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Government-Owned Inventions; Availability for Licensing

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AGENCY:

National Institutes of Health, Public Health Service, DHHS.

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.

Identification of H2-Db and HLA-A2 Specific CD8 Epitopes From Human KDR/VEGFR-2 That Inhibit Angiogenesis by Vaccination

Drs. Samir Khleif and Yujun Dong (NCI).

U.S. Provisional Application No. 60/671,867 filed 15 Apr 2005 (DHHS Reference No. E-158-2005/0-US-01).

Licensing Contact: John Stansberry; (301) 435-5236; stansbej@mail.nih.gov.

Vascular Endothelial Growth Factor Receptor 2 (VEGFR-2/KDR) is a promising target for cancer therapy due to its critical role in tumor associated angiogenesis and vascularization. This invention describes the amino acid sequences of seven short peptides based upon epitopes of human Vascular Endothelial Growth Factor Receptor-2 Start Printed Page 33909(VEGFR-2) that bind human Histocompatibility Leukocyte Antigen A2 (HLA-A2). These peptides can potentially induce Cytotoxic T Lymphocyte (CTL)-mediated lysis of tumor vascularization and inhibit tumor growth. The inventors have demonstrated the principles described in this invention in vivo in mice for VEGFR-2, using murine H2-Db specific peptides instead of HLA-A2. This invention has the potential to inhibit angiogenesis and may be applicable to tumor and autoimmune disease therapy.

In addition to licensing, the technology is available for further development through collaborative research opportunities with the inventors.

Novel Anti-CD30 Antibodies and Recombinant Immunotoxins Containing Disulfide-Stabilized Fv Fragments

Ira H. Pastan et al. (NCI).

U.S. Provisional Application No. 60/387,293 filed 07 Jun 2002 (DHHS Reference No. E-135-2002/0-US-01);

PCT Application No. PCT/US03/18373 filed 07 Jun 2003, which published as WO 03/104432 on 18 Dec 2003 (DHHS Reference No. E-135-2002/1-PCT-01);

U.S. Patent Application filed 03 Dec 2004 (DHHS Reference No. E-135-2002/1-US-02).

Licensing Contact: Jesse S. Kindra; (301) 435-5559; kindraj@mail.nih.gov.

The present invention discloses the creation of new anti-CD30 stalk antibodies and anti-CD30 dsFv-immunotoxins, which have shown good cytotoxic activity.

CD30 is a member of the tumor necrosis factor receptor super family. It is an excellent target due to its high expression in malignant Reed Sternberg cells of Hodgkin's Lymphoma (HL) and in anaplastic large cell lymphomas (ALCL), and due to its expression in only a small subset of normal lymphocytes. Previous attempts to target CD30 include the scFv immunotoxin Ki-4 that has shown specific binding to CD30-positive lymphoma cell lines and killed target cells.

As claimed in this patent application, some of the antibodies do not bind or bind very weakly CD30 released from cells, although they do bind strongly to cell associated CD30. This enhancement further increases the ability of immunotoxins and other immunoconjugates to target and treat lymphomas expressing CD30.

The immunotoxins of the present invention are more stable and have higher affinity for CD30 then their predecessors. Research thus far has shown that the dsFv-immunotoxins are able to kill a variety of CD30-positive lymphoma cell lines in vitro as well as CD30-transfected A431 cells via specific binding to CD30.

In addition to licensing, the technology is available for further development through collaborative research opportunities with the inventors.

Compositions and Methods for Inhibiting Vascular Channels and Methods of Inhibiting Proliferation

Myung Hee Park, Paul M.J. Clement, Hartmut M. Hanauske-Abel, Edith C. Wolff, Hynda K. Kleinman, Bernadette M. Cracchiolo (NIDCR).

U.S. Provisional Application No. 60/314,561 filed 23 Aug 2001 (DHHS Reference No. E-320-2001/0-US-01);

PCT Application No. PCT/US02/26909 filed 23 Aug 2002, which published as WO 03/018014A2 on 06 Mar 2003 (DHHS Reference No. E-320-2001/0-PCT-02);

U.S. Patent Application No. 10/486,671 filed 11 May 2004 (DHHS Reference No. E-320-2001/0-US-03).

Licensing Contact: John Stansberry; (301) 435-5236; stansbej@mail.nih.gov.

Angiogenesis, the recruitment of new blood vessels, is recognized as an important factor in tumor proliferation in many types of cancer. It is generally accepted that therapeutic approaches that inhibit angiogenesis effectively limit, or even prevent, the formation of solid tumors. It has also been shown that anti-angiogenic therapeutics allow conventional radiation therapy and chemotherapy to be more effective.

This invention pertains to certain compounds that inhibit angiogenesis in a previously unrecognized way. These compounds also inhibit the proliferation of cells within intraepithelial neoplasias (clusters of abnormally proliferating epithelial cells that are the origin of cancers). The subject compounds specifically block the formation of the amino acids hypusine and hydroxyproline. The former is the critical residue of eukaryotic translation initiation factor 5A (eIF5A), which is important in cell cycle progression, and hydroxyproline constitutes the critical residue of the collagens. The targeted enzymes are deoxyhypusine hydroxylase and prolyl 4-hydroxylase, respectively.

This invention provides evidence for an important role of eIF-5A in angiogenesis, and discloses a family of compounds with useful clinical properties. Specifically, these compounds include the core structures and potential derivatives of ciclopirox olamine, deferiprone, deferoxamine, and 2,2'-dipyridyl.

Ciclopirox olamine has potential for treatment of oral-pharyngeal cancer, and chemoprevention and treatment of cervical and vulvar cancer. Notably, this drug is FDA-approved in the USA as a topical medication against fungal infections while, in Europe, it is also approved for the treatment of yeast infections of the genital tract. The compound has a known clinical profile and lacks teratogenicity, potentially expediting clinical trials for new cancer treatment indications.

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Dated: June 3, 2005.

Steven M. Ferguson,

Director, Division of Technology Development and Transfer, Office of Technology Transfer, National Institutes of Health.

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[FR Doc. 05-11575 Filed 6-9-05; 8:45 am]

BILLING CODE 4140-01-P