[Federal Register Volume 63, Number 18 (Wednesday, January 28, 1998)]
[Notices]
[Pages 4273-4274]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 98-1967]
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DEPARTMENT OF HEALTH AND HUMAN SERVICES
National Institutes of Health
Government-Owned Inventions; Availability for Licensing
AGENCY: National Institutes of Health, HHS.
ACTION: Notice.
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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.
Novel Attenuated Strains Mycobacterium Tuberculosis
CE Barry, Y. Yuan (NIAID).
Serial No.: 60/025,199 filed 10 July 97.
Licensing Contact: Carol Salata, 301/496-7735 ext 232.
This invention provides for novel attenuated strains of
Mycobacterium tuberculosis and M. bovis. Attenuation is achieved by
down-regulating the expression of the -crystallin heat shock
protein gene (``acr gene''). This gene is essential for virulence of
the organism. Since this strain is isogenic with virulent M.
tuberculosis but for this deletion, the full complement of antigens
remains present and the organism is viable in vitro. The invention
provides for vaccines and methods of vaccinating mammals for protection
against Mycobacterium sp. that cause tuberculosis.
Method of Promoting Tumor Necrosis Using MIG
G Tosato (FDA), J Farber (NIAID), C Sgardari (FDA).
Serial No.: 08/850,914 filed 2 May 97.
Licensing Contact: Jaconda Wagner, 301/496-7735 ext 284.
Monokine induced by IFN- (Mig), which is structurally
related to interferon-inducible protein 10 (IP-10), has been shown to
exhibit antitumor activity. Mig is a member of the chemokine
family. Members of this chemokine family, PF4, PBP, CTAP-III
TG, NAP-2, IL-8 GRO, GRO, GRO, and
IP-10, have been shown to act as an angiogenic or angiostatic factor.
This invention relates to the use of Mig to promote the death of tumor
tissue. It also relates to a method of inhibiting angiogenesis at a
tumor site using Mig.
This research has been published in Blood 1997 Apr 15;89(8):2635-43
and J Leukoc Biol 1997 Mar;61(3):246-57.
A related case is also available for licensing: Serial No. 08/
455,079 filed 31 May 95 entitled ``Interferon-Inducible 10 (IP-10) is a
Potent Inhibitor of Angiogenesis''; inventors are G Tosato, AL
Angiolillo, and C Sgardari.
Formation of Human Bone In Vivo
PG Robey (NIDR), P Bianco (Universita dell Aquilla), Sa Kuznetsov
(NIDR), PH Krebsback (NIDR), DW Rowe (University of Connecticut.
Serial No.: 08/798, 715 filed 12 Feb. 97.
Licensing Contact: Jaconda Wagner, 301/496-7735 ext 284.
This invention provides a model for studying human bone metabolism
in
[[Page 4274]]
vivo. The model system can be used to screen compounds which inhibit or
stimulate bone formation. A protocol using marrow stromal fibroblasts
is also presented. Use of the protocol results in the formation of
self-maintained human bone which supports hematopoiesis. The marrow
stromal fibroblasts combined with the described delivery vehicles can
be implanted into humans to augment bone implants or to repair bone
defects.
This research has been published in J Bone Miner Res 1997
Sep;12(9):1335-47 and Transplantation 1997 Apr 27;63(8):1059-69.
Synthesis and Purification of Hepatitis C Virus Like Particles In
Vitro
TJ Liang and TF Baumert (NIDDK).
Serial No.: 60/030,238 filed 8 Nov 96; PCT/US97/05096 filed 25 Mar.
97.
Licensing Contact: Carol Salata, 301/496-7735 ext 232.
Hepatitis C virus (HCV) is a major causative agent of
posttransfusion and community-acquired hepatitis world-wide. Analysis
of the structural features of HCV has been hampered by the inability to
propagate the virus efficiently in cultural cells and the lack of a
convenient animal model. This invention discloses the production and
purification of HCV-like particles in eukaryotic cells. Infection of
insect cells with a recombinant baculovirus containing the cDNA for the
HCV structural proteins resulted in the formation of HCV-like particles
in cytoplasmic cisternae of the insect cells. Sucrose gradient
purification HCV-like particles exhibited similar biophysical
properties as putative HCV virions. HCV-like particles, purified in
large quantities, may be useful in HCV vaccine development or in
diagnostic kits.
An Enzyme-Linked Immunosorbent Assay (ELISA) to Detect Antibodies to a
Nonstructural Protein of Hepatitis A Virus (HAV)
RH Purcell, T Schultheiss, D Stewart, S Emerson (NIAID).
Serial No.: 60/013, 333 filed 13 Mar. 96; PCT/US97/03428 filed 13
Mar. 97.
Licensing Contact: George Keller, 301/496-7735 ext 246.
The current invention embodies an assay which can differentiate
between an individual who has been vaccinated against Hepatitis A Virus
(HAV), and one who has actually been infected with the virus. HAV
infection results in the production of antibodies against both
structural and nonstructural proteins of the virus. Inactivated HAV
vaccines, which are commonly used for immunization against HAV, cause
the production of antibodies against the structural proteins. Assays
currently in use for determining exposure to HAV measure only
antibodies to structural proteins, and therefore are incapable of
differentiating between individuals who have been infected with HAV and
those who have merely been immunized with the inactivated virus.
The assay embodied in the current invention is capable of detecting
antibodies to the 3C proteinase, which is a nonstructural protein of
HAV. This assay, which utilizes an ELISA for the detection of such
antibodies, should represent a significant improvement over assays
which are currently available.
Restriction Display (RD-PCR) of Differentially Expressed mRNAs
JN Weinstein, J. Buolamwini (NCI).
Serial No.: 60/011, 379 filed 09 Feb 96; PCT/US97/02009 filed 7
Feb. 97.
Licensing Contact: J. Peter Kim, 301/496-7056 ext 264.
This invention provides a kit and methods for detecting gene
expression in cells by reverse transcribing mRNA molecules into cDNA,
and selectively amplifying a subset of the cDNA by a polymerase chain
reaction (PCR) to present a two-dimensional display of the fragments or
for cloning into a vector using restriction enzyme recognition sites
added during the PCR. In one aspect of this invention, only cDNA
corresponding to the 3' end of the mRNA is amplified and displayed or
cloned. In another aspect of the invention, cDNA corresponding to the
entire mRNA molecule is amplified for display or cloning. The method
and kit may be useful in characterizing cells based on their mRNA
content, representing expressed genes, and discovering therapeutics
that alter cellular gene expression by characterizing cells of
different types under a variety of physiological conditions. In
addition to drug discovery, this approach may be used whenever
expression of mRNA is to be assessed, for example, in studies of
malignant transformation, carcinogenesis, immune activation, and
developmental biology.
Selective Elimination of T-Cells that Recognize Specific
Preselected Targets
A Rosenberg (FDA).
Serial No.: 60/002, 964 filed 30 Aug. 95; PCT filed 30 /Aug. 96.
Licensing Contact: Jaconda Wagner, 301/496-7735 ext 284
The invention relates to methods and compositions for the
elimination of T cells that recognize specific preselected targets
which can be used to threat autoimmune diseases and graft rejection.
The invention provides a method for selectively inhibiting or
killing T cells that recognize a specific preselected target molecule
and also for modified killer cells that bear a signal transduction
molecule to which is attached the preselected target molecule.
Recognition of the preselected molecule by a T cell activates the
killer cell which then kills or inhibits the T cell. Where the
preselected molecule is an extracellular domain of an MHC from a
xenograft or an allograft, treatment of the graft recipient with the
modified killer T cells delays or inhibits graft rejection. Similarly,
where the preselected molecule is an MHC that binds the antigenic
determinant of the autoimimune disease, treatment of the organism with
the modified T cells mitigates the autoimmune response directed against
the antigenic determinant.
This research was published in Transpl Immunol 1993; 1(2):93-9.
Dated: January 16, 1998.
Barbara M. McGarey,
Deputy Director, Office of Technology Transfer.
[FR Doc. 98-1967 Filed 1-27-98; 8:45 am]
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