[Federal Register Volume 63, Number 5 (Thursday, January 8, 1998)]
[Notices]
[Pages 1117-1118]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 98-459]
-----------------------------------------------------------------------
DEPARTMENT OF HEALTH AND HUMAN SERVICES
National Institutes of Health
Government-Owned Inventions; Availability for Licensing
AGENCY: National Institutes of Health, HHS.
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.
Hexadecasaccharide-Protein Conjugate Vaccine for Shigella
Dysenteria Type 1
V Pozsgay, JB Robbins, R Schneerson (NICHD)
Serial No. 60/052,869 filed 17 Jul 97
Licensing Contact: Robert Benson, 301/496-7056, ext. 267.
This invention is a conjugate vaccine to prevent infection by
Shigella dysenteria type 1, a human pathogen which causes endemic and
epidemic dysentery worldwide. The conjugate is the first one in which
the polysaccharide antigen has been chemically synthesized and thus has
a known structure. The polysaccharide has a structure resembling the O-
specific polysaccharide portion of the lipopolysaccharide of Shigella
dysenteria type 1. It is expected that the purity of the polysaccharide
will lead to lessened side effects and greater immunogenicity. Mice
immunized with the conjugate of the invention produced antibodies
reactive with the O-specific polysaccharide isolated from Shigella
dysenteria type 1. Synthesis of the hexadecasaccharide is described in
the Journal of the American Chemical Society, June 28, 1995, pp. 6673-
6681.
Cloning of a Gene Mutation for Parkinson's Disease
MH Polymeropoulos, C Lavedan (NHGRI)
Serial No. 60/050, 684 filed 25 June 97
Licensing Contact: Stephen Finley, 301/496-7056 ext. 215.
Parkinson's Disease (PD) affects between 500,000 to one million
persons in the United States alone. The disease is most common in
persons over the age
[[Page 1118]]
of 70. However, one form of PD appears to be hereditary and is probably
responsible for early on-set PD, wherein the symptoms occur before the
age of 60. The newly discovered gene mutation appears to be linked to
the early on-set form of PD. The mutation, a threonine for alanine
substitution, at amino acid position 53 of the human alpha-synuclein
protein effects the secondary structure of the protein and causes an
aggregation of Lewy bodies in the brain. This new mutation is
considered to be a valuable tool in predicting a person's
susceptibility to early on-set PD. Assays developed from this mutation
can also be used for diagnostic purposes.
Non-Nucleoside Inhibitors of Reverse Transcriptase
C Michejda, M Morningstar, T Roth (NCI)
Serial No. 60/038,509 filed 25 Feb 97
Licensing Contact: J. Peter Kim, 301/496-7056 ext. 264.
The present invention is related to non-nucleoside inhibitors of
reverse transcriptase comprising a novel class of substituted
benzimidazole compounds which are potentially effective in the
inhibition of HIV RT and potentially against other infections. The
present invention provides for methods for treating HIV infection
utilizing a compound having anti-reverse transcriptase activity,
wherein said compound comprises at least one substituted benzimidazole.
This technology may present a potent, non-toxic compound which is
effective against wild type RTs and RTs which have undergone mutations
and become resistant to currently used anti-HIV therapies.
Enhanced Suppression of HIV-1 by the Combination of Cytidine
Dideoxynucleoside Analogues and CTP Synthase Inhibitors
W-Y Gao, DG Johns, H. Mitsuya, V Marquez (NCI)
Serial No. 60/033,918 filed 21 Jan 97
Licensing Contract: J. Peter Kim, 301/496-7056 ext. 264.
The present invention provides for compositions and methods to
increase the activity of cytidine-based anti-HIV drugs and to overcome
resistance of human immunodeficiency virus (HIV) to cytidine-based
anti-HIV drugs. More specifically, the invention provides for
composition, methods of preventing or inhibiting the spread of a virus,
methods of treatment, and methods of improving the antiviral activity
of a cytidine dideoxynucleoside analogue drug in patients with viral
infection. Typical drugs suitable for potentiation by this method
include ddC, 3TC, D4C (2', 3'-dideoxycytidine-2', 3'-ene), 5-fluoroddC,
and 3'--fluoroddC. The virus may be HIV-2, HTLV-1, HTLV-2,
SIV, HBV, but most preferably HIV-1.
Interferon-Inducible Protein 10 is a Potent Inhibitor of Angiogenesis
G Tosato, AL Angiolillio, C Sgadari (FDA)
Serial No. 08/455,079 filed 31 May 95
Licensing Contact: Jaconda Wagner, 301/496-7735 ext. 284.
Human Interferon inducible protein 10 (IP-10) is a member of the
chemokine family of molecules. It is a secreted protein with a
molecular weight of approximately 8.6 kD. Previous work has
demonstrated that IP-10 exhibits various activities, including the
inhibition of colony formation by bone marrow hematopoietic cell,
exertion of an antitumor effect, and function as a chemoattractant. In
addition, this work shows that IP-10 is a potent inhibitor of
angiogenesis. Unbalanced angiogenesis is thought to contribute to the
pathogenesis of several diseases including arthritis, psoriasis,
hemangiomas, diabetic retinopathy, and retrolental fibroplasia.
Therefore, IP-10 may be very useful alone or in combination with other
treatments to prevent unbalanced angiogenesis.
This research has been published in Proc. Natl. Acad. Sci. USA 1996
Nov 26;93(24):13791-6 and J. Exp. Med. 1995 Jul 1;182(1):155-62.
A related case is also available for licensing: Serial No. 08/
850,914 filed 02 May 97 entitled ``Method of Promoting Tumor Necrosis
Using Mig''; inventors are G Tosato (FDA), J Farber (NIAID), and C
Sgardari (FDA).
Dominant Negative Deletion Mutants of C-Jun and Their Use in the
Prevention and Treatment of Cancer
NH Colburn, Z Dong, PH Brown, MJ Birrer (NCI)
Serial No. 08/213,433 filed 10 Mar 94
Licensing Contact: Ken Hemby, 301/496-7735 ext. 265.
A number of mutants of the c-jun oncogene have been developed,
which may be particularly useful in the prevention and treatment of
cancer. Numerous studies have shown that tumor promotion is a long-term
process that is partially reversible and that requires chronic exposure
to a tumor promoter, and that subsequent progression of tumors through
invasive and metastatic stages is also a long term process. In recent
years, numerous cellular oncogenes have been implicated in the
transactivation of genes associated with cellular growth and
differentiation. One such cellular ongogene, c-jun, encodes a
phosphoprotein that is a component of the dimeric transcriptional
activator AP-1 along with c-Fos or other Jun or Fos Family proto-
oncoproteins. Several genes that may be involved in tumor promotion or
progression have been shown to be dependent on AP-1 transactivation,
including collagenase and stromelysin (transin). AP-1 inhibiting
dominant negative detection mutants of the c-jun gene have been
developed that, when given to a mammal, may prevent or reverse
carcinogenesis during early or late stages. For the treatment of
cancer, a deletion mutant of the c-jun gene or the protein product may
inhibit the elevated AP-1 transactivation that frequently characterizes
tumor progression and may consequently prevent or reverse the
development or further progression of tumors. This invention also
includes a method for determining whether a tumor promoter induces
transformation via a pathway that depends on induction or elevation of
AP-1 transcriptional activity and AP-1 target gene expression.
Dated: December 23, 1997.
Barbara M. McGarey,
Deputy Director, Office of Technology Transfer.
[FR Doc. 98-459 Filed 1-7-98; 8:45 am]
BILLING CODE 4140-01-M
