[Federal Register Volume 77, Number 97 (Friday, May 18, 2012)]
[Notices]
[Pages 29668-29671]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 2012-12041]
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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.
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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;
[email protected].
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;
[email protected].
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;
[email protected].
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 [email protected].
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,
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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;
[email protected].
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 [email protected].
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;
[email protected].
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]
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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;
[email protected]
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;
[email protected].
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 [email protected].
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;
[email protected].
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