Government-Owned Inventions; Availability for Licensing, 24497-24499 [2012-9776]
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Federal Register / Vol. 77, No. 79 / Tuesday, April 24, 2012 / Notices
provide an addendum to the fourth
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any category.
Respondents: TANF Agencies.
ANNUAL BURDEN ESTIMATES
Instrument
Number of
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Number of
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Average
burden hours
per response
Total burden
hours
ACF–196 ..........................................................................................................
51
4
8
1,632
Estimated Total Annual Burden
Hours: 1,632.
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[FR Doc. 2012–9759 Filed 4–23–12; 8:45 am]
BILLING CODE 4184–01–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
licensing in the U.S. in accordance with
35 U.S.C. 207 to achieve expeditious
commercialization of results of
federally-funded research and
development. Foreign patent
applications are filed on selected
inventions to extend market coverage
mstockstill on DSK4VPTVN1PROD with NOTICES
SUMMARY:
VerDate Mar<15>2010
17:40 Apr 23, 2012
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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.
Small-Molecule Modulators of Lipid
Storage for Treatment of Obesity,
Atherosclerosis, Metabolic Syndrome
and Lipid Storage Diseases
Description of Technology: Lipid
droplets are key organelles involved in
lipid homeostasis. In normal
physiology, these droplets are formed in
response to elevated fatty acid levels,
and are broken down when needed for
energy production. Imbalances in lipid
homeostasis trigger compensatory
alterations in metabolism that can lead
to diseases such as obesity,
atherosclerosis, and metabolic
syndrome. There are also a number of
inherited lipid storage diseases that
result in harmful buildup of various
lipids, such as Gaucher disease, Fabry
disease, and others. Reducing the
accumulation of lipid droplets is a
promising potential strategy for
treatment of such disorders.
This technology describes three novel
structural classes of small-molecule
compounds that significantly reduce the
accumulation of lipid droplets. These
compounds hold promise for the
treatment of diseases associated with
aberrant lipid deposition.
Potential Commercial Applications:
• Treatment of inherited metabolic
diseases such as Gaucher disease, Fabry
disease, and Tay Sachs disease.
• Treatment of obesity and metabolic
disease.
• Treatment of atherosclerosis.
Competitive Advantages: Modulation
of lipid droplet accumulation is a novel
mechanism for treatment of lipid storage
diseases.
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Development Stage:
• Early-stage
• In vitro data available
Inventors: Matthew Boxer et al.
(NCATS).
Intellectual Property: HHS Reference
No. E–277–2011/0—U.S. Provisional
Patent Application No. 61/562,894 filed
22 Nov 2011.
Licensing Contact: Tara L. Kirby,
Ph.D.; 301–435–4426;
tarak@mail.nih.gov.
A Broadly Neutralizing Human AntiHIV Monoclonal Antibody (10E8)
Capable of Neutralizing Most HIV–1
Strains
Description of Technology: This
Human Anti-HIV Monoclonal Antibody
(10E8) has great potential to provide
passive protection from infection, as a
therapeutic vaccine, or as a tool for the
development of vaccine immunogens.
10E8 is one of the most potent HIVneutralizing antibodies isolated thus far
and it can potently neutralize up to 98%
of genetically diverse HIV–1 strains.
10E8 is specific to the membraneproximal external region (MPER) of the
HIV envelope protein, GP41. It is
anticipated that 10E8 could be used in
combination with another human antiHIV–1 monoclonal antibody to provide
an antibody response that neutralizes
nearly all strains of HIV–1.
Additionally, 10E8 is a useful tool for
the design of vaccine immunogens that
can elicit an adaptive immune response
to produces 10E8 like antibodies. This
technology also includes monoclonal
antibodies from the same germ line as
10E8.
Potential Commercial Applications:
• Passive protection to prevent HIV
infection
• Passive protection to prevent motherto-infant HIV transmission
• Topical microbicide to prevent HIV
infection
• Gene-based vectors for anti-gp41
antibody expression
• Therapeutic for the elimination of
HIV infected cells that are actively
producing virus
Competitive Advantages:
E:\FR\FM\24APN1.SGM
24APN1
24498
Federal Register / Vol. 77, No. 79 / Tuesday, April 24, 2012 / Notices
• One of the most potent Human
broadly-neutralizing anti HIV
antibodies isolated to date
• Broad reactivity and high affinity to
most HIV–1 strains
• Activity is highly complementary to
existing broadly neutralizing
antibodies, such as CD4 binding site
antibodies
• Capable of neutralizing all HIV–1
strains, if used in combination with
another anti-HIV monoclonal
antibody
Cytochromes P450 CYP2J and CYP2C
Polyclonal Antibodies and
Recombinant Proteins
metabolize both arachidonic acid and
linoleic acid. The CYP2J and CYP2C
subfamily members have a wide tissue
distribution and may be useful as model
systems for studies of cardiovascular
disease, drug metabolism and toxicity.
Recombinant proteins of mouse
cytochrome P450s CYP2C and CYP2J
have also been expressed and can be
used as controls in immunoblotting, as
well as for metabolism studies.
Potential Commercial Applications:
• These antibodies can be used to
study the expression of the P450s in
various tissues by
immunohistochemistry and
immunoblotting.
• The recombinant proteins can be
used as controls in immunoblotting as
well as for metabolism studies.
Competitive Advantages: The CYP2J
and CYP2C subfamily members have a
wide tissue distribution and may be
useful as model systems for studies of
cardiovascular disease, drug metabolism
and toxicity.
Development Stage: In vitro data
available.
Inventors: Darryl C. Zeldin (NIEHS) et
al.
Publications: Manuscripts in
preparation.
Intellectual Property: HHS Reference
No. E–153–2011/0—Research Material.
Patent protection has not been pursued
for this technology.
Licensing Contact: Fatima Sayyid,
M.H.P.M.; 301–435–4521;
Fatima.Sayyid@nih.hhs.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 antibodies against mouse
cytochrome P450s CYP2J and CYP2C.
For collaboration opportunities, please
contact Elizabeth M. Denholm, Ph.D. at
denholme@niehs.nih.gov.
Description of Technology: The
National Institutes of Health announces
polyclonal antibodies against mouse
cytochrome P450s CYP2J and CYP2C.
Cytochrome P450s catalyze the
metabolism of a wide range of
exogenous compounds, including drugs,
industrial chemicals, environmental
pollutants, and carcinogens. The 2C
family of cytochrome P450 metabolizes
an extensive number of drugs which
include tolbutamide, S-Warfarin,
mephenytoin, diazepam and taxol.
Many of the P450 enzymes are also
active in the NADPH-dependent
oxidation of arachidonic acid to various
eicosanoids found in several species.
The 2J family is expressed at high levels
in the heart and has been shown to
Monoclonal Antibodies Targeting
Human DNA Polymerase beta, a DNA
Repair Enzyme
Description of Technology: Available
for licensing are monoclonal antibodies
targeting human DNA polymerase beta
(Pol B). Pol B is a constitutively
expressed ‘‘housekeeping’’ enzyme that
plays a role in base excision repair
(BER), a cellular defense mechanism
that repairs DNA base damage and loss.
Aberrant Pol B expression is associated
with genomic instability indicating that
Pol B is required for DNA maintenance,
replication and recombination.
These antibodies can be utilized to
elucidate BER’s mechanism of action
and Pol B’s structure and function.
Moreover, the antibodies can be used to
mstockstill on DSK4VPTVN1PROD with NOTICES
Development Stage:
• Pre-clinical
• In vitro data available
• In vivo data available (animal)
Publication: In press.
Intellectual Property: HHS Reference
No. E–253–2011/0—US Provisional
Application No. 61/556,660 filed 07
Nov 2011.
Related Technologies:
• HHS Reference No. E–123–2005/1—
PCT Application No. PCT/US2006/
005613 filed 17 Feb 2006
• HHS Reference No. E–291–2008/0—
US Application No. 13/057,414 filed
03 Feb 2011
Licensing Contact: Cristina
Thalhammer-Reyero, Ph.D., MBA; 301–
435–4507; thalhamc@mail.nih.gov.
Collaborative Research Opportunity:
The National Institute of Allergy and
Infectious Diseases is seeking statements
of capability or interest from parties
interested in collaborative research to
further develop, evaluate or
commercialize vaccine immunogens
capable of eliciting a 10E8-like adaptive
immune response. For collaboration
opportunities, please contact Bill
Ronnenberg at 301–451–3522 or
wronnenberg@niaid.nih.gov.
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detect Pol B in samples with a variety
of techniques including
immunoblotting, ELISA,
immunoprecipitation, and
immunohistochemistry.
Potential Commercial Applications:
• Research tool to elucidate the
mechanism of base excision repair
• Research reagents
Competitive Advantages: Can be
utilized in a variety of applications to
study Pol B.
Development Stage:
• Early-stage
• In vitro data available
Inventors: Samuel Wilson and
Rajendra Prasad (NIEHS).
Publications:
1. Srivastava DK, et al. Phorbol ester
abrogates up-regulation of DNA
polymerase beta by DNA-alkylating
agents in Chinese hamster ovary
cells. J Biol Chem. 1995 Jul
7;270(27):16402–8. [PMID 7608211]
2. Singhal R, et al. DNA polymerase beta
conducts the gap-filling step in
uracil-initiated base excision repair
in a bovine testis nuclear extract. J
Biol Chem. 1995 Jan 13;270(2):949–
57. [PMID 7822335]
3. Prasad R, et al. Specific interaction of
DNA polymerase beta and DNA
ligase I in a multiprotein base
excision repair complex from
bovine testis. J Biol Chem. 1996 Jul
5;271(27):16000–7. [PMID 8663274]
4. Piersen C, et al. Evidence for an imino
intermediate in the DNA
polymerase beta deoxyribose
phosphate excision reaction. J Biol
Chem. 1996 Jul 26;271(30):17811–5.
[PMID 8663612]
5. Sobol R, et al. Regulated overexpression of DNA polymerase beta
mediates early onset cataract in
mice. DNA Repair (Amst). 2003
May 13;2(5):609–22. [PMID
12713817]
6. Poltoratsky V, et al. Down-regulation
of DNA polymerase beta
accompanies somatic
hypermutation in human BL2 cell
lines. DNA Repair (Amst). 2007 Feb
4;6(2):244–53. [PMID 17127106]
Intellectual Property: HHS Reference
No. E–036–2008/0—Research Tool.
Patent protection is not being pursued
for this technology.
Licensing Contact: Jennifer Wong;
301–435–4633; wongje@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 these monoclonal
antibodies. For collaboration
E:\FR\FM\24APN1.SGM
24APN1
Federal Register / Vol. 77, No. 79 / Tuesday, April 24, 2012 / Notices
opportunities, please contact Elizabeth
M. Denholm, Ph.D. at
denholme@niehs.nih.gov.
mstockstill on DSK4VPTVN1PROD with NOTICES
Treatment of Acute and Chronic
Neurological Disorders Using GLP–1,
Exendin-4 and Analogs
Description of Technology: Glucagonlike peptide-1 (GLP–1) and related
peptides, including exendin-4 and
liraglutide, are incretin mimetics that
enhance glucose-dependent insulin
secretion following food ingestion as a
regulator of glucose homeostasis.
Exendin-4 and liraglutide are used
clinically in the safe and effective
treatment of type 2 diabetes to enhance
insulin secretion and maintain a
euglycemic state. These actions are
primarily mediated at the level of the
GLP–1 receptor in the pancreas;
however, these compounds are known
to enter the brain where the GLP–1
receptor also is expressed.
Researchers at the NIH have
discovered the novel use of GLP–1 and
exendin-4 analogs in the treatment of
acute and chronic neurological
disorders and neurodegenerative
diseases. Studies conducted in
extensive cell culture and in mouse
models using these analogs have
demonstrated significant neurotrophic
and neuroprotective actions in models
of several disorders, including
Alzheimer’s disease, Parkinson’s
disease, Huntington’s disease, ALS,
stroke, head trauma and peripheral
neuropathy. These studies have now
been extensively published and
independently validated by other
scientific groups. Furthermore, clinical
studies are ongoing to evaluate the use
of GLP–1 receptor agonists for the
treatment of early Alzheimer’s disease,
Parkinson’s disease and diabetic
neuropathy by several groups within the
US and Europe.
Potential Commercial Applications:
Therapeutics for:
• Neurodegenerative diseases—
Alzheimer’s, Huntington’s,
Parkinson’s, ALS
• Stroke
• Head trauma (traumatic brain injury)
• Peripheral neuropathies
Competitive Advantages:
• Compounds reduce neuronal cell
death, amyloid deposition and
neuroinflammation while promoting
neurogenesis.
• Compounds in this class have
already been shown to be safe and
effective for other indications.
• Extensive in vitro and animal data
are available, and clinical studies are
ongoing.
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• There are extensive publications in
the literature, both from the inventors
and independent groups.
Development Stage:
• Pre-clinical
• Clinical
• In vitro data available
• In vivo data available (animal)
• In vivo data available (human)
Inventors: Nigel Greig, Harold
Halloway, Maire Doyle, Josephine Egan
(all of NIA).
Publications:
1. Li Y, et al. Exendin-4 ameliorates
motor neuron degeneration in
cellular and animal models of
amyotrophic lateral sclerosis. PLoS
One. 2012;7(2):e32008. [PMID
22384126]
2. Li Y, et al. Enhancing the GLP–1
receptor signaling pathway leads to
proliferation and neuroprotection in
human neuroblastoma cells. J
Neurochem. 2010 Jun;113(6):1621–
1631. [PMID 20374430]
3. Li Y, et al. GLP–1 receptor
stimulation reduces amyloid-beta
peptide accumulation and
cytotoxicity in cellular and animal
models of Alzheimer’s disease. J
Alzheimers Dis. 2010;19(4):1205–
1219. [PMID 20308787]
4. Li Y, et al. GLP–1 receptor
stimulation preserves primary
cortical and dopaminergic neurons
in cellular and rodent models of
stroke and Parkinsonism. Proc Natl
Acad Sci USA. 2009 Jan
27;106(4):1285–1290. [PMID
19164583]
5. Martin B, et al. Exendin-4 improves
glycemic control, ameliorates brain
and pancreatic pathologies and
extends survival in a mouse model
of Huntington’s disease. Diabetes.
2009 Feb;58(2):318–328.
[PMID:18984744]
6. Perry T, et al. Evidence of GLP–1mediated neuroprotection in an
animal model of pyridoxineinduced peripheral sensory
neuropathy. Exp Neurol. 2007
Feb;203(2):293–301. [PMID
17125767]
7. Perry T, Greig NH. Enhancing central
nervous system endogenous GLP–1
receptor pathways for intervention
in Alzheimer’s disease. Curr
Alzheimers Res. 2005 Jul;2(3):377–
385. [PMID 15974903]
8. Greig NH, et al. New therapeutic
strategies and drug candidates for
neurodegenerative diseases: p53
and TNF-alpha inhibitors, and
GLP–1 receptor agonists. Ann NY
Acad Sci. 2004 Dec;1035:290–315.
[PMID 15681814]
9. Perry TA, Greig NH. A new
Alzheimer’s disease interventive
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24499
strategy: GLP–1. Curr Drug Targets.
2004 Aug;5(6):565–571. [PMID
15270203]
Listing of additional related
publications available upon request.
Intellectual Property: HHS Reference
No. E–049–2001/0—
• U.S. Patent 7,576,050 issued 18 Aug
2009
• U.S. Patent Application No. 12/
317,042 filed 18 Dec 2008
• Foreign counterparts in Australia,
Canada, Europe, India, and Japan
Licensing Contact: Tara L. Kirby,
Ph.D.; 301–435–4426;
tarak@mail.nih.gov.
Collaborative Research Opportunity:
The National Institute on Aging, Drug
Design and Development Section, is
seeking statements of capability or
interest from parties interested in
collaborative research to further
develop, evaluate or commercialize this
technology. For collaboration
opportunities, please contact Vio Conley
at conleyv@mail.nih.gov.
Dated: April 18, 2012.
Richard U. Rodriguez,
Director, Division of Technology Development
and Transfer, Office of Technology Transfer,
National Institutes of Health.
[FR Doc. 2012–9776 Filed 4–23–12; 8:45 am]
BILLING CODE 4140–01–P
DEPARTMENT OF HEALTH AND
HUMAN SERVICES
National Institutes of Health
Government-Owned Inventions;
Availability for Licensing: Mouse
Models
National Institutes of Health,
Public Health Service, HHS.
ACTION: Notice.
AGENCY:
The inventions listed below
are owned by an agency of the U.S.
Government and are available for
licensing in the U.S. in accordance with
35 U.S.C. 207 to achieve expeditious
commercialization of results of
federally-funded research and
development. Foreign patent
applications are filed on selected
inventions to extend market coverage
for companies and may also be available
for licensing.
FOR FURTHER INFORMATION CONTACT:
Licensing information for the
technologies 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–
SUMMARY:
E:\FR\FM\24APN1.SGM
24APN1
]]>Agencies
[Federal Register Volume 77, Number 79 (Tuesday, April 24, 2012)]
[Notices]
[Pages 24497-24499]
From the Federal Register Online via the Government Printing Office [www.gpo.gov]
[FR Doc No: 2012-9776]
-----------------------------------------------------------------------
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.
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.
Small-Molecule Modulators of Lipid Storage for Treatment of Obesity,
Atherosclerosis, Metabolic Syndrome and Lipid Storage Diseases
Description of Technology: Lipid droplets are key organelles
involved in lipid homeostasis. In normal physiology, these droplets are
formed in response to elevated fatty acid levels, and are broken down
when needed for energy production. Imbalances in lipid homeostasis
trigger compensatory alterations in metabolism that can lead to
diseases such as obesity, atherosclerosis, and metabolic syndrome.
There are also a number of inherited lipid storage diseases that result
in harmful buildup of various lipids, such as Gaucher disease, Fabry
disease, and others. Reducing the accumulation of lipid droplets is a
promising potential strategy for treatment of such disorders.
This technology describes three novel structural classes of small-
molecule compounds that significantly reduce the accumulation of lipid
droplets. These compounds hold promise for the treatment of diseases
associated with aberrant lipid deposition.
Potential Commercial Applications:
Treatment of inherited metabolic diseases such as Gaucher
disease, Fabry disease, and Tay Sachs disease.
Treatment of obesity and metabolic disease.
Treatment of atherosclerosis.
Competitive Advantages: Modulation of lipid droplet accumulation is
a novel mechanism for treatment of lipid storage diseases.
Development Stage:
Early-stage
In vitro data available
Inventors: Matthew Boxer et al. (NCATS).
Intellectual Property: HHS Reference No. E-277-2011/0--U.S.
Provisional Patent Application No. 61/562,894 filed 22 Nov 2011.
Licensing Contact: Tara L. Kirby, Ph.D.; 301-435-4426;
tarak@mail.nih.gov.
A Broadly Neutralizing Human Anti-HIV Monoclonal Antibody (10E8)
Capable of Neutralizing Most HIV-1 Strains
Description of Technology: This Human Anti-HIV Monoclonal Antibody
(10E8) has great potential to provide passive protection from
infection, as a therapeutic vaccine, or as a tool for the development
of vaccine immunogens. 10E8 is one of the most potent HIV-neutralizing
antibodies isolated thus far and it can potently neutralize up to 98%
of genetically diverse HIV-1 strains. 10E8 is specific to the membrane-
proximal external region (MPER) of the HIV envelope protein, GP41. It
is anticipated that 10E8 could be used in combination with another
human anti-HIV-1 monoclonal antibody to provide an antibody response
that neutralizes nearly all strains of HIV-1. Additionally, 10E8 is a
useful tool for the design of vaccine immunogens that can elicit an
adaptive immune response to produces 10E8 like antibodies. This
technology also includes monoclonal antibodies from the same germ line
as 10E8.
Potential Commercial Applications:
Passive protection to prevent HIV infection
Passive protection to prevent mother-to-infant HIV
transmission
Topical microbicide to prevent HIV infection
Gene-based vectors for anti-gp41 antibody expression
Therapeutic for the elimination of HIV infected cells that are
actively producing virus
Competitive Advantages:
[[Page 24498]]
One of the most potent Human broadly-neutralizing anti HIV
antibodies isolated to date
Broad reactivity and high affinity to most HIV-1 strains
Activity is highly complementary to existing broadly
neutralizing antibodies, such as CD4 binding site antibodies
Capable of neutralizing all HIV-1 strains, if used in
combination with another anti-HIV monoclonal antibody
Development Stage:
Pre-clinical
In vitro data available
In vivo data available (animal)
Publication: In press.
Intellectual Property: HHS Reference No. E-253-2011/0--US
Provisional Application No. 61/556,660 filed 07 Nov 2011.
Related Technologies:
HHS Reference No. E-123-2005/1--PCT Application No. PCT/
US2006/005613 filed 17 Feb 2006
HHS Reference No. E-291-2008/0--US Application No. 13/057,414
filed 03 Feb 2011
Licensing Contact: Cristina Thalhammer-Reyero, Ph.D., MBA; 301-435-
4507; thalhamc@mail.nih.gov.
Collaborative Research Opportunity: The National Institute of
Allergy and Infectious Diseases is seeking statements of capability or
interest from parties interested in collaborative research to further
develop, evaluate or commercialize vaccine immunogens capable of
eliciting a 10E8-like adaptive immune response. For collaboration
opportunities, please contact Bill Ronnenberg at 301-451-3522 or
wronnenberg@niaid.nih.gov.
Cytochromes P450 CYP2J and CYP2C Polyclonal Antibodies and Recombinant
Proteins
Description of Technology: The National Institutes of Health
announces polyclonal antibodies against mouse cytochrome P450s CYP2J
and CYP2C. Cytochrome P450s catalyze the metabolism of a wide range of
exogenous compounds, including drugs, industrial chemicals,
environmental pollutants, and carcinogens. The 2C family of cytochrome
P450 metabolizes an extensive number of drugs which include
tolbutamide, S-Warfarin, mephenytoin, diazepam and taxol. Many of the
P450 enzymes are also active in the NADPH-dependent oxidation of
arachidonic acid to various eicosanoids found in several species. The
2J family is expressed at high levels in the heart and has been shown
to metabolize both arachidonic acid and linoleic acid. The CYP2J and
CYP2C subfamily members have a wide tissue distribution and may be
useful as model systems for studies of cardiovascular disease, drug
metabolism and toxicity.
Recombinant proteins of mouse cytochrome P450s CYP2C and CYP2J have
also been expressed and can be used as controls in immunoblotting, as
well as for metabolism studies.
Potential Commercial Applications:
These antibodies can be used to study the expression of
the P450s in various tissues by immunohistochemistry and
immunoblotting.
The recombinant proteins can be used as controls in
immunoblotting as well as for metabolism studies.
Competitive Advantages: The CYP2J and CYP2C subfamily members have
a wide tissue distribution and may be useful as model systems for
studies of cardiovascular disease, drug metabolism and toxicity.
Development Stage: In vitro data available.
Inventors: Darryl C. Zeldin (NIEHS) et al.
Publications: Manuscripts in preparation.
Intellectual Property: HHS Reference No. E-153-2011/0--Research
Material. Patent protection has not been pursued for this technology.
Licensing Contact: Fatima Sayyid, M.H.P.M.; 301-435-4521;
Fatima.Sayyid@nih.hhs.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 antibodies
against mouse cytochrome P450s CYP2J and CYP2C. For collaboration
opportunities, please contact Elizabeth M. Denholm, Ph.D. at
denholme@niehs.nih.gov.
Monoclonal Antibodies Targeting Human DNA Polymerase beta, a DNA Repair
Enzyme
Description of Technology: Available for licensing are monoclonal
antibodies targeting human DNA polymerase beta (Pol B). Pol B is a
constitutively expressed ``housekeeping'' enzyme that plays a role in
base excision repair (BER), a cellular defense mechanism that repairs
DNA base damage and loss. Aberrant Pol B expression is associated with
genomic instability indicating that Pol B is required for DNA
maintenance, replication and recombination.
These antibodies can be utilized to elucidate BER's mechanism of
action and Pol B's structure and function. Moreover, the antibodies can
be used to detect Pol B in samples with a variety of techniques
including immunoblotting, ELISA, immunoprecipitation, and
immunohistochemistry.
Potential Commercial Applications:
Research tool to elucidate the mechanism of base excision
repair
Research reagents
Competitive Advantages: Can be utilized in a variety of
applications to study Pol B.
Development Stage:
Early-stage
In vitro data available
Inventors: Samuel Wilson and Rajendra Prasad (NIEHS).
Publications:
1. Srivastava DK, et al. Phorbol ester abrogates up-regulation of DNA
polymerase beta by DNA-alkylating agents in Chinese hamster ovary
cells. J Biol Chem. 1995 Jul 7;270(27):16402-8. [PMID 7608211]
2. Singhal R, et al. DNA polymerase beta conducts the gap-filling step
in uracil-initiated base excision repair in a bovine testis nuclear
extract. J Biol Chem. 1995 Jan 13;270(2):949-57. [PMID 7822335]
3. Prasad R, et al. Specific interaction of DNA polymerase beta and DNA
ligase I in a multiprotein base excision repair complex from bovine
testis. J Biol Chem. 1996 Jul 5;271(27):16000-7. [PMID 8663274]
4. Piersen C, et al. Evidence for an imino intermediate in the DNA
polymerase beta deoxyribose phosphate excision reaction. J Biol Chem.
1996 Jul 26;271(30):17811-5. [PMID 8663612]
5. Sobol R, et al. Regulated over-expression of DNA polymerase beta
mediates early onset cataract in mice. DNA Repair (Amst). 2003 May
13;2(5):609-22. [PMID 12713817]
6. Poltoratsky V, et al. Down-regulation of DNA polymerase beta
accompanies somatic hypermutation in human BL2 cell lines. DNA Repair
(Amst). 2007 Feb 4;6(2):244-53. [PMID 17127106]
Intellectual Property: HHS Reference No. E-036-2008/0--Research
Tool. Patent protection is not being pursued for this technology.
Licensing Contact: Jennifer Wong; 301-435-4633;
wongje@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 these monoclonal
antibodies. For collaboration
[[Page 24499]]
opportunities, please contact Elizabeth M. Denholm, Ph.D. at
denholme@niehs.nih.gov.
Treatment of Acute and Chronic Neurological Disorders Using GLP-1,
Exendin-4 and Analogs
Description of Technology: Glucagon-like peptide-1 (GLP-1) and
related peptides, including exendin-4 and liraglutide, are incretin
mimetics that enhance glucose-dependent insulin secretion following
food ingestion as a regulator of glucose homeostasis. Exendin-4 and
liraglutide are used clinically in the safe and effective treatment of
type 2 diabetes to enhance insulin secretion and maintain a euglycemic
state. These actions are primarily mediated at the level of the GLP-1
receptor in the pancreas; however, these compounds are known to enter
the brain where the GLP-1 receptor also is expressed.
Researchers at the NIH have discovered the novel use of GLP-1 and
exendin-4 analogs in the treatment of acute and chronic neurological
disorders and neurodegenerative diseases. Studies conducted in
extensive cell culture and in mouse models using these analogs have
demonstrated significant neurotrophic and neuroprotective actions in
models of several disorders, including Alzheimer's disease, Parkinson's
disease, Huntington's disease, ALS, stroke, head trauma and peripheral
neuropathy. These studies have now been extensively published and
independently validated by other scientific groups. Furthermore,
clinical studies are ongoing to evaluate the use of GLP-1 receptor
agonists for the treatment of early Alzheimer's disease, Parkinson's
disease and diabetic neuropathy by several groups within the US and
Europe.
Potential Commercial Applications: Therapeutics for:
Neurodegenerative diseases--Alzheimer's, Huntington's,
Parkinson's, ALS
Stroke
Head trauma (traumatic brain injury)
Peripheral neuropathies
Competitive Advantages:
Compounds reduce neuronal cell death, amyloid deposition
and neuroinflammation while promoting neurogenesis.
Compounds in this class have already been shown to be safe
and effective for other indications.
Extensive in vitro and animal data are available, and
clinical studies are ongoing.
There are extensive publications in the literature, both
from the inventors and independent groups.
Development Stage:
Pre-clinical
Clinical
In vitro data available
In vivo data available (animal)
In vivo data available (human)
Inventors: Nigel Greig, Harold Halloway, Maire Doyle, Josephine
Egan (all of NIA).
Publications:
1. Li Y, et al. Exendin-4 ameliorates motor neuron degeneration in
cellular and animal models of amyotrophic lateral sclerosis. PLoS One.
2012;7(2):e32008. [PMID 22384126]
2. Li Y, et al. Enhancing the GLP-1 receptor signaling pathway leads to
proliferation and neuroprotection in human neuroblastoma cells. J
Neurochem. 2010 Jun;113(6):1621-1631. [PMID 20374430]
3. Li Y, et al. GLP-1 receptor stimulation reduces amyloid-beta peptide
accumulation and cytotoxicity in cellular and animal models of
Alzheimer's disease. J Alzheimers Dis. 2010;19(4):1205-1219. [PMID
20308787]
4. Li Y, et al. GLP-1 receptor stimulation preserves primary cortical
and dopaminergic neurons in cellular and rodent models of stroke and
Parkinsonism. Proc Natl Acad Sci USA. 2009 Jan 27;106(4):1285-1290.
[PMID 19164583]
5. Martin B, et al. Exendin-4 improves glycemic control, ameliorates
brain and pancreatic pathologies and extends survival in a mouse model
of Huntington's disease. Diabetes. 2009 Feb;58(2):318-328.
[PMID:18984744]
6. Perry T, et al. Evidence of GLP-1-mediated neuroprotection in an
animal model of pyridoxine-induced peripheral sensory neuropathy. Exp
Neurol. 2007 Feb;203(2):293-301. [PMID 17125767]
7. Perry T, Greig NH. Enhancing central nervous system endogenous GLP-1
receptor pathways for intervention in Alzheimer's disease. Curr
Alzheimers Res. 2005 Jul;2(3):377-385. [PMID 15974903]
8. Greig NH, et al. New therapeutic strategies and drug candidates for
neurodegenerative diseases: p53 and TNF-alpha inhibitors, and GLP-1
receptor agonists. Ann NY Acad Sci. 2004 Dec;1035:290-315. [PMID
15681814]
9. Perry TA, Greig NH. A new Alzheimer's disease interventive strategy:
GLP-1. Curr Drug Targets. 2004 Aug;5(6):565-571. [PMID 15270203]
Listing of additional related publications available upon request.
Intellectual Property: HHS Reference No. E-049-2001/0--
U.S. Patent 7,576,050 issued 18 Aug 2009
U.S. Patent Application No. 12/317,042 filed 18 Dec 2008
Foreign counterparts in Australia, Canada, Europe, India, and
Japan
Licensing Contact: Tara L. Kirby, Ph.D.; 301-435-4426;
tarak@mail.nih.gov.
Collaborative Research Opportunity: The National Institute on
Aging, Drug Design and Development Section, is seeking statements of
capability or interest from parties interested in collaborative
research to further develop, evaluate or commercialize this technology.
For collaboration opportunities, please contact Vio Conley at
conleyv@mail.nih.gov.
Dated: April 18, 2012.
Richard U. Rodriguez,
Director, Division of Technology Development and Transfer, Office of
Technology Transfer, National Institutes of Health.
[FR Doc. 2012-9776 Filed 4-23-12; 8:45 am]
BILLING CODE 4140-01-P
