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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 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 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.

A Mouse Model of UV-Inducible Cutaneous Malignant Melanoma

Glenn Merlino et al. (NCI)

DHHS Reference No. E-281-00/0

Licensing Contact: Elaine White; 301/496-7056 ext. 282; e-mail: gesee@od.nih.gov

The current invention embodies a genetically engineered mouse harboring a hepatocyte growth factor/scatter factor transgene (“HGF/SF”). The Met signaling pathway, which has been implicated in the development of human melanoma, is chronically Start Printed Page 77653activated in the HGF/SF mice. Upon exposure to a single neonatal dose of erythrogenic UV radiation, the mice develop cutaneous malignant melanoma which is consistent with the epidemiology and pathogenesis of melanomas observed in humans. The mice, therefore, represent a valuable model for studying the development of malignant melanoma in humans, for determining the consequences of ultraviolet radiation, and for assessing the efficacy of therapeutic agents and vaccines against melanoma. While no patent rights are available for this invention, breeding pairs of mice are available for licensing via Biological Materials License Agreements.

Gamma-Glutamyl Transpeptidase Inhibitors: Novel Chemotherapeutic Agents

Robert E. London, Scott A. Gabel (NIEHS)

DHHS Reference No. E-243-00/0 filed 05 Oct 2000

Licensing Contact: Richard Rodriguez; 301/496-7056 ext. 287; e-mail: rodrigur@od.nih.gov

Gamma-glutamyl transpeptidase (GGTP) plays a central role in the metabolism of glutathione. It has been shown to be a marker for neoplasia and cell transformation, and it is induced by the presence of many anti-cancer drugs. Common human epithelial tumors, including, but not necessarily limited to, breast, ovarian and prostate tumors are GGTP-positive. The invention relates to novel inhibitors of GGTP, and their use to treat cancer. In particular, the technology could be used to (1) interfere with glutathione metabolism in GGTP-positive cancers by perhaps altering the cellular orientation of GGTP; (2) potentiate the effects of radiation and chemotherapeutic drugs, in particular, cisplatin, on cancer cells by interfering with cysteine recycling and glutathione regeneration; and (3) reduce renal toxicity for some chemotherapeutic drugs by blocking the metabolism of glutathione-conjugates into toxic agents, e.g., mercapturic acids. The patent application contains composition of matter claims as well as method claims.

Protein Kinase A and the Carney Complex

Constantine A. Stratakis, Lawrence S. Kirschner (NICHD)

DHHS Reference No. 259-00/0 filed 25 Aug 2000

Licensing Contact: Richard Rodriguez; 301/496-7056 ext. 287; e-mail: rodrigur@od.nih.gov

The present invention provides compositions and methods useful in the diagnosis and prognosis of Carney complex (CNC), as well as methods and compositions for the identification of compounds useful in the treatment and/or prevention of CNC. CNC is a multiple endocrine neoplasia syndrome that affects the adrenal cortex, pituitary gland, thyroid gland and gonads. Additionally, compositions and methods are provided for the diagnosis and treatment of conditions associated with skin pigmentation defects, including but not limited to, freckling, as well as endocrine tumors including, but not limited to, adrenal and pituitary tumors. Finally, compositions and methods are provided for the diagnosis and treatment of various types of cancers associated with abnormal protein kinase A activity, and cancers and tumors in which protein kinase A regulatory subunit 1A acts as a tumor-suppressor gene. These actions are possible due to the identification of specific genetic sequences, and the use of this information in assay systems to detect, diagnose and treat the aforementioned conditions.

SH2 Domain Binding Inhibitors

Terrence R. Burke, Yang Gao, Johannes Voight (NCI)

DHHS Reference No. E-262-00/0 filed 22 Aug 2000

Licensing Contact: Richard Rodriguez; 301/496-7056 ext. 287; e-mail: rodrigur@od.nih.gov

Signal transduction, the process of relaying extracellular messages to the intracellular cytoplasm and the nucleus, is critical to normal cellular homeostasis, and protein-tyrosine kinases play a central role in this biological function. Examples of this latter class of enzymes include the PDGF receptor, the FGF receptor, the HGF receptor, members of the EGF receptor family, including the EGF receptor itself and erb-B2, erb-B3 and erb-B4 kinases; the src kinase family, Fak kinase and the Jak kinase family. Protein-tyrosine phosphorylation is known to be involved in modulating the activity of a variety of target enzymes and in the formation of specific complex networks involved in signal transduction via proteins containing specific amino acid sequences, called the Src homology 2, or SH2 domain. A malfunction in this protein-tyrosine phosphorylation through tyrosine kinase overexpression and/or deregulation, can be manifested by various oncogenic and hyperproliferative disorders, such as cancer, inflammation, autoimmune disease, hyperproliferative skin disorders, e.g., psoriasis and allergy/asthma. The disclosed compounds, e.g. peptides, preferably, macrocyclic peptides, are SH2 domain inhibitors with enhanced binding affinity. The claims of the current application are directed to compositions of matter and methods of use which provide for the diagnosis, testing and treatment of the aforementioned disease states.

Use and Targeting of CD98 Light-Chain Proteins in Therapies for Thyroid Hormone Disorders

Yun-Bo Shi (NICHD)

DHHS Reference No. E-054-00/0 filed 30 Jun 2000

Licensing Contact: Marlene Shinn; 301/496-7056 ext. 285; e-mail: shinnm@od.nih.gov

Thyroid hormone disorders are among the most common problems in the Western world. These include hypo-and hyper-thyroidism (including goiter), as well as obesity and developmental abnormalities caused by excess or deficient levels of thyroid hormones during pregnancy.

The NIH announces the discovery of a protein, which is a member of the CD98 light-chain permease family, which acts as a thyroid hormone transporter across vertebrate cell membranes. This protein provides a missing link in the chain by which thyroid hormones in the blood reach the cell nucleus. By utilizing the CDNA of this protein, genomic libraries can be screened for sequences capable of being used as primers for use in diagnostics. Also, by targeting this protein through drug discovery, new treatments for thyroid disorders may be found and developed.

Method of Regulating Interleukin-12 (IL-12) Production by Administering CCR5 Agonists and Antagonists

Sher et al. (NIAID)

PCT/US00/01019 filed 14 Jan 2000

Licensing Contact: J.P. Kim; 301/496-7056 ext. 264; e-mail: kimj@od.nih.gov

Interleukin-12 (IL-12) is a cytokine produced by the body which is necessary for the development of effective cellular immunity against many microbial agents. Increasing IL-12 production has been shown to both enhance the immune clearance of microbial agents as well as augment the protection induced by vaccines. At the same time a number of inflammatory diseases are associated with the excess production of this cytokine. Therefore, methods are needed to both boost IL-12 production for the induction of host resistance as well as suppress it to treat these immunopathologic disorders.

The present invention relates to methods for increasing IL-12 Start Printed Page 77654production in a cell by administering CCR5 agonists and methods for decreasing IL-12 production in a cell administering CCR5 antagonists. The invention also relates to methods for increasing IL-12 production by administering CCR5 agonists and to methods for decreasing IL-12 production in a subject by administering CCR5 antagonists.

Start Signature

Dated: November 11, 2000.

Jack Spiegel,

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

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[FR Doc. 00-31526 Filed 12-11-00; 8:45 am]

BILLING CODE 4140-01-P