[Federal Register: October 24, 2005 (Volume 70, Number 204)]
[Notices]
[Page 61458-61460]
From the Federal Register Online via GPO Access [wais.access.gpo.gov]
[DOCID:fr24oc05-58]
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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 an agency 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.
NIH3T3 Cell Lines Carrying c-Met Mutations Including G3906A, G3522A,
G3810T, T3936C, T3936G, T3997C, C3528T, C3564G, C3831G, A3529T, and
T3640C
Laura S. Schmidt (NCI).
HHS Reference No. E-327-2005/0--Research Tool.
Licensing Contact: John Stansberry; 301/435-5236:
stansbej@mail.nih.gov.
MET is over expressed in a variety of cancers including hereditary
papillary renal cell carcinoma and non-small cell lung cancer. These
cell lines carry naturally-occurring Met mutations and were derived
from the germline of patients with hereditary papillary renal cell
carcinoma. These cell lines can be used as drug discovery research
reagents.
These cell lines were described in part in Schmidt et al., ``Novel
mutations of the MET proto-oncogene in papillary renal carcinomas.
Oncogene. (1999) 18:2343-2350 and Jeffers et al., ``Activating
mutations for the met tyrosine kinase receptor in human cancer.'' PNAS
(1997) 94:11445-11450.
In addition to licensing, the technology is available for further
development through collaborative research opportunities with the
inventors.
[[Page 61459]]
Mouse Fibroblasts Stably Expressing C-Type Lectin Receptors DC-SIGN and
L-SIGN
Vineet N. KewelRamani and Thomas Martin (NCI).
HHS Reference Nos. E-321-2005/0 and E-322-2005/0--Research Tools.
Licensing Contact: Susan Ano; 301/435-5515; anos@mail.nih.gov.
The NIH is pleased to offer for licensing mouse fibroblasts that
stably express the C-type lectin receptors DC-SIGN and L-SIGN (CD209
and CD209L, respectively). L-SIGN and DC-SIGN both exhibit selectivity
for highly mannosylated glycoproteins. DC-SIGN is also selective for
certain Lewis X sugar groups. These types of interactions allow L-SIGN
and DC-SIGN to interact with a wide spectrum of pathogens including
HIV, hepatitis C virus, and SARS coronavirus, which appear to use L-
SIGN and DC-SIGN to facilitate their replication. In addition to HIV,
HCV, and SARS, pathogens such as Ebola virus, some herpes viruses, and
tuberculosis interact with DC-SIGN. In contrast to primary cells
expressing L-SIGN and DC-SIGN, the subject fibroblasts are resilient,
adhere to coated tissue culture plates, grow rapidly and continually
express high levels of their respective receptor. The subject materials
could be used to study the interaction of pathogens with L-SIGN or DC-
SIGN and to screen for compounds that block these interactions.
Additionally, the materials could be used for the development of
antibodies or compounds through rational design that interacted with L-
SIGN or DC-SIGN. The NIH3T3/DC-SIGN and NIH3T3/L-SIGN cells are further
described in Journal of Virology, 2002, vol. 26(12), pages 5905-5914.
The subject technologies are available for licensing from the NIH
through biological materials license agreements.
Murine Mast Cell Line Useful for Toxicity and Immunopotency Screens
Michael Potter (NCI).
HHS Reference No. E-274-2005/0--Research Tool.
Licensing Contact: John Stansberry; 301/435-5236;
stansbej@mail.nih.gov.
The technology is a mouse cell line (P815) that could be useful for
screening biological and chemical agents for toxicity and
immunopotency. Specifically, the cell line is useful for screening for
toxic effects of immunopotentiators including Mycobacterium bovis,
Bacillus Calmette-Gurerin strain, zymosan, lipopolysaccharide and
dextran sulfate. The cell line may also have application in screening
other compounds.
The cell line may also prove useful for studies of cancer and tumor
immunology as injection of mice with P815 leads to progressive tumors.
The P815 tumors express cell surface antigens that could provide a
model for cancer vaccine development.
Mutated Pseudomonas Exotoxins with Reduced Antigenicity
Ira H. Pastan et al. (NCI).
U.S. Provisional Patent Application filed 29 Jul 2005 (HHS Reference
No. E-262-2005/0-US-01).
Licensing Contact: Jesse S. Kindra; 301-435-5559; kindraj@mail.nih.gov.
The use of Pseudomonas exotoxins (PE) for treatment of solid
tumors, in particular, has been limited because of the development of
neutralizing antibodies to the immunotoxin after the first
administration. These antibodies develop before most protocols would
call for a second administration of the immunotoxin, and therefore
render further use of the immunotoxins ineffective against solid tumors
in previously exposed patients.
The studies underlying this novel invention reveal that the
predominant immune response of patients to PE-immunotoxins is the PE
portion of the immunotoxin. This finding indicates that reducing the
antigenicity of the PE molecules used for immunotoxins would reduce the
overall antigenicity of the immunotoxin, and increase their utility.
Therefore, this invention relates to mutated Pseudomonas exotoxins
(PE) that have reduced antigenicity compared to PEs containing the
native sequence. The PEs of this invention have one or more individual
mutations that reduce antibody binding to one or more epitopes of PE.
In addition to licensing, the technology is available for further
development through collaborative research opportunities with the
inventors.
Methods and Materials for Identifying Polymorphic Variants, Diagnosing
Susceptibilities, and Treating Disease
Lawrence C. Brody (NHGRI) et al.
PCT Application No. PCT/US05/21288 filed 16 Jun 2005 (HHS Reference No.
E-149-2005/0-PCT-01).
Licensing Contact: Marlene Shinn-Astor; 301/435-4426;
shinnm@mail.nih.gov.
This invention relates to materials and methods associated with
polymorphic variants in two enzymes involved in folate-dependent and
one-carbon metabolic pathways important in pregnancy-related
complications and neural tube birth defects: MTHFD1 (5,10-
methylenetrahydrofolate dehydrogenase, 5,10-methenyltetrahydrofolate
cyclohydrolase, 10-formyltetrahydrofolate synthase) and
methylenetetrahydrofolate dehydrogenase (NADP+ dependent) 1-like
(MTHFD1L). These enzymes are extremely important in the promotion of
DNA synthesis, a process that is critical for normal placental and
fetal development.
Recently, the inventors have discovered that a MTHFD1 polymorphism
is also a strong maternal genetic risk factor for placental abruption,
premature separation of a normally implanted placenta. This
polymorphism may also be a risk factor for first and second trimester
miscarriages. Diagnostic and therapeutic methods are provided in this
invention involving the correlation of polymorphic variants in MTHFD1
and other genes with relative susceptibility for various pregnancy-
related and other complications such as cancer, cardiovascular disease,
and developmental anomalies. Both nutrient status and genetic
background are independent yet interacting risk factors for impaired
folate metabolism. However, the mechanisms that lead to pathology or
the mechanisms whereby folate prevents these disorders are unknown.
Therefore, a diagnostic and therapeutic invention of this kind would
significantly improve the detection and treatment of disorders
associated with folate metabolism.
For further information, see Brody et al., July 28, 2005, ``A
polymorphism in the MTHFD1 gene increases a mother's risk of having an
unexplained second trimester pregnancy loss,'' Mol. Hum. Reprod.
10.1093/molehr/gah204.
In addition to licensing, the technology is available for further
development through collaborative research opportunities with the
inventors.
AAV5 Vector and Uses Thereof
John A. Chiorini, Robert M. Kotin (NHLBI).
U.S. Provisional Application No. 60/087,029 filed 28 May 1998 (HHS
Reference No. E-127-1998/0-US-01).
U.S. Patent Application No. 09/717,789 filed 21 Nov 2000 (HHS Reference
No. E-127-1998/0-US-07).
U.S. Patent Application Serial No. 11/184,380 filed 19 Jul 2005 (HHS
Reference No. E-127-1998/0-US-08).
Licensing Contact: Jesse S. Kindra; 301/435-5559; kindraj@mail.nih.gov.
The invention described and claimed in this patent application
provides for novel vectors and viral particles which
[[Page 61460]]
comprise adeno-associated virus serotype 5 (AAV5). AAV5 is a single-
stranded DNA virus of either plus or minus polarity which, like other
AAV serotypes (e.g., AAV4, AAV2) requires a helper virus for
replication. AAV type 2 has the interesting and potentially useful
ability to integrate into human chromosome 19 q 13.3-q ter. This
activity is dependent on the non-structural, Rep, proteins of AAV2. The
Rep proteins of AAV types 2 and 5 are dissimilar and are not able to
substitute in DNA replication of the heterologous serotype.
AAV5 offers several advantages which make it attractive for use in
gene therapy: 1. Increased production (10-50 fold greater than AAV2);
2. distinct integration locus when compared to AAV2; 3. Rep protein and
ITR regions do not complement other AAV serotypes; and 4. appears to
utilize different cell surface attachment molecules than those of AAV
type 2.
In addition to licensing, the technology may be available for
further development through collaborative research opportunities with
the inventors.
The Use of Nitroxides in the Prophylactic and Therapeutic Treatment of
Cancer Due to Genetic Defects
James Mitchell, Angelo Russo, Anne Deluca and Murali Cherukuri (NCI).
U.S. Patent Application No. 09/424,519 filed 03 Mar 2000, claiming
priority to 27 May 1997 (HHS Reference No. E-167-1997/0-US-07).
Licensing Contact: George Pipia; 301/435-5560; pipiag@mail.nih.gov.
The invention is a method for preventing or treating cancer,
especially cancers associated with defects in the p53 gene. This gene
is generally considered to be a tumor-suppressor gene, and in a large
percentage of malignancies including pancreatic, colon, lung, and
breast, the gene is found to be inactive in the cancer. It is believed
that many individuals have genetic defects in p53 predisposing them to
cancer.
The invention involves the use of certain nitroxides as agents to
slow the appearance or progression of tumors associated with p53
knockout. Thus, these compounds could serve as preventative agents for
people predisposed to cancer, or as therapeutic agents for certain
cancers. As nitroxides have already been identified as antioxidants,
such agents could become part of a cancer prevention and anti-aging
regimen. A new method of use for these compounds now include their use
in imaging, which correlates functional information about the tumor
with magnetic resonance imaging data.
Dated: October 13, 2005.
Steven M. Ferguson,
Director, Division of Technology Development and Transfer, Office of
Technology Transfer, National Institutes of Health.
[FR Doc. 05-21118 Filed 10-21-05; 8:45 am]
BILLING CODE 4140-01-P