[Federal Register: August 2, 2004 (Volume 69, Number 147)]
[Notices]               
[Page 46169-46170]
From the Federal Register Online via GPO Access [wais.access.gpo.gov]
[DOCID:fr02au04-57]                         

-----------------------------------------------------------------------

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.

-----------------------------------------------------------------------

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.

Griffithsin, Glycosylation-Resistant Griffithsin, and Related 
Conjugates, Compositions, Nucleic Acids, Vectors, Host Cells, Methods 
of Production and Methods of Using

    Drs. Barry O'Keefe, Michael Boyd, and Toshiyuki Mori (NCI); U.S. 
Provisional Application No. 60/576,056 filed 01 Jun 2004 (DHHS 
Reference No. E-106-2003/0-US-01); Licensing Contact: Sally Hu; 301/
435-5606; hus@mail.nih.gov.
    This invention provides: (1) Isolated and purified antiviral 
peptides or antiviral proteins named griffithsin; (2) purified nucleic 
acid encoding griffithsin or a fragment thereof; (3) vectors comprising 
such a nucleic acid; a host cell comprising such a nucleic acid or 
vector; (4) a conjugate comprising all or part (such as an antiviral 
part) of the griffithsin; (5) antibodies that bind griffithsin; (6) 
methods of producing griffithsin and a conjugate thereof; (7) methods 
of inhibiting prophylactically and therapeutically a viral infection 
e.g., HIV, influenza; and, (8) vaccine development and screening 
assays. Since picomolar concentrations of griffithsin irreversibly 
inactivate human clinical isolates of HIV and the griffithsin protein 
can also target other retroviruses (e.g. FIV, SIV and HTLV) and non-
retroviruses (influenza, measles, ebola) having envelope constituents 
similar to HIV, this invention may represent potential new therapeutic 
or prophylactic applications against viruses, including the causative 
agent for AIDS.

Activation of Nerve Growth Factor Receptor Trophic Functions

    Lino Tessarollo et al. (NCI); U.S. Provisional Application No. 60/
509,158 filed 07 Oct 2003 (DHHS Reference No. E-013-2003/0-US-01); 
Licensing Contact: Norbert Pontzer; 301/435-5502, 
pontzern@mail.nih.gov.

[[Page 46170]]

    Neurotrophins, such as Nerve Growth Factor (NGF), are crucial to 
the maintenance and survival of neurons of the peripheral and central 
nervous system. Although these actions have potential therapeutic use 
in the treatment of a number of neurodegenerative diseases, problems 
with peripheral administration of these fairly large molecules limits 
their clinical usefulness. Survival signaling of neurotrophins is 
mediated mainly through binding to cell surface Trk tyrosine kinase 
receptors. The juxtamembrane region of the NGF TrkA receptor binds two 
key adapter proteins, Shc and FRS-2/SNT, which become tyrosine 
phosphorylated and provide a scaffold for other signaling proteins. The 
binding of FRS-2/SNT to TrkA is also affected by a neighboring three 
amino acid KFG domain conserved in all Trk receptors. These inventors 
found that deletion of the three KFG amino acids affects binding and 
activation of the adaptor proteins FRS-2/SNT and Shc. This effect 
increases the general ability to activate downstream TrkA activated 
signaling pathways in response to NGF. This molecular phenotype leads 
biologically to a trophic effect on the cholinergic neurons of the 
basal forebrain and of the striatum in vivo. This invention provides a 
target for selecting small drugs that mimic the effect of KFG domain 
deletion and thus promote trophic effects in degenerative diseases.

Compositions and Methods for Diagnostics and Therapeutics for 
Hydrocephalus

    Perry J. Blackshear, Darryl C. Zeldin, Joan P. Graves, Deborah J. 
Stumpo (NIEHS); U.S. Provisional Patent Application No. 60/374,184 
filed 19 Apr 2002 (DHHS Reference No. E-163-2002/0-US-01); U.S. 
Provisional Patent Application No. 60/388,266 filed 13 Jun 2002 (DHHS 
Reference No. E-163-2002/1-US-01); PCT Application No. PCT/US03/12348 
filed 18 Apr 2003, which published as WO 03/088919 on 30 Oct 2003 (DHHS 
Reference No. E-163-2002/2-PCT-01); Licensing Contact: Pradeep Ghosh; 
301/435-5282; ghoshpr@mail.nih.gov.
    Congenital hydrocephalus is a public health problem and a 
significant population suffers from this birth defect in the United 
States. It has been estimated that a significant number of patients 
with congenital hydrocephalus also suffer from aqueductal stenosis. 
Congenital hydrocephalus has an adverse effect on developing brain and 
may persist as neurological defects in children and adults. Some of 
these defects may manifest in form of mental retardation, cerebral 
palsy, epilepsy and visual disabilities. The cost of treatment for such 
disorders may exceed $100 million annually. Efficient diagnostics to 
determine the risks of development of hydrocephalus are lacking in the 
market.
    This invention relates to RFX4--v3 proteins and nucleic acids 
encoding the RFX4--v3 proteins. RFX4--v3 proteins are associated with 
congenital hydrocephalus. Congenital hydrocephalus is a common birth 
defect and many cases of hydrocephalus are caused by chromosome X-
linked genetic mutations. The present invention provides assays for the 
detection of RFX4--v3 polymorphisms associated with congenital 
hydrocephalus that may lead to the determination of an individual's 
risk of developing disease states and conditions. Therefore, the 
present invention would be most useful in developing diagnostic tests 
for abnormalities that may lead to the development of hydrocephalus and 
thus, has a market potential of substantial significance.

    Dated: July 23, 2004.
Steven M. Ferguson,
Director, Division of Technology Development and Transfer, Office of 
Technology Transfer, National Institutes of Health.
[FR Doc. 04-17467 Filed 7-30-04; 8:45 am]

BILLING CODE 4140-01-P