National Institutes of Health, Public Health Service, HHS.
This is notice, in accordance with 35 U.S.C. 209(c)(1) and 37 CFR part 404.7(a)(1)(i), that the National Institutes of Health, Department of Health and Human Services, is contemplating the grant of an exclusive patent license to practice the inventions embodied in U.S. Provisional Patent Application No. 60/850,132, filed October 6, 2006, now abandoned (HHS Ref. No. E-227-2006/0-US-01); U.S. Provisional Patent Application No. 60/864,153, filed November 02, 2006, now abandoned (HHS Ref. No. E-227-2006/1-US-01); U.S. Provisional Patent Application No. 60/888,754, filed February 07, 2007, now abandoned (HHS Ref. No. E-227-2006/2-US-01); U.S. Provisional Patent Application No. 60/910,549, filed April 06, 2007, now abandoned (HHS Ref. No. E-227-2006/3-US-01); U.S. Provisional Patent Application No. 60/956,375, filed August 16, 2007, now abandoned (HHS Ref. No. E-227-2006/4-US-01); PCT Patent Application No. PCT/2007/080647, filed October 5, 2007, now abandoned (HHS Ref. No. E-227-2006/5-PCT-01); U.S. Patent Application No. 12/444,364, filed October 5, 2007 (HHS Ref. No. E-227-2006/5-US-02); Canadian Patent Application (not yet determined) (HHS Ref. No. E-227-2006/5-CA-03); Australian Patent Application No. 2007319576, filed October 5, 2007 (HHS Ref. No. E-227-2006/5-AU-04); and European Patent Application No. 07868382.8, filed October 5, 2007 (HHS Ref. No. E-227-2006/5-EP-05), all of which are entitled “Prevention of Tissue Ischemia, Related Methods and Compositions”, developed by Dr. David Roberts (NCI), Dr. Jeffrey Isenberg, and Dr. William Frazier. The patent rights in these inventions have been assigned to the United States of America. The prospective exclusive license territory may be “worldwide”, and the field of use may be limited to: (1) “The use of antibodies including humanized antibodies reacting with CD47 or related antigens, precursors, or molecules, and isolated and/or recombinant fragments, and conjugates Start Printed Page 34767with an affinity for CD47 for the preservation or resuscitation of organs and tissues for transplantation”; (2) “the use of antibodies including humanized antibodies reacting with CD47 or related antigens, precursors, or molecules, and isolated and/or recombinant fragments, and conjugates with an affinity for CD47 for treating or preventing vascular diseases, including but not limited to, pulmonary hypertension, sickle cell disease, myocardial infarction, stroke, and tissue ischemia resulting from trauma and surgical procedures”; (3) “the use of antisense oligonucleotides or RNA formulations of stabilized composition to reduce expression of CD47 for treating wounds and/or burns and for use in reconstructive surgery”; and (4) “use of small molecules antagonists of CD47 for treating or preventing vascular diseases including, but not limited to, thrombosis, hypertension, peripheral artery disease, renal artery disease, and ischemia resulting from atherosclerosis” to Vasculox, Inc., having an office in at least St. Louis, Missouri, U.S.A. The patent rights in these inventions have been assigned to the United States of America.
Only written comments and/or applications for a license which are received by the NIH Office of Technology Transfer on or before September 15, 2009 will be considered.
Requests for copies of the patent application, inquiries, comments, and other materials relating to the contemplated exclusive license should be directed to: Charlene A. Sydnor, Ph.D., Licensing and Patenting Manager, Office of Technology Transfer, National Institutes of Health, 6011 Executive Boulevard, Suite 325, Rockville, MD 20852-3804; Telephone: (301) 435-4689; Facsimile: (301) 402-0220; E-mail: firstname.lastname@example.org.End Preamble Start Supplemental Information
Nitric Oxide (NO) plays an important role as a major intrinsic vasodilator, and increases blood flow to tissues and organs. Disruption of this process leads to peripheral vascular disease, ischemic heart disease, stroke, diabetes and many more significant diseases. The inventors have discovered that the matrix protein thrombospondin1 (TSP1) blocks the beneficial effects of NO, and prevents it from dilating blood vessels and increasing blood flow to organs and tissues. Additionally, they discovered that this regulation requires TSP1 interaction with its cell receptor, CD47. Relief of this inhibition in genetically altered mice lacking either TSP1 or CD47 results in dramatically improved blood flow and increased tissue oxygenation. Further, by using reagents such as monoclonal antibodies and peptides that block TSP1-CD47 interaction, or agents such as antisense oligonucleotides or morpholinos that reduce the level of CD47 or TSP1, blood flow can dramatically increase to ischemic tissues in vivo. Inhibition of TSP1 signaling at the level of CD47 expression and/or activation significantly improves the survival of tissue in an ischemic environment.
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 part 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 establishes that the grant of the license would not be consistent with the requirements of 35 U.S.C. 209 and 37 CFR part 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: July 10, 2009.
Richard U. Rodriguez,
Director, Division of Technology Development and Transfer, Office of Technology Transfer, National Institutes of Health.
[FR Doc. E9-17038 Filed 7-16-09; 8:45 am]
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