Government-Owned Inventions; Availability for Licensing, 61714-61717 [2011-25734]
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Federal Register / Vol. 76, No. 193 / Wednesday, October 5, 2011 / Notices
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Dated: September 30, 2011.
Leslie Kux,
Acting Assistant Commissioner for Policy.
[FR Doc. 2011–25684 Filed 10–4–11; 8:45 am]
BILLING CODE 4160–01–P
DEPARTMENT OF HEALTH AND
HUMAN SERVICES
National Institutes of Health
Proposed Collection; Comment
Request; STAR METRICS (Science and
Technology for America’s
Reinvestment: Measuring the EffecTs
of Research on Innovation,
Competitiveness and Science)
In compliance with the
requirement of Section 3506(c)(2)(A) of
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for opportunity for public comment on
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Management and Budget (OMB) for
review and approval.
Proposed Collection: Title: STAR
METRICS (Science and Technology for
America’s Reinvestment: Measuring the
EffecTs of Research on Innovation,
SUMMARY:
Competitiveness and Science). Type of
Information Collection Request:
Reinstatement of OMB number 0925–
0616, expiration date 01/31/2011. Need
and Use of Information Collection: The
aim of STAR METRICS is twofold. The
goal of STAR METRICS is to continue
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participating universities and Federal
agencies with a reliable and consistent
means to account for the number of
scientists and staff that are on research
institution payrolls, supported by
Federal funds. In subsequent
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economic outcomes (such as job
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(such as citations and patents) as well
as on social and health outcomes.
Frequency of Response: Quarterly.
Affected Public: Universities and other
research institutions. Type of
Respondents: University administrators.
The annual reporting burden is as
follows: Estimated Number of
Respondents: 100. Estimated Number of
Responses per Respondent: 4. Average
Burden Hours per Response: 2.5.
Estimated Total Annual Burden Hours
Requested: 1,315. The annualized cost
to respondents is estimated to be
$65,750. There are no Capital Costs to
report. There are no Operating or
Maintenance Costs to report.
A.12–1 ESTIMATES ANNUAL BURDEN HOURS
Number of
respondents
Form
Frequency of
response
Average time
per response
(in hours)
Annual hour
burden
7
100
1
4
45
2.5
315
1000
Total ..........................................................................................................
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Stage 1: One time data input ..........................................................................
Stage 2: Ongoing quarterly data input ............................................................
........................
........................
........................
1,315
Request for Comments: Written
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are to respond, including the use of
appropriate automated, electronic,
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mechanical, or other technological
collection techniques or other forms of
information technology.
To
request more information on the
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FOR FURTHER INFORMATION CONTACT:
PO 00000
Dated: September 27, 2011.
Stefano Bertuzzi,
Office of the Director, Office of Science Policy
Analysis, Office of Science Policy, National
Institutes of Health.
[FR Doc. 2011–25732 Filed 10–4–11; 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:
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Federal Register / Vol. 76, No. 193 / Wednesday, October 5, 2011 / Notices
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.
SUMMARY:
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.
ADDRESSES:
mstockstill on DSK4VPTVN1PROD with NOTICES
Platform Technology Using Ubiquitin
To Improve the Delivery and Efficacy of
Cytosolic Targeted Toxins
Description of Technology: Targeted
toxins (TT) are hybrid protein drugs
consisting of ligands that bind to the
surface of cancer cells and deliver
polypeptide toxins that kill malignant
cells by inactivating cytosolic protein
synthesis and inducing cell death. A
major challenge in the construction of
targeted toxins is reducing the
nonspecific binding of the toxin moiety
to normal tissues and increasing the
cytotoxicity of the treatment.
To address these issues, the NIH
inventors have identified that the
protein ubiquitin, a small protein in
eukaryotic cells that plays a role in
protein recycling, can separate the
targeting moiety and the catalytic
moiety of a TT in the cytosol of cells.
By decoupling the two moieties, the
cytotoxicity of the TT treatment can be
greatly increased since the catalytic
domain remains longer in the cytosol.
This technology would be highly useful
for all TT and immunotoxins that access
the cytosol to either affect cytosolic
targets or traffic to further sites of
action. To validate this approach, the
inventors have tested ubiquitin variants
within a TT consisting of anthrax toxin
lethal factor N-terminus (LFn) and
Pseudomonas exotoxin A catalytic
domain (PEIII). Here, they show that the
intracellular release of the PEIII
(catalytic moiety) is achievable and that
ubiquitination of the TT controls the
persistence of the TTs in the cytosol and
thus controls the observed cytotoxicity.
Potential Commercial Applications:
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• Chimeric or fusion molecules for
increasing the efficacy and cytotoxicity
of targeted toxins and immunotoxins.
• Methods for cytosol delivery of
targeted toxins to target cells.
Competitive Advantages:
• Broadly applicable to all cytotoxic
immunoconjugates.
• Increased stability and cytotoxicity
of the TT without affecting the delivery
or specificity of the treatment.
• Therapeutic access to the cytosol
and/or trafficking to further sites of
action such as the nucleus.
• Rapid cytosolic release of the
catalytic moiety and degradation of the
targeting moiety.
Development Stage:
• Pre-clinical
• In vitro data available
Inventors: Christopher Bachran
(NIAID), Stephen Leppla (NIAID), Shihui Liu (NIAID), Thomas Morley
Publications:
1. Tcherniuk S, et al. Construction of
tumor-specific toxins using ubiquitin
fusion technique. Mol Ther. 2005
Feb;11(2):196–204. [PMID 15668131]
2. Wang F. Selective cytotoxicity to
HER2-positive tumor cells by a
recombinant e23sFv-TD-tBID protein
containing a furin cleavage sequence.
Clin Cancer Res. 2010 Apr
15;16(8):2284–2294. [PMID 20371697]
3. Heisler I. A cleavable adapter to
reduce nonspecific cytotoxicity of
recombinant immunotoxins. Int J
Cancer. 2003 Jan 10;103(2):277–282.
[PMID 12455044]
Intellectual Property: HHS Reference
No. E–150–2011/0—U.S. Provisional
Application No. 61/473,450 filed 08
April 2011
Related Technologies:
• HHS Reference No. E–293–1999—
Mutated Anthrax Toxin Protective
Antigen Proteins That Specifically
Target Cells Containing High Amounts
of Cell-Surface Metalloproteinases or
Plasminogen Activator Receptors
(Leppla/NIAID)
• HHS Reference No. E–070–2007—
Human Cancer Therapy Using
Engineered Metalloproteinase-Activated
Anthrax Lethal Toxin That Target
Tumor Vasculature (Leppla/NIAID)
• HHS Reference No. E–059–2004—
Multimeric Protein Toxins to Target
Cells Having Multiple Identifying
Characteristics (Leppla/NIAID)
Licensing Contact: Whitney Hastings;
301–451–7337; hastingw@mail.nih.gov
NOX5 Immunogenic Peptides and
Monoclonal Antibodies for the
Detection of Cancer and Inflammatory
Responses
Description of Technology: The
membrane-associated NADPH oxidase 5
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(NOX5) protein is expressed in various
fetal tissues, uterus, testis, spleen,
lymph nodes and endothelial cells. In
addition, the reactive oxygen species
(ROS) generated by NOX5 have been
shown to participate in signaling
cascades regulating proliferation in
several cancers and pre-cancerous
conditions, such as hairy cell leukemia,
melanoma, prostate cancer, and Barret’s
esophagus. Further, excess ROS
produced by NOX5 has been associated
with coronary artery disease,
inflammation, and atherosclerosis.
The present invention discloses the
identification and characterization of a
purified monoclonal antibody against
NOX5 protein. This NOX5 antibody can
detect endogenous levels of NOX5 in
human cells and could aid in studies
and diagnostic tests of NOX5-based
redox signaling involved in cancer, cell
growth and differentiation, as well as
angiogenic and inflammatory responses.
In addition, the NOX5 antibody may
have therapeutic applications (e.g. antiinflammatory, antiangiogenic, or
antiproliferative activity) by interfering
with NOX5 activation at the cell surface.
Potential Commercial Applications:
• Diagnostic for the detection of
NOX5 in human cells and NOX5-based
redox signaling
• Antibody can be used in ELISA,
Western Blot, Immunofluorescence,
Immunoprecipitation and
Immunohistochemistry
• Tool to aid in the understanding of
NOX5’s functional significance in
human physiology and pathophysiology
• Possible therapeutic for the
treatment of various human diseases
associated with NOX5 and/or ROS
Competitive Advantages:
• Antibody is the only mouse
monoclonal commercially available to
the best of our knowledge
• Antibody is highly specific in
recognizing the NOX5 protein with
greater efficiency and the accurate
detection compared to other Nox5
antibodies
Development Stage: Pre-clinical
Inventors: James H. Doroshow,
Krishnendu K. Roy, Smitha Antony
(NCI)
Publications:
1. Kamiguti AS, et al. Expression and
activity of NOX5 in the circulating
malignant B cells of hairy cell leukemia.
J Immunol. 2005 Dec 15;175(12):8424–
8430. [PMID: 16339585]
2. Brar SS, et al. NOX5 NAD(P)H
oxidase regulates growth and apoptosis
in DU 145 prostate cancer cells. Am J
Physiol Cell Physiol. 2003
Aug;285(2):C353–C369. [PMID:
12686516]
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Federal Register / Vol. 76, No. 193 / Wednesday, October 5, 2011 / Notices
3. Hong J, et al. Bile acid reflux
contributes to development of
esophageal adenocarcinoma via
activation of phosphatidylinositolspecific phospholipase Cgamma2 and
NADPH oxidase NOX5–S. Cancer Res.
2010 Feb 1;70(3):1247–1255. [PMID:
20086178]
Intellectual Property: HHS Reference
No. E–149–2011/0—U.S. Provisional
Application No. 61/471,596 filed 04
April 2011
Licensing Contact: Whitney Hastings;
301–451–7337; hastingw@mail.nih.gov
mGluR5 Tumor Mouse Model
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Description of Technology: Glutamate
receptor mGluR5 has been reported to
function in the brain. There were no
prior reports of it being involved in
melanoma. The NIH investigators have
discovered that when over expressed in
transgenic animals, mGluR5 induces
melanoma. The establishment of an
mGluR5 tumor mouse model will
provide a unique opportunity to help
elucidate the mechanisms underlying
tumor formation, and allow the study of
aggressive melanoma in animals and a
screen of potential therapeutics. Such
an mGluR5 tumor mouse model is
established at the National Institutes of
Health and is available for licensing.
Potential Commercial Applications:
• Drug screening for melanoma
therapeutics
• Research Tool
Competitive Advantage: Tumor
mouse model only available from the
NIH lab.
Development Stage:
• Prototype
• Pre-clinical
• In vivo data available (animal)
Inventors: Katherine W. Roche and
Kyu Yeong Choi (NINDS)
Publication: Choi KY, et al.
Expression of the metabotropic
glutamate receptor 5 (mGluR5) induces
melanoma in transgenic mice. Proc Natl
Acad Sci USA 2011; published ahead of
print September 6, 2011, doi:10.1073/
pnas.1107304108.
Intellectual Property: HHS Reference
No. E–123–2010/0—Research Tool.
Patent protection is not being pursued
for this technology.
Licensing Contact: Betty Tong, Ph.D.;
301–594–6565; tongb@mail.nih.gov
Monoclonal Antibodies to FCRL5
(CD307e/IRTA2/FcRH5) as
Therapeutics and Diagnostics for B-cell
Cancers
Description of Technology: The Fc
receptor-like (FCRL) genes (also known
as CD307, IRTA, FcRH, IFGP or SPAP)
encode cell membrane proteins that are
believed to play roles in immunity and
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B cell differentiation. Some FCRL genes
have been implicated in B cell
lymphomas and multiple myelomas.
Data suggest that the FCRL1–5 proteins
are expressed differently on malignant B
cells as well as subpopulations of
normal B cells. Due to this differential
expression, FCRL proteins represent
potential targets for the treatment of
cancers of a B cell origin.
This technology relates to the
development of novel monoclonal
antibodies for a specific member of the
FCRL protein family: FCRL5. FCRL5 is
normally induced on mature B cells
upon activation, but its expression is
deregulated in multiple myeloma and
Burkitt’s lymphoma. Due to the
correlation of FCRL5 overexpression
and B cell malignancies, antibodies to
FCRL5 may have value as a therapeutic
or diagnostic tool. Specifically, the
antibodies can be used as therapeutic
agents by themselves or they can be
attached to a cytotoxic agent such as
Pseudomonas exotoxin A. Alternatively,
the antibodies can be used to detect the
deregulation of FCRL5 as a means of
diagnosing B cell malignancies.
Potential Commercial Applications:
• Detection or diagnosis of B cell
cancers using monoclonal antibodies to
FCRL5
• Treatment of B cell cancers using
monoclonal antibodies to FCRL5 for
inducing antibody-dependent cell death
• Treatment of B cell cancers using
monoclonal antibodies to FCRL5 for
targeting cytotoxic agents specifically to
cancer cells (e.g., immunotoxins)
Competitive Advantages:
• No cross-reactivity with other FCRL
proteins demonstrates strong selectivity
as both a therapeutic and diagnostic
agent
• Targeted therapeutics such as
monoclonal antibodies and
immunotoxins decrease non-specific
killing of healthy, essential cells,
resulting in fewer side-effects and
healthier patients
Development Stage: Pre-clinical
Inventors: Ira H. Pastan et al. (NCI)
Publications:
1. Ise T, et al. Elevation of soluble
CD307 (IRTA2/FcRH5) protein in the
blood and expression on malignant cells
of patients with multiple myeloma,
chronic lymphocytic leukemia, and
mantle cell lymphoma. Leukemia. 2007
Jan; 21(1):169–174. [PMID 17051241]
2. Ise T, et al. Immunoglobulin
superfamily receptor translocation
associated 2 protein on lymphoma cell
lines and hairy cell leukemia cells
detected by novel monoclonal
antibodies. Clin Cancer Res. 2005 Jan
1;11(1):87–96. [PMID 15671532]
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Intellectual Property: HHS Reference
No. E–287–2004/1—U.S. Patent
7,999,077 issued 16 Aug 2011
Licensing Contact: David A.
Lambertson, Ph.D.; 301–435–4632;
lambertsond@mail.nih.gov
Potent Inhibitory RNAs for NonSurgical Treatment of Salivary Gland
Cancers
Description of Technology: In the
U.S., approximately 40,000 cases of
head and neck cancer, including
salivary gland tumors, are diagnosed
each year. Surgery with post-operative
radiotherapy is the most common
treatment for salivary gland tumors.
However, complete removal is difficult
due to the three-dimensional growth
pattern of these tumors which impedes
a surgeon’s ability to determine once the
tumor has been fully removed. Both
surgeons and patients desire minimal
surgical approaches for cosmetic
reasons, as well as to preserve nerve
function in the facial area. Thus a
significant need exists for non-surgical
approaches to treating salivary gland
tumors.
Researchers at the National Cancer
Institute, NIH, have discovered that
mucoepidermoid (MEC) salivary gland
tumors arise from a chromosomal
rearrangement which generates a fusion
oncogene, Mect1–Maml2, that functions
to alter Notch and CREB signaling
pathways. An RNAi vector has been
developed that selectively suppresses
the oncogene and inhibits growth of
certain MEC tumor cell lines containing
the oncogene by at least 90%. The RNAi
vector has no effect on cells that do not
express the oncogene. This ability of the
RNAi vectors to block the ‘‘gain-offunction’’ activity of the acquired
Mect1–Maml2 oncogene suggests new
possibilities for the diagnosis and
therapy of these cancers.
Potential Commercial Applications:
• Diagnosis of MEC salivary gland
tumors
• Treatment of MEC salivary gland
tumors
Competitive Advantages:
• Non-surgical
• Selective
• Potent
• Can be used in combination with
other known treatments, such as
radiation and chemotherapy
Development Stage:
• Pre-clinical
• In vitro data available
Inventors: Frederic Kaye (formerly
NCI), Takefumi Komiya (NCI)
Publications:
1. Tonon G, et al. t(11;19)(q21;p13)
translocation in mucoepidermoid
carcinoma creates a novel fusion
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Federal Register / Vol. 76, No. 193 / Wednesday, October 5, 2011 / Notices
product that disrupts a Notch signaling
pathway. Nat Genet. 2003
Feb;33(2):208–213. [PMID 12539049]
2. Martins C, et al. A study of
MECT1–MAML2 in mucoepidermoid
carcinoma and Warthin’s tumor of
salivary glands. J Mol Diagn. 2004
Aug;6(3):205–210. [PMID 15269296]
3. Coxon A, et al. Mect1–Maml2
fusion oncogene linked to the aberrant
activation of cyclic AMP/CREB
regulated genes. Cancer Res. 2005 Aug
15;65(16):7137–7144. [PMID 16103063]
4. Komiya T, et al. Sustained
expression of Mect1–Maml2 is essential
for tumor cell growth in salivary gland
cancers carrying the t(11;19)
translocation. Oncogene. 2006 Oct
5;25(45):6128–6132. [PMID 16652146]
5. Kaye FJ. Emerging biology of
malignant salivary gland tumors offers
new insights into the classification and
treatment of mucoepidermoid cancer.
Clin Cancer Res. 2006 Jul 1;12(13):3878–
3881. [PMID 16818681]
6. Tirado Y, et al. CRTC1/MAML2
fusion transcript in high grade
mucoepidermoid carcinomas of salivary
and thyroid glands and Warthin’s
tumors: implications for histogenesis
and biologic behavior. Genes
Chromosomes Cancer. 2007
Jul;46(7):708–715. [PMID 17437281]
7. Komiya T, et al. Enhanced activity
of the CREB co-activator Crtc1 in LKB1
null lung cancer. Oncogene. 2010 Mar
18;29(11):1672–1680. [PMID 20010869]
Intellectual Property: HHS, Reference
No. E–086–2003/0 —
• U.S. Patent No. 7,553,822 issued 30
June 2009
• U.S. Patent Application No. 12/
493,901 filed 29 June 2009
Licensing Contact: Patrick McCue,
Ph.D.; 301–435–5560;
mccuepat@mail.nih.gov
Dated: September 29, 2011.
Richard U. Rodriguez,
Director, Division of Technology Development
and Transfer, Office of Technology Transfer,
National Institutes of Health.
[FR Doc. 2011–25734 Filed 10–4–11; 8:45 am]
BILLING CODE 4140–01–P
DEPARTMENT OF HEALTH AND
HUMAN SERVICES
mstockstill on DSK4VPTVN1PROD with NOTICES
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.
SUMMARY:
VerDate Mar<15>2010
19:11 Oct 04, 2011
Jkt 226001
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.
Humanized Monoclonal Antibodies
Efficient for Neutralization of TickBorne Encephalitis Virus (TBEV)
Description of Technology: TBEV
causes serious illnesses from meningitis
to meningo-encephalitis, totaling 3,000
cases of hospitalization in Europe and
between 5,000–10,000 cases in Russia
reported every year. The Far Eastern
hemorrhagic TBEV strains are
associated with a mortality rate
(between 1–2%), higher than other
strains isolated in the Siberia or Western
Europe. There is a high proportion (up
to 46%) of TBEV patients with
temporary or permanent neurological
sequelae. The number of TBEV
infections has increased steadily and
TBEV cases have been reported in new
areas, probably reflecting an increased
spread of vector tick species. Prevention
of TBEV infections has been carried out
in a few countries in Europe by
immunization using an inactivated
TBEV vaccine. The vaccine carries a
high manufacturing cost and requires a
regimen of multiple doses, and for this
reason, vaccination is not generally
carried out. The materials disclosed are
humanized monoclonal antibodies
derived from TBEV-neutralizing Fab
antibodies isolated from infected
chimpanzees by repertoire cloning. One
antibody in particular, MAb 2E6, has
been demonstrated to bind to and
neutralize a TBEV/dengue type 4 virus
chimera (via interaction with the TBEV
antigenic determinants) as well as the
related Langat virus. Protection against
TBEV/DEN–4 infection and Langat
infection has been demonstrated using
animal models of infection. The
antibodies disclosed, in particular MAb
2E6, have the potential for use as
prophylactic and therapeutic agents
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against TBEV and Langat virus.
Additionally, these antibodies may be
suitable as diagnostic reagents for the
detection of TBEV and/or Langat virus.
Potential Commercial Applications:
• TBEV Prophylaxis.
• TBEV Therapy.
• TBEV Diagnostics.
Competitive Advantages:
• Cost effective alternative to existing
vaccine.
• Fully humanized antibody.
• Strongly neutralizing antibody.
• Efficient production methods.
Development Stage:
• Pre-clinical.
• In vitro data available.
• In vivo data available (animal).
Inventors: C. J. Lai, Robert Purcell,
Alexander Pletnev (NIAID).
Intellectual Property: HHS Reference
No. E–231–2011/0—Research Tool.
Patent protection is not being pursued
for this technology.
Licensing Contact: Peter Soukas; 301–
435–4646; soukasp@mail.nih.gov
Collaborative Research Opportunity:
The NIAID is seeking statements of
capability or interest from parties
interested in collaborative research to
further develop, evaluate or
commercialize TBEV monoclonal
antibodies. For collaboration
opportunities, please contact Wade
Williams at 301–827–0258.
Rapid Molecular Assays for Specific
Detection and Quantitation of Loa Loa
Microfilaremia
Description of Technology: The risk of
fatal reactions in some infected
individuals administered drug
treatments for Loa loa infection, and the
lack of accurate, convenient, diagnostics
for this infection have thwarted efforts
to eradicate the disease. Time
consuming, labor intensive and training
intensive microscope-based analysis of
blood samples is the standard available
diagnostic for Loa loa infection. This
new assay technology introduces an
easy to use, species-specific, highly
sensitive, diagnostic that is able to be
performed with minimal training.
Positive test results may be indicated by
an easily visualized color change and
this test may be run without the need
for expensive equipment such as a
thermocycler. Because this test is rapid,
cost efficient, labor efficient, accurate,
and simple to run and read, it may be
readily incorporated into portable pointof-care formats. These attributes make it
ideally suited for use in locations where
Loa loa infection is endemic. These
advantages may lead to this technology
becoming the new standard for
diagnosis of Loa loa infections and a
valuable tool, in control programs, to
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]]>Agencies
[Federal Register Volume 76, Number 193 (Wednesday, October 5, 2011)]
[Notices]
[Pages 61714-61717]
From the Federal Register Online via the Government Printing Office [www.gpo.gov]
[FR Doc No: 2011-25734]
-----------------------------------------------------------------------
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.
-----------------------------------------------------------------------
[[Page 61715]]
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.
Platform Technology Using Ubiquitin To Improve the Delivery and
Efficacy of Cytosolic Targeted Toxins
Description of Technology: Targeted toxins (TT) are hybrid protein
drugs consisting of ligands that bind to the surface of cancer cells
and deliver polypeptide toxins that kill malignant cells by
inactivating cytosolic protein synthesis and inducing cell death. A
major challenge in the construction of targeted toxins is reducing the
nonspecific binding of the toxin moiety to normal tissues and
increasing the cytotoxicity of the treatment.
To address these issues, the NIH inventors have identified that the
protein ubiquitin, a small protein in eukaryotic cells that plays a
role in protein recycling, can separate the targeting moiety and the
catalytic moiety of a TT in the cytosol of cells. By decoupling the two
moieties, the cytotoxicity of the TT treatment can be greatly increased
since the catalytic domain remains longer in the cytosol. This
technology would be highly useful for all TT and immunotoxins that
access the cytosol to either affect cytosolic targets or traffic to
further sites of action. To validate this approach, the inventors have
tested ubiquitin variants within a TT consisting of anthrax toxin
lethal factor N-terminus (LFn) and Pseudomonas exotoxin A catalytic
domain (PEIII). Here, they show that the intracellular release of the
PEIII (catalytic moiety) is achievable and that ubiquitination of the
TT controls the persistence of the TTs in the cytosol and thus controls
the observed cytotoxicity.
Potential Commercial Applications:
Chimeric or fusion molecules for increasing the efficacy
and cytotoxicity of targeted toxins and immunotoxins.
Methods for cytosol delivery of targeted toxins to target
cells.
Competitive Advantages:
Broadly applicable to all cytotoxic immunoconjugates.
Increased stability and cytotoxicity of the TT without
affecting the delivery or specificity of the treatment.
Therapeutic access to the cytosol and/or trafficking to
further sites of action such as the nucleus.
Rapid cytosolic release of the catalytic moiety and
degradation of the targeting moiety.
Development Stage:
Pre-clinical
In vitro data available
Inventors: Christopher Bachran (NIAID), Stephen Leppla (NIAID),
Shi-hui Liu (NIAID), Thomas Morley
Publications:
1. Tcherniuk S, et al. Construction of tumor-specific toxins using
ubiquitin fusion technique. Mol Ther. 2005 Feb;11(2):196-204. [PMID
15668131]
2. Wang F. Selective cytotoxicity to HER2-positive tumor cells by a
recombinant e23sFv-TD-tBID protein containing a furin cleavage
sequence. Clin Cancer Res. 2010 Apr 15;16(8):2284-2294. [PMID 20371697]
3. Heisler I. A cleavable adapter to reduce nonspecific
cytotoxicity of recombinant immunotoxins. Int J Cancer. 2003 Jan
10;103(2):277-282. [PMID 12455044]
Intellectual Property: HHS Reference No. E-150-2011/0--U.S.
Provisional Application No. 61/473,450 filed 08 April 2011
Related Technologies:
HHS Reference No. E-293-1999--Mutated Anthrax Toxin
Protective Antigen Proteins That Specifically Target Cells Containing
High Amounts of Cell-Surface Metalloproteinases or Plasminogen
Activator Receptors (Leppla/NIAID)
HHS Reference No. E-070-2007--Human Cancer Therapy Using
Engineered Metalloproteinase-Activated Anthrax Lethal Toxin That Target
Tumor Vasculature (Leppla/NIAID)
HHS Reference No. E-059-2004--Multimeric Protein Toxins to
Target Cells Having Multiple Identifying Characteristics (Leppla/NIAID)
Licensing Contact: Whitney Hastings; 301-451-7337;
hastingw@mail.nih.gov
NOX5 Immunogenic Peptides and Monoclonal Antibodies for the Detection
of Cancer and Inflammatory Responses
Description of Technology: The membrane-associated NADPH oxidase 5
(NOX5) protein is expressed in various fetal tissues, uterus, testis,
spleen, lymph nodes and endothelial cells. In addition, the reactive
oxygen species (ROS) generated by NOX5 have been shown to participate
in signaling cascades regulating proliferation in several cancers and
pre-cancerous conditions, such as hairy cell leukemia, melanoma,
prostate cancer, and Barret's esophagus. Further, excess ROS produced
by NOX5 has been associated with coronary artery disease, inflammation,
and atherosclerosis.
The present invention discloses the identification and
characterization of a purified monoclonal antibody against NOX5
protein. This NOX5 antibody can detect endogenous levels of NOX5 in
human cells and could aid in studies and diagnostic tests of NOX5-based
redox signaling involved in cancer, cell growth and differentiation, as
well as angiogenic and inflammatory responses. In addition, the NOX5
antibody may have therapeutic applications (e.g. anti-inflammatory,
antiangiogenic, or antiproliferative activity) by interfering with NOX5
activation at the cell surface.
Potential Commercial Applications:
Diagnostic for the detection of NOX5 in human cells and
NOX5-based redox signaling
Antibody can be used in ELISA, Western Blot,
Immunofluorescence, Immunoprecipitation and Immunohistochemistry
Tool to aid in the understanding of NOX5's functional
significance in human physiology and pathophysiology
Possible therapeutic for the treatment of various human
diseases associated with NOX5 and/or ROS
Competitive Advantages:
Antibody is the only mouse monoclonal commercially
available to the best of our knowledge
Antibody is highly specific in recognizing the NOX5
protein with greater efficiency and the accurate detection compared to
other Nox5 antibodies
Development Stage: Pre-clinical
Inventors: James H. Doroshow, Krishnendu K. Roy, Smitha Antony
(NCI)
Publications:
1. Kamiguti AS, et al. Expression and activity of NOX5 in the
circulating malignant B cells of hairy cell leukemia. J Immunol. 2005
Dec 15;175(12):8424-8430. [PMID: 16339585]
2. Brar SS, et al. NOX5 NAD(P)H oxidase regulates growth and
apoptosis in DU 145 prostate cancer cells. Am J Physiol Cell Physiol.
2003 Aug;285(2):C353-C369. [PMID: 12686516]
[[Page 61716]]
3. Hong J, et al. Bile acid reflux contributes to development of
esophageal adenocarcinoma via activation of phosphatidylinositol-
specific phospholipase Cgamma2 and NADPH oxidase NOX5-S. Cancer Res.
2010 Feb 1;70(3):1247-1255. [PMID: 20086178]
Intellectual Property: HHS Reference No. E-149-2011/0--U.S.
Provisional Application No. 61/471,596 filed 04 April 2011
Licensing Contact: Whitney Hastings; 301-451-7337;
hastingw@mail.nih.gov
mGluR5 Tumor Mouse Model
Description of Technology: Glutamate receptor mGluR5 has been
reported to function in the brain. There were no prior reports of it
being involved in melanoma. The NIH investigators have discovered that
when over expressed in transgenic animals, mGluR5 induces melanoma. The
establishment of an mGluR5 tumor mouse model will provide a unique
opportunity to help elucidate the mechanisms underlying tumor
formation, and allow the study of aggressive melanoma in animals and a
screen of potential therapeutics. Such an mGluR5 tumor mouse model is
established at the National Institutes of Health and is available for
licensing.
Potential Commercial Applications:
Drug screening for melanoma therapeutics
Research Tool
Competitive Advantage: Tumor mouse model only available from the
NIH lab.
Development Stage:
Prototype
Pre-clinical
In vivo data available (animal)
Inventors: Katherine W. Roche and Kyu Yeong Choi (NINDS)
Publication: Choi KY, et al. Expression of the metabotropic
glutamate receptor 5 (mGluR5) induces melanoma in transgenic mice. Proc
Natl Acad Sci USA 2011; published ahead of print September 6, 2011,
doi:10.1073/pnas.1107304108.
Intellectual Property: HHS Reference No. E-123-2010/0--Research
Tool. Patent protection is not being pursued for this technology.
Licensing Contact: Betty Tong, Ph.D.; 301-594-6565;
tongb@mail.nih.gov
Monoclonal Antibodies to FCRL5 (CD307e/IRTA2/FcRH5) as Therapeutics and
Diagnostics for B-cell Cancers
Description of Technology: The Fc receptor-like (FCRL) genes (also
known as CD307, IRTA, FcRH, IFGP or SPAP) encode cell membrane proteins
that are believed to play roles in immunity and B cell differentiation.
Some FCRL genes have been implicated in B cell lymphomas and multiple
myelomas. Data suggest that the FCRL1-5 proteins are expressed
differently on malignant B cells as well as subpopulations of normal B
cells. Due to this differential expression, FCRL proteins represent
potential targets for the treatment of cancers of a B cell origin.
This technology relates to the development of novel monoclonal
antibodies for a specific member of the FCRL protein family: FCRL5.
FCRL5 is normally induced on mature B cells upon activation, but its
expression is deregulated in multiple myeloma and Burkitt's lymphoma.
Due to the correlation of FCRL5 overexpression and B cell malignancies,
antibodies to FCRL5 may have value as a therapeutic or diagnostic tool.
Specifically, the antibodies can be used as therapeutic agents by
themselves or they can be attached to a cytotoxic agent such as
Pseudomonas exotoxin A. Alternatively, the antibodies can be used to
detect the deregulation of FCRL5 as a means of diagnosing B cell
malignancies.
Potential Commercial Applications:
Detection or diagnosis of B cell cancers using monoclonal
antibodies to FCRL5
Treatment of B cell cancers using monoclonal antibodies to
FCRL5 for inducing antibody-dependent cell death
Treatment of B cell cancers using monoclonal antibodies to
FCRL5 for targeting cytotoxic agents specifically to cancer cells
(e.g., immunotoxins)
Competitive Advantages:
No cross-reactivity with other FCRL proteins demonstrates
strong selectivity as both a therapeutic and diagnostic agent
Targeted therapeutics such as monoclonal antibodies and
immunotoxins decrease non-specific killing of healthy, essential cells,
resulting in fewer side-effects and healthier patients
Development Stage: Pre-clinical
Inventors: Ira H. Pastan et al. (NCI)
Publications:
1. Ise T, et al. Elevation of soluble CD307 (IRTA2/FcRH5) protein
in the blood and expression on malignant cells of patients with
multiple myeloma, chronic lymphocytic leukemia, and mantle cell
lymphoma. Leukemia. 2007 Jan; 21(1):169-174. [PMID 17051241]
2. Ise T, et al. Immunoglobulin superfamily receptor translocation
associated 2 protein on lymphoma cell lines and hairy cell leukemia
cells detected by novel monoclonal antibodies. Clin Cancer Res. 2005
Jan 1;11(1):87-96. [PMID 15671532]
Intellectual Property: HHS Reference No. E-287-2004/1--U.S. Patent
7,999,077 issued 16 Aug 2011
Licensing Contact: David A. Lambertson, Ph.D.; 301-435-4632;
lambertsond@mail.nih.gov
Potent Inhibitory RNAs for Non-Surgical Treatment of Salivary Gland
Cancers
Description of Technology: In the U.S., approximately 40,000 cases
of head and neck cancer, including salivary gland tumors, are diagnosed
each year. Surgery with post-operative radiotherapy is the most common
treatment for salivary gland tumors. However, complete removal is
difficult due to the three-dimensional growth pattern of these tumors
which impedes a surgeon's ability to determine once the tumor has been
fully removed. Both surgeons and patients desire minimal surgical
approaches for cosmetic reasons, as well as to preserve nerve function
in the facial area. Thus a significant need exists for non-surgical
approaches to treating salivary gland tumors.
Researchers at the National Cancer Institute, NIH, have discovered
that mucoepidermoid (MEC) salivary gland tumors arise from a
chromosomal rearrangement which generates a fusion oncogene, Mect1-
Maml2, that functions to alter Notch and CREB signaling pathways. An
RNAi vector has been developed that selectively suppresses the oncogene
and inhibits growth of certain MEC tumor cell lines containing the
oncogene by at least 90%. The RNAi vector has no effect on cells that
do not express the oncogene. This ability of the RNAi vectors to block
the ``gain-of-function'' activity of the acquired Mect1-Maml2 oncogene
suggests new possibilities for the diagnosis and therapy of these
cancers.
Potential Commercial Applications:
Diagnosis of MEC salivary gland tumors
Treatment of MEC salivary gland tumors
Competitive Advantages:
Non-surgical
Selective
Potent
Can be used in combination with other known treatments,
such as radiation and chemotherapy
Development Stage:
Pre-clinical
In vitro data available
Inventors: Frederic Kaye (formerly NCI), Takefumi Komiya (NCI)
Publications:
1. Tonon G, et al. t(11;19)(q21;p13) translocation in
mucoepidermoid carcinoma creates a novel fusion
[[Page 61717]]
product that disrupts a Notch signaling pathway. Nat Genet. 2003
Feb;33(2):208-213. [PMID 12539049]
2. Martins C, et al. A study of MECT1-MAML2 in mucoepidermoid
carcinoma and Warthin's tumor of salivary glands. J Mol Diagn. 2004
Aug;6(3):205-210. [PMID 15269296]
3. Coxon A, et al. Mect1-Maml2 fusion oncogene linked to the
aberrant activation of cyclic AMP/CREB regulated genes. Cancer Res.
2005 Aug 15;65(16):7137-7144. [PMID 16103063]
4. Komiya T, et al. Sustained expression of Mect1-Maml2 is
essential for tumor cell growth in salivary gland cancers carrying the
t(11;19) translocation. Oncogene. 2006 Oct 5;25(45):6128-6132. [PMID
16652146]
5. Kaye FJ. Emerging biology of malignant salivary gland tumors
offers new insights into the classification and treatment of
mucoepidermoid cancer. Clin Cancer Res. 2006 Jul 1;12(13):3878-3881.
[PMID 16818681]
6. Tirado Y, et al. CRTC1/MAML2 fusion transcript in high grade
mucoepidermoid carcinomas of salivary and thyroid glands and Warthin's
tumors: implications for histogenesis and biologic behavior. Genes
Chromosomes Cancer. 2007 Jul;46(7):708-715. [PMID 17437281]
7. Komiya T, et al. Enhanced activity of the CREB co-activator
Crtc1 in LKB1 null lung cancer. Oncogene. 2010 Mar 18;29(11):1672-1680.
[PMID 20010869]
Intellectual Property: HHS, Reference No. E-086-2003/0 --
U.S. Patent No. 7,553,822 issued 30 June 2009
U.S. Patent Application No. 12/493,901 filed 29 June 2009
Licensing Contact: Patrick McCue, Ph.D.; 301-435-5560;
mccuepat@mail.nih.gov
Dated: September 29, 2011.
Richard U. Rodriguez,
Director, Division of Technology Development and Transfer, Office of
Technology Transfer, National Institutes of Health.
[FR Doc. 2011-25734 Filed 10-4-11; 8:45 am]
BILLING CODE 4140-01-P
