[Federal Register Volume 68, Number 216 (Friday, November 7, 2003)]
[Notices]
[Pages 63112-63113]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 03-28055]


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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 invention listed below is owned by an agency of the U.S. 
Government and is 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 
application 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 application.

Isolation of Hybridomas Producing Monoclonal Antibodies (MAbs) 
Inhibitory to Human CYP2J2

Dr. Darryl Zeldin (NIEHS), Dr. Harry Gelboin (NCI), et al.
DHHS Reference No. E-337-2003/0--Research Tool.
Licensing Contact: Marlene Shinn-Astor; 301/435-4426; 
[email protected].

    Cytochromes P450 catalyze the NADPH-dependent oxidation of 
arachidonic acid to various eicosanoids found in several species. The 
eicosanoids are biosynthesized in numerous tissues including pancreas, 
intestine, kidney, heart, and lung where they are involved in many 
different biological activities.
    The NIH announces three specific monoclonal antibodies that 
strongly inhibit and/or immunoblot the human cytochrome P450 2J2 
(CYP2J2). MAb 6-5-20-8 selectively inhibits CYP2J2-mediated arachidonic 
acid metabolism by more than 80% and also immunoblots the enzyme. MAb 
6-2-16-1 also selectively inhibits arachidonic acid metabolism by more 
than 80%, but does not immunoblot the enzyme. MAb 5-3-2-2 is not 
inhibitory, but selectively immunoblots the enzyme. These antibodies 
can be used to identify and quantify inter-individual variation in 
physiological functions and to study pharmacological drug metabolism in 
various tissues.
    This research is also described in: Sun et al., Circ. Res. 90: 
1020-1027, 2002; King et al., Mol. Pharmacol. 61: 840-852, 2002; Yang 
et al., Mol. Pharmacol. 60: 310-320, 2001; Zeldin, J. Biol. Chem. 276: 
36059-36062, 2001; Node et al., J. Biol. Chem. 276: 15983-15989, 2001; 
Node et al., Science 285: 1276-1279, 1999; Wu et al., J. Biol. Chem. 
271: 3460-3468.

TNF-[alpha] Converting Enzyme Inhibitory Agents and Stimulatory Agents

Dr. Stewart Levine et al. (NHLBI).
U.S. Provisional Patent Application filed 24 Sep 2003 (DHHS Reference 
No. E-208-2003/0-US-01).
Licensing Contact: Marlene Shinn-Astor; 301/435-4426; 
[email protected].


[[Page 63113]]


    The action of Tumor Necrosis Factor alpha (TNF-[alpha]) has been 
implicated in such diseases as arthritis, sepsis, ulcerative colitis, 
multiple sclerosis, Crohn's disease, septic shock, graft rejection, 
cachexia, insulin resistance, post-ischemic reperfusion injury, tumor 
metastasis, tissue ulceration, abnormal wound healing, periodontal 
disease, bone disease, proteinuria, aneurismal aortic disease, 
degenerative cartilage loss, demyelinating diseases of the nervous 
system, and HIV infection. TNF-[alpha] converting enzyme (TACE) or ADAM 
17 (A Disintegrin And Metalloprotease) is a member of a family of zinc 
metalloproteases, and is an important regulator of inflammation, immune 
regulation, and cellular proliferation as a consequence of its ability 
to catalyze the activation of TNF-[alpha] from a membrane bound to a 
soluble form.
    The NIH announces the identification of a protein, corresponding to 
the amino-terminus of the TACE prodomain, that possesses a TACE 
inhibitory activity that is independent of a cysteine-switch mechanism. 
This TACE inhibitory protein could be used as a new therapeutic agent 
against chronic inflammatory diseases that are mediated by TNF-[alpha].

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

Anita Roberts (NCI).
U.S. Provisional Patent Application No. 60/441,297 filed 17 Jan 2003 
(DHHS Reference No. E-062-2003/0-US-01).
Licensing Contact: Marlene Shinn-Astor; 301/435-4426; 
[email protected].

    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-
[beta]) 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-[beta]-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: October 28, 2003.
Steven M. Ferguson,
Director, Division of Technology Development and Transfer, Office of 
Technology Transfer, National Institutes of Health.
[FR Doc. 03-28055 Filed 11-6-03; 8:45 am]
BILLING CODE 4140-01-P