[Federal Register Volume 69, Number 190 (Friday, October 1, 2004)]
[Notices]
[Pages 58929-58930]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 04-22148]


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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, HHS.

ACTION: Notice.

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SUMMARY: The inventions listed below are owned by an agency 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 writing to the indicated 
licensing contact at the Office of Technology Transfer, National 
Institutes of Health, 6011 Executive Boulevard, Suite 325, Rockville, 
Maryland 20852-3804; telephone: (301) 496-7057; fax: (301) 402-0220. A 
signed Confidential Disclosure Agreement will be required to receive 
copies of the patent applications.

Cytonectin, Cytonectin Gene and Cytonectin Inhibitors and Binding 
Ligands and Their Use in the Diagnosis and Treatment of Disease

Soni J. Anderson et al. (NCI)

U.S. Provisional Application No. 60/553,977 Filed 18 Mar 2004 (DHHS 
Reference No. E-128-2004/0-US-01); U.S. Provisional Application No. 60/
578,068 Filed 09 Jun 2004 (DHHS Reference No. E-128-2004/1-US-01)
    Licensing Contact: Fatima Sayyid; (301) 435-4521; 
<a href="/cdn-cgi/l/email-protection#a1d2c0d8d8c8c5c7e1ccc0c8cd8fcfc8c98fc6ced7"><span class="__cf_email__" data-cfemail="4e3d2f3737272a280e232f27226020272660292138">[email protected]</span></a>.
    Cytonectin is a 35K molecular weight protein that displays ion-
independent adherence properties, is expressed in a variety of organs 
and tissues and is evolutionarily conserved from human to rodent and 
avian species. Within the body it is thought to serve the function of 
``super glue'' contributing to cell-cell interactions and 3-dimensional 
tissue structure and a physiologic ``do not attack'' signal molecule 
that prevents tissue destruction by cells of monocyte lineage including 
odontoclasts in secondary teeth. It also plays an important role in the 
pathology associated with cancer, arthritis, Alzheimer's and 
Parkinson's disease.
    The present invention relates to cytonectin, to polynucleotides 
that encode cytonectin, to inhibitors and antibodies that bind to 
cytonectin and to the use of compositions in the diagnosis and 
treatment of cytonectin-related diseases and conditions.

Genetic Fingerprint of Acute Stroke

Alison E. Baird (NINDS)

U.S. Provisional Application No. 60/575,279 Filed 27 May 2004 (DHHS 
Reference No. E-306-2003/0-US-01)
    Licensing Contact: Fatima Sayyid; (301) 435-4521; 
<a href="/cdn-cgi/l/email-protection#8af9ebf3f3e3eeeccae7ebe3e6a4e4e3e2a4ede5fc"><span class="__cf_email__" data-cfemail="5f2c3e2626363b391f323e36337131363771383029">[email protected]</span></a>.
    Stroke is the third leading cause of death and the leading cause of 
adult disability in developed countries. Despite the prevalence and 
burden of this disease, stroke precipitants and pathophysiological 
mechanisms in individual patients are often unknown. It is also 
difficult to accurately predict whether a stroke will lead to only 
minor neurological sequelae or more serious medical consequences. 
Although animal experiments in focally ischemic brain tissue have 
indicated that there are alterations in gene expression following a 
stroke, gene expression profiling has not yet been applied to clinical 
human stroke, primarily because brain tissue samples are inaccessible 
and rarely justified.
    The present provisional patent application discloses methods of 
determining whether a subject had an ischemic stroke, methods of 
determining the prognosis of a subject who had an ischemic stroke, as 
well as methods of determining an appropriate treatment regimen for a 
subject who had an ischemic stroke.

Inhibition of Smad3 To Prevent Fibrosis and Improve Wound Healing

Anita B. Roberts et al. (NCI)

U.S. Patent Application No. 10/299,886 Filed 18 Nov 2002 (DHHS 
Reference No. E-070-2000/0-US-06), claiming priority to PCT Application 
No. PCT/US00/13725 Filed 19 May 2000 (DHHS Reference No. E-070-2000/0-
PCT-01)
    Licensing Contact: Marlene Shinn-Astor; (301) 435-4426; 
<a href="/cdn-cgi/l/email-protection#582b3031363635183539313476363130763f372e"><span class="__cf_email__" data-cfemail="98ebf0f1f6f6f5d8f5f9f1f4b6f6f1f0b6fff7ee">[email protected]</span></a>.
    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-beta) 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-beta 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.

[[Page 58930]]

    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.

Use of Smad3 Inhibitor in the Treatment of Fibrosis Dependent on 
Epithelial to Mesenchymal Transition as in the Eye and Kidney

Anita B. Roberts (NCI)

PCT Application No. PCT/US04/03563 Filed 16 Jan 2004 (DHHS Reference 
No. E-062-2003/3-PCT-01)
    Licensing Contact: Marlene Shinn-Astor; (301) 435-4426; 
<a href="/cdn-cgi/l/email-protection#a8dbc0c1c6c6c5e8c5c9c1c486c6c1c086cfc7de"><span class="__cf_email__" data-cfemail="d1a2b9b8bfbfbc91bcb0b8bdffbfb8b9ffb6bea7">[email protected]</span></a>.
    Fibroid scar tissue has been associated with wound healing of the 
epithelial layer following tissue damage created by surgery or other 
means. Examples of which include the opaque scar tissue associated with 
cataract surgery and the fibroid scar tissue produced in several kidney 
diseases such as is seen in unilateral ureteral obstruction.
    Smad2 and Smad3 are highly homologous cytoplasmic proteins which 
function to mediate signals from Transforming Growth Factor Beta (TGF-
B) and activin receptors to promoters of target genes found in the 
nucleus. The NIH announces a technology wherein Smad 3 is now 
implicated in TGF-B-dependent transdifferentiation of epithelial cells 
to mesenchymal cells (EMT), which blocks the endpoint of fibrosis at an 
early stage of differentiation of epithelial cell precursors into 
interstitial fibroblasts. In particular, fibrosis was blocked following 
wounding of the lens of the eye and damage created to the kidney. It is 
believed that an inhibitor of Smad 3 could be used to block fibrosis 
following cataract surgery and lens implantation in patients, as well 
as slowing the progression of end-stage renal disease.

    Dated: September 22, 2004.
Steven M. Ferguson,
Director, Division of Technology Development and Transfer, Office of 
Technology Transfer, National Institutes of Health.
[FR Doc. 04-22148 Filed 9-30-04; 8:45 am]
BILLING CODE 4140-01-P


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