National Institutes of Health, Public Health Service, DHHS.
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.
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; firstname.lastname@example.org.
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, email@example.com. Start Printed 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; firstname.lastname@example.org.
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.Start Signature
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