National Institutes of Health, Public Health Service, DHHS.
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.
Licensing information and copies of the U.S. patent applications listed below may be obtained by contacting Richard U. Rodriguez, M.B.A., at the Office of Technology Transfer, National Institutes of Health, 6011 Executive Boulevard, Suite 325, Rockville, Maryland 20852-3804; telephone: 301/496-7056 ext. 287; fax: 301/402-0220; e-mail: email@example.com. A signed Confidential Disclosure Agreement will be required to receive copies of the patent applications.
Identification of a Novel Amplified Gene, MB1, at 17q23
Anne H Kallioniemi, Maarit T Barlund, Outi M Monni, Juha T Kononen, Olli P Kallioniemi (NHGRI)
DHHS Reference No. E-038-00/0 filed 13 Dec 1999
DNA amplification at 17q23 is one of the most common genetic alterations in breast cancer. Genes affected by this amplification may have a critical role in Start Printed Page 21775breast cancer development and progression and may provide targets for anti-cancer therapy. The inventors have identified a novel gene from the amplified region, named MB1, which has no homology to any known genes. MB1 is amplified in about 9% of primary breast tumors and is overexpressed in breast cancer cell lines with amplification. MB1 may define a critically important breast cancer gene which could have significance for development of improved diagnostics against breast cancer.
The Use of Recombinant Cholera Toxin-B for the Treatment of Inflammatory Bowel Disease
Warren Strober, Monica Boirivant, Ivan J Fuss, Brian L Kelsall (NIAID)
Serial No. 60/165,111 filed 12 Nov 1999
The present invention provides methods of treating or preventing inflammation in a subject, comprising administering to the subject an effective amount of cholera toxin subunit B (CT-B). In particular, the present invention provides methods of decreasing the activity of interferon-gamma in a subject, decreasing the activity of IL-12 in a subject, and treating or preventing a Th1 T-cell mediated autoimmune disorder.Start Signature
Dated: April 18, 2000.
Director, Division of Technology Development and Transfer, Office of Technology Transfer, National Institutes of Health.
[FR Doc. 00-10181 Filed 4-21-00; 8:45 am]
BILLING CODE 4140-01-P