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Government-Owned Inventions; Availability for Licensing

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AGENCY:

National Institutes of Health, Public Health Service, HHS.

ACTION:

Notice.

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 Start Printed Page 58061listed 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: 301/594-7700; fax: 301/402-0220. A signed Confidential Disclosure Agreement will be required to receive copies of the patent applications.

Antiproliferative Actions of Human IGF Binding Protein-3 Mutants That Do Not Bind IGF-I or IGF-II

M.M. Rechler (NIDDK), DHHS Reference No. E-048-02/0 filed Dec 17, 2001.

Licensing Contact: Brenda Hefti, 301/496-7736 ext. 206, e-mail: heftib@od.nih.gov; or Richard Rodriguez, 301/496-7056 ext. 287, e-mail: rodrigur@od.nih.gov.

Recent epidemiological studies indicate that increased serum insulin-like growth factor binding protein-3 (IGFBP-3) is associated with decreased risk of prostate, breast, lung and colorectal cancers, and childhood leukemia. IGFBP-3 can inhibit cell growth and stimulate death through formation of complexes with IGF-I and IGF-II that prevent activation of the IGF-I receptor to stimulate proliferation and survival.

The current invention embodies a novel mechanism of action for IGFBP-3: direct inhibition of cell growth and stimulation of cell death through a mechanism that is independent of IGF-I, IGF-II and the IGF-I receptor. In the current invention, human IGFBP-3 has been genetically modified so that its affinity for IGF-I and IGF-II is greatly reduced, and it can act only through this novel direct mechanism. These human IGFBP-3 mutants still can inhibit DNA synthesis and stimulate apoptosis, and have been shown to induce apoptosis in human prostate cancer cells. The current invention could selectively exert antiproliferative action without interfering with IGF actions, and may have therapeutic uses as an antitumor agent.

A Novel DNA Methyltransferase Assay System With High Throughput/Automation Potential

K. Robertson, T. Yokochi (NCI), DHHS Reference No. E-030-02/0 filed Jan 14, 2002.

Licensing Contact: Brenda Hefti, 301/496-7736 ext. 206, e-mail: heftib@od.nih.gov; or Richard Rodriguez, 301/496-7056 ext. 287, e-mail: rodrigur@od.nih.gov.

It is now believed that unregulated cell growth is due to aberrant gene expression in cells caused by deletion, mutation, or silencing of one or more critical growth regulatory proteins. The latter method, gene silencing, is mediated by DNA methylation, or the addition of methyl groups to cytosine residues at critical gene expression control regions.

The current invention embodies a novel and highly sensitive assay for detecting DNA methyltransferase activity, which catalyzes the addition of methyl groups to DNA. Treatment with DNA methyltransferase inhibitors in a clinical setting might lead to expression of silenced gene(s) and restoration of controlled cell growth. Huge numbers of compounds must be screened to identify ones that are active against DNA methyltransferases. The assay embodied in the current invention represents the first such assay adaptable for high-throughput and/or automated screening of potential DNA methyltransferase inhibitors. This assay also is fast, easy, reproducible, and highly sensitive.

HGC-1, A Gene Encoding a Member of the Olfactomedin-Related Protein Family

Griffin P. Rodgers, Wen-Li Liu, Jiachang Zhang (NIDDK), DHHS Reference No. E-166-01/0 filed Dec 07, 2001.

Licensing Contact: Brenda Hefti, 301/496-7736 ext. 206, e-mail: heftib@od.nih.gov; or Richard Rodriguez, 301/496-7056 ext. 287, e-mail: rodrigur@od.nih.gov.

The current technology embodies a newly identified gene, Human Granulocyte Colony-Stimulating Factor-Stimulated-Clone-1 (hGC-1), that has been cloned and characterized, and its protein sequence has been deduced. The gene is expressed in the bone marrow, prostate, small intestine, colon, and stomach, and has been mapped to chromosome 13 in a region that contains a tumor suppressor gene cluster. The gene is found to be selectively present in normal human myeloid lineage cells and is believed to play a role in allowing lymphocytes to differentiate properly. It is believed that the gene may be used as a selective marker for human prostate cancer, multiple myeloma, B-cell chronic lymphocytic leukemia and other types of cancer and can be used diagnostically as well as in therapeutic screening activities.

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Dated: September 3, 2002.

Jack Spiegel,

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

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[FR Doc. 02-23334 Filed 9-12-02; 8:45 am]

BILLING CODE 4140-01-P