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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 Start Printed Page 30323Institutes 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; thalhamc@mail.nih.gov.

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; kindraj@mail.nih.gov.

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; heftib@mail.nih.gov.

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; heftib@mail.nih.gov.

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; heftib@mail.nih.gov.

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; heftib@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.

The immunotoxins of the present invention are more stable and have higher affinity for CD30 then their predecessors. Research thus far has Start Printed Page 30324shown 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.

Start Signature

Dated: May 20, 2004.

Steven M. Ferguson,

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

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[FR Doc. 04-11970 Filed 5-26-04; 8:45 am]

BILLING CODE 4140-01-P