Government-Owned Inventions; Availability for Licensing, 29668-29671 [2012-12041]
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29668
Federal Register / Vol. 77, No. 97 / Friday, May 18, 2012 / Notices
(NIH) National Institute on Drug Abuse
(NIDA), and in partnership with the
Food and Drug Administration (FDA).
Using annual interviews and the
collection of bio-specimens from adults,
the study is designed to establish a
population-based framework for
monitoring and evaluating the
behavioral and health impacts of
regulatory provisions by FDA as it meets
its mandate under the Family Smoking
Prevention and Tobacco Control Act
(FSPTCA) to regulate tobacco-product
advertising, labeling, marketing,
constituents, ingredients, and additives.
These regulatory changes are expected
to influence tobacco-product risk
perceptions, exposures, and use patterns
in the short term, and to reduce tobaccorelated morbidity and mortality in the
long term. By measuring and accurately
reporting tobacco product use behaviors
and health effects associated with these
regulatory changes, this study will
provide an empirical evidence base to
inform the development,
implementation, and evaluation of
tobacco-product regulations in the U.S.
Frequency of Response: Annually.
Affected Public: Individuals or
households. Type of Respondents:
Youth (ages 12–17) and Adults (ages
18+). The annual reporting burden for
the field test is presented in Table 1,
and the annual reporting burden for the
baseline data collection is presented in
Table 2. The annualized cost to
respondents for the field test is
estimated at: $24,495; and the
annualized cost to respondents for the
baseline data collection is: $1,947,567.
There are no Capital Costs to report.
There are no Operating or Maintenance
Costs to report.
TABLE 1—PATH STUDY FIELD TEST HOUR BURDEN ESTIMATES
Estimated
number of
respondents
Type of respondents
Estimated
number of
responses per
respondent
Average
burden hours
per response
Estimated total
annual burden
hours
requested
Adults—Household Screener ..........................................................................
Adults—Individual Screener ............................................................................
Adults—Extended Interview .............................................................................
Adults—Tobacco Use Form ............................................................................
Youth—Extended Interview .............................................................................
Adult—Parent Interview ...................................................................................
1,295
840
590
590
100
100
1
1
1
1
1
1
22/60
6/60
1 26/60
2/60
55/60
24/60
479
84
844
18
92
40
Total ..........................................................................................................
3,515
1
........................
1,557
TABLE 2—PATH STUDY BASELINE HOUR BURDEN ESTIMATES
Estimated
number of
respondents
Type of respondents
Estimated
number of
responses per
respondent
Average
burden hours
per response
Estimated total
annual burden
hours
requested
100,983
63,000
42,730
42,730
16,857
16,857
1
1
1
1
1
1
22/60
6/60
1 26/60
2/60
55/60
24/60
37,364
6,300
61,104
1,282
15,508
6,743
Total ..........................................................................................................
mstockstill on DSK4VPTVN1PROD with NOTICES
Adults—Household Screener ..........................................................................
Adults—Individual Screener ............................................................................
Adults—Extended Interview .............................................................................
Adults—Tobacco Use Form ............................................................................
Youth—Extended Interview .............................................................................
Adult—Parent Interview ...................................................................................
283,157
1
........................
128,301
Request for Comments: Written
comments and/or suggestions from the
public and affected agencies are invited
on one or more of the following points:
(1) Whether the proposed collection of
information is necessary for the proper
performance of the function of the
agency, including whether the
information will have practical utility;
(2) The accuracy of the agency’s
estimate of the burden of the proposed
collection of information, including the
validity of the methodology and
assumptions used; (3) Ways to enhance
the quality, utility, and clarity of the
information to be collected; and (4)
Ways to minimize the burden of the
collection of information on those who
are to respond, including the use of
appropriate automated, electronic,
mechanical, or other technological
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18:21 May 17, 2012
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collection techniques or other forms of
information technology.
To
request more information on the
proposed project or to obtain a copy of
the data collection plans and
instruments, contact Kevin P. Conway,
Ph.D., Deputy Director, Division of
Epidemiology, Services, and Prevention
Research, National Institute on Drug
Abuse, 6001 Executive Blvd., Room
5185; 301–443–8755; email
PATHprojectofficer@mail.nih.gov.
Comments Due Date: Comments
regarding this information collection are
best assured of having their full effect if
received within 60-days of the date of
this publication.
FOR FURTHER INFORMATION CONTACT:
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Dated: May 11, 2012.
Helio Chaves,
Deputy Executive Officer (OM Director),
NIDA.
[FR Doc. 2012–12017 Filed 5–17–12; 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.
ACTION: Notice.
AGENCY:
The inventions listed below
are owned by an agency of the U.S.
Government and are available for
SUMMARY:
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Federal Register / Vol. 77, No. 97 / Friday, May 18, 2012 / Notices
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.
FOR FURTHER INFORMATION CONTACT:
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.
Java Applet for Modeling Human
Metabolism and Energy Expenditure for
Adaptive Dieting and Exercise
Regimens
Description of Technology: Known
methods for predicting weight loss fail
to account for slowing of metabolism as
weight is lost and therefore overestimate
the degree of weight loss. While this
limitation of the 3500 Calorie per pound
rule has been known for some time, it
was not clear how to dynamically
account for the metabolic slowing. The
invention provides a Java applet for
modeling of human metabolism to
improve the weight change predictions.
The model has been validated using
previously published human data and
the model equations have been
published. A web-based implementation
of the published dynamic model has
been created to allow users to perform
simulations for planning weight loss
interventions in adults and accounts for
individual differences in metabolism
and body composition.
mstockstill on DSK4VPTVN1PROD with NOTICES
Potential Commercial Applications
• Obesity.
• Weight Loss.
Competitive Advantages: Personalized
predictions.
Development Stage: Prototype.
Inventors: Kevin Hall, Carson Chou,
Dhruva Chandramohan (all of NIDDK).
Intellectual Property: HHS Reference
No. E–160–2012/0—Research Tool.
Patent protection is not being pursued
for this technology.
Licensing Contact: Michael
Shmilovich, Esq.; 301–435–5019;
shmilovm@mail.nih.gov.
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29669
Antagonist of A3 Adenosine Receptor
Fluorescent Probes for the Study of
Diseases Such as Cancer, Autoimmune
Conditions, Dry Eye and Other
Indications that Involve A3 Signaling
predicted to benefit from combined
HDAC inhibitor/mTOR inhibitor
therapy. Additional information is
available upon request.
Description of Technology: Small
molecule drugs, A3AR-selective
agonists, are currently in advanced
clinical trials for the treatment of
hepatocellular carcinoma, autoimmune
inflammatory diseases, such as
rheumatoid arthritis, psoriasis, and dry
eye disease, and other conditions. This
molecular probe may serve as a
companion tool to identify and stratify
patient populations based on the
prevalence of the target A3 adenosine
receptors.
Potential Commercial Applications:
Useful tools to study prevalence of this
receptor on neutrophils which is
predictive of response to the agonist
drugs.
Competitive Advantages: Drug
screening at this receptor is often done
currently using radiolabeled agonists or
antagonists of the human A3AR of
nanomolar affinity. This method would
avoid the use of radioisotopes in this
part of the research and development
process.
• Development of a clinical
diagnostic test to identify cancer
patients who would benefit most from
mTOR and HDAC combination therapy.
• Use as a surrogate biomarker related
to drug response.
• Development of therapeutics
targeting several cancers, including
multiple myeloma.
Development Stage
• Early-stage.
• In vitro data available.
Inventors: Kenneth A. Jacobson, et al.
(NIDDK).
Publication: Novel Fluorescent
Antagonist as a Molecular Probe in A3
Adenosine Receptor Binding Assays
Using Flow Cytometry, manuscript
submitted for publication.
Intellectual Property: HHS, Reference
No. E–073–2012/0—U.S. Provisional
Application 61/590,596 filed 25 Jan
2012 (Note: a separate license may be
required for the fluorescent portion of
the molecule.)
Licensing Contact: Betty B. Tong,
Ph.D.; 301–594–6565;
tongb@mail.nih.gov.
Methods for Selection of Cancer
Patients and Predicting Efficacy of
Combination Therapy With Histone
Deacetylase (HDAC) and mTOR
Inhibitors
Description of Technology: Available
for licensing is a novel gene signature of
thirty-seven drug responsive genes that
links changes in gene expression to the
clinically desirable outcome of
improved overall survival. Expression of
these genes has been linked to prognosis
in several cancers, including, but not
limited to multiple myeloma, lung,
breast, and melanoma. Patients
identified by this signature would be
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Potential Commercial Applications
Competitive Advantages
• Implements a smaller gene set
compared to current diagnostic gene
signatures.
• Provides a basis for the
development of a diagnostic for patient
stratification or a response measurement
related to the combined use of mTOR
and HDAC inhibitors for cancer
treatment.
Development Stage
• Early-stage.
• In vitro data available.
• In vivo data available (animal).
Inventors: Beverly Mock et al. (NCI).
Intellectual Property: HHS Reference
No. E–013–2012/0—U.S. Provisional
Application No. 61/558,402 filed 10
Nov 2011.
Licensing Contact: Patrick McCue,
Ph.D.; 301–435–5560;
mccuepat@mail.nih.gov.
Collaborative Research Opportunity:
The NCI 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 Methods for Selecting
Cancer Patients for HDACi/mTORi
Combination Therapy. For collaboration
opportunities, please contact John
Hewes, Ph.D. at hewesj@mail.nih.gov.
GLI-Similar 3(GLIS3) Knock Out (KO)
Mice as Models to Screen Therapeutics
for Diabetes, Polycystic Kidney Disease,
and Hypothyroidism
Description of Technology: GLIsimilar (Glis) 1–3 proteins constitute a
¨
subfamily of the Kruppel-like zinc
finger transcription factors that are
closely related to the Gli family.
Mutations in human GLIS3 have been
implicated in a syndrome characterized
by neonatal diabetes and congenital
hypothyroidism (NDH) and in some
patients accompanied by polycystic
kidney disease, glaucoma, and liver
fibrosis. To further identify and study
the physiological functions of GLIS3,
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Federal Register / Vol. 77, No. 97 / Friday, May 18, 2012 / Notices
NIEHS investigators generated mice in
which GLIS3 is ubiquitously knocked
out (GLIS3–KO) or conditionally
knocked out in a cell type-specific
manner. GLIS3–KO mice develop
polycystic kidney disease,
hypothyroidism, and neonatal diabetes,
as indicated by the development of
hyperglycemia and hypoinsulinemia.
The pancreatic endocrine cells,
particularly insulin-producing
pancreatic beta cells, are greatly
diminished in these mice. The pancreasselective knockout mice GLIS3(Pdx1Cre) develop severe diabetes within 2–
3 months, much later than the GLIS3–
KO mice. The kidney-selective knockout
of GLIS3 (GLIS3(Ksp-Cre) mice lack
expression of GLIS3 in the collecting
ducts and develop severe polycystic
kidney disease within a period of 2–4
months. These mice can be used as
models to screen therapeutics for
diabetes, polycystic kidney disease, and
hypothyroidism.
Related Technologies
Potential Commercial Applications
Description of Technology: Available
for licensing and commercial
development are a novel influenza virus
microarray and methods for using the
microarray for the identification of
existing and new types and subtypes of
human influenza viruses. There are
three types of influenza viruses, type A,
B and C. Influenza types A or B viruses
cause epidemics of disease almost every
winter, with type A causes major
pandemic periodically. Influenza type A
viruses are further divided into subtypes
based on two proteins on the surface of
the virus. These proteins are called
hemagglutinin (H) and neuraminidase
(N). There are 16 known HA subtypes
and 9 known NA subtypes of influenza
A viruses. Each subtype may have
different combination of H and N
proteins. Although there are only three
known A subtypes of influenza viruses
(H1N1, H1N2, and H3N2) currently
circulating among humans, many other
different strains are circulating among
birds and other animals and these
viruses do spread to humans
occasionally. There is a requirement for
sensitive and rapid diagnostic
techniques in order to improve both the
diagnosis of infections and the quality
of surveillance systems. This microarray
platform tiles the genomes of all
types/subtypes of influenza viruses, and
is capable of correctly identifying all 3
types/subtypes of influenza viruses from
an influenza vaccine sample.
• Therapeutic target in the
management of diabetes, polycystic
kidney disease, and hypothyroidism.
• Models to test therapeutic drugs for
diabetes, polycystic kidney disease, and
hypothyroidism.
Competitive Advantages
• Provides opportunity to discover
upstream signals that regulate GLIS3
activity.
• Can be used in stem cell therapy in
diabetes treatment.
• Excellent model to study the role of
GLIS3 in neonatal diabetes.
Development Stage
• Early-stage.
• Pre-clinical.
• In vivo data available (animal).
Inventors: Anton M Jetten, Hong Soon
Kang, Kristin Lichti-Kaiser (all of
NIEHS).
mstockstill on DSK4VPTVN1PROD with NOTICES
Publications
1. Kang HS, et al. Transcription factor
Glis3, a novel critical player in the
regulation of pancreatic beta-cell
development and insulin gene
expression. Mol Cell Biol. 2009
Dec;29(24):6366–79. [PMID 19805515]
2. Kang HS, et al. Glis3 is associated
with primary cilia and Wwtr1/TAZ and
implicated in polycystic kidney disease.
Mol Cell Biol. 2009 May;29(10): 2556–
69. [PMID 19273592]
Intellectual Property: HHS Reference
No. E–303–2011/0—Research Tool.
Patent protection is not being pursued
for this technology.
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• HHS Reference No. E–253–2010/0
—An In-Vitro Cell System Useful for
Identification of RORgamma
Antagonists.
• HHS Reference No. E–222–2009/0
—RORgamma (RORC) Deficient Mice
Which Are Useful for the Study of
Lymph Node Organogenesis and
Immune Responses.
Licensing Contact: Suryanarayana
Vepa, Ph.D., J.D.; 301–435–5020;
vepas@mail.nih.gov.
Collaborative Research Opportunity:
The NIEHS is seeking statements of
capability or interest from parties
interested in collaborative research to
further develop, evaluate or
commercialize GLIS3 Knock Out Mice.
For collaboration opportunities, please
contact Elizabeth M. Denholm, Ph.D. at
denholme@niehs.nih.gov.
Microarray for Detection and Subtyping
of Human Influenza Viruses
Potential Commercial Applications
• Detection and identification of
human influenza viruses.
• Efficient discovery of new subtypes
of influenza viruses.
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• Diagnosis of influenza outbreaks.
Competitive Advantages: Technology
can detect multiple types and subtypes
of influenza virus.
Development Stage
• Pre-clinical.
• In vitro data available.
Inventors: Xiaolin Wu, David J.
Munroe, Cassio S. Baptista, Elizabeth
Shannon (all of NCI).
Intellectual Property: HHS Reference
No. E–208–2006/0—U.S. Patent
Application No. 11/936,530 filed 07
Nov 2007.
Licensing Contact: Kevin W. Chang,
Ph.D.; 301–435–5018;
changke@mail.nih.gov.
M3 Muscarinic Receptor Knockout
Mice (Chrm3 tm1Jwe) for the Study of
Obesity and Other Metabolic Disorders
Description of Mouse: The five
Muscarinic Acetylcholine (ACh)
receptors are G-protein coupled
receptors (M1R–M5R). M3 muscarinic
ACh receptors are present in the central
nervous system and the periphery.
M3R knockout mice are viable and
fertile, and have no major
morphological abnormalities. They have
a lean phenotype due to a combination
of reduced caloric intake and increased
energy expenditure. Because of their
lean phenotype, M3R knockout mice
have improved glucose tolerance and
increased insulin sensitivity.
Pharmacological blockade of central
M3Rs may be a novel strategy for the
treatment of obesity and associated
metabolic disorders.
In the airway, vagally-mediated
bronchoconstriction responses were
abolished in M3R knockout mice in
vivo, suggesting that M3R antagonists
may be useful in the treatment of
chronic obstructive pulmonary disease
(COPD) and asthma. Studies with M3R
knockout mice also have shown that the
M3R is the major muscarinic receptor
mediating ACh-induced glandular
secretion from exocrine and endocrine
glands, including the secretion of
insulin from pancreatic beta cells.
Potential Commercial Applications:
Animal model to study COPD and
metabolism.
Competitive Advantages: M3R
knockout mice are viable and fertile,
and have no major morphological
abnormalities.
Development Stage: Pre-clinical.
¨
Developer of Mouse: Jurgen Wess,
Ph.D. (NIDDK).
Publication: Yamada M, et al. Mice
lacking the M3 muscarinic acetylcholine
receptor are hypophagic and lean.
Nature. 2001 Mar 8;410(6825):207–12.
[PMID 11242080]
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18MYN1
Federal Register / Vol. 77, No. 97 / Friday, May 18, 2012 / Notices
Intellectual Property: HHS Reference
No. E–346–2004/2—Research Tool.
Patent protection is not being pursued
for this technology.
Related Technologies
• HHS Reference No. E–346–2004/
0—M1 Muscarinic receptor KO
(Chrm1tm1Jwe) Mice.
• HHS Reference No. E–346–2004/
1—M2 Muscarinic receptor KO (Chrm2
tm1Jwe) Mice.
Licensing Contact: Jaime M. Greene,
M.S.; 301–435–5559;
greenejaime@mail.nih.gov
mstockstill on DSK4VPTVN1PROD with NOTICES
Use of E-Selectin Tolerization as
Treatment for Immunological and
Vascular-Related Disorders
Description of Technology: This
technology relates to the mucosal
delivery (e.g. intranasal) of an E-selectin
fragment as a tolerization agent for the
prevention and treatment of
immunological and vascular-related
disorders, including stroke and multiple
sclerosis (MS) as well as rare or orphan
diseases involving vascular modulated
disorders.
E-selectin is an adhesion molecule
that is expressed on endothelial cells
lining blood vessels in response to
certain localized cytokines, making the
endothelial surface pro-coagulant, proinflammatory and/or immunoreactive.
Such changes on the endothelial surface
have been linked to the development of
vascular-related disorders like stroke, as
well as immune regulated diseases such
as MS.
Intranasal administration of
E-selectin, using a tolerizing dosing
schedule, induces an immunological
tolerance to E-selectin. T regulatory
cells become targeted to activating blood
vessel segments, where they release
immunomodulatory cytokines such as
IL–10. This release of cytokines
suppresses local pro-coagulant, proinflammatory and immunoreactive
effects. Thus, administration of
E-selectin as a tolerizing agent will
provide a targeted therapeutic approach,
impacting only affected sites in the
endothelium.
Potential Commercial Applications:
Treatment of diseases biologically based
on vascular initiated immune
regulation. Such disorders include
prevention of secondary stroke, MS,
Alzheimer’s, Parkinson’s, rheumatoid
arthritis, type 1 diabetes, and psoriasis.
Competitive Advantages
• Low doses utilized thus minimizing
potential side effects.
• Animal data are available, with
further studies currently on-going.
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• Administration through the
intranasal route represents a less
invasive mode of delivery.
• FDA pre-IND meetings have been
held and FDA communications are
ongoing.
Development Stage
• Pre-clinical.
• In vitro data available.
• In vivo data available (animal).
Inventors: John M. Hallenbeck, Maria
Spatz, Hidetaka Takeda, Hideaki Wakita
(all of NINDS)
Publications
1. Li X, et al. Intranasal delivery of
E-selectin reduces atherosclerosis in
ApoE-/- mice. PLoS One.
2011;6(6):e20620. Epub 2011 Jun 20.
[PMID 21701687]
2. Hallenbeck J. How inflammation
modulates central nervous system vessel
activation and provides targets for
intervention—a personal perspective.
Ann N Y Acad Sci. 2010 Oct;1207:1–7.
doi: 10.1111/j.1749–6632.2010.05785.x.
[PMID 20955418]
3. Ishibashi S, et al. Mucosal tolerance
to E-selectin promotes the survival of
newly generated neuroblasts via
regulatory T-cell induction after stroke
in spontaneously hypertensive rats. J
Cereb Blood Flow Metab. 2009
Mar;29(3):606–20. [PMID 19107136]
4. Wakita H, et al. Mucosal
tolerization to E-selectin protects against
memory dysfunction and white matter
damage in a vascular cognitive
impairment model. J Cereb Blood Flow
Metab. 2008 Feb;28(2):341–53. [PMID
17637705]
5. Nakayama T, et al. Intranasal
administration of E-selectin to induce
immunological tolerization can
suppress subarachnoid hemorrhageinduced vasospasm implicating immune
and inflammatory mechanisms in its
genesis. Brain Res. 2007 Feb
9;1132(1):177–84. [PMID 17188657]
6. Illoh K, et al. Mucosal tolerance to
E-selectin and response to systemic
inflammation. J Cereb Blood Flow
Metab. 2006 Dec;26(12):1538–50. [PMID
16596122]
7. Chen Y, et al. Mucosal tolerance to
E-selectin provides cell-mediated
protection against ischemic brain injury.
Proc Natl Acad Sci U S A. 2003 Dec
9;100(25):15107–12. [PMID 14645708]
8. Takeda H, et al. Induction of
mucosal tolerance to E-selectin prevents
ischemic and hemorrhagic stroke in
spontaneously hypertensive genetically
stroke-prone rats. Stroke. 2002
Sep;33(9):2156–63. [PMID 12215580]
Intellectual Property
• HHS Reference No. E–237–1999/
0—
PO 00000
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29671
—U.S. Patent No. 7,261,896 issued 28
Aug 2007.
—U.S. Patent Application No. 11/
820,326 filed 19 Jun 2007.
• HHS Reference No. E–237–1999/
1—
—U.S. Patent No. 7,897,575 issued 01
Mar 2011.
—U.S. Patent Application No.
12,859,048 filed 18 Aug 2010.
• and Foreign counterparts in
Australia, Canada, Europe, and Japan
Licensing Contact: Tara Kirby, Ph.D.;
301–435–4426; tarak@mail.nih.gov.
Collaborative Research Opportunity:
The Stroke Branch, NINDS/NIH, is
seeking statements of capability or
interest from parties interested in
collaborative research to further
develop, evaluate or commercialize the
applications of E-selectin tolerization in
treatment of neurological based disease.
For collaboration opportunities, please
contact Laurie Arrants, NINDS at
arrantsl@ninds.nih.gov.
Nucleic Acids and Methods for
Expression of the Rat FceRI beta
Subunit, Which Plays a Critical Role in
Allergy and the Immune Response
Description of Technology: FceRI is
the high-affinity receptor for the Fc
region of immunoglobulin E (IgE), and
plays an important role in the allergic
response and inflammation. It controls
the production of important
immunomodulatory molecules, such as
cytokines and histamine.
This technology describes nucleic
acids encoding the beta subunit of rat
FceRI, as well as vectors and transgenic
cells including such nucleic acids. Also
described are methods of expressing
functional rat FceRI in a host cell. These
may be useful in studies of allergy and
the immune response.
Potential Commercial Applications:
Research studies of allergy and the
immune response.
Development Stage
• Early-stage.
• In vitro data available.
Inventors: Jean-Pierre Kinet and
Henry Metzger (NIAMS).
Intell ectual Property: HHS Reference
No. E–247–1988/4—U.S. Patent No.
6,165,744 issued 26 Dec 2000.
Licensing Contact: Tara L. Kirby,
Ph.D.; 301–435–4426;
tarak@mail.nih.gov.
Dated: May 14, 2012.
Richard U. Rodriguez,
Director, Division of Technology Development
and Transfer, Office of Technology Transfer,
National Institutes of Health.
[FR Doc. 2012–12041 Filed 5–17–12; 8:45 am]
BILLING CODE 4140–01–P
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]]>Agencies
[Federal Register Volume 77, Number 97 (Friday, May 18, 2012)]
[Notices]
[Pages 29668-29671]
From the Federal Register Online via the Government Printing Office [www.gpo.gov]
[FR Doc No: 2012-12041]
-----------------------------------------------------------------------
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
[[Page 29669]]
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.
FOR FURTHER INFORMATION CONTACT: 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.
Java Applet for Modeling Human Metabolism and Energy Expenditure for
Adaptive Dieting and Exercise Regimens
Description of Technology: Known methods for predicting weight loss
fail to account for slowing of metabolism as weight is lost and
therefore overestimate the degree of weight loss. While this limitation
of the 3500 Calorie per pound rule has been known for some time, it was
not clear how to dynamically account for the metabolic slowing. The
invention provides a Java applet for modeling of human metabolism to
improve the weight change predictions. The model has been validated
using previously published human data and the model equations have been
published. A web-based implementation of the published dynamic model
has been created to allow users to perform simulations for planning
weight loss interventions in adults and accounts for individual
differences in metabolism and body composition.
Potential Commercial Applications
Obesity.
Weight Loss.
Competitive Advantages: Personalized predictions.
Development Stage: Prototype.
Inventors: Kevin Hall, Carson Chou, Dhruva Chandramohan (all of
NIDDK).
Intellectual Property: HHS Reference No. E-160-2012/0--Research
Tool.
Patent protection is not being pursued for this technology.
Licensing Contact: Michael Shmilovich, Esq.; 301-435-5019;
shmilovm@mail.nih.gov.
Antagonist of A3 Adenosine Receptor Fluorescent Probes for
the Study of Diseases Such as Cancer, Autoimmune Conditions, Dry Eye
and Other Indications that Involve A3 Signaling
Description of Technology: Small molecule drugs, A3AR-
selective agonists, are currently in advanced clinical trials for the
treatment of hepatocellular carcinoma, autoimmune inflammatory
diseases, such as rheumatoid arthritis, psoriasis, and dry eye disease,
and other conditions. This molecular probe may serve as a companion
tool to identify and stratify patient populations based on the
prevalence of the target A3 adenosine receptors.
Potential Commercial Applications: Useful tools to study prevalence
of this receptor on neutrophils which is predictive of response to the
agonist drugs.
Competitive Advantages: Drug screening at this receptor is often
done currently using radiolabeled agonists or antagonists of the human
A3AR of nanomolar affinity. This method would avoid the use
of radioisotopes in this part of the research and development process.
Development Stage
Early-stage.
In vitro data available.
Inventors: Kenneth A. Jacobson, et al. (NIDDK).
Publication: Novel Fluorescent Antagonist as a Molecular Probe in
A3 Adenosine Receptor Binding Assays Using Flow Cytometry, manuscript
submitted for publication.
Intellectual Property: HHS, Reference No. E-073-2012/0--U.S.
Provisional Application 61/590,596 filed 25 Jan 2012 (Note: a separate
license may be required for the fluorescent portion of the molecule.)
Licensing Contact: Betty B. Tong, Ph.D.; 301-594-6565;
tongb@mail.nih.gov.
Methods for Selection of Cancer Patients and Predicting Efficacy of
Combination Therapy With Histone Deacetylase (HDAC) and mTOR Inhibitors
Description of Technology: Available for licensing is a novel gene
signature of thirty-seven drug responsive genes that links changes in
gene expression to the clinically desirable outcome of improved overall
survival. Expression of these genes has been linked to prognosis in
several cancers, including, but not limited to multiple myeloma, lung,
breast, and melanoma. Patients identified by this signature would be
predicted to benefit from combined HDAC inhibitor/mTOR inhibitor
therapy. Additional information is available upon request.
Potential Commercial Applications
Development of a clinical diagnostic test to identify
cancer patients who would benefit most from mTOR and HDAC combination
therapy.
Use as a surrogate biomarker related to drug response.
Development of therapeutics targeting several cancers,
including multiple myeloma.
Competitive Advantages
Implements a smaller gene set compared to current
diagnostic gene signatures.
Provides a basis for the development of a diagnostic for
patient stratification or a response measurement related to the
combined use of mTOR and HDAC inhibitors for cancer treatment.
Development Stage
Early-stage.
In vitro data available.
In vivo data available (animal).
Inventors: Beverly Mock et al. (NCI).
Intellectual Property: HHS Reference No. E-013-2012/0--U.S.
Provisional Application No. 61/558,402 filed 10 Nov 2011.
Licensing Contact: Patrick McCue, Ph.D.; 301-435-5560;
mccuepat@mail.nih.gov.
Collaborative Research Opportunity: The NCI 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
Methods for Selecting Cancer Patients for HDACi/mTORi Combination
Therapy. For collaboration opportunities, please contact John Hewes,
Ph.D. at hewesj@mail.nih.gov.
GLI-Similar 3(GLIS3) Knock Out (KO) Mice as Models to Screen
Therapeutics for Diabetes, Polycystic Kidney Disease, and
Hypothyroidism
Description of Technology: GLI-similar (Glis) 1-3 proteins
constitute a subfamily of the Kr[uuml]ppel-like zinc finger
transcription factors that are closely related to the Gli family.
Mutations in human GLIS3 have been implicated in a syndrome
characterized by neonatal diabetes and congenital hypothyroidism (NDH)
and in some patients accompanied by polycystic kidney disease,
glaucoma, and liver fibrosis. To further identify and study the
physiological functions of GLIS3,
[[Page 29670]]
NIEHS investigators generated mice in which GLIS3 is ubiquitously
knocked out (GLIS3-KO) or conditionally knocked out in a cell type-
specific manner. GLIS3-KO mice develop polycystic kidney disease,
hypothyroidism, and neonatal diabetes, as indicated by the development
of hyperglycemia and hypoinsulinemia. The pancreatic endocrine cells,
particularly insulin-producing pancreatic beta cells, are greatly
diminished in these mice. The pancreas-selective knockout mice
GLIS3(Pdx1-Cre) develop severe diabetes within 2-3 months, much later
than the GLIS3-KO mice. The kidney-selective knockout of GLIS3
(GLIS3(Ksp-Cre) mice lack expression of GLIS3 in the collecting ducts
and develop severe polycystic kidney disease within a period of 2-4
months. These mice can be used as models to screen therapeutics for
diabetes, polycystic kidney disease, and hypothyroidism.
Potential Commercial Applications
Therapeutic target in the management of diabetes,
polycystic kidney disease, and hypothyroidism.
Models to test therapeutic drugs for diabetes, polycystic
kidney disease, and hypothyroidism.
Competitive Advantages
Provides opportunity to discover upstream signals that
regulate GLIS3 activity.
Can be used in stem cell therapy in diabetes treatment.
Excellent model to study the role of GLIS3 in neonatal
diabetes.
Development Stage
Early-stage.
Pre-clinical.
In vivo data available (animal).
Inventors: Anton M Jetten, Hong Soon Kang, Kristin Lichti-Kaiser
(all of NIEHS).
Publications
1. Kang HS, et al. Transcription factor Glis3, a novel critical
player in the regulation of pancreatic beta-cell development and
insulin gene expression. Mol Cell Biol. 2009 Dec;29(24):6366-79. [PMID
19805515]
2. Kang HS, et al. Glis3 is associated with primary cilia and
Wwtr1/TAZ and implicated in polycystic kidney disease. Mol Cell Biol.
2009 May;29(10): 2556-69. [PMID 19273592]
Intellectual Property: HHS Reference No. E-303-2011/0--Research
Tool. Patent protection is not being pursued for this technology.
Related Technologies
HHS Reference No. E-253-2010/0 --An In-Vitro Cell System
Useful for Identification of RORgamma Antagonists.
HHS Reference No. E-222-2009/0 --RORgamma (RORC) Deficient
Mice Which Are Useful for the Study of Lymph Node Organogenesis and
Immune Responses.
Licensing Contact: Suryanarayana Vepa, Ph.D., J.D.; 301-435-5020;
vepas@mail.nih.gov.
Collaborative Research Opportunity: The NIEHS is seeking statements
of capability or interest from parties interested in collaborative
research to further develop, evaluate or commercialize GLIS3 Knock Out
Mice. For collaboration opportunities, please contact Elizabeth M.
Denholm, Ph.D. at denholme@niehs.nih.gov.
Microarray for Detection and Subtyping of Human Influenza Viruses
Description of Technology: Available for licensing and commercial
development are a novel influenza virus microarray and methods for
using the microarray for the identification of existing and new types
and subtypes of human influenza viruses. There are three types of
influenza viruses, type A, B and C. Influenza types A or B viruses
cause epidemics of disease almost every winter, with type A causes
major pandemic periodically. Influenza type A viruses are further
divided into subtypes based on two proteins on the surface of the
virus. These proteins are called hemagglutinin (H) and neuraminidase
(N). There are 16 known HA subtypes and 9 known NA subtypes of
influenza A viruses. Each subtype may have different combination of H
and N proteins. Although there are only three known A subtypes of
influenza viruses (H1N1, H1N2, and H3N2) currently circulating among
humans, many other different strains are circulating among birds and
other animals and these viruses do spread to humans occasionally. There
is a requirement for sensitive and rapid diagnostic techniques in order
to improve both the diagnosis of infections and the quality of
surveillance systems. This microarray platform tiles the genomes of all
types/subtypes of influenza viruses, and is capable of correctly
identifying all 3 types/subtypes of influenza viruses from an influenza
vaccine sample.
Potential Commercial Applications
Detection and identification of human influenza viruses.
Efficient discovery of new subtypes of influenza viruses.
Diagnosis of influenza outbreaks.
Competitive Advantages: Technology can detect multiple types and
subtypes of influenza virus.
Development Stage
Pre-clinical.
In vitro data available.
Inventors: Xiaolin Wu, David J. Munroe, Cassio S. Baptista,
Elizabeth Shannon (all of NCI).
Intellectual Property: HHS Reference No. E-208-2006/0--U.S. Patent
Application No. 11/936,530 filed 07 Nov 2007.
Licensing Contact: Kevin W. Chang, Ph.D.; 301-435-5018;
changke@mail.nih.gov.
M3 Muscarinic Receptor Knockout Mice (Chrm3 tm1Jwe) for the Study of
Obesity and Other Metabolic Disorders
Description of Mouse: The five Muscarinic Acetylcholine (ACh)
receptors are G-protein coupled receptors (M1R-M5R). M3 muscarinic ACh
receptors are present in the central nervous system and the periphery.
M3R knockout mice are viable and fertile, and have no major
morphological abnormalities. They have a lean phenotype due to a
combination of reduced caloric intake and increased energy expenditure.
Because of their lean phenotype, M3R knockout mice have improved
glucose tolerance and increased insulin sensitivity. Pharmacological
blockade of central M3Rs may be a novel strategy for the treatment of
obesity and associated metabolic disorders.
In the airway, vagally-mediated bronchoconstriction responses were
abolished in M3R knockout mice in vivo, suggesting that M3R antagonists
may be useful in the treatment of chronic obstructive pulmonary disease
(COPD) and asthma. Studies with M3R knockout mice also have shown that
the M3R is the major muscarinic receptor mediating ACh-induced
glandular secretion from exocrine and endocrine glands, including the
secretion of insulin from pancreatic beta cells.
Potential Commercial Applications: Animal model to study COPD and
metabolism.
Competitive Advantages: M3R knockout mice are viable and fertile,
and have no major morphological abnormalities.
Development Stage: Pre-clinical.
Developer of Mouse: J[uuml]rgen Wess, Ph.D. (NIDDK).
Publication: Yamada M, et al. Mice lacking the M3 muscarinic
acetylcholine receptor are hypophagic and lean. Nature. 2001 Mar
8;410(6825):207-12. [PMID 11242080]
[[Page 29671]]
Intellectual Property: HHS Reference No. E-346-2004/2--Research
Tool. Patent protection is not being pursued for this technology.
Related Technologies
HHS Reference No. E-346-2004/0--M1 Muscarinic receptor KO
(Chrm1tm1Jwe) Mice.
HHS Reference No. E-346-2004/1--M2 Muscarinic receptor KO
(Chrm2 tm1Jwe) Mice.
Licensing Contact: Jaime M. Greene, M.S.; 301-435-5559;
greenejaime@mail.nih.gov
Use of E-Selectin Tolerization as Treatment for Immunological and
Vascular-Related Disorders
Description of Technology: This technology relates to the mucosal
delivery (e.g. intranasal) of an E-selectin fragment as a tolerization
agent for the prevention and treatment of immunological and vascular-
related disorders, including stroke and multiple sclerosis (MS) as well
as rare or orphan diseases involving vascular modulated disorders.
E-selectin is an adhesion molecule that is expressed on endothelial
cells lining blood vessels in response to certain localized cytokines,
making the endothelial surface pro-coagulant, pro-inflammatory and/or
immunoreactive. Such changes on the endothelial surface have been
linked to the development of vascular-related disorders like stroke, as
well as immune regulated diseases such as MS.
Intranasal administration of E-selectin, using a tolerizing dosing
schedule, induces an immunological tolerance to E-selectin. T
regulatory cells become targeted to activating blood vessel segments,
where they release immunomodulatory cytokines such as IL-10. This
release of cytokines suppresses local pro-coagulant, pro-inflammatory
and immunoreactive effects. Thus, administration of E-selectin as a
tolerizing agent will provide a targeted therapeutic approach,
impacting only affected sites in the endothelium.
Potential Commercial Applications: Treatment of diseases
biologically based on vascular initiated immune regulation. Such
disorders include prevention of secondary stroke, MS, Alzheimer's,
Parkinson's, rheumatoid arthritis, type 1 diabetes, and psoriasis.
Competitive Advantages
Low doses utilized thus minimizing potential side effects.
Animal data are available, with further studies currently
on-going.
Administration through the intranasal route represents a
less invasive mode of delivery.
FDA pre-IND meetings have been held and FDA communications
are ongoing.
Development Stage
Pre-clinical.
In vitro data available.
In vivo data available (animal).
Inventors: John M. Hallenbeck, Maria Spatz, Hidetaka Takeda,
Hideaki Wakita (all of NINDS)
Publications
1. Li X, et al. Intranasal delivery of E-selectin reduces
atherosclerosis in ApoE-/- mice. PLoS One. 2011;6(6):e20620. Epub 2011
Jun 20. [PMID 21701687]
2. Hallenbeck J. How inflammation modulates central nervous system
vessel activation and provides targets for intervention--a personal
perspective. Ann N Y Acad Sci. 2010 Oct;1207:1-7. doi: 10.1111/j.1749-
6632.2010.05785.x. [PMID 20955418]
3. Ishibashi S, et al. Mucosal tolerance to E-selectin promotes the
survival of newly generated neuroblasts via regulatory T-cell induction
after stroke in spontaneously hypertensive rats. J Cereb Blood Flow
Metab. 2009 Mar;29(3):606-20. [PMID 19107136]
4. Wakita H, et al. Mucosal tolerization to E-selectin protects
against memory dysfunction and white matter damage in a vascular
cognitive impairment model. J Cereb Blood Flow Metab. 2008
Feb;28(2):341-53. [PMID 17637705]
5. Nakayama T, et al. Intranasal administration of E-selectin to
induce immunological tolerization can suppress subarachnoid hemorrhage-
induced vasospasm implicating immune and inflammatory mechanisms in its
genesis. Brain Res. 2007 Feb 9;1132(1):177-84. [PMID 17188657]
6. Illoh K, et al. Mucosal tolerance to E-selectin and response to
systemic inflammation. J Cereb Blood Flow Metab. 2006 Dec;26(12):1538-
50. [PMID 16596122]
7. Chen Y, et al. Mucosal tolerance to E-selectin provides cell-
mediated protection against ischemic brain injury. Proc Natl Acad Sci U
S A. 2003 Dec 9;100(25):15107-12. [PMID 14645708]
8. Takeda H, et al. Induction of mucosal tolerance to E-selectin
prevents ischemic and hemorrhagic stroke in spontaneously hypertensive
genetically stroke-prone rats. Stroke. 2002 Sep;33(9):2156-63. [PMID
12215580]
Intellectual Property
HHS Reference No. E-237-1999/0--
--U.S. Patent No. 7,261,896 issued 28 Aug 2007.
--U.S. Patent Application No. 11/820,326 filed 19 Jun 2007.
HHS Reference No. E-237-1999/1--
--U.S. Patent No. 7,897,575 issued 01 Mar 2011.
--U.S. Patent Application No. 12,859,048 filed 18 Aug 2010.
and Foreign counterparts in Australia, Canada, Europe, and
Japan
Licensing Contact: Tara Kirby, Ph.D.; 301-435-4426;
tarak@mail.nih.gov.
Collaborative Research Opportunity: The Stroke Branch, NINDS/NIH,
is seeking statements of capability or interest from parties interested
in collaborative research to further develop, evaluate or commercialize
the applications of E-selectin tolerization in treatment of
neurological based disease. For collaboration opportunities, please
contact Laurie Arrants, NINDS at arrantsl@ninds.nih.gov.
Nucleic Acids and Methods for Expression of the Rat Fc[egr]RI beta
Subunit, Which Plays a Critical Role in Allergy and the Immune Response
Description of Technology: Fc[egr]RI is the high-affinity receptor
for the Fc region of immunoglobulin E (IgE), and plays an important
role in the allergic response and inflammation. It controls the
production of important immunomodulatory molecules, such as cytokines
and histamine.
This technology describes nucleic acids encoding the beta subunit
of rat Fc[egr]RI, as well as vectors and transgenic cells including
such nucleic acids. Also described are methods of expressing functional
rat Fc[egr]RI in a host cell. These may be useful in studies of allergy
and the immune response.
Potential Commercial Applications: Research studies of allergy and
the immune response.
Development Stage
Early-stage.
In vitro data available.
Inventors: Jean-Pierre Kinet and Henry Metzger (NIAMS).
Intell ectual Property: HHS Reference No. E-247-1988/4--U.S. Patent
No. 6,165,744 issued 26 Dec 2000.
Licensing Contact: Tara L. Kirby, Ph.D.; 301-435-4426;
tarak@mail.nih.gov.
Dated: May 14, 2012.
Richard U. Rodriguez,
Director, Division of Technology Development and Transfer, Office of
Technology Transfer, National Institutes of Health.
[FR Doc. 2012-12041 Filed 5-17-12; 8:45 am]
BILLING CODE 4140-01-P
