Notice (B): Government-Owned Inventions; Availability for Licensing

Federal Register: March 5, 2010 (Volume 75, Number 43)            
                  Page 10280-10281

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.

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    Related Publication: Unpublished.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; 
sstand@od.nih.gov.

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; 
Fatima.Sayyid@nih.hhs.gov.

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; 
tarak@mail.nih.gov.
    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 
steroids@helix.nih.gov 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; vepas@mail.nih.gov.
    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 jwess@helix.nih.gov 
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