[Federal Register Volume 70, Number 111 (Friday, June 10, 2005)]
[Notices]
[Pages 33908-33909]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 05-11575]


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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 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; 
[email protected].
    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

[[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; 
[email protected].

    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; 
[email protected].

    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.

    Dated: June 3, 2005.
Steven M. Ferguson,
Director, Division of Technology Development and Transfer, Office of 
Technology Transfer, National Institutes of Health.
[FR Doc. 05-11575 Filed 6-9-05; 8:45 am]
BILLING CODE 4140-01-P