[Federal Register Volume 69, Number 103 (Thursday, May 27, 2004)]
[Notices]
[Pages 30322-30324]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 04-11970]


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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

[[Page 30323]]

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.

AT8, a Hybridoma Cell Line Producing a Monoclonal Antibody (MAb) 
Specific for Ly49G, a Mouse Natural Killer (NK) Cell Receptor

Andrew J. Makrigiannis (NCI).
DHHS Reference No. E-131-2004/0--Research Material.
Licensing Contact: Cristina Thalhammer-Reyero; 301/435-4507; 
[email protected].

    This MAb is useful for identifying and isolating specific 
subpopulations of mouse NK cells using flow cytometry and fluorescence 
activated cell sorting (FACS). The AT8 antibody is also useful as a 
reagent to study the innate immune system using mouse models. This 
antibody has been described in Makrigiannis et al., ``Independent 
Control of Ly49g Alleles: Implications for NK Cell Repertoire Selection 
and Tumor Cell Killing,'' J. Immunol. 2004 172:1414-1425.

Materials and Methods for Inhibiting Wip1

Dmitry Bulavin, Galina BeLova, Albert J. Fornace, Jr. (NCI).
U.S. Patent Application filed 12 Mar 2004 (DHHS Reference No. E-340-
2003/0-US-01), a CIP of PCT/US03/08997 filed 21 Mar 2003, which 
published as WO 03/083103 on 01 Oct 2003 (DHHS Reference No. E-002-
2002/0-PCT-02).
Licensing Contact: Jesse S. Kindra; 301/435-5559; [email protected].

    Wild-type p53-induced phosphatase 1 (Wip1) is a MG2+-
dependent serine/threonine protein phosphatase that is expressed in 
response to ionizing or ultra-violate radiation in a manner that is 
dependent on the tumor suppressor gene product p53. Wip1 has been shown 
to dephosphorylate and inactivate p38 MAP kinase, which in its 
activated state functions to activate p53 for the induction of 
apoptosis and transcription in response to environmental stress, 
thereby rendering Wip1 anti-apoptotic.
    Further studies have indicated that Wip1 is a candidate proto-
oncogene involved in tumorigenesis. Therefore, Wip1 represents an 
attractive new target for cancer therapy. Accordingly, the present 
invention relates to methods and compositions of inhibiting Wip1 in a 
cell. Inhibition of Wip1 would be expected to reduce tumor cell 
viability either alone or in combination with cytotoxic agents.

Genes Expressed in Prostate Cancer and Methods of Use

Ira Pastan, Tapan Bera, and Byungkook Lee (NCI).
U.S. Provisional Patent Application No. 60/461,399 filed 08 Apr 2003 
(DHHS Reference No. E-148-2003/0-US-01); PCT Application has been 
filed.
Licensing Contact: Brenda Hefti; 301/435-4632; [email protected].

    This invention is a novel gene, called New Gene Expressed in 
Prostate (NGEP). This gene appears to be expressed only in prostate. 
This gene has two known splice variants of significantly different 
size. The shorter splice variant encodes a cytoplasmic protein, while 
the longer splice variant encodes a plasma membrane protein.
    This patent application contains claims to the polypeptide, NGEP, 
nucleotides encoding NGEP, antibodies that bind NGEP polypeptides, and 
methods of using these polypeptides, polynucleotides, and antibodies.
    The presence of the protein on the cell surface and the selective 
expression in prostate and prostate cancer make this a potential target 
for prostate cancer diagnostics and therapeutics. Potential 
therapeutics could be gene-based, vaccines, antibodies, or 
immunoconjugates. Further information can be obtained by viewing a 
recent publication by the inventors (PNAS v.104 no.9, p.3050-3064, 
March 2, 2004).

BASE, a New Cancer Gene, and Uses Thereof

Ira Pastan, Kristi Egland, James Vincent, Byungkook Lee, and Robert 
Strausberg (NCI).
PCT Application No. PCT/US03/39476 filed 10 Dec 2003 (DHHS Reference 
No. E-321-2002/0-PCT-02).
Licensing Contact: Brenda Hefti; 301/435-4632; [email protected].

    The present invention identifies a new gene expressed in breast 
cancers. The gene undergoes alternative splicing, and is expressed as 
one of two polypeptides. Both splice variants appear to be secreted 
proteins, and therefore good potential therapeutic targets. The patent 
application claims BASE polypeptides, nucleic acids, gene therapy and 
vaccine uses, and antibodies. This novel gene target might be useful as 
a breast cancer marker for diagnostics, or as a target for breast 
cancer therapeutics.

IL-21 Critically Regulates Immunoglobulin Production

Warren J. Leonard, Katsutoshi Ozaki, and Rosanne Spolski (NHLBI).
U.S. Provisional Patent Application 60/393,215 filed 01 Jul 2002 (DHHS 
Reference No. E-211-2002/0-US-01); PCT/US03/20370 filed 26 Jun 2003, 
which published as WO 04/003156 on 08 Jan 2004 (DHHS Reference No. E-
211-2002/0-PCT-02).
Licensing Contact: Brenda Hefti; 301/435-4632; [email protected].

    The invention includes a mouse in which the IL-21 receptor gene is 
disrupted by homologous recombination, the disruption being sufficient 
to prevent expression of the IL-21 receptor and thus to inhibit the 
action of IL-21. The invention also includes a mouse in which both the 
IL-21 receptor gene and the IL-4 gene are simultaneously disrupted in 
fashions being sufficient to inhibit the action of IL-21 and the 
production of IL-4. In a homozygous state, these mutations produce a 
mouse that has diminished B cell function.
    This invention also relates to the use of agents that inhibit the 
interaction of IL-21 with the IL-21 receptor to modulate an immune 
response. This invention may be used to alter B cell activity, to treat 
a subject with Job's disorder, to treat an allergic reaction in a 
subject, or prevent an allergic reaction in a subject.

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).
Licensing Contact: Brenda Hefti; 301/435-4632; [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.
    The immunotoxins of the present invention are more stable and have 
higher affinity for CD30 then their predecessors. Research thus far has

[[Page 30324]]

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

    Dated: May 20, 2004.
Steven M. Ferguson,
Director, Division of Technology Development and Transfer, Office of 
Technology Transfer, National Institutes of Health.
[FR Doc. 04-11970 Filed 5-26-04; 8:45 am]
BILLING CODE 4140-01-P