Government-Owned Inventions; Availability for Licensing, 36553-36554 [2011-15477]

Agencies

• DEPARTMENT OF HEALTH AND HUMAN SERVICES
• National Institutes of Health

[Federal Register Volume 76, Number 120 (Wednesday, June 22, 2011)]
[Notices]
[Pages 36553-36554]
From the Federal Register Online via the Government Printing Office [www.gpo.gov]
[FR Doc No: 2011-15477]


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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.

Mouse Model for Cerebral Cavernous Malformation, an Inherited Brain 
Disorder

    Description of Technology: Cerebral Cavernous Malformation (CCM) is 
a brain disease affecting up to 0.5% of the worldwide population. CCM 
is characterized by grossly dilated vessels prone to leaking and 
hemorrhage which result in severe headaches, seizures, and strokes. 
Inherited forms of the disease are due to mutations in one of three 
loci, CCM1, CCM2, and CCM3. Prior efforts to develop mice with targeted 
null mutations in Ccm1, Ccm2, or Ccm3 have been unsuccessful, as such 
mutations result in embryonic death.
    The inventors have developed the first mouse model available for 
the study of CCM, in which mouse Ccm2 can be conditionally deleted in 
blood-accessible and endothelial cells, resulting in neurological 
defects, ataxia, and brain hemorrhages consistent with the human 
disease. The model was generated through a cross of C57BL/6 Ccm2-floxed 
mice with C57BL/6 MX-1-Cre mice, which permits inducible ablation by 
polyinosinic:polycytidylic acid (pIpC).
    Inventors: Ulrich Siebenlist (NIAID) and Yoh-suke Mukoyama (NHLBI).
    Related Publications: In preparation.
    Patent Status: HHS Reference No. E-158-2011/0--Research Material. 
Patent protection is not being pursued for this technology.
    Licensing Status: Available for licensing under a Biological 
Materials License Agreement.
    Licensing Contact: Tara L. Kirby, PhD; 301-435-4426; 
tarak@mail.nih.gov.

System to Increase Consistency and Reduce Variations in Contrast and 
Sensitivity in MRI Imaging

    Description of Technology: The technology relates to the field of 
MRI. More specifically, the invention describes and claims system and 
methods related to the use of non-linear B0 shims to improve 
excitation flip angle uniformity in high field MRI. The disclosed 
system and methods can be used in conjunction with existing multi-
dimension excitation methods, including those that use parallel 
excitation to improve contrast and sensitivity in gradient echo 
magnetic resonance imaging. The technology is designed to overcome 
shortcomings associated with high field MRI, namely RF flip angle 
inhomogeneity due to wavelength effects that can lead to spatial 
variations in contrast and sensitivity.
    Applications: High field MRI.
    Advantages: The present system and methods will improve performance 
of high field MRI:
     Improve the transmit profile homogeneity, and therefore 
the uniformity of MRI images.
     The method is applicable to all MRI scanning with poor B1 
uniformity. This includes situations when B1 variations are caused by 
the coil B1 profile, by the dielectric properties of the object 
(wavelength effects), or by a combination of both.
     The method is applicable with currently available single 
or multi-channel B1 coils.
    Development Status:
     Proof of principle has been demonstrated on a prototype 
device.
     Demonstration of the application to human imaging is 
currently underway.
    Inventors: Jeff Duyn (NINDS).
    Relevant Publication: Duan Q, van Gelderen P, Duyn J. B0 
based shimming of RF flip angle in MRI. Submitted to Magnetic Resonance 
in Medicine.
    Patent Status: U.S. Provisional Application No. 61/473,610 filed 08 
Apr 2011 (HHS Reference No. E-129-2011/0-US-01).
    Licensing Status: Available for licensing and commercial 
development.
    Licensing Contacts:
     Uri Reichman, PhD, MBA; 301-435-4616; UR7a@nih.gov.
     John Stansberry, PhD; 301-435-5236; js852e@nih.gov.

Polyclonal Antibodies Against RGS7, a Regulator of G Protein Signaling, 
for Research and Diagnostic Use

    Description of Technology: Investigators at the National Institutes 
of Health have generated a polyclonal antibody against the Regulator of 
G protein Signaling Protein 7 (RGS7). The RGS7 protein regulates 
neuronal G protein signaling pathways and inhibits signal transduction 
by increasing the GTPase activity of G protein alpha. RGS7 may play an 
important role in synaptic vesicle exocytosis and in the

[[Page 36554]]

rapid regulation of neuronal excitability and the cellular responses to 
stimulation. This polyclonal antibody was generated by using a purified 
fusion protein containing the regulator of guanine nucleotide-binding 
protein signaling (RGS) C-terminal region of bovine RGS. The antibody 
specifically recognizes RGS7 of mouse, rat, and human origin. The 
antibody is useful for studying the expression, functions, and 
interactions of RGS7 by Western blot and immunofluorescence analysis.
    Applications:
     Basic research tool for the study of RGS7. Reagent for 
diagnostic applications such as Western Blotting, ELISA, 
immunofluorescence and immunohistochemistry in fixed tissue samples.
     Reagent for biochemical techniques such as 
immunoprecipitation. Development of diagnostics or therapeutics for 
diseases of the nervous system linked to RGS protein-regulated 
signaling including Parkinson's disease, schizophrenia, seizure 
disorders, multiple sclerosis, and opiate addiction.
    Inventors: William F. Simonds and Jianhua Zhang (NIDDK).

Relevant Publications

    1. Rojkova AM, Woodard GE, Huang TC, Combs CA, Zhang JH, Simonds 
WF. Ggamma subunit-selective G protein beta 5 mutant defines regulators 
of G protein signaling protein binding requirement for nuclear 
localization. J Biol Chem. 2003 Apr 4;278(14):12507-12512. [PMID: 
12551930]
    2. Nini L, Waheed AA, Panicker LM, Czapiga M, Zhang JH, Simonds WF. 
R7-binding protein targets the G protein beta 5/R7-regulator of G 
protein signaling complex to lipid rafts in neuronal cells and brain. 
BMC Biochem. 2007 Sep 19;8:18. [PMID: 17880698]
    3. Panicker LM, Zhang JH, Posokhova E, Gastinger MJ, Martemyanov 
KA, Simonds WF. Nuclear localization of the G protein beta 5/R7-
regulator of G protein signaling protein complex is dependent on R7 
binding protein. J Neurochem. 2010 Jun;113(5):1101-1112. [PMID: 
20100282]
    Patent Status: HHS Reference No. E-077-2011/0--Research Tool. 
Patent protection is not being pursued for this technology.
    Licensing Status: This technology is available as a research tool 
under a Biological Materials License.
    Licensing Contact: Jaime Greene, M.S.; 301-435-5559; 
greenejaime@mail.nih.gov.
    Collaborative Research Opportunity: The NIDDK Metabolic Diseases 
Branch is seeking statements of capability or interest from parties 
interested in collaborative research to further develop, evaluate, or 
commercialize polyclonal antibodies against the Regulator of G protein 
Signaling Protein 7 (RGS7). Please contact Anna Z. Amar at 301-451-2305 
or aa54d@nih.gov for more information.

Oligonucleotide Compounds that Enhance Immunity to Cancer and Reduce 
Autoimmunity

    Description of Technology: Suppressive cells, including macrophages 
and other myeloid-derived suppressor cells, regulatory T cells, and 
dendritic cells (DCs), have been attributed to tumor growth. DCs in 
particular are known to be associated with the induction of T cell 
tolerance in cancer, but molecular mechanisms that control DC 
dysfunction are complex and a better understanding of DC mechanisms in 
tumors is needed. Recently FOXO3, originally identified as a tumor 
suppressor, was associated with DC dysfunction. Additionally, 
therapeutics targeting FOXO3 are known to be effective at killing many 
tumors types, synergize with traditional therapies, and show efficacy 
against tumors that are otherwise resistant to conventional treatments.
    The researchers at the NIH have demonstrated for the first time 
that FOXO3 expression by DC coincides with expression of suppressive 
genes that negatively regulate T cell function. They have also 
demonstrated that silencing FOXO3 simultaneously changes DC function, 
eliminating tolerogenicity and enhancing their immunostimulatory 
capacity. Specifically, the inventors have developed siRNAs or 
oligonucleotides that enhance an immune response and neutralize the 
activity of FOXO3 in DCs by converting suppressive cells into 
immunostimulatory cells. This novel approach could be applied to cancer 
vaccines, where dendritic cells could be treated with these small 
molecules prior to use in clinical therapies. Alternatively, small 
molecules that stimulate FOXO3 expression could be used for inducing 
immune suppression for autoimmune diseases like type I diabetes or 
multiple sclerosis.

Applications

     An adjuvant to neutralize FOXO3 and elicit a more potent 
response to cancer immune-based therapies, either at the time of 
vaccination or during an on-going anti-tumor immune response.
     Suppressing an immune response through the induction of 
FOXO3 expression to prevent tissue-specific autoimmune diseases like 
type I Diabetes or Multiple sclerosis, where known target antigens have 
been identified.

Advantages

     The ability to treat multiple tumor types linked to FOXO3 
expression.
     siRNAs can be delivered to different organs with minimal 
cytotoxicity.
     Through the modulation of FOXO3 gene expression, 
therapeutics for both cancer and autoimmune diseases can be developed.
    Development Status: Pre-clinical proof of principle.
    Inventors: Arthur A. Hurwitz (NCI) et al.
    Publication: Watkins SK, Zhu Z, Riboldi E, Shafer-Weaver KA, 
Stagliano KE, Sklavos MM, Ambs S, Yagita H, Hurwitz AA. FOXO3 programs 
tumor-associated DCs to become tolerogenic in human and murine prostate 
cancer. J Clin Invest. 2011 Apr 1;121(4):1361-1372. [PubMed: 21436588]

Patent Status

     U.S. Provisional Application No. 61/293,098 filed January 
7, 2010 (HHS Reference No. E-086-2010/0-US-01).
     PCT Application No. PCT/US2011/020315 filed January 6, 
2011 (HHS Reference No. E-086-2010/0-PCT-02).
    Licensing Status: Available for licensing.
    Licensing Contact: Whitney Hastings; 301-451-7337; 
hastingw@mail.nih.gov.
    Collaborative Research Opportunity: The National Cancer Institute 
Cancer and Inflammation Program is seeking statements of capability or 
interest from parties interested in collaborative research to further 
develop, evaluate, or commercialize agents that both block FOXO3 
function and enforce FOXO3 expression. Please contact John Hewes, PhD 
at 301-435-3121 or hewesj@mail.nih.gov for more information.

    Dated: June 14, 2011.
Richard U. Rodriguez,
Director, Division of Technology Development and Transfer, Office of 
Technology Transfer, National Institutes of Health.
[FR Doc. 2011-15477 Filed 6-21-11; 8:45 am]
BILLING CODE 4140-01-P