Agency information collection activities: owned; availability for licensing,

[Federal Register: December 30, 1998 (Volume 63, Number 250)]

[Notices]

[Page 71934-71935]

From the Federal Register Online via GPO Access [wais.access.gpo.gov]

[DOCID:fr30de98-68]

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 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 filedon 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 contacting Susan S. Rucker, J.D., Patent and licensing Specialist, Office of Technology Transfer, National Institutes of Health, 6011 Executive Boulevard, Suite 325, Rockville, Maryland 20852-3804; telephone 301/496-7057 ext. 245; fax: 301/402-0220; e-mail: sr156v@nih.gov. A signed Confidential Disclosure Agreement will be required to receive copies of the patent applications.

cDNA Encoding A Gene, BOG (B5T Over-Expressed Gene), And Its Protein Product

SS Thorgeirsson, JT Woitach, M Zhang (NCI) Serial Nos. 60/079,567 filed27 Mar 98and 60/075,922 filed25 Feb 98.

These applications describe a newly identified gene, termed BOG (B5t Over-Expressed Gene), and its protein product. Rat, murine and human homologs of the gene are described. Human BOG has been mapped to chromosome 20 and murine BOG to chromosome 2.

The applications describe the binding of the BOG gene product with the gene product pRb, of the well-known tumor suppressor gene RB ( retinoblastoma susceptibility gene). The complex formed between Rb and BOG typically does not contain E2F-1 in vivo. This binding property suggests that cells which are transformed/transfected with cDNA or other functional nucleotide sequences which encode the BOG gene product will be useful as tools for studying cell cycle control and oncogenesis.

Studies using rat liver epithelial cell (RLE) lines which are resistant to the growth inhibitory effects of TGF-‹greek-b›1 and primary liver tumors have been shown to over-express BOG. In addition, when normal RLE continuously over-express BOG the cells become transformed and the transformed cells are able to form hepatolblastoma- like tumors when transplanted into nude mice. BOG antisense nucleotides can be used to restore sensitivity to TGF-‹greek-b› in cells which over-express BOG. Therefore, biologics derived from BOG may be useful as diagnostics or therapeutics.

Thymosin ‹greek-a›1 Promotes Tissue Repair, Angiogenesis and Cell Migration

KM Malinda, HD Kleinman (NIDCR), RK Maheshwari, and A Goldstein, Serial Nos. 09/186,476 filed04 Nov 98, 60/069,590 filed12 Dec 97, and 60/065,032 filed10 Nov 97.

These applications describe the use of the compound thymosin ‹greek-a›1 as an agent for promoting wound healing. Thymosin ‹greek-a›1 is a small, 28 mer, peptide which can be made by chemical synthesis or recombinantly. Studies using a punch model for wounds in rats have shown that providing thymosin ‹greek-a›1 either intraperitoneally or topically accelerates wound healing. In addition, thmosin ‹greek-a›1 has been shown to promote endothelial and keratinoctye cell migration in vivo and to promote angiogenesis in vivo.

This work has been published in J. Immunol. 160(2); 1001-6 (Jan 15, 1998).

Double-Stranded RNA Dependent Protein Kinase Derived Peptides To Promote Proliferation of Cells and Tissues in a Controlled Manner

DP Bottaro (NCI), R Petryshyn (EM), Serial No. PCT/US97/14350 filed 29 Jul 97 and 60/023,307 filed30 Jul 97

These applications describe a number of peptides having a minimum size of eight (8) amino acids which act as

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antagonists of PKR (Protein Kinase R). PKR is a critical enzyme in the interferon signaling pathway which has been implicated in cross-talk between the interferon signaling pathway and the TNF-‹greek-a› apoptosis signaling pathway. The peptide antagonists described herein may be use to inhibit apoptosis or to stimulate cell proliferation under conditions of cell cycle arrest, reduced growth or quiescence leading to possible applications in wound healing, cell culture, or skin grafts.

A portion of this work has appeared in Virology 222 (1): 193-200 (August 1, 1996).

AAV4 Vector and Uses Thereof

JA Chiorini, RM Kotin, B Safer (NHLBI), Serial No. 60/025,934 filed 09 Sept 96 and PCT/US97/16266

These patent applications describe the cloning and characterization of the full-length genome of adeno-associated virus type 4 (AAV4). AAV4, like other members of the AAV family may be useful as a vector for gene therapy.

When compared to AAV2 AAV4 may be better suited as a vector due to its larger size which permits efficient encapsidation of a larger recombinant genome, its greater buoyant density which allows for easier separation of AAV4 from contaminating helper virus. Other characteristics of AAV4 which distinguish it from AAV2 and AAV3 are its expanded promoter region, its distinct capsid protein, its different tissue tropism and its ability to bind hemagluttinin (HA). While AAV4 has several distinguishing characteristics from AAV2 and AAV3 it also shares significant homology, greater than 90%, with the Rep proteins of AAV2 and AAV3.

Studies using a lacZ reporter gene suggest that AAV4 can transduce human, monkey, and rat cells. Other studies comparing transduction efficiencies in a number of cell lines, competition cotransduction experiments and the effect of trypsin on transduction efficiency suggest that the cellular receptor for AAV4 is distinct from that of AAV2.

This research has been published in J. Virology 71(9): 6823-33 (Sept 1997) and as PCT Publication 98/11244 (March 19, 1998).

Dated: December 21, 1998. Jack Spiegel, Ph.D., Director, Division of Technology Development and Transfer Office of Technology Transfer.

[FR Doc. 98-34529Filed12-29-98; 8:45 am]

BILLING CODE 4140-01-M