors have used a Lyn -/- mouse model that develops an
autoimmune disease exhibiting some features of human SLE. Using this
model the inventors identified basophils and self-reactive IgEs as
important components in the development of autoantibody-mediated kidney
disease. The inventors found that depletion of basophils or the absence
of IgE causes a considerable reduction in autoantibody production and
preserves kidney function in the Lyn -/- mice. The inventors' work
demonstrates that IgE immune complexes can activate basophils and that
removal of self-reactive IgEs that form functional circulating immune
complexes prevents kidney disease. Further, the inventors have shown
that basophils are contributors to the production of the self-reactive
antibodies that cause lupus-like nephritis in the Lyn -/- mice.
Accordingly, reducing circulating IgE levels or reducing basophil
activation may be of therapeutic benefit.
Potential Commercial Applications: Further research and development
of therapeutic approach to treat lupus nephritis.
Competitive Advantages: Current treatment of lupus has not advanced
for many years. This finding is of importance for its potential in
advancing treatment of the disease.
Development Stage:
Early-stage
Pre-clinical
Inventors: Juan Rivera and Nicolas Charles (NIAMS).
Publications:
1. Charles N, et al. Basophils and the T helper 2 environment can
promote the development of lupus nephritis. Nat Med. 2010
Jun;16(6):701-707. [PMID 20512127].
2. Brightbill HD, et al. Antibodies specific for a segment of human
membrane IgE deplete IgE-producing B cells in humanized mice. J Clin
Invest. 2010 Jun;120(6):2218-2229. [PMID 20458139].
3. Mack M, et al. Basophils and mast cells in renal injury. Kidney
Int. 2009 Dec;76(11):1142-1147. [PMID 19692999].
4. Busse W, et al. Omalizumab, anti-IgE recombinant humanized
monoclonal antibody for the treatment of severe allergic asthma. J
Allergy Clin Immunol. 2001 Aug;108(2):184-90. [PMID: 11496232].
Intellectual Property: HHS Reference No. E-216-2010/0--PCT
Application No. PCT/US2010/058077 filed 24 Nov 2010.
Licensing Contact: Jaime M. Greene; 301-435-5559;
greenejaime@mail.nih.gov.
Collaborative Research Opportunity: The National Institute of
Arthritis and Musculoskeletal and Skin Diseases is seeking statements
of capability or interest from parties interested in collaborative
research to further develop, evaluate or commercialize the technology
for the use of anti-IgE in the treatment of Lupus Nephritis. For
collaboration opportunities, please contact Cecilia Pazman at
pazmance@mail.nih.gov.
Dated: March 27, 2012.
Richard U. Rodriguez,
Director, Division of Technology Development and Transfer, Office of
Technology Transfer, National Institutes of Health.
[FR Doc. 2012-7709 Filed 3-29-12; 8:45 am]
BILLING CODE 4140-01-P
