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Government-Owned Inventions; Availability for Licensing

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National Institutes of Health, Public Health Service, DHHS.




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.


Licensing information and copies of the U.S. patent applications Start Printed Page 46648listed 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.

Methods and Structures for Microengineering Neocartilage Scaffolds

Erik Petersen and Richard Spencer (NIA),

DHHS Reference No. E-175-01/0 filed 27 Apr 2001,

Licensing Contact: Marlene Shinn; 301-496-7056 ext. 285; e-mail:

Therapy for joint damage due to trauma, congenital abnormality, or osteoarthritis has in the past only been limited to the replacement of the joint with a prosthesis. Recently, autologous transplantation of chondrocytes has begun to be performed, however, there are several hurdles that have needed to be overcome, including problems with cell loss and heterogeneous development of tissue density.

The NIH announces a new method of growing chondrocytes on a two-dimensional surface patterned biocompatible scaffold. These scaffolds consist of creating uniform contoured surfaces using photolithographic methods and then covering the surface with a polysaccharide gel. The gel is then allowed to cure and then is removed from the template. Chondrocytes that have been isolated from explants are then applied to the surface and attach to the gel. Once attached, the cells create an extracellular matrix within the gel and layers of neocartilage are created within the square depressions. Functional tissue is thereby produced which can be used as grafts and/or implants in humans.

Agents Useful for Reducing Amyloid Precursor Protein and Treating Dementia and Methods of Use Thereof

Nigel H. Greig et al. (NIA),

Serial No. 60/245,329 filed 02 Nov 2000,

Licensing Contact: Norbert Pontzer; 301/496-7736 ext. 284; e-mail:

Alzheimer's disease (AD) is a progressive neurodegenerative condition leading to loss of memory and other cognitive functions. Alzheimer's disease is characterized pathologically by the appearance of senile plaques, primarily composed of amyloid β protein (Aβ), and neurofibrillary tangles in the CNS. Treatments reducing potentially toxic Aβ may thus prevent the occurrence and progression of Alzheimer's disease. As Aβ is derived from the larger β amyloid precursor protein (βAPP), reducing the production of βAPP should provide a therapy for the treatment of Alzheimer's disease.

The production of βAPP is regulated by cytokines, muscarinic receptors, and some cholinesterase inhibitors. The latter also have some utility in treating the symptoms of Alzheimer's disease. The agents and methods disclosed and claimed in this patent application reduce the production of βAPP and Aβ in vivo and in vitro without cholinergic side effects or other toxicity. The agents are structurally related to a known anti-cholinesterase agent in current clinical assessment, but are devoid of anticholinesterase activity and associated side effects. They likely act on a recently described translational regulatory element on βAPP mRNA. Further information as to how these agents effect βAPP processing can be found in the Proceedings of the National Academy of Sciences, Volume 98(13), Pages 7605-7610, June 19, 2001.

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Dated: August 29, 2001.

Jack Spiegel,

Director, Division of Technology, Development and Transfer, Office of Technology Transfer, National Institutes of Health.

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[FR Doc. 01-22355 Filed 9-5-01; 8:45 am]