[Federal Register: October 25, 2000 (Volume 65, Number 207)]
[Notices]
[Page 63874-63875]
From the Federal Register Online via GPO Access [wais.access.gpo.gov]
[DOCID:fr25oc00-96]
-----------------------------------------------------------------------
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:
shinnm@od.nih.gov.
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:
shinnm@od.nih.gov.
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:
berkleyd@od.nih.gov.
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:
kimj@od.nih.gov.
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