[Federal Register Volume 65, Number 174 (Thursday, September 7, 2000)]
[Notices]
[Pages 54286-54287]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 00-22881]


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DEPARTMENT OF HEALTH AND HUMAN SERVICES

National Institutes of Health


Government-Owned Inventions; Availability for Licensing

AGENCY: National Institutes of Health, Public Health Service, DHHS.

ACTION: Notice.

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SUMMARY: 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.

ADDRESSES: 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: 
[email protected]. 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-) 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- 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.

[[Page 54287]]

Anti--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 
-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.

    Dated: August 29, 2000.
Jack Spiegel,
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