99-30065. Government-Owned Inventions; Availability for Licensing  

  • [Federal Register Volume 64, Number 222 (Thursday, November 18, 1999)]
    [Notices]
    [Pages 63049-63050]
    From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
    [FR Doc No: 99-30065]
    
    
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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, DHHS.
    
    ACTION: Notice.
    
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    SUMMARY: The inventions listed below are owned by agencies 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.
    
    Peptide Inhibitor of Cyclin Dependent Kinase 4 (cdk4) Derived from 
    MyoD
    
    BM Paterson, J Zhang (NCI).
    Serial No. 60/139,934 filed 18 Jun 1999.
    Licensing Contact: Susan S. Ricker; 301/496-7056 ext. 245; e-mail: 
    sr156v@nih.gov.
    
        This invention pertains to cell cycle regulation and the activity 
    of the GI cyclin-dependent kinase 4 (CDK4). The invention describes a 
    15 amino acid peptide and variants thereof derived from MyoD, which is 
    an inhibitor of the CDK4. CDK4 is one of a number of cyclin-dependent 
    kinases which control progression through the cell cycle through their 
    ability to phosphorylate particular substrates at the correct phase of 
    the cell cycle. CDK4 has been shown to be involved in cell cycle 
    control through its ability to regulate the activity of the 
    retinoblastoma protein, pRb, an activator of genes essential for cell 
    division.
        Inhibitors of the cyclin-dependent kinases (CKIs), such as the 
    peptides described in this invention, prevent cell cycle progression 
    and induce cells to exit the cell cycle into the Go state. The peptides 
    described in this invention prevent the phosphorylation of pRb by cdk4, 
    an obligate step for entry into the cell cycle. Osteosarcomas and 
    habdosarcomas are two types of tumors known to over-express pRb. The 
    inhibitor described in this invention may be useful in treating these 
    cancers or other diseases which have been specifically linked to over-
    expression of active pRb.
        Background material related to this invention has been published 
    [Zhang. J. et al. EMBO J 18(4): 926-33 (Feb. 15, 1999)].
    
    Chromatographic Separation of Proteins by Ammonium Sulfate 
    Precipitation
    
    Yoichiro Ito (NHLBI)
    Serial No. 09/263,609 filed 05 Mar. 99
    Licensing Contact: John Fahner-Vihtelic; 301/496-7735 ext.
    270; e-mail: jf36z@nih.gov
    
        Recently, a field flow fractionation apparatus and method for the 
    chromatographic separation of proteins have been developed. Unique in 
    design, the fractionation apparatus contains two spiral channels, a 
    reagent channel and a sample channel carved into two mating disks 
    separated by a semi-permeable membrane. The primary advantage to this 
    design is that it allows proteins passing through the sample channel to 
    be fractioned according to their ability to precipitate out in the 
    presence of an exponential ammonium sulfate concentration gradient in 
    the reagent channel. Protein elution is achieved by repetitive 
    precipitation, and takes place along the sample channel without the 
    tedious manual labor required by conventional fractionation procedures. 
    This method can also utilize other precipitation reagents such as NaCl, 
    ethanol and polyethylene glycols. Applications would include 
    purification of monoclonal antibodies (IgM and IgG) from a culture 
    medium and ascitic fluid and affinity separation of recombinant enzymes 
    from E. coli  lysate. A working prototype is undergoing additional 
    refinement.
    
    Calcium Channel Compositions and Methods of Use Thereof
    
    Michael I. Lerman et al. (NCI)
    Serial No. 60/114,359 filed 30 Dec 1998
    Licensing Contact: Susan S. Rucker; 301/496-7056 ext. 245;
    e-mail sr156v@nih.gov
    
        The invention described in this patent application relates to the 
    identification, isolation and cloning of a three cDNAs identified 
    during a search of the short arm of chromosome 3 for a tumor suppressor 
    gene (TSG) associated with lung, breast and other cancers. The cDNAs 
    are alternate isoforms which encode a protein which functions as a
    
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    L-type voltage-dependent calcium channel. Type L-voltage dependent 
    calcium channels represent one of five families of calcium channels, L, 
    R, P, N, Q, which have been identified. Type L voltage-dependent 
    calcium channels are found in a wide variety of tissues including the 
    brain, muscle and the endocrine system.
        The gene has been mapped to the short arm of chromosome 3 at 
    3p21.3. The gene, which corresponds to this cDNAs is an alpha2delta 
    (2) subunit, and has been shown to be deleted in lung 
    and breast cancer. The scientists have demonstrated that the expression 
    of this calcium channel has been shut off in lung cancer cells and 
    hypothesize that this may lead to a malignant phenotype. Possible 
    applications of this technology include its use in drug screening 
    assays; its use as an early diagnostic marker and/or as a prognostic or 
    treatment indicator; its use in gene therapy where defective cells 
    would be reconstructed with the gene and as a therapeutic agent for 
    clearing autoantibodies which develop toward the alpha2delta subunit in 
    the disease Lambert-Eton myasthenia syndrome.
    
    Hepatitus C Virus (HCV) Envelope Protein Modified for Expression on 
    the Host Cell Surface and Use of DNA Constructs Encoding the 
    Modified Protein as a Vaccine and of Host Cells Expressing the 
    Protein in Diagnostic and Screening Assays
    
    Xavier Forns, Suzanne U. Emerson, Jens Bukh, Robert H. Purcell (NIAID)
    Serial No. 60/089,779 filed 18 Jun 1998
    Licensing Contact: J. Peter Kim; 301/496-7056 ext. 264;
    e-mail: jk41n@nih.gov
    
        Hepatitis C virus (HCV) is a single stranded RNA virus responsible 
    for the majority of non-A non-B hepatitis. Hepatitis C virus (HCV) has 
    a worldwide distribution and is a major cause of liver cirrhosis and 
    hepatocellular carcinoma in the U.S., Europe, and Japan. For this 
    reason, development of a vaccine against hepatitis C is of great 
    importance.
        The present invention provides for hepatitis C virus (HCV) vaccines 
    and diagnostic assays. The invention provides chimeric genes, 
    expression vectors which comprise these chimeric genes, and DNA based 
    vaccines which employ the expression vectors as immunogens to produce 
    protective antibodies to HCV in a mammal. The invention further 
    provides for diagnostic assays to screen sera for the presence of 
    antibodies to HCV envelope proteins, as antigens in the screening of 
    phage display combinatorial libraries, and as reagents to develop 
    tissue culture systems suitable for testing anti-HCV envelope 
    antibodies for neutralizing activity.
    
    Human FRP and Fragments Thereof Including Methods for Using Them
    
    US Rubin (NCI), PW Finch, SA Aaronson, and X He
    Serial No. 09/087, 031 field 29 May 1998
    Licensing Contact: Susan S. Rucker; 301/496-7056 ext 245; e-mail: 
    sr156v@nih.gov
    
        This application relates to signal transduction pathways and 
    mechanisms. More particularly, the application describes the isolation, 
    cloning of the cDNA encoding, and characterization of a human protein 
    denoted ``Frizzled Related Protein'' or FRP. FRP, also known as sFRP-1, 
    is a secreted protein which contains an N-terminal cysteine-rich domain 
    (CRD) which is a similar to the CRDs of the frizzled family of membrane 
    anchored Wnt receptors. sFRP-1 lacks any transmembrane region or 
    cytoplasmic domain characteristic of molecules capable of transducing a 
    signal within a cell but is preferentially distributed to the cell 
    surface or matrix.
        Wnt signaling has been implicated in the development of cancers and 
    various organs. sFRP-1 has been demonstrated to antagonize Wnt 
    signaling and therefore may function as an inhibitor of Wnt activity or 
    otherwise modulate Wnt signaling. In addition, others have suggested 
    that sFRP-1 plays a role in regulating apoptosis by sensitizing cells 
    to apoptotic agents and modulating levels of -catenin. The 
    gene encoding sFRP-1 is found on the short arm of chromosome 8 at 
    8p11.1-12. RNA transcripts have been identified in multiple adult 
    tissues such as the heart, kidney, ovary, prostate, testis, small 
    intestine and colon but have not been detected in a number of other 
    tissues.
        In view of this sFRP-1 derived products may be useful in further 
    study of sFRP-1--Wnt interactions, drug screening assays, the 
    development of diagnostics for cancer or other conditions which are 
    related to Wnt signaling, or may be developed as therapeutic agents 
    themselves. Recombinant FRP, expression vectors containing FRP cDNA and 
    cDNA containing the full length FRP coding sequence are available. 
    Limited quantities of rabbit polyclonal antisera which specifically 
    binds FRP is also available.
        This work has appeared, in part, in Finch, PW, et al. PNAS 94(13): 
    6770-75 (June 24, 1997) and has been published as WO 98/54325 (Dec. 3, 
    1998).
    
    Use of Lipoxygenase Inhibitors as Anti-Cancer Therapeutic and 
    Intervention Agents
    
    James L. Mulshine, Marti Jett (NCI)
    Serial No. 08/704,569 filed 03 Dec 96
    Licensing Contact: Girish Barua; 301/496-7056 ext. 263; email 
    gb18t@nih.gov
    
        We have reported that S-Lipoxygenase inhibitors can treat or 
    prevent certain epithelial cancers such as lung cancer, breast cancer, 
    and head and neck cancer. This is believed to occur from the 
    interruption of the 5-lipoxygenase pathway which results in increased 
    tumor cell apoptosis. We have demonstrated this effect for the growth 
    factor-induced stimulation in several model systems so we propose this 
    as a robust anti-promotional chemoprevention approach as well.
        Suitable 5-lipoxygenase inhibitors useful for the methods of the 
    present invention include 2-(12-Hydroxydodeca-5, 10-dinyl) 3,5,6-
    trimethyl-1,4benzoquinone and derivatives thereof; Nordihydroguiaretic 
    acid and derivatives and 3-[1-(4-chlorobenzy)-3-t-butylthio-t-
    isopropyl-indol-2-yl] -2, 2-dimethylpropionic acid and derivatives 
    thereof. Also intended to be encompassed by this are hydroxyurea 
    derivatives as inhibitors of 5-lipoxygenase for use in the prevention 
    and treatment of the cancers mentioned above.
    
        Dated: November 9, 1999.
    Jack Spiegel,
    Director, Division of Technology Development and Transfer, Office of 
    Technology Transfer, National Institutes of Health.
    [FR Doc. 99-30065 Filed 11-17-99; 8:45 am]
    BILLING CODE 4140-01-M
    
    
    

Document Information

Published:
11/18/1999
Department:
National Institutes of Health
Entry Type:
Notice
Action:
Notice.
Document Number:
99-30065
Pages:
63049-63050 (2 pages)
PDF File:
99-30065.pdf