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

Federal Register: October 3, 2008 (Volume 73, Number 193)             
                  Page 57635-57637

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

[[Page 57636]]

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.

Matriptase Hypomorphic Mouse Model of a Human Ichthyosis

    Description of Technology: Available for licensing are mice with 
greatly reduced levels of matriptase, a membrane protease involved in 
epithelial development, immune function, and carcinogenesis. These mice 
were created to study autosomal recessive ichthyosis with hypotricosis 
(ARIH), an inherited human disease that has been linked to a mutation 
in the ST14 gene that encodes matriptase. These mice manifest the same 
defects seen in people afflicted by ARIH, so it can be an effective 
model for studying the role of matriptase in disorders that affect skin 
development.
    Applications:
     Research tool for skin development research.
     Model to develop and test therapeutics for treating skin 
disorders, including skin cancer.
     Model immunity and allergy.
    Advantages: Well characterized animal model closely related to a 
human genetic disorder.
    Market: Ichthyosis is a series of genetic skin diseases 
characterized by dry, thickened, scaling skin that affects more than 
one million Americans. Presently, there is no cure for ichthyosis, only 
treatments to help manage symptoms.
    Development Status: Well characterized mouse model of human ARIH.
    Inventors: Thomas H. Bugge (NIDCR) et al.
    Publication: K List et al. Autosomal ichthyosis with hypotrichosis 
syndrome displays low matriptase proteolytic activity and is 
phenocopied in ST14 hypomorphic mice. J Biol Chem. 2007 Dec 
14;282(50):36714-36723.
    Patent Status: HHS Reference No. E-323-2008/0--Biological Material. 
Patent protection is not being pursued for this technology.
    Licensing Status: Available for non-exclusive licensing under a 
Biological Materials License Agreement.
    Licensing Contact: Adaku Nwachukwu, J.D.; 301-435-5560; 
madua@mail.nih.gov.
    Collaborative Research Opportunity: The National Institute of 
Dental and Craniofacial Research, Oral and Pharyngeal Cancer Branch, is 
seeking statements of capability or interest from parties interested in 
collaborative research to further develop, evaluate, or commercialize 
this technology. Please contact David W. Bradley, Ph.D. at 301-402-0540 
or bradleyda@nidcr.nih.gov for more information.

Prostatic Adenocarcinoma Cells Expressing or Lacking the Tumor 
Suppressor Gene PTEN

    Description of Technology: PTEN is a tumor suppressor gene that is 
frequently deleted or mutated in a variety of human cancers, including 
prostate, breast, endometrial, lung, and ovarian cancers. In prostate 
cancer cells, PTEN deletion is the most common event observed. The loss 
of PTEN is thought to play and important role in tumor cell 
proliferation and metastasis due to a lack of control of the signaling 
pathways that mediate cellular processes such as apoptosis and 
migration. Previously PTEN had been shown to downregulate cyclin D1 
expression as well as regulate p53 protein levels and transcriptional 
activity, and recently the inventors of this technology have shown that 
PTEN decreases surface IGF-IR protein levels in prostate cancer cell 
lines in an Akt-independent manner.
    PC3 cells are prostate cancer cells that lack PTEN gene. This 
technology describes PC3 cells that overexpress the PTEN gene. These 
cell lines can be used to study the role of the PTEN gene in cancer 
growth and metastasis.
    Market:
     Prostate cancer is the most common type of cancer found in 
American men, and it has been estimated that there were more than 
230,000 new cases in the U.S. in 2007. Prostate cancer is also the 
second leading cause of cancer death in men.
     In the U.S. over 2 million women have been treated for 
breast cancer, with more than 200,000 women diagnosed in the year 2007 
alone. Breast cancer is the second leading cause of cancer death in 
women.
    Development Status: The technology is currently in the pre-clinical 
stage of development.
    Inventors: Derek LeRoith and Michael Quon (NIDDK).
    Publication: H Zhao et al. PTEN inhibits cell proliferation and 
induces apoptosis by downregulating cell surface IGF-IR expression in 
prostate cancer cells. Oncogene 2004 Jan 22;23(3):786-794.
    Patent Status: HHS Reference No. E-292-2008/0--Research Tool. 
Patent protection is not being pursued for this technology.
    Licensing Status: Available for licensing.
    Licensing Contact: Whitney A. Hastings; 301-451-7337; 
hastingw@mail.nih.gov.

Fully Human Anti-Human NKG2D Monoclonal Antibody

    Description of Technology: Available for licensing is a fully human 
monoclonal antibody (KYK-2.0 IgG1) with high specificity and affinity 
to human NKG2D, a stimulatory or costimulatory receptor located on the 
cell surface of natural killer (NK) cells and CD8+ T cells. NKG2D plays 
a role in mediating immune responses in autoimmune and infectious 
diseases and cancer and it makes NKG2D an attractive target for 
therapeutic intervention. Nonetheless, monoclonal antibodies to NKG2D 
that are suitable for clinical investigations have not been available. 
In solution, KYK-2.0 IgG1 interferes with the cytolytic activity of 
human NK cells. When immobilized, KYK-2.0 IgG1 induces human NK cell 
activation. The dual antagonistic and agonistic activity promises a 
broad range of therapeutic applications.
    Application: Therapeutic fully human monoclonal antibody for a 
variety of indications including autoimmune and infectious diseases, 
cancer, and transplantation.
    Advantage: The dual antagonistic and agonistic activity in concert 
with low immunogenicity suggests broad and potent therapeutic utility 
of KYK-2.0 IgG1 and its derivatives.
    Development Status: The technology is currently in the pre-clinical 
stage of development.
    Market:
     Monoclonal antibody market is one of the fastest growing 
and most lucrative sectors of the pharmaceutical industry with a 48.1% 
growth between 2003 and 2004.
     Monoclonal antibody market is estimated to be worth $30.3 
billion in 2010.
    Inventors: Christoph Rader and Ka Yin Kwong (NCI)
    Related Publication: KY Kwong, S Baskar, H Zhang, CL Mackall, C 
Rader. Generation, affinity maturation, and characterization of a human 
anti-human NKG2D monoclonal antibody with dual antagonistic and 
agonistic activity. J Mol

[[Page 57637]]

Biol., in press (available online 2008 Sep 16, doi:10.1016/
j.jmb.2008.09.008).
    Patent Status: U.S. Provisional Application No. 61/086,027 filed 04 
Aug 2008 (HHS Reference No. E-211-2008/0-US-01).
    Licensing Status: Available for exclusive or non-exclusive 
licensing.
    Licensing Contact: Jennifer Wong; 301-435-4633; 
wongje@mail.nih.gov.
    Collaborative Research Opportunity: The Experimental 
Transplantation and Immunology Branch, Center for Cancer Research, 
National Cancer Institute is seeking statements of capability or 
interest from parties interested in collaborative research to further 
develop, evaluate, or commercialize the fully human anti-human NKG2D 
monoclonal antibody KYK-2.0 IgG1. Please contact John D. Hewes, Ph.D. 
at 301-435-3121 or hewesj@mail.nih.gov for more information.

Methods for the Detection and Treatment of Lung Cancer

    Description of Technology: Lung cancer is the third most common 
malignant disease and the first leading cause of cancer death in the 
western world. Non-small cell lung cancer (NSCLC) is one of the leading 
causes of death accounting for nearly 30% of all cancer deaths. Despite 
considerable research, lung cancer remains difficult to diagnose and 
treat effectively. Current chemotherapeutic regimens provide poor 
survival benefits and the unmet clinical need among lung cancer 
patients is very high. The prognosis is very bleak since most patients 
are diagnosed with lung cancer at a late stage.
    The inventors have discovered that approximately 20% of common 
adult NSCLC have an aberrant activation of CRTC gene members with 
marked induction of CRTC regulated genes. CRTC activation is linked 
with the loss of LKB1/STK11 kinases which results in CRTC 
underphosphorylation and enhanced nuclear localization. As the LKB1/
STK11 signaling pathways has been exploited in potential cancer 
therapeutic treatments, this novel unrecognized consequence the loss of 
LKB1/STK11 function associated with aberrant CRTC activation in cancer 
offers new candidate diagnostic and therapeutic targets for NSCLC.
    Applications:
     Novel cancer diagnostics and therapeutic treatments.
     Method to detect and treat lung cancer.
    Development Status: The technology is currently in the pre-clinical 
stage of development.
    Market:
     Lung cancer is the leading cause of cancer deaths among 
both men and women in the U.S.
     The NSCLC market was estimated to be worth US$3.7 billion 
in 2006 and will increase by 17% by 2012.
    Inventors: Frederic Kaye and Amy Coxon (NCI).
    Patent Status: U.S. Provisional Application No.61/036,830 filed 13 
Mar 2008 (HHS Reference No. E-069-2008/0-US-01).
    Licensing Status: Available for exclusive or non-exclusive 
licensing.
    Licensing Contact: Jennifer Wong; 301-435-4633; 
wongje@mail.nih.gov.

Human Perilipin Proteins

    Description of Technology: Perilipins are important regulators of 
lipid storage in fat cells. These proteins stabilize fat droplets and 
control their breakdown by controlling access of lipid-degrading 
enzymes. Since these proteins are central to the storage and breakdown 
of body fat it very likely that they are crucial for the regulation of 
body weight. Perilipin expression is elevated in obese animals and 
humans. Mutations in the perilipin gene are associated with increased 
risk of obesity in women. Importantly, when the perilipin gene is 
inactivated the obesity of model mice is reversed. Therefore, perilipin 
could be a good candidate for therapeutic targeting to treat obesity in 
humans.
    This NIH invention claims DNA sequences of splice variants that 
code for human perilipin protein isoforms and methods of expressing the 
recombinant protein in bacteria or mammalian cells. It also claims 
substantially purified perilipin proteins and methods for detecting 
their presence in a biological sample.
    Applications:
     Drug development for obesity.
     Diagnostics for detection of perilipins.
     Antigens for antibody production.
     Markers for identifying true adipocytes.
    Advantages:
     Cloned DNA sequences ready for protein expression.
     Isoforms allow greater flexibility in designing 
therapeutics.
    Development Status: Pre-clinical.
    Inventors: Constantine Londos, Andrew S. Greenberg, Alan R. Kimmel, 
John J. Egan (NIDDK).
    Related Publication: AS Greenberg et al. Perilipin, a major 
hormonally regulated adipocyte-specific phosphoprotein associated with 
the periphery of lipid storage droplets. J Biol Chem. 1991 Jun 
15;266(17):11341-11346.
    Patent Status:
     U.S. Patent No. 6,074,842 issued 13 Jun 2000 (HHS 
Reference No. E-111-1991/0-US-03).
     U.S. Patent No. 5,585,462 issued 17 Dec 1996 (HHS 
Reference No. E-111-1991/1-US-01).
    Licensing Status: Available for exclusive or non-exclusive 
licensing.
    Licensing Contact: Surekha Vathyam, PhD; 301-435-4076; 
vathyams@mail.nih.gov.

     Dated: September 29, 2008.
Richard U. Rodriguez,
Director, Division of Technology Development and Transfer, Office of 
Technology Transfer, National Institutes of Health.
[FR Doc. E8-23436 Filed 10-2-08; 8:45 am]

BILLING CODE 4140-01-P