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 Marlene Shinn, J.D., at the Office of Technology Transfer, National Institutes of Health, 6011 Executive Boulevard, Suite 325, Rockville, Maryland 20852-3804; telephone: 301/496-7056 ext. 285; fax: 301/402-0220; e-mail: firstname.lastname@example.org. A signed Confidential Disclosure Agreement will be required to receive copies of the patent applications.
Inhibition of Smad3 To Prevent Fibrosis and Improve Wound Healing
Anita B. Roberts et al. (NCI)
DHHS Reference No. E-070-00/0 filed 19 May 2000; PCT/US00/13725
Millions of dollars are spent each year to heal chronic non-healing wounds and in the treatment of severe burn patients. The NIH announces a new technology that may lead to improved approaches to treatment of burn patients and the reduction of scarring and more rapid closure of both acute (surgical) and chronic wounds (e.g., diabetic, decubitus, and venus statis ulcers).
Smad2 and Smad3 are highly homologous cytoplasmic proteins which function to transduce signals from Transforming Growth Factor-beta (TGF-β) and activin receptors to promoters of target genes found in the nucleus. This new technology indicates that interference with specific signaling pathways downstream of TGF-β may be more selective and have a better outcome than approaches aimed at blocking all effects of this pleiotropic cytokine. Specifically, it is proposed that elimination or inhibition of Smad3 may interfere with fibrogenic mechanisms and reduce the accumulation of scar tissue associated with high dose radiation and wound healing, while increasing the rate of re-epithelialization of wounds.
Although this technology is still in an early stage, our researchers have obtained solid evidence of the involvement of Smad3 in these processes by use of a Smad3 null mouse model which they have developed. Based on these results, it is believed that antisense Smad3 or small molecule inhibitors of Smad3 will have clinical applications in wound healing, in improving growth and reducing unwanted fibrosis of autologous skin grafts for treatment of burn patients, and in treatment of radiation fibrosis and other fibrotic diseases associated with chronic inflammation. In addition, the discovery of inhibitors to Smad3 signaling may lead to radiation dose escalation and accelerated tumor cell death while reducing the side effects associated with radiation therapy. Start Printed Page 54287
Anti-γ-H2A Antibody and Method for Detecting DNA Double-Stranded Breaks
William M. Bonner, Efthimia P. Rogakou (NCI)
Serial No. 09/351,721 filed 12 Jul 1999
There presently exist assays for determining DNA breakage due to stresses such as radiation and toxins. These include the TUNEL assay and single cell gel electrophoresis, among others. The difficulty in using these and other assays arises in that a great number of DNA breaks are necessary for adequate detection of the breakage. Since only 40 double-stranded breaks in the DNA leads to cell death, it is evident that there is a need for an assay with greater specificity.
The NIH announces a new technology which relates to such an improvement over current DNA detection assays, with the ability to be sensitive enough to detect a single DNA double-stranded break in a cell's nucleus. This method for detection uses antibodies directed against a synthetic phosphorylated peptide containing the mammalian γ-H2AX C-terminal sequence for deletion of DNA double-stranded breaks. It centers on the activity of the H2A histone. In response to a DNA break, H2A can become phosphorylated in great numbers and provide protection for the break site to assist in repair. The antibody and method available show specificity for this occurrence and thus allow detection at levels much lower than are presently needed by other detection techniques. Use of such technology could be widespread, both as a diagnostic tool and with specific DNA breakage-related disease and syndrome research.Start Signature
Dated: August 29, 2000.
Director, Division of Technology Development and Transfer, Office of Technology Transfer, National Institutes of Health.
[FR Doc. 00-22881 Filed 9-6-00; 8:45 am]
BILLING CODE 4140-01-P