Prospective Grant of Co-Exclusive License: Use Fully Human and/or Humanized Monoclonal Antibodies Against IGF-I and/or IGF-II for the Treatment of Human Cancers

AGENCY:

National Institutes of Health, Public Health Service, HHS.

ACTION:

Notice.

SUMMARY:

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 a co-exclusive patent license to practice the inventions embodied in U.S. Patent Application No. 12/296,328 entitled, “Human IGF-I-Specific and IGF-I and IGF-II Cross-Reactive Human Monoclonal Antibodies” and all foreign counterparts [HHS Ref. No. E-336-2005/0] to Trubion Pharmaceuticals, Inc., which is located in Seattle, Washington. The patent rights in this invention have been assigned to the United States of America.

The prospective co-exclusive license territory may be worldwide and the field of use may be limited to the use of the antibodies and their method of use in the Licensed Patent Rights for the treatment of human cancers.

DATES:

Only written comments and/or applications for a license which are received by the NIH Office of Technology Transfer on or before April 27, 2009 will be considered. This notice updates the Federal Register Notice published in 73 FR 32719, June 10, 2008.

ADDRESSES:

Requests for copies of the patent application, inquiries, comments, and other materials relating to the contemplated co-exclusive license should be directed to: Whitney A. Hastings, M.S., Licensing and Patenting Manager, Office of Technology Transfer, National Institutes of Health, 6011 Executive Boulevard, Suite 325, Rockville, MD 20852-3804. Telephone: (301) 451-7337; Facsimile: (301) 402-0220; E-mail: hastingw@mail.nih.gov.

SUPPLEMENTARY INFORMATION:

The type 1 insulin-like growth factor (IGF) receptor (IGF1R) is over-expressed by many tumors and mediates proliferation, motility, and protection from apoptosis. Agents that inhibit IGF1R expression or function can potentially block tumor growth and metastasis. Its major ligands, IGF-I and IGF-II, are over-expressed by multiple tumor types. Previous studies indicate that inhibition of IGF-I and/or IGF-II binding to its cognizant receptor negatively modulates signal transduction through the IGF pathway and concomitant cell growth. Therefore, use of humanized or fully human antibodies against IGFs represents a valid approach to inhibit tumor growth.

The above identified patent applications discloses three (3) novel fully human monoclonal antibodies designated m705, m706, and m708, which are specific for insulin-like growth factor (IGF)-I. Two (2) of the three (3) antibodies, m705 and m706 are specific for IGF-I and do not cross react with IGF-II and insulin while, m708 cross reacts with IGF-II.

These antibodies can be used to prevent binding of IGF-I to its concomitant receptor IGFIR, consequently, modulating diseases such as cancer. Additional embodiments describe methods for treating various human diseases associated with aberrant cell growth and motility including breast, prostate, and leukemia carcinomas. Thus, these novel antibodies may provide a therapeutic intervention for multiple carcinomas without the negative side effects associated with insulin inhibition.

The prospective co-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 co-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 establishes 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 co-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.