[Federal Register Volume 63, Number 229 (Monday, November 30, 1998)]
[Notices]
[Pages 65798-65799]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 98-31730]


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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, Public Health Service, DHHS.

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 contacting Dennis H. Penn, 
Pharm.D., Technology Licensing Specialist, Office of Technology 
Transfer, National Institutes of Health, 6011 Executive Boulevard, 
Suite 325, Rockville, Maryland 20852-3804; telephone: 301/496-7056 ext. 
211; fax: 301/402-0220. A signed Confidential Disclosure Agreement will 
be required to receive copies of the patent applications.

A Mitochondrial-Specific ATP-Binding Transporter Gene (ABC7) Is An 
Iron Transporter In An Interhited Ataxia-Anemia Syndrome

MC Dean, R Allikmets, AA Hutchinson (NCI)
DHHS Reference No. E-181-98/0 filed Oct 23, 1998

    The gene responsible for the rare genetic disease, X-linked 
siderblastic anemia and ataxia (XLSA/A) has been identified and linked 
to a mutation of the ATP-Binding transporter gene (ABC7). Two sequence 
changes which correspond to amino acid changes at positions 50 and 396 
were detected. This gene may prove useful as a diagnostic for XLSA/A 
carriers or as a means to rule out XLSA/A from other siderblastic 
anemias. ABC7, an iron transporter, may prove to be a valuable tool for 
studying the function and regulation of muscle cells and the loss of 
motor function associated with many diseases with faculty iron 
metabolism, i.e. neuromuscular disease, cardiac disorders and 
neurological disorders.

Compsitions And Uses of FIG-alpha Gene

J Dean, L Liang, S soyal (NIDDK)
Serial No. 60/069,037 filed Dec. 12, 1997

    This application related to an isolated and purified polynucleotide 
encoding an isolated and purified polypeptide associated with the 
expression of zona pellucida genes. The mouse zona pellucida is 
composed of three glycoproteins, ZP1, ZP2 and ZP3, encoded by single-
copy genes whose expression is temporarlly and spatially restricted to 
oocytes. All three proteins are required for the formation of the 
extracellular zona matrix and female mice with a single disrupted zona 
gene lack a zona and are infertile. An E-box (CANNTG), located 
approximately 200 bp upstream of the transcription start site of the 
ZP1, ZP2 and ZP3, forms a protein-DNA complex present in oocytes and, 
to a much lesser extent, in testes. The integrity of this E-box in ZP2 
and ZP3 promoters is required for expression of luciferase reporter 
genes microinjected into growing oocytes. The presence of the 
ubiquitous transcription factor E12 in the complex was used to identify 
a novel basic helix-loop-helix protein FIG (Factor In the 
Germline alpha) whose expression was limited to oocytes within the 
ovary.)
    This invention relates to the molecular characterization of 
FIG, a novel germ cell specific bHLB transcription factor that 
binds as a heterodimer with E12 to the E-box in the promoter region of 
all three mouse zona pellucida genes and has the ability to 
transactivate reporter gene constructs in vitro. FIG is 
critical for folliculogenesis and has a role in the coordinate, oocyte-
specific expression of the three zona pellucida genes, the products of 
which for an extracellular matrix required for fertilization and early 
development. This invention also relates to monoclonal and polyclonal 
antibodies, which recognize the FIG polypeptide.

[[Page 65799]]

Ureido Derivatives Of Poly-4-Amino-2-Carboxy-1-Methyl Pyrrole 
Compounds For Treatment Of inflammation

OM Zac Howard (SAIC), JJ Oppenheim (NCI), WJ Murphy (SAIC), EA 
Sausville (NCI)
Serial No. 60/067,526 filed Dec 4, 1997

    Inflammatory reactions arising from a variety of medical conditions 
may have serious medical consequences when poorly controlled. Such 
inflammatory reactions contribute to a variety of disease states such 
as arthritis, asthma, non-bacterial medicated respiratory distress 
syndrome, reperfusion injury, and blunt force trauma. Accordingly, 
there is a need for new methods of diminished inflammation, especially 
acute inflammation.
    This invention describes a method of inhibiting inflammation, 
particularly non-TNF dependent inflammation, by administering 
pharmacologically active ureido derivatives of distamycin. Since TNF is 
only one of many inducers of chemokines, this invention provides a more 
inclusive method for treatment of many inflammatory conditions, 
including conditions in which TNF does not play a substantial 
deleterious role in the pathology of the condition.

Therapeutic Chemokine Antagonists

JJ Oppenheim, JM Wang, OY Chertov, LO Arthur, F Ruscetti (NCI)
DHHS Reference No. E-170-96/0 filed Sep 06, 1996; PVT/US97/15594 filed 
Sep 05, 1997

    This invention relates to a new class of chemoattractant 
antagonists, which are therapeutic candidates for treating disease 
conditions involving recruitment of inflammatory cells. These 
chemoattractant antagonists are comprised of a group consisting of 
gp120, gp41, domains and variants of gp41 and gp120.
    Chemoattractants include the subgroup of chemokines and are known 
to mediate chemotaxis and other pro-inflammatory phenomena. The 
chemoattractants are generally short peptides. The family of chemokines 
is subdivided into distinct subfamilies, C-X-C and C-C, based on the 
arrangements of the first two cysteines of the primary amino acid 
sequence.
    Members of the chemokine subfamily have remarkable similarities in 
their structural organization and biochemical properties. These 
homologies are consistent with the similarities observed in their 
biological effects, both in vitro and in vivo. These properties have 
prompted speculation that chemokines are mediators in autoimmune and 
allergic disorders.

    Dated: November 16, 1998.
Jack Spiegel,
Director, Division of Technology Development and Transfer, Office of 
Technology Transfer.
[FR Doc. 98-31730 Filed 11-27-98; 8:45 am]
BILLING CODE 4140-01-M