Skip to Content

Notice

Government-Owned Inventions; Availability for Licensing

Document Details

Information about this document as published in the Federal Register.

Published Document

This document has been published in the Federal Register. Use the PDF linked in the document sidebar for the official electronic format.

Start Preamble

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.

NAG-1: A Non-Steroidal Anti-Inflammatory Drug Related Gene Which Has Anti-Tumorigenic Properties

Thomas E. Eling, Seung Joon Baek (NIEHS)

DHHS Reference No. E-170-00/0 filed 08 Sep 2000

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

Non-steroidal anti-inflammatory drugs (NSAIDs) are widely used in the treatment of inflammatory disease, and their anti-inflammatory effects are believed to result from their ability to inhibit the formation of prostaglandins by prostaglandin H synthase (COX). Two forms of prostaglandin H have been identified, COX-1 and COX-2. The former seems to be constitutively expressed in a variety of tissues while the high expression of the latter has been reported in colorectal tumors. NSAIDs have been shown to be effective in reducing human colorectal cancers and possibly breast and lung cancers. While the exact mechanism(s) by which NSAIDs function has not been elucidated, they could potentially play a critical role in detecting, diagnosing and treating inflammatory diseases as well as cancer. The present invention relates to screening methods for the identification of agonistic and/or antagonistic agents for the activation of the promoter region of NAG-1. Additional claims are directed to 1) the Start Printed Page 75724DNA sequence of NAG-1, 2) compositions containing the NAG-1 sequence and 3) methods for treating cancer patients using NAG-1.

Novel MHC Class II Restricted T Cell Epitopes from the Cancer Antigen, NY-ESO-1

DHHS Reference No. E-090-00/0 filed 28 Jan 2000 and

MHC Class II Restricted CD4+ T Cell Epitopes From NY-ESO-1 Presented by DP

DHHS Reference No. E-227-00/0 filed 29 Sep 2000

Wang et al. (NCI)

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

NY-ESO-1 is a known tumor antigen which is expressed on a broad range of tumor types, including melanoma, breast, bladder, ovarian, prostate, head and neck cancers, neuroblastoma, and small cell lung cancer. The above-referenced inventions embody the identification of a number of novel immunogenic peptide epitopes, and analogs thereof, which are derived from the NY-ESO-1 tumor antigen.

DHHS Reference No. E-090-00/0 serves to identify novel MHC Class II restricted epitopes of NY-ESO-1 which are recognized by CD4+ T cells. DHHS Reference No. E-227-00/0 embodies the identification of two additional immunogenic peptide epitopes of NY-ESO-1. The latter two epitopes are presented by HLA-DP4, a prevalent MHC Class II allele present in 43-70% of Caucasians. The inventors also determined that the DP allele is highly associated with the NY-ESO-1 antibody production. In addition, one of these epitopes has dual HLA A2 and DP4 specificity, thereby has the potential to generate both CD4+ and CD8+ tumor specific T cells. These epitopes may be of great value as prophylactic and/or therapeutic cancer vaccines for use against a number of common cancers.

T-Cell Epitope of MAGE-12 and Related Nucleic Acids, Vectors, Cells, Compositions, and Methods of Inducing an Immune Response to Cancer

Monica Panelli, Francesco Marincola, Maria Bettinotti (NCI)

DHHS Reference No. E-056-00/0 filed 03 Mar 2000

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

The current invention embodies the identification of a T-cell epitope from the cancer-specific antigen MAGE-12. The MAGE family of genes encodes human tumor specific antigens (TSA), and various genes of this family are expressed by tumors of different histologies (melanoma, lung, colon, breast, laryngeal cancer, sarcomas, certain leukemias) and not by normal cells (except testis and placenta). The MAGE-12 peptide which is the subject of the current invention is a specific epitope within MAGE-12 (residues170-178) which is recognized by tumor infiltrating lymphocytes in the context of HLA-Cw0702 (a common HLA type in the Caucasian population). This T-cell epitope is advantageous in that it represents a novel tumor rejection antigen for use as a peptide vaccine against melanoma or other cancer types expressing MAGE-12 and may therefore be of great value for use in cancer immunotherapy.

Secreted Frizzled Related Protein, sFRP, Fragments and Methods of Use Thereof

JS Rubin, A Uren (both of NCI), and F Reichsman, S Cumberledge

Serial No. 09/546,043 filed 10 April 00

Licensing Contact: Susan S. Rucker; 301/496-7056 ext 245; e-mail: ruckers@od.nih.gov

This application relates to signal transduction pathways and mechanisms. More particularly, the application describes various active fragments of the secreted Wnt binding protein sFRP-1 (s ecreted F rizzled R elated P rotein-1). The sFRP-1 fragments described are capable of binding to Wnt and therefore are able to modulate Wnt activity. The fragments may or may not contain the cysteine rich domain (CRD) of sFRP-1 suggesting that the CRD is not essential for Wnt binding. In addition, in contrast to earlier findings employing higher levels of sFRP-1, the ability of sFRP-1 to enhance Wnt signaling at low levels is also described suggesting biphasic regulation of Wnt signaling by sFRP-1. The sFRP-1 fragments described herein may be useful in the further study of Wnt signaling as well as targets for the development of small molecules which can modulate Wnt signaling. PHS also owns additional intellectual property related to sFRP-1 which is described in US Patent Application Serial Number 09/087,031 and which has been published as WO 98/54325 (12/03/1998).

This work has appeared, in part, in Uren, A et al. JBC 275(6): 4374-4382 (Feb 11, 2000).

Start Signature

Dated: November 22, 2000.

Jack Spiegel,

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

End Signature End Preamble

[FR Doc. 00-30714 Filed 12-1-00; 8:45 am]

BILLING CODE 4140-01-P