National Institutes of Health, Public Health Service, DHHS.
This is notice, in accordance with 35 U.S.C. § 209 (c) (1) and 37 CFR § 404.7 (a) (1) (i), that the National Institutes of Health, Department of Health and Human Services is contemplating the grant of an exclusive license to practice the inventions embodied in PCT Patent Application S/N PCT/US99/27817 (filed November 23, 1999) based on U.S. Patent Application 60/109,957 (filed November 25, 1998), entitled “Antagonists of the αEβ7 Integrin as Therapeutic Agents for Inflammatory Diseases”, to BioSeek, Inc., having a place of business in San Francisco, CA. The patent rights in these inventions have been assigned to the United States of America.
The prospective exclusive license territory will be worldwide and the field of use may be limited to αEβ7-related human therapeutics for the treatment of inflammatory diseases.
Only written comments and/or license applications which are received by the National Institutes of Health on or before August 11, 2000 will be considered.
Requests for copies of the patent, inquiries, comments and other materials relating to the contemplated exclusive license should be directed to: Vasant Gandhi, J.D., Ph.D., Technology Licensing Specialist, Office of Technology Transfer, National Institutes of Health, 6011 Executive Boulevard, Start Printed Page 36837Suite 325, Rockville, MD 20852-3804; Telephone: (301) 496-7056, X224; Facsimile (301) 402-0220; E-mail email@example.com.End Preamble Start Supplemental Information
The pathogenesis of inflammatory reactions may depend upon the traffic of inflammatory mediating cells from sites of induction to sites of inflammation. This trafficking is known to be mediated, in part, by the interaction of the integrin, α4β7, and the addressin, mucosa adressin cell adhesion molecule-1. This homing, which governs the entry of cells into tissues, is accompanied by additional adhesion molecule-ligand interactions that ensure the retention of cells in the target tissue.
The inventors believe the integrin, αEβ7, may play a role in retaining intraepithelial lymphocytes in the intraepithelial site via its interaction with E-cadherin. Experiments have shown in IL-2-/- mice, that administration of anti-αEβ7 can prevent colonic inflammation and reverse pre-existing inflammation. This data is important because it strongly suggests that both entry and retention of cells are necessary for the induction and maintenance of colitis in these IL-2-/- mice. The present technology relates to methods for treating inflammatory reactions for but not necessarily limited to: autoimmune diseases, graft-versus-host disease and transplantation rejections.
The prospective exclusive license: will be royalty-bearing and will comply with the terms and conditions of 35 U.S.C. § 209 and 37 CFR 404.7. The prospective exclusive license may be granted unless within sixty (60) days from the date of this published notice, the NIH receives written evidence and argument that establish that the grant of the license would not be consistent with the requirements of 35 U.S.C. § 209 and 37 CFR 404.7.
Applications for a license in the field of use filed in response to this notice will be treated as objections to the grant of the contemplated exclusive license. Comments and objections submitted to this notice will not be made available for public inspection and, to the extent permitted by law, will not be released under the Freedom of Information Act, 5 U.S.C. § 552.Start Signature
Dated: June 1, 2000.
Director, Division of Technology Development and Transfer, Office of Technology Transfer.
[FR Doc. 00-14749 Filed 6-9-00; 8:45 am]
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