[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 <greek-a>-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-<greek-g> (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 <greek-a> chemokine 
family. Members of this chemokine family, PF4, PBP, CTAP-III 
<greek-b>TG, NAP-2, IL-8 GRO<greek-a>, GRO<greek-b>, GRO<greek-g>, 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]
BILLING CODE 4140-01-M