Government-Owned Inventions; Availability for Licensing, 3273-3275 [2012-1264]
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Federal Register / Vol. 77, No. 14 / Monday, January 23, 2012 / Notices
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Dated: January 13, 2012.
Glenda Conroy,
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[FR Doc. 2012–1267 Filed 1–20–12; 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
licensing in the U.S. in accordance with
35 U.S.C. 207 to achieve expeditious
commercialization of results of
federally-funded research and
development. Foreign patent
applications are filed on selected
inventions to extend market coverage
for companies and may also be available
for licensing.
ADDRESSES: Licensing information and
copies of the U.S. patent applications
listed below may be obtained by writing
to the indicated licensing contact at the
Office of Technology Transfer, National
Institutes of Health, 6011 Executive
Boulevard, Suite 325, Rockville,
Maryland 20852–3804; telephone: (301)
496–7057; fax: (301) 402–0220. A signed
Confidential Disclosure Agreement will
be required to receive copies of the
patent applications.
TKELLEY on DSK3SPTVN1PROD with NOTICES
SUMMARY:
Enhancement of Cancer Imaging and
Treatment With Somatostatin Analogs
Description of Technology: Available
for licensing is a novel method using
short-term treatment with a
glucocorticoid antagonist to increase the
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expression of somatostatin receptors in
tumor cells and improve rates of tumor
identification in patients with high
cortisol levels.
Tumors express up to five different
receptors for somatostatin analogs on
their surface. This enables somatostatin
and its analogs to bind to the tumor
cells. When the compound has a
radioactive or radiopharmaceutical
‘‘tag’’ it can allow the cell to be killed
(via radiation) or imaged (via the
radiopharmaceutical). Somatostatin
analogs have variable affinity for the
five somatostatin receptors (types 1–5).
As a result, if tumors express less of the
more avid receptors, imaging or
treatment with the analogs is less likely
to be successful. There is a large
variability in functional type 2 receptor
expression in these tumors. High
cortisol levels (such as those seen in
Cushing’s syndrome) cause the type 2
receptor level to decrease, which (with
type 5) is the primary binding site for
1111n-DTPA-D-Phe-pentetreotide, which
is used to image tumors (in an
octreotide nuclear medicine scan).
Potential Commercial Applications:
Tumor imaging and
radiopharmaceutical therapy using
somatostatin analogs.
Competitive Advantages: Allows
conversion of a negative to positive
octreotide scan in patients with active
hypercortisolism.
Development Stage: Pilot.
Inventors: Lynnette Nieman (NICHD),
et al.
Intellectual Property: HHS Reference
No. E–252–2011/0—U.S. Provisional
Application No. 61/533,664 filed 12 Sep
2011.
Licensing Contact: Patrick McCue,
Ph.D.; (301) 435–5560;
mccuepat@mail.nih.gov.
and a PARP inhibitor in the target
cancer cell. The high levels of GSH/GST
are often a feature of cancer cells. The
compound is predicted to have strong
synergy with other anticancer
therapeutics.
PARP Inhibitor/NO Donor Dual
Prodrugs as Anticancer Agents
Description of Technology: Scientists
at NIH have developed a hybrid prodrug
molecule with enhanced biological
activity as anticancer agent. Novel
cancer therapeutic strategies are in high
demand. Diazeniumdiolate-based nitric
oxide (NO)-releasing prodrugs are a
growing class of promising anticancer
agents. Poly (ADP-ribose) polymerase
(PARP) inhibitors have also emerged as
a promising class of therapeutic
compounds for cancer. The twocomponent prodrug described in the
instant invention is expected to deliver
DNA damaging agent (NO release) along
with an inhibitor of DNA repair (PARP
inhibitor) simultaneously to a cancer
cell. The prodrugs are activated by
glutathione/glutathione S-transferase
(GSH/GST) and release cytotoxic NO
Description of Technology: Ataxia
telangiectasia (A–T) is a rare
neurodegenerative disease that is caused
by mutations in the Ataxia
Telangiectasia Mutated (ATM) gene,
which is the chief activator of the
cellular response to double stranded
DNA breaks. Defects in this gene can
lead to abnormal cell death, particularly
in the brain and in the immune system,
and the disease is also characterized by
hypersensitivity to radiation and other
DNA-damaging agents, as well as a
predisposition to lymphoma. There is
currently no effective treatment for this
disease.
Investigators at the National Human
Genome Research Institute (NHGRI)
have shown that ATM-null cells treated
with rottlerin, a small molecule protein
kinase inhibitor, respond to double
stranded DNA breaks by activating an
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Potential Commercial Applications
• Cancer therapeutics.
• Cancer therapeutics in combination
with other anticancer therapies.
Competitive Advantages:
Combination of DNA damaging agent
and DNA repair inhibitor in one
molecule has advantage over both
individual drug treatments.
Development Stage
• Prototype.
• Early-stage.
• Pre-clinical.
• In vitro data available.
Inventors: Anna E. Maciag, Larry K.
Keefer, and Joseph E. Saavedra (NCI).
Publication: PARP Inhibitor/NO
Donor Dual Prodrugs as Anticancer
Agents, manuscript in preparation.
Intellectual Property: HHS Reference
No. E–220–2011/0—U.S. Patent
Application No. 61/549,862 filed 21 Oct
2011.
Related Technologies
• HHS Reference No. E–093–1996/
3—U.S. Patent No. 6,610,660 issued 26
Aug 2003.
• HHS Reference No. E–025–2010/
0—PCT Application No. PCT/US2010/
056446 filed 12 Nov 2010, which
published as WO 2011/060215 on 19
May 2011
Licensing Contact: Betty B. Tong,
Ph.D.; (301) 594–6565;
tongb@mail.nih.gov.
Small Molecule Drugs for Treatment of
Ataxia Telangiectasia or DNA Damage
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Federal Register / Vol. 77, No. 14 / Monday, January 23, 2012 / Notices
alternate DNA repair pathway.
Similarly, ATM-null mice demonstrate
increased protection from radiation
when treated with this compound.
Thus, rottlerin or related compounds
may be an effective treatment for A–T or
other diseases resulting from DNA
damage.
Potential Commercial Applications:
Therapy for ataxia telangiectasia or
other diseases resulting from DNA
damage.
function and regulating antibody
production.
• Model to study IL–21’s pathology in
autoimmunity, immunodeficiency,
allergy, and cancer.
Competitive Advantages: Mouse
model that constitutively expresses
human IL–21, without the negative side
effects of growth retardation and high
toxicity present in other human IL–21
transgenic mice.
Competitive Advantages
• There is currently no therapy for
ataxia telangiectasia.
• Rottlerin is a readily-obtained,
small molecule compound.
• Pre-clinical.
• In vivo data available (animal).
Inventors: Warren Leonard and
Katsutoshi Ozaki (NHLBI).
Publication: Ozaki K, et al. Regulation
of B cell differentiation and plasma cell
generation by IL–21, a novel inducer of
Blimp-1 and Bcl-6. J Immunol. 2004
Nov 1;173(9):5361–5371. [PMID
15494482].
Intellectual Property: HHS Reference
No. E–231–2010/0—Research Tool.
Patent protection is not being pursued
for this technology.
TKELLEY on DSK3SPTVN1PROD with NOTICES
Development Stage
• Early-stage.
• In vitro data available.
• In vivo data available (animal).
Inventors: Wei Zheng et al. (NCTT).
Intellectual Property: HHS Reference
No. E–038–2011/0—U.S. Provisional
Application No. 61/524,177 filed 16
Aug 2011.
Licensing Contact: Tara L. Kirby,
Ph.D.; (301) 435–4426;
tarak@mail.nih.gov.
Transgenic Human Interleukin-21
Mouse Model
Description of Technology: Available
for licensing is a mouse model that
constitutively expresses human
interleukin-21 (IL–21). Traditionally,
human IL–21 transgenic mouse models
are difficult to produce as those with
high IL–21 levels exhibit growth
retardation and die before sexual
maturity. The investigators generated
transgenic mice that express human IL–
21, which can stimulate murine cells in
vitro thereby providing an accurate
model to elucidate IL–21’s role in
immunity, immune disorders, and
cancer.
IL–21 is a type I cytokine whose
receptor is expressed on T, B, and
natural killer cells. IL–21 has
pleiotropic actions ranging from
augmenting the proliferation of T cells
to driving the differentiation of B cells
into memory cells and terminally
differentiated plasma cells. Moreover,
IL–21 has anti-tumor activity by
augmenting natural killer cell activity.
This mouse model allows studying
human IL–21 in vivo and its role in a
variety of diseases such as
autoimmunity, immunodeficiency,
allergy, and cancer.
Potential Commercial Applications
• Model to study human IL–21 in
vivo.
• Research tool to elucidate IL–21’s
role in T, B, and natural killer cell
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Development Stage
Related Technologies
• HHS Reference No. E–211–2002/
1—U.S. Patent 7,332,645 issued 19 Feb
2008; U.S. Patent Application No. 11/
958,540 filed 18 Dec 2007.
• HHS Reference No. E–120–2003/
1—U.S. Patent 7,993,919 issued 09 Aug
2011.
• HHS Reference No. E–120–2003/
2—U.S. Patent 7,378,276 issued 27 May
2008; U.S. Patent Application No. 12/
126,166 filed 23 May 2008.
• HHS Reference No. E–137–2002/
0—U.S. Patent Application No. 10/
508,978 filed 19 Nov 2004; U.S. Patent
Application No. 12/651,858 filed 04 Jan
2010.
Licensing Contact: Jennifer Wong;
(301) 435–4633; wongje@mail.nih.gov.
Method for Producing Significant
Amounts of B19 Virus for Development
of Killed or Attenuated Vaccines
Description of Technology: Human
parvovirus B19 (B19) is a common
infection of children and adults and is
the cause of fifth disease. B19
selectively infects erythroid progenitor
cells of bone marrow, fetal liver and a
small number of specialized cell lines.
These specific cell lines demonstrate
limited infectibility and commonly
produce little or no virus following
initial inoculation with B19. Current
methods for producing infectious B19
require phlebotomy of infrequently
available infected donors. The available
technology describes a method of
producing pure populations of human
erythroid progenitor cells that are fully
permissive to B19 infection. The ability
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to efficiently generate significant
amounts of infectious B19V in cells is
useful for the development of killed or
attenuated vaccines, therapeutics and
efficient diagnostic tools for prevention
and treatment of B19V.
Potential Commercial Applications
• Human parvovirus B19 diagnostic.
• Vaccine manufacture.
• Research and development of antiparvovirus agents.
Competitive Advantages: Method
produces pure populations of human
erythroid progenitor cells that are fully
permissive of B19 infection.
Development Stage
• Pre-clinical.
• In vitro data available.
Inventors: Susan Wong and Neal S.
Young (NHLBI).
Publications
1. Giarratana MC, et al. Ex vivo
generation of fully mature human red
blood cells from hematopoietic stem
cells. Nat Biotechnol. 2005 Jan;
23(1):69–74. [PMID 15619619].
2. Freyssinier JM, et al. Purification,
amplification and characterization of a
population of human erythroid
progenitors. Br J Haematol. 1999 Sep;
106(4):912–922. [PMID 10519992].
Intellectual Property: HHS Reference
No. E–188–2006/0—U.S. Patent
Application No. 12/301,960 filed 21
Nov 2008.
Licensing Contact: Kevin W. Chang,
Ph.D.; (301) 435–5018;
changke@mail.nih.gov.
Collaborative Research Opportunity:
The NHLBI Hematology Branch is
seeking statements of capability or
interest from parties interested in
collaborative research to further
develop, evaluate or commercialize
novel methods to produce parvovirus
B19 and use as diagnostic or vaccine.
For collaboration opportunities, please
contact Dr. Neal Young at (301) 496–
5093 or youngns@mail.nih.gov.
HIV Therapeutics Utilizing Peptide
Secreting Commensal Bacteria
Description of Technology: Available
for licensing and commercial
development is a patent estate covering
genetically engineered commensal
bacteria compositions and their
methods of use that secrete HIV
infectivity interfering peptides with the
aid of co-expressed translocation
mediators such as HylB, HylD or tolC
gene products. The bacteria can be, for
example, Escherichia coli, and are
preferably those that colonize the
gastrointestinal or genitourinary tracts.
The secreted anti-HIV peptide can be a
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Federal Register / Vol. 77, No. 14 / Monday, January 23, 2012 / Notices
functional inhibitory fragment from the
C-terminus of HIV, SHIV or SIV, or an
inhibitory peptide derived from the Nterminus receptor-binding domain of
SIV gp41, HIV–1 gp41, or HIV–2 gp41.
The secreted anti-HIV peptide can also
be a peptide from the allosteric domain
of gp120, an extracellular loop of CCR5,
an anti-CD4 immunoglobulin, a mimetic
of CD4, an alpha-defensin or thetadefensin, a CD38 fragment homologous
to the V3 loop of gp120, polphemusin
II (a CXCR4 antagonist), a RANTES
peptide that binds to CCR5 or an HIV
surface binding peptide such as
cyanovirin.
Potential Commercial Applications:
HIV therapeutics.
Competitive Advantages: Utilizes
naturally occurring commensal bacteria.
Development Stage
• Pre-clinical.
• In vivo data available (animal).
Inventor: Dean H. Hamer (NCI).
Publications
1. Lagenaur LA, et al. Prevention of
vaginal SHIV transmission in macaques
by a live recombinant Lactobacillus.
Mucosal Immunol. 2011 Nov;4(6):648–
657. [PMID 21734653].
2. Rao S, et al. Toward a live
microbial microbicide for HIV:
commensal bacteria secreting an HIV
fusion inhibitor peptide. Proc Natl Acad
Sci U S A. 2005 Aug 23;102(34):11993–
11998. [PMID 16040799].
Intellectual Property
HHS Reference No. E–233–2004/0—
• U.S. Patent Application No. 11/
710,512 filed 26 Feb 2007.
• Various international issued
patents.
Licensing Contact: Michael
Shmilovich, Esq.; (301) 435–5019;
shmilovm@mail.nih.gov.
Dated: January 17, 2012.
Richard U. Rodriguez,
Director, Division of Technology Development
and Transfer, Office of Technology Transfer,
National Institutes of Health.
[FR Doc. 2012–1264 Filed 1–20–12; 8:45 am]
BILLING CODE 4140–01–P
TKELLEY on DSK3SPTVN1PROD with NOTICES
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:
VerDate Mar<15>2010
17:58 Jan 20, 2012
Jkt 226001
The inventions listed below
are owned by an agency of the U.S.
Government and are available for
licensing in the U.S. in accordance with
35 U.S.C. 207 to achieve expeditious
commercialization of results of
federally-funded research and
development. Foreign patent
applications are filed on selected
inventions to extend market coverage
for companies and may also be available
for licensing.
ADDRESSES: Licensing information and
copies of the U.S. patent applications
listed below may be obtained by writing
to the indicated licensing contact at the
Office of Technology Transfer, National
Institutes of Health, 6011 Executive
Boulevard Suite 325, Rockville,
Maryland 20852–3804; telephone: (301)
496–7057; fax: (301) 402–0220. A signed
Confidential Disclosure Agreement will
be required to receive copies of the
patent applications.
SUMMARY:
Thioxothiazolidinone Derivatives—A
Novel Class of Anti Cancer Agents
Description of Technology: The
invention provides for a novel class of
heterocyclic compounds (i.e.
thioxothiazolidinone derivatives) that
exhibit anticancer activity in a unique
mechanism. More specifically, the
compounds of the invention act as
inhibitors of the enzyme human tyrosyl
DNA phosphodiesterase1 (Tdp1), a DNA
repair enzyme involved in
topoisomerase1 (Top1) mediated DNA
damage, such as damage induced by the
Top1 inhibitors and chemotherapeutic
agents, camptothecins. As such, these
compounds can serve as potentiators of
camptothecins. The experimental data
indeed point at a synergistic effect
achieved in a combination therapy of
the thioxothiazolidinone derivatives of
the invention and the established
anticancer agents camptothecins.
Moreover, due to this synergistic effect,
a lower therapeutic dose of the latter
may be needed, resulting in reduced
side effects. In addition, it is possible
that the Tdp1 inhibitors of the invention
may be effective as anti tumor agents on
their own. This is based on the fact that
Tdp1 is involved also in repairing DNA
damage resulting from oxygen radicals,
and the observation that tumors contain
excess free radicals.
Potential Commercial Applications
• Effective cancer therapy in
combination with camptothecins.
• Cancer therapy as standalone anti
cancer agents.
Competitive Advantages: The
compounds of the invention act in
unique mechanism that can enhance the
therapeutic efficacy of the anticancer
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3275
drugs camptothecins, and at the same
time can serve as standalone anticancer
agents.
Development Stage: In vitro data
available.
Inventors: Yves G. Pommier (NCI) et
al.
Publications
1. Marchand C, et al. Identification of
phosphotyrosine mimetic inhibitors of
human tyrosyl-DNA phosphodiesterase
I by a novel AlphaScreen highthroughput assay. Mol Cancer Ther.
2009 Jan;8(1):240–248. [PMID
19139134].
2. Dexheimer TS, et al. Tyrosyl-DNA
phosphodiesterase as a target for
anticancer therapy. Anticancer Agents
Med Chem. 2008 May;8(4):381–389.
[PMID 18473723].
3. Dexheimer TS, et al. 4–Pregnen-21ol-3,20-dione-21-(4bromobenzenesufonate) (NSC 88915)
and related novel steroid derivatives as
tyrosyl-DNA phosphodiesterase (Tdp1)
inhibitors. J Med Chem. 2009 Nov
26;52(22): 7122–7131. [PMID 19883083].
Intellectual Property: HHS Reference
No. E–239–2011/0—U.S. Provisional
Patent Application No. 61/545,308 filed
10 Oct 2011.
Licensing Contact: Uri Reichman,
Ph.D., MBA; (301) 435–4616;
reichmau@mail.nih.gov.
Monospecific and Bispecific Human
Monoclonal Antibodies Targeting IGF–
II
Description of Technology: The type 1
insulin-like growth factor (IGF) receptor
(IGF1R) is over-expressed by many
tumors and mediates proliferation,
motility, and protection from apoptosis.
Agents that inhibit IGF1R expression or
function can potentially block tumor
growth and metastasis. Its major ligands,
IGF–I, and IGF–II are over-expressed by
multiple tumor types. Previous studies
indicate that inhibition of IGF–I, and/or
IGF–II binding to its cognizant receptor
negatively modulates signal
transduction through the IGF pathway
and concomitant cell proliferation and
growth. Therefore, use of humanized or
fully human antibodies against IGFs
represents a valid approach to inhibit
tumor growth. The present invention
discloses two monoclonal antibodies,
designated m610.27 and m630, and a
bispecific monoclonal antibody, m660,
generated by linking domains from
m610.27 and m630. All three antibodies
display high affinities for IGF–I and
IGF–II in the pM to nM range. The
antibodies inhibited signal transduction
mediated by the IGF–1R interaction
with IGF–I and IGF–II and blocked
phosphorylation of IGF–IR and the
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]]>Agencies
[Federal Register Volume 77, Number 14 (Monday, January 23, 2012)]
[Notices]
[Pages 3273-3275]
From the Federal Register Online via the Government Printing Office [www.gpo.gov]
[FR Doc No: 2012-1264]
-----------------------------------------------------------------------
DEPARTMENT OF HEALTH AND HUMAN SERVICES
National Institutes of Health
Government-Owned Inventions; Availability for Licensing
AGENCY: National Institutes of Health, Public Health Service, HHS.
ACTION: Notice.
-----------------------------------------------------------------------
SUMMARY: The inventions listed below are owned by an agency of the U.S.
Government and are available for licensing in the U.S. in accordance
with 35 U.S.C. 207 to achieve expeditious commercialization of results
of federally-funded research and development. Foreign patent
applications are filed on selected inventions to extend market coverage
for companies and may also be available for licensing.
ADDRESSES: Licensing information and copies of the U.S. patent
applications listed below may be obtained by writing to the indicated
licensing contact at the Office of Technology Transfer, National
Institutes of Health, 6011 Executive Boulevard, Suite 325, Rockville,
Maryland 20852-3804; telephone: (301) 496-7057; fax: (301) 402-0220. A
signed Confidential Disclosure Agreement will be required to receive
copies of the patent applications.
Enhancement of Cancer Imaging and Treatment With Somatostatin Analogs
Description of Technology: Available for licensing is a novel
method using short-term treatment with a glucocorticoid antagonist to
increase the expression of somatostatin receptors in tumor cells and
improve rates of tumor identification in patients with high cortisol
levels.
Tumors express up to five different receptors for somatostatin
analogs on their surface. This enables somatostatin and its analogs to
bind to the tumor cells. When the compound has a radioactive or
radiopharmaceutical ``tag'' it can allow the cell to be killed (via
radiation) or imaged (via the radiopharmaceutical). Somatostatin
analogs have variable affinity for the five somatostatin receptors
(types 1-5). As a result, if tumors express less of the more avid
receptors, imaging or treatment with the analogs is less likely to be
successful. There is a large variability in functional type 2 receptor
expression in these tumors. High cortisol levels (such as those seen in
Cushing's syndrome) cause the type 2 receptor level to decrease, which
(with type 5) is the primary binding site for \111\1n-DTPA-D-Phe-
pentetreotide, which is used to image tumors (in an octreotide nuclear
medicine scan).
Potential Commercial Applications: Tumor imaging and
radiopharmaceutical therapy using somatostatin analogs.
Competitive Advantages: Allows conversion of a negative to positive
octreotide scan in patients with active hypercortisolism.
Development Stage: Pilot.
Inventors: Lynnette Nieman (NICHD), et al.
Intellectual Property: HHS Reference No. E-252-2011/0--U.S.
Provisional Application No. 61/533,664 filed 12 Sep 2011.
Licensing Contact: Patrick McCue, Ph.D.; (301) 435-5560;
mccuepat@mail.nih.gov.
PARP Inhibitor/NO Donor Dual Prodrugs as Anticancer Agents
Description of Technology: Scientists at NIH have developed a
hybrid prodrug molecule with enhanced biological activity as anticancer
agent. Novel cancer therapeutic strategies are in high demand.
Diazeniumdiolate-based nitric oxide (NO)-releasing prodrugs are a
growing class of promising anticancer agents. Poly (ADP-ribose)
polymerase (PARP) inhibitors have also emerged as a promising class of
therapeutic compounds for cancer. The two-component prodrug described
in the instant invention is expected to deliver DNA damaging agent (NO
release) along with an inhibitor of DNA repair (PARP inhibitor)
simultaneously to a cancer cell. The prodrugs are activated by
glutathione/glutathione S-transferase (GSH/GST) and release cytotoxic
NO and a PARP inhibitor in the target cancer cell. The high levels of
GSH/GST are often a feature of cancer cells. The compound is predicted
to have strong synergy with other anticancer therapeutics.
Potential Commercial Applications
Cancer therapeutics.
Cancer therapeutics in combination with other anticancer
therapies.
Competitive Advantages: Combination of DNA damaging agent and DNA
repair inhibitor in one molecule has advantage over both individual
drug treatments.
Development Stage
Prototype.
Early-stage.
Pre-clinical.
In vitro data available.
Inventors: Anna E. Maciag, Larry K. Keefer, and Joseph E. Saavedra
(NCI).
Publication: PARP Inhibitor/NO Donor Dual Prodrugs as Anticancer
Agents, manuscript in preparation.
Intellectual Property: HHS Reference No. E-220-2011/0--U.S. Patent
Application No. 61/549,862 filed 21 Oct 2011.
Related Technologies
HHS Reference No. E-093-1996/3--U.S. Patent No. 6,610,660
issued 26 Aug 2003.
HHS Reference No. E-025-2010/0--PCT Application No. PCT/
US2010/056446 filed 12 Nov 2010, which published as WO 2011/060215 on
19 May 2011
Licensing Contact: Betty B. Tong, Ph.D.; (301) 594-6565;
tongb@mail.nih.gov.
Small Molecule Drugs for Treatment of Ataxia Telangiectasia or DNA
Damage
Description of Technology: Ataxia telangiectasia (A-T) is a rare
neurodegenerative disease that is caused by mutations in the Ataxia
Telangiectasia Mutated (ATM) gene, which is the chief activator of the
cellular response to double stranded DNA breaks. Defects in this gene
can lead to abnormal cell death, particularly in the brain and in the
immune system, and the disease is also characterized by
hypersensitivity to radiation and other DNA-damaging agents, as well as
a predisposition to lymphoma. There is currently no effective treatment
for this disease.
Investigators at the National Human Genome Research Institute
(NHGRI) have shown that ATM-null cells treated with rottlerin, a small
molecule protein kinase inhibitor, respond to double stranded DNA
breaks by activating an
[[Page 3274]]
alternate DNA repair pathway. Similarly, ATM-null mice demonstrate
increased protection from radiation when treated with this compound.
Thus, rottlerin or related compounds may be an effective treatment for
A-T or other diseases resulting from DNA damage.
Potential Commercial Applications: Therapy for ataxia
telangiectasia or other diseases resulting from DNA damage.
Competitive Advantages
There is currently no therapy for ataxia telangiectasia.
Rottlerin is a readily-obtained, small molecule compound.
Development Stage
Early-stage.
In vitro data available.
In vivo data available (animal).
Inventors: Wei Zheng et al. (NCTT).
Intellectual Property: HHS Reference No. E-038-2011/0--U.S.
Provisional Application No. 61/524,177 filed 16 Aug 2011.
Licensing Contact: Tara L. Kirby, Ph.D.; (301) 435-4426;
tarak@mail.nih.gov.
Transgenic Human Interleukin-21 Mouse Model
Description of Technology: Available for licensing is a mouse model
that constitutively expresses human interleukin-21 (IL-21).
Traditionally, human IL-21 transgenic mouse models are difficult to
produce as those with high IL-21 levels exhibit growth retardation and
die before sexual maturity. The investigators generated transgenic mice
that express human IL-21, which can stimulate murine cells in vitro
thereby providing an accurate model to elucidate IL-21's role in
immunity, immune disorders, and cancer.
IL-21 is a type I cytokine whose receptor is expressed on T, B, and
natural killer cells. IL-21 has pleiotropic actions ranging from
augmenting the proliferation of T cells to driving the differentiation
of B cells into memory cells and terminally differentiated plasma
cells. Moreover, IL-21 has anti-tumor activity by augmenting natural
killer cell activity. This mouse model allows studying human IL-21 in
vivo and its role in a variety of diseases such as autoimmunity,
immunodeficiency, allergy, and cancer.
Potential Commercial Applications
Model to study human IL-21 in vivo.
Research tool to elucidate IL-21's role in T, B, and
natural killer cell function and regulating antibody production.
Model to study IL-21's pathology in autoimmunity,
immunodeficiency, allergy, and cancer.
Competitive Advantages: Mouse model that constitutively expresses
human IL-21, without the negative side effects of growth retardation
and high toxicity present in other human IL-21 transgenic mice.
Development Stage
Pre-clinical.
In vivo data available (animal).
Inventors: Warren Leonard and Katsutoshi Ozaki (NHLBI).
Publication: Ozaki K, et al. Regulation of B cell differentiation
and plasma cell generation by IL-21, a novel inducer of Blimp-1 and
Bcl-6. J Immunol. 2004 Nov 1;173(9):5361-5371. [PMID 15494482].
Intellectual Property: HHS Reference No. E-231-2010/0--Research
Tool. Patent protection is not being pursued for this technology.
Related Technologies
HHS Reference No. E-211-2002/1--U.S. Patent 7,332,645
issued 19 Feb 2008; U.S. Patent Application No. 11/958,540 filed 18 Dec
2007.
HHS Reference No. E-120-2003/1--U.S. Patent 7,993,919
issued 09 Aug 2011.
HHS Reference No. E-120-2003/2--U.S. Patent 7,378,276
issued 27 May 2008; U.S. Patent Application No. 12/126,166 filed 23 May
2008.
HHS Reference No. E-137-2002/0--U.S. Patent Application
No. 10/508,978 filed 19 Nov 2004; U.S. Patent Application No. 12/
651,858 filed 04 Jan 2010.
Licensing Contact: Jennifer Wong; (301) 435-4633;
wongje@mail.nih.gov.
Method for Producing Significant Amounts of B19 Virus for Development
of Killed or Attenuated Vaccines
Description of Technology: Human parvovirus B19 (B19) is a common
infection of children and adults and is the cause of fifth disease. B19
selectively infects erythroid progenitor cells of bone marrow, fetal
liver and a small number of specialized cell lines. These specific cell
lines demonstrate limited infectibility and commonly produce little or
no virus following initial inoculation with B19. Current methods for
producing infectious B19 require phlebotomy of infrequently available
infected donors. The available technology describes a method of
producing pure populations of human erythroid progenitor cells that are
fully permissive to B19 infection. The ability to efficiently generate
significant amounts of infectious B19V in cells is useful for the
development of killed or attenuated vaccines, therapeutics and
efficient diagnostic tools for prevention and treatment of B19V.
Potential Commercial Applications
Human parvovirus B19 diagnostic.
Vaccine manufacture.
Research and development of anti-parvovirus agents.
Competitive Advantages: Method produces pure populations of human
erythroid progenitor cells that are fully permissive of B19 infection.
Development Stage
Pre-clinical.
In vitro data available.
Inventors: Susan Wong and Neal S. Young (NHLBI).
Publications
1. Giarratana MC, et al. Ex vivo generation of fully mature human
red blood cells from hematopoietic stem cells. Nat Biotechnol. 2005
Jan; 23(1):69-74. [PMID 15619619].
2. Freyssinier JM, et al. Purification, amplification and
characterization of a population of human erythroid progenitors. Br J
Haematol. 1999 Sep; 106(4):912-922. [PMID 10519992].
Intellectual Property: HHS Reference No. E-188-2006/0--U.S. Patent
Application No. 12/301,960 filed 21 Nov 2008.
Licensing Contact: Kevin W. Chang, Ph.D.; (301) 435-5018;
changke@mail.nih.gov.
Collaborative Research Opportunity: The NHLBI Hematology Branch is
seeking statements of capability or interest from parties interested in
collaborative research to further develop, evaluate or commercialize
novel methods to produce parvovirus B19 and use as diagnostic or
vaccine. For collaboration opportunities, please contact Dr. Neal Young
at (301) 496-5093 or youngns@mail.nih.gov.
HIV Therapeutics Utilizing Peptide Secreting Commensal Bacteria
Description of Technology: Available for licensing and commercial
development is a patent estate covering genetically engineered
commensal bacteria compositions and their methods of use that secrete
HIV infectivity interfering peptides with the aid of co-expressed
translocation mediators such as HylB, HylD or tolC gene products. The
bacteria can be, for example, Escherichia coli, and are preferably
those that colonize the gastrointestinal or genitourinary tracts. The
secreted anti-HIV peptide can be a
[[Page 3275]]
functional inhibitory fragment from the C-terminus of HIV, SHIV or SIV,
or an inhibitory peptide derived from the N-terminus receptor-binding
domain of SIV gp41, HIV-1 gp41, or HIV-2 gp41. The secreted anti-HIV
peptide can also be a peptide from the allosteric domain of gp120, an
extracellular loop of CCR5, an anti-CD4 immunoglobulin, a mimetic of
CD4, an alpha-defensin or theta-defensin, a CD38 fragment homologous to
the V3 loop of gp120, polphemusin II (a CXCR4 antagonist), a RANTES
peptide that binds to CCR5 or an HIV surface binding peptide such as
cyanovirin.
Potential Commercial Applications: HIV therapeutics.
Competitive Advantages: Utilizes naturally occurring commensal
bacteria.
Development Stage
Pre-clinical.
In vivo data available (animal).
Inventor: Dean H. Hamer (NCI).
Publications
1. Lagenaur LA, et al. Prevention of vaginal SHIV transmission in
macaques by a live recombinant Lactobacillus. Mucosal Immunol. 2011
Nov;4(6):648-657. [PMID 21734653].
2. Rao S, et al. Toward a live microbial microbicide for HIV:
commensal bacteria secreting an HIV fusion inhibitor peptide. Proc Natl
Acad Sci U S A. 2005 Aug 23;102(34):11993-11998. [PMID 16040799].
Intellectual Property
HHS Reference No. E-233-2004/0--
U.S. Patent Application No. 11/710,512 filed 26 Feb 2007.
Various international issued patents.
Licensing Contact: Michael Shmilovich, Esq.; (301) 435-5019;
shmilovm@mail.nih.gov.
Dated: January 17, 2012.
Richard U. Rodriguez,
Director, Division of Technology Development and Transfer, Office of
Technology Transfer, National Institutes of Health.
[FR Doc. 2012-1264 Filed 1-20-12; 8:45 am]
BILLING CODE 4140-01-P
