[Federal Register Volume 65, Number 207 (Wednesday, October 25, 2000)]
[Notices]
[Pages 63874-63875]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 00-27356]


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

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 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.

A Cultured Cell Line which Expresses the GLU4 Glucose Transporter 
Isoform Labeled with a Short Hemaglutinin Peptide and a Modified 
Green Fluorescence Protein

Samuel W. Cushman (NIDDK), DHHS Reference No. E-264-00/0 filed 26 Jul 
2000; Licensing Contact: Marlene Shinn; 301/496-7056 ext. 285; email: 
[email protected].
    The aforementioned invention is currently available through a 
Biological Materials License as a research tool. Insulin regulates 
glucose uptake by inducing the translocation of GLUT4, a glucose 
transporter isoform expressed in fat and muscle, from intracellular 
components to the plasma membrane. The NIH announces the discovery of a 
cell line that expresses the GLUT4 glucose transporter isoform with a 
short hemaglutin peptide (HA) and a modified green fluorescent protein 
(GFP). The HA peptide is recognized by a specific antibody when GLUT4 
is in the plasma membrane but not when GLUT4 is sequestered inside the 
cell. The modified GFP can be detected by its fluorescence whether it 
is inside the cell or on the cell surface. This allows the HA label to 
quantitate the GLUT4 subcellular distribution and the GFP label, the 
total GLUT4 expression. Therefore, this invention can be used in high 
through-put screening, as an assay reagent, and it may aid specifically 
in ascertaining compounds that have the insulin-like effect of 
stimulating GLU4 translocation from an intracellular compartment to the 
cell surface.

Dmt-tic Di- and Tri-Peptidic Derivatives and Related Compositions 
and Methods of Use

Lawrence H. Lazarus (NIEHS), DHHS Reference No. E-103-00/0 filed 24 Mar 
2000; Licensing Contact: Marlene Shinn; 301/496-7056 ext. 285; e-mail: 
[email protected].
    A major obstacle in the treatment of many cancers involves the 
clinical manifestation of drug resistance. Currently, toxic substances 
are used in clinical and therapeutic settings to inhibit glycoproteins 
in the cell membrane of some cancer cells that have the ability to pump 
out of the cell drugs that would be potentially lethal. The most common 
of these glycoproteins is the 170-kd ATP-dependent transmembrane efflux 
pump. The multidrug resistance (MDR1) phenotype, however, is not the 
sole source of drug resistance since MDR1 is a member of a superfamily 
of proteins structurally related to the transmembrane P-glycoproteins.
    NIH scientists have prepared a series of -opiod analogs of 
Dmt-tic (2',6'-dimethyl-L-tyrosine-1,2,3,4-tetrahydroisoquinoline-3-
carboxylic acid). At least one of the analogs, which is biologically 
stable and exerts no known side effects, has been observed to inhibit 
the ability of MDR1 to pump out a fluorescent probe from the cell 
membrane. Thus, these analogs might represent novel chemosensitizing 
agents to treat both hematologic malignancies (lymphomas) and solid 
tumors (e.g. breast and colon) without toxic effects in patients.
    In addition, this invention provides more potent -opioid 
antagonists and -opiod antagonists with duel binding

[[Page 63875]]

affinity and biological activity toward -opiod and -
opiod receptors. These compounds therefore, have the potential to treat 
opiate and alcohol abuse, neurological diseases, neuropeptide or 
neurotransmitter imbalances, neurological and immune dysfunction, graft 
rejections through immunosuppression with antagonists, pain control 
through short half-life agonists, and shock and brain injuries.

Scratch Wound Assay Device

Katherine Malinda et al. (NINR), Serial No. 09/496,134 filed 01 Feb 
2000; Licensing Contact: Dale Berkley; 301/496-7735 ext. 223; e-mail: 
[email protected].
    Tissue wounds undergo a complex and ordered series of events to 
repair tissue. These events may include infiltration of inflammatory 
immune cells as part of the process to remove and destroy necrotic 
tissue, increased vascularization by angiogenic factors, and increased 
cell proliferation and extracellular matrix deposition. Although the 
basic process of tissue repair has been characterized, the individual 
steps and factors necessary to carry out this complex series of events 
are not yet well understood or fully identified. Accordingly, there is 
a need to develop a way of reproducibly injuring a layer of cells to 
study the effects of different compounds of treatments on the ability 
of the remaining cells to repair the damaged area.
    The present invention provides a device that reproducibly makes a 
wound of a desired size in a cell layer grown on a cell culture 
material. The device allows researchers to use small volumes of cells 
and test materials suggesting its use as a tool in high throughput 
screening of compounds. This provides researchers with a faster, more 
accurate way of screening large numbers of factors and determining the 
effects of cell growth and migration agents in model wounds produced in 
the cell, organ, or tissue layer.

Method of in vitro T cell Differentiation of CD34+ Progenitor Cells

Ruiz et al. (NIAID), DHHS Reference No. E-206-98/0 filed 29 Oct 1999; 
Licensing Contact: J. P. Kim; 301/496-7056 ext. 264; e-mail: 
[email protected].
    The present invention relates to a human in vitro system for 
inducing the growth and de novo differentiation of T cells from CD34+ 
progenitor cells in the presence of various cytokine cocktails and 
lymph node stroma. The mature T cells which are generated may be used 
to treat individuals with primary or acquired T cell 
immunodeficiencies, including HIV infection.

    Dated: October 13, 2000.
Jack Spiegel,
Director, Division of Technology, Development and Transfer, Office of 
Technology Transfer, National Institutes of Health.
[FR Doc. 00-27356 Filed 10-24-00; 8:45 am]
BILLING CODE 4140-01-P