Government-Owned Inventions; Availability for Licensing, 32937-32940 [E9-16300]
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Centers for Public Health Preparedness
(CPHP) Program. The purpose of the
CPHP Program is to strengthen terrorism
and emergency preparedness by linking
academic expertise to state and local
health agency needs. The program
brings together colleges and universities
with a common focus on public health
preparedness to establish a national
network of education and training
resources. Of these institutions, 27 are
accredited Schools of Public Health
funded through a five-year Cooperative
Agreement for years 2004–2009. This
program addresses the public health
goals described in ‘‘A National Strategy
for Terrorism Preparedness and
Response: 2003–2008 Strategic Plan,’’
specifically Imperative Five, a
Competent and Sustainable Workforce.
Critical objectives under this Imperative
are to: (1) Increase the number and type
of professionals that comprise a
preparedness and response workforce;
(2) deliver certification and
competency-based training and
education; (3) recruit and retain the
highest quality workforce; and (4)
evaluate the impact of training to ensure
learning has occurred.
CDC requests OMB approval for a
period of one year to collect information
beginning in the fall of 2009. CDC is
undertaking a summative evaluation of
the CPHP Program encompassing the
period of the current Cooperative
Agreement. In order to complete this
evaluation, CDC is proposing three data
collection instruments to gather
information describing the program’s
processes and outcomes. These are: (1)
CPHP Interview Instrument; (2) CPHP
Customer/Partner Survey Instrument;
and (3) CPHP Customer/Partner FollowUp Interview Instrument. Collectively,
these instruments are needed in order to
gather, process, aggregate, evaluate, and
disseminate CPHP program information.
The information will be used by CDC to
document progress toward meeting
established program goals and
objectives, to evaluate outcomes
generated by the collective work of the
27 Centers, to inform the development
of a new public health preparedness
education and training cooperative
agreement program, and to respond to
data inquiries made by CDC and other
agencies of the federal government.
The CPHP Interview Instrument will
be used to guide a telephone interview
process with key CPHP staff. Questions
will gather perceptions about the CPHP
Program from the perspective of CPHP
staff. It is estimated that there will be a
total of 81 respondents with an
estimated time for data collection of 90
minutes. The CPHP Customer/Partner
Survey Instrument will be used to
gather information from representatives
of organizations that have received
training or technical assistance from the
CPHP Program. It will be administered
electronically with an option for paper
copy administration. It is estimated that
there will be one request per respondent
and a total of 171 respondents with an
estimated time for data collection of 20
minutes. The CPHP Customer/Partner
Follow-Up Interview Instrument will be
used to gather more in-depth
information on the same categories of
questions from the Survey Instrument. It
is estimated that there will be a total of
20 respondents with an estimated time
for data collection of 45 minutes. The
annualized estimated burden hours are
193.5.
There are no costs to respondents
except their time.
ESTIMATED ANNUALIZED BURDEN HOURS
Number of
respondents
Type of respondent
Form name
CPHP PIs, PCs, and Evaluators ..........................
CPHP Interview Instrument.
CPHP Customer/Partner Survey Instrument.
CPHP Customer/Partner Follow-Up Interview Instrument.
CPHP Customers and Partners ...........................
CPHP Customers and Partners ...........................
Dated: July 2, 2009.
Marilyn I. Radke,
Reports Clearance Officer, Centers for Disease
Control and Prevention.
[FR Doc. E9–16225 Filed 7–8–09; 8:45 am]
1.5
121.5
171
1
20/60
57
20
1
45/60
15
National Institutes of Health
ADDRESSES:
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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.
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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
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Total burden
(in hours)
1
DEPARTMENT OF HEALTH AND
HUMAN SERVICES
Government-Owned Inventions;
Availability for Licensing
Average burden per response
(in hours)
81
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.
BILLING CODE 4163–18–P
Number of
responses per
respondent
be required to receive copies of the
patent applications.
Immunogenic Peptide from NGEP
Protein for Developing Prostate Cancer
Vaccines
Description of Technology: The NGEP
protein is only present in the prostate
and is typically overexpressed on
prostate cancer cells. Hence, as a novel
prostate tumor-associated antigen (TAA)
it is a good target for developing active
immunotherapies to kill prostate cancer
cells. For example, NGEP could be used
in a vaccine to activate an individual’s
immune system to recognize and kill
NGEP-expressing prostate cancer cells.
However, TAAs typically are not very
effective in inciting an immune
response. This can be overcome by
identifying portions (epitopes) of the
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TAA that are more immunologically
active.
Investigators at the NIH have
identified a small peptide fragment of
the NGEP protein (NGEP CTL peptide
epitope) that is very effective in
activating cytotoxic lymphocytes,
causing them to destroy prostate cancer
cells and has great potential for
development of a variety of active
immunotherapy strategies, such as
vector-based cancer vaccines, to treat
and prevent prostate cancer. In addition,
it could be used for developing sensitive
immunoassays for measuring the
immune response of a prostate cancer
patient during immunotherapy.
Applications:
• Peptide cancer vaccine.
• Vector-based cancer vaccine.
• Liposome-based cancer vaccine.
• Cellular cancer vaccine.
• In vitro diagnostic for monitoring
the immune response of prostate cancer
patients during cancer vaccine trials.
Advantages:
• Small biologic therapeutic.
• Can be chemically synthesized or
produced recombinantly.
• DNA encoded peptide allows
molecular engineering.
• Can be used as a tumor antigen with
the clinically proven TRICOM-based
vaccine technology.
Development Status: Early stage.
Market: Prostate cancer is the secondleading cause of cancer death in men. It
is estimated that in the United States
there will be 192,280 new cases of
prostate cancer and 27,360 deaths due
to prostate cancer in 2009.
Inventors: Jeffrey Schlom et al. (NCI).
Publications: No publications directly
related to this technology.
Patent Status: U.S. Provisional
Application No. 61/170,900 filed 20 Apr
2009 (HHS Reference No. E–042–2009/
0–US–01).
Licensing Status: Available for
licensing.
Licensing Contact: Sabarni Chatterjee,
PhD; 301–435–5587;
chatterjeesa@mail.nih.gov.
Collaborative Research Opportunity:
The National Cancer Institute, Center for
Cancer Research, Laboratory of Tumor
Immunology and Biology, is seeking
statements of capability or interest from
parties interested in collaborative
research to further develop, evaluate, or
commercialize this technology. Please
contact Kevin Brand, J.D. at 301–451–
4566 or brandk@mail.nih.gov for more
information.
Gene Expression Signature Predictive
of Response to Chemotherapy
Description of Technology:
Combination cisplatin and fluorouracil
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(CF) is a reference chemotherapy
regimen for metastatic gastric cancer.
However, to date, no genome-wide
studies have identified distinctions in
gene expression that predict which
subjects with metastatic disease will
benefit from this therapy and which
subjects will not exhibit a therapeutic
response to chemotherapy. Given the
toxicity of chemotherapy, however,
defining parameters that identify those
subjects who will likely benefit from
chemotherapy is of paramount
importance. Early identification of nonresponders would provide opportunities
to explore alternate or novel therapeutic
approaches. Thus, a need exists to
identify methods of predicting a
subject’s response to chemotherapy
prior to receiving the treatment.
Scientists at the National Institutes of
Health have discovered a three-gene
signature that can be used to determine
the chemotherapy response in patients
with cancer. By measuring the
expression of three cancer-specific
genes it can be determined if a patient
with an epithelial cancer such as gastric,
bladder, head and neck, esophageal or
cervical cancers, will respond to CF
treatment. The inventors have
demonstrated that examining these
expression levels has high fidelity in
identifying CF treatment nonresponders. Further, the invention
describes a mechanism that can help
patients identified as non-responders
become responsive to treatment.
Therefore these methods have the
potential to reduce fatalities caused by
metastatic gastric cancer by identifying
patients early on who are nonresponsive to standard CF treatment and
customizing a new treatment plan
which may be better suited to their
individual needs.
Applications:
• Prognostic testing of epithelial
cancer patients.
• Customized treatment for gastric
cancer patients identified as CF
treatment non-responders.
Advantages:
• Expression levels of cancer-specific
genes can be used to determine if
metastatic gastric cancer patients are
responsive to combination cisplatin and
fluorouracil (CF) treatment.
• Fatalities due to metastatic gastric
cancer may be reduced by customizing
the treatment of non-responders.
Market: In 2008, it is estimated that
there will be 21,500 new cases and
10,880 deaths from gastric cancer in the
United States.
Development Status: Patient tissue
sample data available.
Inventors: Jeffrey E. Green and Hark
Kyun Kim (NCI).
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Patent Status: U.S. Provisional
Application No. 61/195,123 filed 03 Oct
2008 (HHS Reference No. E–282–2008/
0–US–01).
Licensing Status: Available for
licensing.
Licensing Contact: Surekha Vathyam,
PhD; 301–435–4076;
vathyams@mail.nih.gov.
Collaborative Research Opportunity:
The National Cancer Institute, Center for
Cancer Research, Laboratory of Cancer
Biology and Genetics, is seeking
statements of capability or interest from
parties interested in collaborative
research to further develop, evaluate, or
commercialize Gene Expression
Signature Predictive of Response to
Chemotherapy. Please contact John D.
Hewes, PhD at 301–435–3121 or
hewesj@mail.nih.gov for more
information.
Therapeutic Applications of a p53
Isoform in Regenerative Medicine,
Aging, and Cancer
Description of Technology: p53 plays
a critical role in carcinogenesis and
aging as a key regulator of cell cycle
progression, senescence and apoptosis.
The inventors have discovered that a
natural variant of p53 (D133p53)
inhibits p53-dependent cell senescence.
Utilizing D133p53 siRNAs, the inventors
have data demonstrating that siRNAtreated human fibroblast undergo cell
senescence, thereby indicating that
D133p53 inhibition could be a novel
approach for cell senescence-mediated
anti-proliferative therapy, including
anti-cancer treatments. Alternatively,
enhanced expression with D133p53 can
extend the replicative lifespan of normal
human cells. This technology may
provide a new method in the field of
regenerative medicine for aging-related
degenerative disease.
Also available for licensing are
D133p53 siRNAs and shRNA vectors, as
well as a D133p53 overexpression
vector, which can be used for cancer
and age-related degenerative
therapeutics. The shRNA can be stably
integrated into the cellular genome for
long-term D133p53 inhibition.
The inventors have also discovered
that another p53 variant (p53b)
accelerates p53-dependent cell
senescence, and developed a vector for
overexpressing p53b, which could be
used for cell senescence-mediated antiproliferative therapy.
Applications:
• Method to treat cancer.
• Method to treat aging related
disorders.
• Method to promote tissue
regeneration.
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Federal Register / Vol. 74, No. 130 / Thursday, July 9, 2009 / Notices
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• Pharmaceutical compositions to
inhibit cancer or promote cell
regeneration.
Advantages:
• Ability to treat a wide variety of
cancers and age-related diseases as p53
is present in normal cells.
• shRNA therapeutics are stably
integrated into genome for long-term
treatment.
Development Status: The technology
is currently in the pre-clinical stage of
development.
Market:
• An estimated 1,479,350 new cancer
diagnoses in the U.S. in 2009.
• Cancer is the second leading cause
of death in United States.
• It is estimated that the cancer
therapeutic market would double to $50
billion a year in 2010 from $25 billion
in 2006.
Inventors: Curtis C. Harris (NCI) et al.
Relevant Publications:
1. K Fujita et al. p53 isoforms,
D133p53 and p53b, are endogenous
regulators of replicative cellular
senescence. Nat Cell Biol., in press.
2. International Agency Research on
Cancer Conference, Lyon, France,
November 13, 2007.
Patent Status:
• U.S. Provisional Application No.
60/987,340 filed 12 Nov 2007 (HHS
Reference No. E–033–2008/0–US–01).
• PCT Application No. PCT/US2008/
080648 filed 21 Oct 2008 (HHS
Reference No. E–033–2008/0–PCT–02).
Licensing Status: Available for
licensing.
Licensing Contact: Jennifer Wong;
301–435–4633; wongje@mail.nih.gov.
Collaborative Research Opportunity:
The National Cancer Institute,
Laboratory of Human Carcinogenesis, is
seeking statements of capability or
interest from parties interested in
collaborative research to further
develop, evaluate, or commercialize this
technology. Please contact
Curtis_Harris@nih.gov for more
information.
Novel Compounds that Specifically Kill
Multi-Drug Resistant Cancer Cells
Description of Invention: One of the
major hindrances to successful cancer
chemotherapy is the development of
multi-drug resistance (MDR) in cancer
cells. MDR is frequently caused by the
increased expression or activity of ABC
transporter proteins in response to the
toxic agents used in chemotherapy.
Research has generally been directed to
overcoming MDR by inhibiting the
activity of ABC transporters. However,
compounds that inhibit ABC transporter
activity often elicit strong and
undesirable side-effects, restricting their
usefulness as therapeutics.
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Investigators at the NIH previously
identified that the compound NSC73306
had the ability to specifically kill cancer
cells that overexpressed an ABC
transporter responsible for MDR.
Importantly, this ‘‘MDR-selective
compound’’ is not an inhibitor of ABC
transporters, reducing the likelihood of
undesirable side-effects if used as a
therapeutic.
Using NSC 73306 as a model, new
MDR-selective compounds have been
created with improved solubility and
selectivity. These new MDR-selective
compounds can also selectively kill
MDR cancer cells, with their efficacy
correlating directly with the level of
ABC transporter expression. Recent
evidence also shows that these new
MDR-selective compounds have the
ability to decrease the expression of
ABC transporters, potentially resensitizing the cancer cells to
chemotherapeutic agents. Thus, MDRselective compounds represent a
powerful strategy for treating multi-drug
resistant cancers as a direct
chemotherapeutic and as agents that can
re-sensitize MDR cancer cells for
treatment with additional
chemotherapeutic agents.
Applications:
• Treatment of cancers associated
with multi-drug resistance, either alone
or in combination with other
therapeutics.
• Development of a pharmacophore
for improved effectiveness in treating
cancers associated with multi-drug
resistance.
• Re-sensitization of multi-drug
resistant cancer cells to
chemotherapeutic agents.
Advantages:
• MDR-selective compounds
capitalize on one of the most common
drawbacks to cancer therapies (MDR) by
using it as an advantage for treating
cancer.
• The compositions do not inhibit the
activity of ABC transporters, thereby
reducing the chance of undesired sideeffects during treatment.
• The effects of MDR-selective
compounds correlate with the level of
ABC transporter expression, allowing
healthy cells which do not express high
levels of ABC transporters to better
survive treatments.
• Increased specificity allows the new
MDR-selective compounds to be tailored
to treating cancers associated with the
overexpression and hyperactivity of
particular ABC transporters.
• Increased solubility of the new
MDR-selective compounds allows
greater access to cancer cells, thereby
increasing therapeutic effectiveness.
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32939
Development Status: Preclinical stage
of development.
Patent Status: PCT Application No.
PCT/US2009/000861 (HHS Reference
No. E–017–2008/0–PCT–02).
Inventors: Matthew D. Hall et al.
(NCI).
For more information, see:
• MD Hall et al. Synthesis, activity,
and pharmacophore development for
isatin-beta-thiosemicarbazones with
selective activity toward multidrugresistant cells. J Med Chem. 2009 May
28;52(10):3191–3204.
• US Patent Application Publication
20080214606 A1 (US Patent Application
11/629,233).
Licensing Status: Available for
licensing.
Licensing Contact: David A.
Lambertson, PhD; 301–435–4632;
lambertsond@mail.nih.gov.
Collaborative Research Opportunity:
The National Cancer Institute,
Laboratory of Cell Biology, is seeking
statements of capability or interest from
parties interested in collaborative
research to further develop, evaluate, or
commercialize the agents described
here. Please contact John D. Hewes, PhD
at 301–435–3121 or
hewesj@mail.nih.gov for more
information.
Methods for Treating Cancer in
Humans Using IL–21
Description of Invention: The present
invention discloses the use of IL–21 for
cancer therapy, cancer prevention, and
method to induce apoptosis. When
compared to similar cytokines, IL–21
has shown substantial anticancer
activity and reduced toxicity in murine
models.
IL–21 belongs to the class I family of
cytokines and is closely related to IL–2
and IL–15. Some cancer patients have
shown significant response to
administration of IL–2. However, IL–2
has also been associated with severe
toxicity leading to a variety of
undesirable side effects. This invention
attempts to resolve the toxicity concerns
and presents a new therapy for cancer
prevention and treatment.
Applications: Method to treat and
prevent cancer.
Advantages: Targeted therapy to
minimize negative side effects of IL–2
cancer therapeutics.
Development Status: Pre-clinical.
Inventors: Patrick Hwu (formerly
NCI), Gang Wang (formerly NCI),
Warren J. Leonard (NHLBI), Rosanne
Spolski (NHLBI), et al.
Related Publications:
1. R Spolsi and WJ Leonard.
Interleukin-21: Basic biology and
implications for cancer and
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autoimmunity. Annu Rev Immunol.
2008;26:57–79.
2. WJ Leonard and R Spolski.
Interleukin-21: A modulator of
lymphoid proliferation, apoptosis and
differentiation. Nat Rev Immunol. 2005
Sep;5(9):688–698.
3. G Wang et al. In vivo antitumor
activity of interleukin 21 mediated by
natural killer cells. Cancer Res. 2003
Dec15;63(24):9016–9022.
Patent Status: U.S. Patent Application
No. 10/508,978 filed 19 Nov 2004 (HHS
Reference No. E–137–2002/0–US–03).
Licensing Status: Available for
licensing.
Licensing Contact: Jennifer Wong;
301–435–4633; wongje@mail.nih.gov.
Dated: July 1, 2009.
Richard U. Rodriguez,
Director, Division of Technology Development
and Transfer, Office of Technology Transfer,
National Institutes of Health.
[FR Doc. E9–16300 Filed 7–8–09; 8:45 am]
BILLING CODE 4140–01–P
DEPARTMENT OF HEALTH AND
HUMAN SERVICES
National Institutes of Health
Government-Owned Inventions;
Availability for Licensing
rmajette on DSK29S0YB1 with NOTICES
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.
qPCR Assay for Detection of JC Virus
Description of Invention: JC Virus
causes a fatal disease in the brain called
progressive multifocal
leukoencephalopathy (PML) that occurs
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in many patients with
immunocompromised conditions. For
example, more than five percent (5%) of
AIDS patients develop PML.
Additionally, these conditions include,
but are not limited to, cancers such as
leukemias and lymphomas, organ
transplants such as kidney, heart and
autoimmune conditions with treatment
that modulates the immune system such
as Multiple Sclerosis (MS), rheumatoid
arthritis, psoriasis, and systemic lupus
erythematosus. The finding of JCV DNA
in the patients with neurological
symptoms of PML is a diagnostic
criterion and is needed to confirm the
diagnosis of PML to rule out other
neurological conditions.
This technology describes a qPCR
assay that utilizes viral DNA standards
and testing samples to detect the
presence of the JC viral genome in
patients’ cerebrospinal fluid and blood,
blood products, and tissue samples from
biopsy or autopsy.
Application: Development of JC Virus
(JCV) diagnostics, calibration of existing
JCV assays.
Advantages: Assay is sensitive,
reproducible and highly specific
because the amount of JCV DNA in
cerebrospinal fluid or blood or blood
product samples may be very small.
Development Status: Materials and
assay have been developed and tested.
Inventors: Eugene O. Major and
Caroline Ryschkewitsch (NINDS).
Publications
1. ML Landry et al. False negative
PCR despite high levels of JC virus DNA
in spinal fluid: Implications for
diagnostic testing. J Clin Virol. 2008
Oct;43(2):247–249.
2. C Ryschkewitsch et al. Comparison
of PCR-southern hybridization and
quantitative real-time PCR for the
detection of JC and BK viral nucleotide
sequences in urine and cerebrospinal
fluid. J Virol Methods. 2004
Nov;121(2):217–221.
3. T Yousry et al. Evaluation of
patients treated with natalizumab for
progressive multifocal
leukoencephalopathy. N Engl J Med.
2006 Mar 2;354(9):924–933.
Patent Status: HHS Reference No. E–
152–2009/0—Research Material. Patent
protection is not being pursued for this
technology.
Licensing Status: Available for
licensing.
Licensing Contact: Peter A. Soukas,
J.D.; 301–435–4646;
soukasp@mail.nih.gov.
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A Locking Device for Permanently
Securing Surgical Suture Loops
Description of Invention: This
technology relates to a device that can
be used to non-invasively secure
surgical suture loops when combined
with a percutaneous delivery system. It
has been shown to be effective in
correcting mitral valve regurgitation
(MVR) in an animal model. During the
procedure, a guidewire is
percutaneously conveyed to the atrium
of the heart and is used to secure the
‘‘cerclage’’ suture encircling the mitral
valve annulus, which is delivered using
a delivery catheter. The locking device
is advanced over the suture by the
delivery catheter and it permanently
secures the suture and maintains the
tension on the annulus once the
delivery system is removed. This
locking device, in combination with the
percutaneous procedure, allows for
more complete coaptation of the valve
leaflets and correction of MVR without
the need for open heart surgery and its
associated risks. The locking device is
also adjustable, allowing the user to
vary the tension on the suture if further
tightening or loosening is required. It is
also MRI compatible and all follow-up
studies can be performed under MRI.
This invention has demonstrated its
ability to correct MVR in animals where
the locking device was observed to
maintain the correct position and
tension after implantation. This device
has the potential to replace the
traditional loop and knot method used
for surgical correction of MVR, and may
also be useful for other conditions that
require permanently secured suture
loops.
Applications: Non-invasive and
effective correction of MVR and other
conditions; Tensioning device for
securing suture loops.
Advantages: Technology amenable to
a non-invasive technique; Control of
tension on surgical sutures.
Development Status: Early stage.
Inventor: Ozgur Kocaturk (NHLBI).
Patent Status: U.S. Provisional
Application No. 61/157,267 filed 04 Mar
2009 (HHS Reference No. E–048–2009/
0–US–01).
Licensing Status: Available for
licensing.
Licensing Contact: Jeffrey A. James,
Ph.D.; 301–435–5474;
jeffreyja@mail.nih.gov.
Collaborative Research Opportunity:
The National Heart, Lung and Blood
Institute Cardiac Catheterization Lab is
seeking statements of capability or
interest from parties interested in
collaborative research to further
develop, evaluate, or commercialize the
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]]>Agencies
[Federal Register Volume 74, Number 130 (Thursday, July 9, 2009)]
[Notices]
[Pages 32937-32940]
From the Federal Register Online via the Government Printing Office [www.gpo.gov]
[FR Doc No: E9-16300]
-----------------------------------------------------------------------
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.
Immunogenic Peptide from NGEP Protein for Developing Prostate Cancer
Vaccines
Description of Technology: The NGEP protein is only present in the
prostate and is typically overexpressed on prostate cancer cells.
Hence, as a novel prostate tumor-associated antigen (TAA) it is a good
target for developing active immunotherapies to kill prostate cancer
cells. For example, NGEP could be used in a vaccine to activate an
individual's immune system to recognize and kill NGEP-expressing
prostate cancer cells. However, TAAs typically are not very effective
in inciting an immune response. This can be overcome by identifying
portions (epitopes) of the
[[Page 32938]]
TAA that are more immunologically active.
Investigators at the NIH have identified a small peptide fragment
of the NGEP protein (NGEP CTL peptide epitope) that is very effective
in activating cytotoxic lymphocytes, causing them to destroy prostate
cancer cells and has great potential for development of a variety of
active immunotherapy strategies, such as vector-based cancer vaccines,
to treat and prevent prostate cancer. In addition, it could be used for
developing sensitive immunoassays for measuring the immune response of
a prostate cancer patient during immunotherapy.
Applications:
Peptide cancer vaccine.
Vector-based cancer vaccine.
Liposome-based cancer vaccine.
Cellular cancer vaccine.
In vitro diagnostic for monitoring the immune response of
prostate cancer patients during cancer vaccine trials.
Advantages:
Small biologic therapeutic.
Can be chemically synthesized or produced recombinantly.
DNA encoded peptide allows molecular engineering.
Can be used as a tumor antigen with the clinically proven
TRICOM-based vaccine technology.
Development Status: Early stage.
Market: Prostate cancer is the second-leading cause of cancer death
in men. It is estimated that in the United States there will be 192,280
new cases of prostate cancer and 27,360 deaths due to prostate cancer
in 2009.
Inventors: Jeffrey Schlom et al. (NCI).
Publications: No publications directly related to this technology.
Patent Status: U.S. Provisional Application No. 61/170,900 filed 20
Apr 2009 (HHS Reference No. E-042-2009/0-US-01).
Licensing Status: Available for licensing.
Licensing Contact: Sabarni Chatterjee, PhD; 301-435-5587;
chatterjeesa@mail.nih.gov.
Collaborative Research Opportunity: The National Cancer Institute,
Center for Cancer Research, Laboratory of Tumor Immunology and Biology,
is seeking statements of capability or interest from parties interested
in collaborative research to further develop, evaluate, or
commercialize this technology. Please contact Kevin Brand, J.D. at 301-
451-4566 or brandk@mail.nih.gov for more information.
Gene Expression Signature Predictive of Response to Chemotherapy
Description of Technology: Combination cisplatin and fluorouracil
(CF) is a reference chemotherapy regimen for metastatic gastric cancer.
However, to date, no genome-wide studies have identified distinctions
in gene expression that predict which subjects with metastatic disease
will benefit from this therapy and which subjects will not exhibit a
therapeutic response to chemotherapy. Given the toxicity of
chemotherapy, however, defining parameters that identify those subjects
who will likely benefit from chemotherapy is of paramount importance.
Early identification of non-responders would provide opportunities to
explore alternate or novel therapeutic approaches. Thus, a need exists
to identify methods of predicting a subject's response to chemotherapy
prior to receiving the treatment.
Scientists at the National Institutes of Health have discovered a
three-gene signature that can be used to determine the chemotherapy
response in patients with cancer. By measuring the expression of three
cancer-specific genes it can be determined if a patient with an
epithelial cancer such as gastric, bladder, head and neck, esophageal
or cervical cancers, will respond to CF treatment. The inventors have
demonstrated that examining these expression levels has high fidelity
in identifying CF treatment non-responders. Further, the invention
describes a mechanism that can help patients identified as non-
responders become responsive to treatment. Therefore these methods have
the potential to reduce fatalities caused by metastatic gastric cancer
by identifying patients early on who are non-responsive to standard CF
treatment and customizing a new treatment plan which may be better
suited to their individual needs.
Applications:
Prognostic testing of epithelial cancer patients.
Customized treatment for gastric cancer patients
identified as CF treatment non-responders.
Advantages:
Expression levels of cancer-specific genes can be used to
determine if metastatic gastric cancer patients are responsive to
combination cisplatin and fluorouracil (CF) treatment.
Fatalities due to metastatic gastric cancer may be reduced
by customizing the treatment of non-responders.
Market: In 2008, it is estimated that there will be 21,500 new
cases and 10,880 deaths from gastric cancer in the United States.
Development Status: Patient tissue sample data available.
Inventors: Jeffrey E. Green and Hark Kyun Kim (NCI).
Patent Status: U.S. Provisional Application No. 61/195,123 filed 03
Oct 2008 (HHS Reference No. E-282-2008/0-US-01).
Licensing Status: Available for licensing.
Licensing Contact: Surekha Vathyam, PhD; 301-435-4076;
vathyams@mail.nih.gov.
Collaborative Research Opportunity: The National Cancer Institute,
Center for Cancer Research, Laboratory of Cancer Biology and Genetics,
is seeking statements of capability or interest from parties interested
in collaborative research to further develop, evaluate, or
commercialize Gene Expression Signature Predictive of Response to
Chemotherapy. Please contact John D. Hewes, PhD at 301-435-3121 or
hewesj@mail.nih.gov for more information.
Therapeutic Applications of a p53 Isoform in Regenerative Medicine,
Aging, and Cancer
Description of Technology: p53 plays a critical role in
carcinogenesis and aging as a key regulator of cell cycle progression,
senescence and apoptosis. The inventors have discovered that a natural
variant of p53 ([Delta]133p53) inhibits p53-dependent cell senescence.
Utilizing [Delta]133p53 siRNAs, the inventors have data demonstrating
that siRNA-treated human fibroblast undergo cell senescence, thereby
indicating that [Delta]133p53 inhibition could be a novel approach for
cell senescence-mediated anti-proliferative therapy, including anti-
cancer treatments. Alternatively, enhanced expression with
[Delta]133p53 can extend the replicative lifespan of normal human
cells. This technology may provide a new method in the field of
regenerative medicine for aging-related degenerative disease.
Also available for licensing are [Delta]133p53 siRNAs and shRNA
vectors, as well as a [Delta]133p53 overexpression vector, which can be
used for cancer and age-related degenerative therapeutics. The shRNA
can be stably integrated into the cellular genome for long-term
[Delta]133p53 inhibition.
The inventors have also discovered that another p53 variant
(p53[beta]) accelerates p53-dependent cell senescence, and developed a
vector for overexpressing p53[beta], which could be used for cell
senescence-mediated anti-proliferative therapy.
Applications:
Method to treat cancer.
Method to treat aging related disorders.
Method to promote tissue regeneration.
[[Page 32939]]
Pharmaceutical compositions to inhibit cancer or promote
cell regeneration.
Advantages:
Ability to treat a wide variety of cancers and age-related
diseases as p53 is present in normal cells.
shRNA therapeutics are stably integrated into genome for
long-term treatment.
Development Status: The technology is currently in the pre-clinical
stage of development.
Market:
An estimated 1,479,350 new cancer diagnoses in the U.S. in
2009.
Cancer is the second leading cause of death in United
States.
It is estimated that the cancer therapeutic market would
double to $50 billion a year in 2010 from $25 billion in 2006.
Inventors: Curtis C. Harris (NCI) et al.
Relevant Publications:
1. K Fujita et al. p53 isoforms, [Delta]133p53 and p53[beta], are
endogenous regulators of replicative cellular senescence. Nat Cell
Biol., in press.
2. International Agency Research on Cancer Conference, Lyon,
France, November 13, 2007.
Patent Status:
U.S. Provisional Application No. 60/987,340 filed 12 Nov
2007 (HHS Reference No. E-033-2008/0-US-01).
PCT Application No. PCT/US2008/080648 filed 21 Oct 2008
(HHS Reference No. E-033-2008/0-PCT-02).
Licensing Status: Available for licensing.
Licensing Contact: Jennifer Wong; 301-435-4633;
wongje@mail.nih.gov.
Collaborative Research Opportunity: The National Cancer Institute,
Laboratory of Human Carcinogenesis, is seeking statements of capability
or interest from parties interested in collaborative research to
further develop, evaluate, or commercialize this technology. Please
contact Curtis_Harris@nih.gov for more information.
Novel Compounds that Specifically Kill Multi-Drug Resistant Cancer
Cells
Description of Invention: One of the major hindrances to successful
cancer chemotherapy is the development of multi-drug resistance (MDR)
in cancer cells. MDR is frequently caused by the increased expression
or activity of ABC transporter proteins in response to the toxic agents
used in chemotherapy. Research has generally been directed to
overcoming MDR by inhibiting the activity of ABC transporters. However,
compounds that inhibit ABC transporter activity often elicit strong and
undesirable side-effects, restricting their usefulness as therapeutics.
Investigators at the NIH previously identified that the compound
NSC73306 had the ability to specifically kill cancer cells that
overexpressed an ABC transporter responsible for MDR. Importantly, this
``MDR-selective compound'' is not an inhibitor of ABC transporters,
reducing the likelihood of undesirable side-effects if used as a
therapeutic.
Using NSC 73306 as a model, new MDR-selective compounds have been
created with improved solubility and selectivity. These new MDR-
selective compounds can also selectively kill MDR cancer cells, with
their efficacy correlating directly with the level of ABC transporter
expression. Recent evidence also shows that these new MDR-selective
compounds have the ability to decrease the expression of ABC
transporters, potentially re-sensitizing the cancer cells to
chemotherapeutic agents. Thus, MDR-selective compounds represent a
powerful strategy for treating multi-drug resistant cancers as a direct
chemotherapeutic and as agents that can re-sensitize MDR cancer cells
for treatment with additional chemotherapeutic agents.
Applications:
Treatment of cancers associated with multi-drug
resistance, either alone or in combination with other therapeutics.
Development of a pharmacophore for improved effectiveness
in treating cancers associated with multi-drug resistance.
Re-sensitization of multi-drug resistant cancer cells to
chemotherapeutic agents.
Advantages:
MDR-selective compounds capitalize on one of the most
common drawbacks to cancer therapies (MDR) by using it as an advantage
for treating cancer.
The compositions do not inhibit the activity of ABC
transporters, thereby reducing the chance of undesired side-effects
during treatment.
The effects of MDR-selective compounds correlate with the
level of ABC transporter expression, allowing healthy cells which do
not express high levels of ABC transporters to better survive
treatments.
Increased specificity allows the new MDR-selective
compounds to be tailored to treating cancers associated with the
overexpression and hyperactivity of particular ABC transporters.
Increased solubility of the new MDR-selective compounds
allows greater access to cancer cells, thereby increasing therapeutic
effectiveness.
Development Status: Preclinical stage of development.
Patent Status: PCT Application No. PCT/US2009/000861 (HHS Reference
No. E-017-2008/0-PCT-02).
Inventors: Matthew D. Hall et al. (NCI).
For more information, see:
MD Hall et al. Synthesis, activity, and pharmacophore
development for isatin-beta-thiosemicarbazones with selective activity
toward multidrug-resistant cells. J Med Chem. 2009 May 28;52(10):3191-
3204.
US Patent Application Publication 20080214606 A1 (US
Patent Application 11/629,233).
Licensing Status: Available for licensing.
Licensing Contact: David A. Lambertson, PhD; 301-435-4632;
lambertsond@mail.nih.gov.
Collaborative Research Opportunity: The National Cancer Institute,
Laboratory of Cell Biology, is seeking statements of capability or
interest from parties interested in collaborative research to further
develop, evaluate, or commercialize the agents described here. Please
contact John D. Hewes, PhD at 301-435-3121 or hewesj@mail.nih.gov for
more information.
Methods for Treating Cancer in Humans Using IL-21
Description of Invention: The present invention discloses the use
of IL-21 for cancer therapy, cancer prevention, and method to induce
apoptosis. When compared to similar cytokines, IL-21 has shown
substantial anticancer activity and reduced toxicity in murine models.
IL-21 belongs to the class I family of cytokines and is closely
related to IL-2 and IL-15. Some cancer patients have shown significant
response to administration of IL-2. However, IL-2 has also been
associated with severe toxicity leading to a variety of undesirable
side effects. This invention attempts to resolve the toxicity concerns
and presents a new therapy for cancer prevention and treatment.
Applications: Method to treat and prevent cancer.
Advantages: Targeted therapy to minimize negative side effects of
IL-2 cancer therapeutics.
Development Status: Pre-clinical.
Inventors: Patrick Hwu (formerly NCI), Gang Wang (formerly NCI),
Warren J. Leonard (NHLBI), Rosanne Spolski (NHLBI), et al.
Related Publications:
1. R Spolsi and WJ Leonard. Interleukin-21: Basic biology and
implications for cancer and
[[Page 32940]]
autoimmunity. Annu Rev Immunol. 2008;26:57-79.
2. WJ Leonard and R Spolski. Interleukin-21: A modulator of
lymphoid proliferation, apoptosis and differentiation. Nat Rev Immunol.
2005 Sep;5(9):688-698.
3. G Wang et al. In vivo antitumor activity of interleukin 21
mediated by natural killer cells. Cancer Res. 2003 Dec15;63(24):9016-
9022.
Patent Status: U.S. Patent Application No. 10/508,978 filed 19 Nov
2004 (HHS Reference No. E-137-2002/0-US-03).
Licensing Status: Available for licensing.
Licensing Contact: Jennifer Wong; 301-435-4633;
wongje@mail.nih.gov.
Dated: July 1, 2009.
Richard U. Rodriguez,
Director, Division of Technology Development and Transfer, Office of
Technology Transfer, National Institutes of Health.
[FR Doc. E9-16300 Filed 7-8-09; 8:45 am]
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