National Institutes of Health (at bottom of this page)
63 Navy Inventions Offered for Licensing
SUMMARY: The inventions listed below
are assigned to the United States Government as represented by the Secretary
of the Navy and are made available for licensing by the Department of the Navy.
Copies of patents cited are available from the Commissioner of
Patents and Trademarks, Washington, DC 20231, for $3.00 each. Requests for copies
of patents must include the patent number.
Copies of patent applications cited are available from the National Technical
Information Service (NTIS), Springfield, Virginia 22161 for
$6.95 each ($10.95 outside North American Continent).
Requests for copies of patent applications must include the patent application
serial number. Claims are deleted from the copies of patent applications sold
to avoid premature disclosure. The following patents and patent applications
are available for
licensing:
FOR FURTHER INFORMATION CONTACT: Mr. John G. Wynn, Staff Patent Attorney, Office of Naval Research (Code 00CC), Arlington, VA 22217-5660, telephone (703) 696-4004.
Nine Inventions Offered by the National Institutes of Health
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.
1. Methods of Inhibiting Cancer Cells With
ADNF III Antisense Oligonucleotides
I Gozes, R Zamostiano, E Gelber, A Pinhasov, M Bassan (all of Tel Aviv University),
DE Brenneman (NICHD) Serial No.: 09/364,609 filed 30 Jul 1999. Licensing Contact:
Susan S. Rucker; 301/496_7056 ext. 245; e_mail: sr156v@nih.gov.
This application describes methods of inhibiting the proliferation of cells using an antisense oligonucleotide derived from the polypeptide Activity Dependent Neurotrophic Factor III (ADNF III)/Activity Dependent Neuroprotective Protein (ADNP). Preferred antisense oligonucleotides are complementary to the 5' region of ADNF III/ADNP. The ability of such antisense oligonucleotides to inhibit cell proliferation has been demonstrated in in vitro models such as the HT29 colon cancer cell line. Based on the location of ADNF III/ADNP on chromosome 20 at 20q13, a region which has been shown via CGH to be associated with breast, ovary, colon, head and neck, brain and pancreatic cancers, ADNF III/ADNP antisense molecules might also be expected to be useful in treating one or more of these cancers.
2. Orally Active Peptides That Prevent Cell
Damage and Death
DE Brenneman, CY Spong (both of NICHD), I Gozes, A Pinhasov, E Giladi (all of
Tel Aviv University) Serial No.: 60/149,956 filed 18 Aug. 1999. Licensing Contact:
Susan S. Rucker; 301/496_7056 ext. 245; e_mail: sr156v@nih.gov.
This application describes two peptides which are orally active and which have been shown in in vitro assays to protect against neuronal cell death. In animal model systems for Alzheimer's disease and Fetal Alcohol Syndrome the peptide have also been demonstrated to be useful. The first peptide is D_SAL, a D_isomer of the peptide SAL (SALLRSIPA) derived from Activity Dependent Neurotrophic Factor I (ADNF I). The second peptide is D_NAP, a D_isomer of the peptide NAP (NAPVSIPQ) derived from a related protein Activity Dependent Neuroprotective Protein (ADNP)/Activity Dependent Neurotrophic Factor III (ADNF III). The peptides may be used alone or in combination. The peptides may be constructed solely of D_isomers of their amino acids or combinations of D and L amino acids. Other diseases involving neuronal cell death where D_SAL or D_NAP may be useful include Huntington's disease, epilepsy, Parkinson's disease and Tourette's syndrome.
3. 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)].
4. 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.
5. 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 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 (<greek_a>2<greek_d>) 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.
6. 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.
7. 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 <greek_b>_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).
8. 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.
9. Extracelular cAMP_Dependent Protein Kinase
in the Diagnosis and Prognosis of Cancer and Methods of Treatment
Inventor: Dr. Yoon S. Cho_Chung (NCI). U.S. Patent Application Serial
No.: 60/140,288 filed June 18, 1999. DHHS Ref. No.: E_110_99/0
It has been discovered that expression of extracellular_PKA (ECPKA) is serum is a measure of hormone_dependency of breast cancer. In view of this discovery, this invention provides a method of determining whether or not breast cancer in a give patient is hormone_dependent or hormone_independent. Current methods of determining hormone_dependency in breast cancer involve biopsy and examination of the breast cancer tissue for the presence of estrogen and/or progesterone receptors, which can be detected in the tissue by an immunohistochemical assay using a monoclonal antibody, by a biochemical assay using dextran_coated charcoal, and by other means. Such methods are disadvanageous due to inaccuracies (As much as 30_40% of results are false positives or false negatives), a lack of consensus as to the minimum number of cells required to have an estrogen and/or progesterone receptor for determination of hormone_dependent cancer, and required biopsy. The present invention seeks to overcome such disadvantages by providing a more accurate assay for the hormone dependency or independency of breast cancer which does not require biopsy The determination of whether a breast cancer is hormone_dependent or hormone_independent has meaningful implications for the selection of treatment strategy and the prognosis of the disease. For example, if the breast cancer is hormone_dependent, the treatment may include hormone therapy involving administration of anti_estrogen drugs, the destruction of ovary function, or the removal of the ovaries. In the case of hormone_independence the absence of estrogen receptors in the primary tumor indicates a higher rate of recurrence and a shorter survival rate. In this instance the treatment will likely include the administration of chemotherapeutic drugs. This invention provides a method of diagnosing cancer in a patient. The method involves assaying a sample of serum or other body fluids from the patient for the presence of ECPKA. An elevated level of ECPKA in the sample compared to the level in a control sample is indicative of cancer in the patient. The invention also includes a method of assaying a sample of serum or other body fluids from the patient for the presence of ECPKA in which (i) A reduction in the level of ECPKA in the sample as compared to the level in an earlier sample from the patient indicates an improvement in the patient's prognosis, (ii) no change in the level of ECPKA in the sample as compared to the level of ECPKA in an earlier sample from the patient, indicates no change in the patient's condition, or (iii) an increase in the level of ECPKA in the sample as compared to the level in an earlier sample from the patient, indicating a worsening of the patient's condition. As alluded to above, the invention also involves a method of determining whether a diagnosed breast cancer is hormone_dependent or hormone_independent. This method involves assaying a serum or other body fluid sample from the patient for the presence of ECPKA versus a control sample. An elevated level of ECPKA indicates that the breast cancer is hormone_dependent. Finally, the invention provides a method for the treatment of cancer. This method involves reducing the level of ECPKA by delivering the RII<greek_b> subunit of PKA_II to target cancer cells to down_regulate the expression of ECPKA and inhibit cancer cell growth. The above mentioned Invention is available, including any available foreign intellectual property rights, for licensing.
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