[Federal Register Volume 75, Number 43 (Friday, March 5, 2010)]
[Notices]
[Pages 10280-10281]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 2010-4758]
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DEPARTMENT OF HEALTH AND HUMAN SERVICES
National Institutes of Health
Government-Owned Inventions; Availability for Licensing
AGENCY: National Institutes of Health, Public Health Service, HHS.
ACTION: Notice.
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SUMMARY: The inventions listed below are owned by an agency of the U.S.
Government and are available for 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.
Monoclonal Antibody to Mouse Toll-Like Receptor 3 (TLR3) Extracellular
Domain
Description of Invention: The best available antibody for labeling
cells expressing mouse TLR3 is now available for licensing. It is a rat
IgG2a monoclonal antibody that was generated to the extracellular
domain of mouse TLR3 and specifically binds mouse TLR3 in permeabilized
cells. TLR3 is located in endosomes and recognizes double-stranded RNA,
a molecular signature of many viruses. This antibody would be of
interest to anyone studying TLR3 distribution and localization in
studies related to innate immunity and dendritic cell function.
Applications:
Fluorescence-Activated Cell Sorting (FACS).
Immunofluorescence.
Immunocytochemistry.
Inventors: David M. Segal, Yan Wang, Ivett Jelinek (NCI).
Related Publication: Unpublished.
Patent Status: HHS Reference No. E-038-2010/0--Research Tool.
Patent protection is not being pursued for this technology.
Licensing Status: This technology is available as a research tool
(hybridoma) under a Biological Materials License.
Licensing Contact: Steve Standley, Ph.D.; 301-435-4074;
[email protected].
Haptoglobin for Control of the Blood Pressure Response to Plasma Free
Hemoglobin
Description of Invention: Release of hemoglobin into the blood is a
central pathophysiologic event contributing to morbidity and mortality
in chronic and acute hemolytic anemias and severe malaria. These
toxicities arise from hemoglobin-related scavenging of nitric oxide, a
blood vessel vasodilator, and peroxidative chain reactions that lead to
damage of the surrounding tissues. Animal models have demonstrated both
an attenuation of the hypertensive response due to nitric oxide
scavenging and a prevention of peroxidative toxicity.
Compartmentalization of hemoglobin, rather than short-lived nitric
oxide-based drugs, may represent a new therapeutic paradigm in
countering the pathophysiological side effects associated with free
hemoglobin.
This technology identifies haptoglobin and haptoglobin mimetics as
potential therapeutics for high blood pressure and intravascular
toxicity due to release of hemoglobin from red blood cells. It provides
a novel process in which free hemoglobin is compartmentalized within
the haptoglobin molecule. Therapeutic proof-of-principle has been
demonstrated for this technology in dog and guinea pig models.
Potential Applications and Advantages:
[[Page 10281]]
A therapeutic for high blood pressure and intravascular
toxicity resulting from free hemoglobin in the blood (as associated
with hemolytic anemias such as sickle cell disease, paroxysmal
nocturnal hemoglobinuria, and thalassemia, as well as cerebral
malaria).
Compartmentalization of hemoglobin may minimize toxicities
associated with cell-free hemoglobin, in contrast to currently
available nitric oxide-based drugs which seek to counterbalance but not
minimize these toxicities.
Development Status: Pre-clinical stage.
Inventors: Abdu I. Alayash (FDA) et al.
Publication: FS Boretti et al. Sequestration of extracellular
hemoglobin within a haptoglobin complex decreases its hypertensive and
oxidative effects in dogs and guinea pigs. J Clin Invest. 2009
Aug;119(8):2271-2280. [PubMed: 19620788]
Patent Status: U.S. Provisional Application No. 61/226,602 filed 17
Jul 2009 (HHS Reference No. E-256-2009/0-US-01)
Licensing Status: Available for licensing.
Licensing Contact: Fatima Sayyid, M.H.P.M.; 301-435-4521;
[email protected].
A Biomarker and Therapeutic Target for Ovarian Cancer
Description of Invention: This technology provides methods of
diagnosing or treating certain ovarian cancers using STAMP, a steroid
cofactor.
According to the American Cancer Society, ovarian cancer is the
ninth most common cancer in the United States, but is the fifth most
deadly, with an estimated 14,600 deaths in 2009; the 10-year survival
rate for this cancer is less than 40 percent. The majority of ovarian
cancer cases are diagnosed at late-stage disease, due to the difficulty
in detecting this cancer in its early stages, when symptoms are subtle.
There are currently no effective methods for early-stage diagnosis
of ovarian cancer. Diagnosis is usually made through a combination of
physical examination, ultrasound imaging, and a blood test for the
tumor marker CA-125. The CA-125 test only returns a true positive
result for about 50% of early-stage ovarian cancers, and may be
elevated in other conditions not related to cancer, so it is not an
adequate early detection tool when used alone.
The inventors previously discovered STAMP, a steroid cofactor that
modulates glucocorticoid receptor-mediated gene induction and
repression. The inventors have now shown that STAMP mRNA levels are
elevated in ovarian cancer samples, including early-stage cancers. They
have also found that in a subset of ovarian cancer cell lines,
introduction of STAMP siRNAs slows cell proliferation. These findings
suggest that STAMP may be useful as a biomarker to detect early stage
cancer in ovarian tissues, and is also promising as a therapeutic
target for a subset of ovarian cancers.
Applications:
Development of an early-stage diagnostic test for ovarian
cancer.
Development of an siRNA-based therapy for ovarian cancer.
Development Status: Discovery stage.
Market: Ovarian cancer is the fifth most-deadly cancer in the
United States, and over 21,000 new U.S. cases were diagnosed in 2009.
Inventors: S. Stoney Simons et al. (NIDDK).
Related Publications: In preparation.
Patent Status: U.S. Provisional Application No. 61/185,503 filed 09
Jun 2009 (HHS Reference No. E-226-2009/0-US-01).
Licensing Status: Available for licensing.
Licensing Contact: Tara Kirby, PhD; 301-435-4426;
[email protected].
Collaborative Research Opportunity: The National Institute of
Diabetes and Digestive and Kidney Disease Steroid Hormones Section is
seeking statements of capability or interest from parties interested in
collaborative research to further develop, evaluate, or commercialize
STAMP, a steroid cofactor. Please contact S. Stoney Simons at
[email protected] for more information.
Conditional V2 Vasopressin Receptor Mutant Mice as a Model To Study X-
linked Nephrogenic Diabetes Insipidus (XNDI)
Description of Invention: X-linked nephrogenic diabetes insipidus
(XNDI) is a severe kidney disease caused by inactivating mutations in
the V2 vasopressin receptor (V2R) gene that result in the loss of renal
urine-concentrating ability. At present, no specific pharmacological
therapy has been developed for XNDI, primarily due to the lack of
suitable animal models. This technology provides a unique and viable
animal model of XNDI. NIH investigators have generated mice in which
the V2R gene could be conditionally deleted during adulthood by
administration of 4-OH-tamoxifen. Radioligand-binding studies confirmed
the lack of V2R-binding sites in kidneys following 4-OH-tamoxifen
treatment, and further analysis indicated that upon V2R deletion, adult
mice displayed all characteristic symptoms of XNDI, including polyuria,
polydipsia, and resistance to the antidiuretic actions of vasopressin.
Gene expression analysis suggested that activation of renal EP4
PGE2 receptors might compensate for the lack of renal V2R activity in
XNDI mice. Strikingly, both acute and chronic treatment of the mutant
mice with a selective EP4 receptor agonist greatly reduced all major
manifestations of XNDI, including changes in renal morphology. These
physiological improvements were most likely due to a direct action on
EP4 receptors expressed on collecting duct cells. These findings
illustrate the usefulness of V2R mutant mice for elucidating and
testing new strategies for the potential treatment of humans with XNDI.
Inventors: J[uuml]rgen Wess et al. (NIDDK)
Publication: Li JH, Chou CL, Li B, Gavrilova O, Eisner C,
Schnermann J, Anderson SA, Deng CX, Knepper MA, Wess J. A selective EP4
PGE2 receptor agonist alleviates disease in a new mouse model of X-
linked nephrogenic diabetes insipidus. J Clin Invest. 2009 Oct
1;119(10):3115-3126. [PubMed: 19729836]
Patent Status: HHS Reference Nos. E-174-2009/0 & E-175-2009/0--
Research Tool. Patent protection is not being pursued for this
technology.
Licensing Status: Available for licensing under a Biological
Materials License Agreement.
Licensing Contact: Suryanarayana (Sury) Vepa, Ph.D., J.D.; 301-435-
5020; [email protected].
Collaborative Research Opportunity: The National Institute of
Diabetes and Digestive and Kidney Diseases, Laboratory of Bioorganic
Chemistry, Molecular Signalling Section, is seeking statements of
capability or interest from parties interested in collaborative
research to further develop, evaluate, or commercialize this
technology. Please contact Dr. J[uuml]rgen Wess at [email protected]
for more information.
Dated: March 1, 2010.
Richard U. Rodriguez,
Director, Division of Technology Development and Transfer, Office of
Technology Transfer, National Institutes of Health.
[FR Doc. 2010-4758 Filed 3-4-10; 8:45 am]
BILLING CODE 4140-01-P