Government-Owned Inventions; Availability for Licensing, 52889-52892 [E7-18192]
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<galactosyltransferases having increased
enzymatic activity relative to [beta](1,4)galactosyltransferases produced in the
absence of the amino acid segments.
Applications: Synthesis of
polysaccharide antigens for conjugate
vaccines, glycosylation of monoclonal
antibodies, and as research tools.
Development Stage: The enzymes
have been synthesized and preclinical
studies have been performed.
Inventors: Pradman K. Qasba,
Boopathy Ramakrishnan, Elizabeth
Boeggeman (NCI).
Patent Status: U.S. and Foreign Rights
Available (HHS Reference No. E–230–
2002/2).
Licensing Status: Available for
exclusive or non-exclusive licensing.
Licensing Contact: Peter A. Soukas,
J.D.; 301/435–4646;
soukasp@mail.nih.gov.
Collaborative Research Opportunity:
The National Cancer Institute’s
Nanobiology Program is seeking
statements of capability or interest from
parties interested in collaborative
research to further develop, evaluate, or
commercialize the use of galactose and
modified galactose to be linked to an Nacetylglucosamine that may itself be
linked to a variety of other molecules.
Please contact John D. Hewes, PhD. at
301–435–3121 or hewesj@mail.nih.gov
for more information.
representation of the heart position.
RaMP tracks fast-moving blood volume
during systole as a marker for the heart
position, while suppressing stationary
or slow moving spins. This approach
allows cardiac navigation in two
orthogonal directions simultaneously,
eliminates the need to obtain empirical
correlations between the diaphragm and
the heart, and increases tracking
reliability among individual patients.
The method uses a spoiled-Fast Low
Angle Shot (FLASH) navigator and
incorporates an alternating pair of
bipolar velocity-encoding gradients.
Data at 1.5T indicate that RaMP is
capable of correcting bulk motion of the
heart over multiple cardiac cycles to
within +/¥1.43 mm in the superiorinferior direction and +/¥0.84 mm in
the anterior-posterior direction.
Applications:
Reduction of MR image artifacts due
to respiration motion.
Real-time tracking of cardiac motion.
Market: Magnetic Resonance Imaging.
Development Status: Late-stage
technology.
Inventors: Vinay M. Pai and Han Wen
(NHLBI).
Patent Status: U.S. Patent Application
No. 10/244,903 filed 16 Sep 2002 (HHS
Reference No. E–164–2002/0–US–01).
Licensing Status: Available for
exclusive or non-exclusive licensing.
Licensing Contact: Chekesha S.
Clingman, Ph.D.; 301/435–5018;
clingmac@mail.nih.gov.
Collaborative Research Opportunity:
The NHLBI is seeking statements of
capability or interest from parties
interested in collaborative research to
further develop, evaluate, or
commercialize this technology. Please
contact Lili Portilla at 301–594–4273 or
via e-mail at Lilip@nih.gov for more
information.
Rapid Motion Perception MRI
Navigator Method
Description of Technology: Available
for licensing and commercial
development is a non-breathhold flow
sensitive navigator technique for
reducing respiratory motion artifacts in
magnetic resonance (MR) images. The
method, called Rapid Motion Perception
(RaMP), tracks bulk translational motion
of the heart in real-time. The position of
the blood volume is a direct
DEPARTMENT OF HEALTH AND
HUMAN SERVICES
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Dated: September 7, 2007.
Steven M. Ferguson,
Director, Division of Technology Development
and Transfer, Office of Technology Transfer,
National Institutes of Health.
[FR Doc. E7–18189 Filed 9–14–07; 8:45 am]
BILLING CODE 4140–01–P
National Institutes of Health
Government-Owned Inventions;
Availability for Licensing
National Institutes of Health,
Public Health Service, HHS.
ACTION: Notice.
AGENCY:
SUMMARY: The inventions listed below
are owned by an agency of the U.S.
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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.
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.
ADDRESSES:
New and Improved Chemotherapy
Adjuvants: Folate Based Inactivators of
O6-alkylguanine-DNA alkyltransferase
(alkyltransferase)
Description of Technology: O6Benzylguanine derivatives, some O6benzylpyrimidines, and related
compounds are known to be inactivators
of the human DNA repair protein O6alkylguanine-DNA alkyltransferase
(alkyltransferase). This repair protein is
the primary source of resistance many
tumor cells develop when exposed to
chemotherapeutic agents that modify
the O6-position of DNA guanine
residues. Therefore, inactivation of this
protein can bring about a significant
improvement in the therapeutic
effectiveness of these chemotherapy
drugs. The prototype inactivator O6benzylguanine is currently in clinical
trials in the United States as an adjuvant
in combination with the
chloroethylating agent 1, 3-bis (2chloroethyl)-1-nitrosourea (BCNU) and
the methylating agent temozolomide. A
similar alkyltransferase inactivator, O6(4-bromothenyl) guanine is in clinical
trials in the UK.
This technology is directed to the
discovery of a new class of potent
alkyltransferase inactivators, based on
folate ester derivatives of O6-benzyl-2′deoxyguanosine and of O6-[4(hydroxymethyl)benzyl] guanine. All
the folate ester derivatives of O6-benzyl2′-deoxyguanosine were able to
sensitize human tumor cells to killing
by 1, 3-bis (2-chloroethyl)-1-nitrosourea
with O6-benzyl-3′-O-[g-folyl]-2′deoxyguanosine being the most active.
The 3′ ester was found to be more potent
than the 5′ ester and was more than an
order of magnitude more active than O6-
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benzylguanine, which is currently in
clinical trials.
Applications
Promising candidates as
chemotherapy adjuvants for the
treatment of cancer.
Therapeutic application for drug
resistant tumors where acquired
resistance is caused by O6-alkylguanineDNA alkyltransferase.
Advantages
The folate ester derivatives are highly
water soluble.
Conjugation of folic acid to an
alkyltransferase inactivating compound
should allow targeting of delivery to
cells that express folate receptor as
many tumor cells are known to do.
Development Status: The technology
is currently in the pre-clinical stage of
development.
Inventors: Drs. Gary Pauly (NCI),
Robert C. Moschel (NCI), Sahar
Javanmard (NCI), et al.
Patent Status: This technology
consists of U.S. Provisional Application
No. 60/915,510 foreign equivalents,
entitled ‘‘Inactivators of O6Alkylguanine-DNA Alkyltransferase’’
(HHS Reference No. E–200–2007/0).
Related Technology: HHS Reference
No. E–274–2003/0, entitled ‘‘2-AminoO4-Substituted Pteridines and Their Use
as Inactivators of O6-Alkylguanine-DNA
Alkyltransferase’’.
Licensing Status: Available for
exclusive and non-exclusive licensing.
Licensing Contact: Adaku
Nwachukwu, J.D.; 301/435–5560;
madua@mail.nih.gov.
jlentini on PROD1PC65 with NOTICES
Papilloma Pseudovirus for Detection
and Therapy of Tumors
Description of Technology: There is
extensive literature on the use of viral
vectors, particularly those based on the
adenovirus and AAV, to increase the
potency of anti-tumor gene therapy.
However, these approaches have had
limited success because of limited antitumor effects and unacceptable toxicity.
This invention describes the use of
papillomavirus pseudoviruses (PsV) as a
gene transfer technology and a tumor
diagnostic method. Preliminary studies
showed that PsV bind to cells that were
transplanted with human ovarian tumor
(Shin-3) while normal tissues were not
affected. PsV does not infect several
other normal intact tissues but
continues to selectively infect
additional cell types that are damaged.
Additionally, the inventors have
constructed oligoT PsV vectors that can
be engineered to express certain
cytotoxic genes to induce tumor
regression and simultaneous increase
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human papilloma virus’
immunogenicity. This technology could
be an effective anti-tumor therapy
because it has shown increased
infection of compromised cells with an
inability to infect normal cells thereby
reducing potential toxicity to patients.
In addition to a potential anti-cancer
therapeutic, this technology could also
be used as a diagnostic tool in the
detection of tumor masses. Detection
can be achieved through the use of
fluorescent dye coupled particles of PsV
that have preferential binding to tumor
tissues and not normal tissues.
Applications
Method to treat and selectively target
cancer with limited toxicity.
Method to accurately diagnose cancer.
Anti-tumor therapeutic vaccines.
Anti-tumor cytoxic gene therapy
constructs.
Market
An estimated 1,444,920 new cancer
cases in 2007.
600,000 cancer deaths in the U.S. in
2006.
It is estimated that market for cancer
drugs would double to $50 billion a year
in 2010 from $25 billion in 2006.
Development Status: The technology
is currently in the pre-clinical stage of
development.
Inventors: Jeffrey Roberts, John T.
Schiller, Douglas R. Lowy (NCI).
Publications
1. CB Buck, et al. Generation of HPV
pseudovirions using transfection and
their use in neutralization assays.
Methods Mol Med. 2005;119:445–462.
2. CB Buck, et al. Efficient
intracellular assembly of papillomaviral
vectors. J Virol. 2004 Jan;78(2):751–757.
Patent Status: U.S. Provisional
Application No. 60/928,495 filed 08
May 2007 (HHS Reference No. E–186–
2007/0–US–01).
Licensing Status: Available for
exclusive or non-exclusive licensing.
Licensing Contact: Jennifer Wong;
301/435–4633; wongje@mail.nih.gov.
New Synthetic Variants of 2-(4isothiocyanatobenzyl)-6methyldiethylenetriamine Pentaacetic
Acid (1B4M–DTPA): Novel
Macromolecular MRI Contrast Agents
Description of Technology: The
present invention describes the
synthesis and use of two protected
variants of the 2-(4isothiocyanatobenzyl)-6methyldiethylenetriamine pentaacetic
acid (1B4M–DTPA) (also known as the
commercial bifunctional chelator,
tiuxetan), bearing either an
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isothiocyanate or a succinimidyl ester
moiety, respectively. These molecules
were synthesized for the following uses:
(1) Use in the introduction of the
chelator to the N-terminus of peptides,
aptamers, PNA, etc. wherein
deprotection or cleavage from resin or
solid phase support of the product is
possible and (2) introduction of the
chelator to macromolecular structures
such as dendrimer wherein this is
accomplished in organic solvents
eliminating the gross inefficiency of the
prior aqueous methods.
In both uses, the elimination or delay
of any aqueous chemistry steps in the
synthesis process obviates the
possibilities of contamination by
spurious metals. Metal contaminations
could compromise latter radiolabeling
or can also hinder the introduction of
paramagnetic ions such as Gd(II1) for
MRI applications. The chemistry used
in this synthetic process is very flexible
and provides the basis for an extensive
list of conjugation functional groups to
be introduced.
Comparative MR imaging with these
dendrimer based molecules revealed
equivalent enhancement of the vessels
and organs such as the kidney and liver.
Applications
Useful in the conjugation of nearly all
peptides for targeting antigens/peptides
associated with cancers.
Useful for modification of
macromolecules such as dendrimer,
carbon tubes, etc., for labeling with
radioactive metal ions suitable for
imaging and/or therapy and
paramagnetics for MRI.
Advantages
The chemistry is very flexible and
provides the basis for an extensive list
of conjugation functional groups to be
introduced.
The elimination of aqueous chemistry
steps obviates the possibilities of
contamination by spurious metals that
could compromise subsequent
radiolabeling.
The elimination of aqueous steps aids
in the introduction of paramagnetic ions
such as Gd(III) for MRI applications.
The general synthesis process
provides a procedure for preparing
dendrimer-based MR agents with higher
yields and efficiency while enhancing
versatility.
Benefits: In spite of advances in
cancer therapeutics and diagnostics,
more than 600,000 cancer deaths are
estimated to occur in 2007. Early and
accurate detection is a key component
of successful clinical management of
cancer. This technology can contribute
to the development of better MRI agents
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for diagnosing cancer and thus improve
overall survival and quality of life of
patients suffering from cancer.
Inventors: Drs. Martin Brechbiel and
Heng Xu (NCI).
Development Status: Synthesis
process and data available.
Patent Status: U.S. Provisional
Application No. 60/864,503 filed 06
Nov 2006 (HHS Reference No. E–226–
2006/0–US–01).
Publication: H Xu, CA Regino, M
Bernardo, Y Koyama, H Kobayashi, PL
Choyke, MW Brechbiel. Toward
improved syntheses of dendrimer-based
magnetic resonance imaging contrast
agents: New bifunctional
diethylenetriaminepentaacetic acid
ligands and nonaqueous conjugation
chemistry. J Med Chem. 2007 Jul
12;50(14):3185–3193. Epub 2007 Jun 7.
Licensing Contact: Mojdeh Bahar;
301/435–2950; baharm@mail.nih.gov.
Methods and Compositions for Treating
FUS1 Related Disorders
Description of Technology: The FUS1
gene residing in the 3p21.3 chromosome
region may function as a tumor
suppressor gene. In animal models,
disruption of FUS1 is associated with an
increased frequency of spontaneous
vascular tumors and signs of
autoimmune disease. The investigators
have in vivo data that demonstrate that
FUS1 null mutants show a consistent
defect in NK cell maturation that
correlate with changes in the expression
of IL–15. Injection of IL–15 into FUS1
knockout mice completely rescued the
NK cell maturation defect suggesting
that FUS1 plays an important role in the
development and activation of the
mammalian immune system.
Applications
Method to treat cancer, autoimmune
diseases, and immune disorders such as
HIV.
Method to boost immunity in
conjunction with cancer and immune
disorder therapies.
Method to diagnose FUS1 related
disorders.
Animal model to study anti-tumor
response and autoimmunity.
jlentini on PROD1PC65 with NOTICES
Market
An estimated 1,444,920 new cancer
diagnoses in the U.S. in 2007.
600,000 deaths caused by cancer in
the U.S. in 2006.
Cancer is the second leading cause of
death in United States.
It is estimated that market for cancer
drugs would double to $50 billion a year
in 2010 from $25 billion in 2006.
An estimated 8.5 million Americans
are afflicted with autoimmune diseases.
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Development Status: The technology
is currently in the pre-clinical stage of
development.
Inventors: Michael I. Lerman, et al.
(NCI).
Publication: AV Ivanova, et al.
Autoimmunity, spontaneous
tumourigenesis, and IL–15 insufficiency
in mice with a targeted disruption of the
tumour suppressor gene Fus1. J Path.
2007 Apr;211(5):591–601.
Patent Status: PCT Patent Application
No. PCT/US2006/026533 (HHS
Reference No. E–137–2005/0–PCT–02).
Licensing Status: Available for
exclusive or non-exclusive licensing.
Licensing Contact: Jennifer Wong;
301/435–4633; wongje@mail.nih.gov.
Collaborative Research Opportunity:
The National Cancer Institute Basic
Research Laboratory is seeking
statements of capability or interest from
parties interested in collaborative
research to further develop, evaluate, or
commercialize cancer and immune
disorder therapies Please contact John
D. Hewes, Ph.D. at 301–435–3121 or
hewesj@mail.nih.gov for more
information.
Tumor Suppressor Genes
Description of Technology: Members
of the inhibitor of growth (ING) family
of tumor suppressor genes are involved
in the regulation of diverse processes
including cell cycle progression,
apoptosis, and DNA repair as important
cofactors of p53. ING members contain
a highly evolutionary conserved
sequence common in chromatinregulating proteins, and there are
overlapping functions between ING
family members in negative regulation
of cell growth as well as a dependent
regulation between various ING
members and p53.
Available for licensing are
compositions for new tumor suppressor
designated p28ING5, p33ING2, and
p47ING3 (pING). Overexpression of
these proteins has been shown to inhibit
cell proliferation in human cancer cells
lines, and these characteristics suggest
that they may have important
implications in cancer diagnosis and
therapy. These compositions include
nucleic acids, polypeptides, and
antibodies that specifically bind to their
respective ING members. Also claimed
are cancer diagnostic and treatment
methods.
Applications
Methods to treat and diagnose cancer
with pING compositions.
Methods to identify pING modulating
agents.
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Research tool to study cell cycle
regulation and p53 pathways. pING
compositions.
Market
Cancer is the second leading cause of
death in United States.
An estimated 600,000 deaths caused
by cancer in 2006.
Development Status: The technology
is currently in the pre-clinical stage of
development.
Inventors: Curtis C. Harris (NCI), et al.
Publications
1. T Okano, et al. Alterations in novel
candidate tumor suppressor genes, ING1
and ING2 in human lung cancer. Oncol
Rep. 2006 Mar;15(3):545–549.
2. H Kataoka, et al. ING1 represses
transcription by direct DNA binding and
through effects on p53. Cancer Res. 2003
Sep 15;63(18):5785–5792.
3. M Nagashima, et al. A novel PHDfinger motif protein, p47ING3,
modulates p53-mediated transcription,
cell cycle control, and apoptosis.
Oncogene. 2003 Jan 23;22(3):343–350.
4. M Nagashima, et al. DNA damageinducible gene p33ING2 negatively
regulates cell proliferation through
acetylation of p53. Proc Natl Acad Sci
USA. 2001 Aug 14;98(17):9671–9676.
Patent Status
U.S. Patent No. 6,790,948 issued 14 Sep
2004 (HHS Reference No. E–272–
1998/0–US–02)
U.S. Patent Application No. 10/868,270
filed 14 Jun 2004 (HHS Reference No.
E–272–1998/0–US–03)
PCT Patent Application No. PCT/
US2001/04425 filed 09 Feb 2001
(HHS Reference No. E–254–1999/
0–PCT–02)
U.S. Patent Application No. 10/203,532
filed 02 Aug 2002 (HHS Reference No.
E–254–1999/0–US–03)
PCT Patent Application No. PCT/
US2003/02174 filed 23 Jul 2003 (HHS
Reference No. E–300–2001/0–PCT–
02)
U.S. Patent Application No. 10/502,431
filed 22 Jul 2004 (HHS Reference No.
E–300–2001/0–US–03)
Licensing Status: Available for
exclusive or non-exclusive licensing.
Licensing Contact: Jennifer Wong;
301/435–4633; wongje@mail.nih.gov.
Peptide Inhibitor of Cyclin Dependent
Kinase 4 (CDK4) Derived From MyoD
Description of Technology: This
invention pertains to cell cycle
regulation and the activity of the G1
cyclin-dependent kinase 4 (CDK4). The
invention describes a 15 amino acid
peptide and variants thereof derived
from muscle determination factor,
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MyoD, which is an inhibitor of the
CDK4. CDK4 is one of a number of
cyclin-dependent kinases which control
progression through the cell cycle
through their ability to phosphorylate
particular substrates at the correct phase
of the cell cycle. CDK4 has been shown
to be involved in cell cycle control
through its ability to regulate the
activity of the retinoblastoma protein,
pRb, an activator of genes essential for
cell division.
Inhibitors of the cyclin-dependent
kinases, such as the peptides described
in this invention, prevent cell cycle
progression and induce cells to exit the
cell cycle into the Go state. The peptides
described in this invention prevent the
phosphorylation of pRb by CDK4, an
obligate step for entry into the cell
cycle. Osteosarcomas and
habdosarcomas are two types of tumors
known to over-express pRb. The
inhibitor described in this invention
may be useful in treating these cancers
or other diseases which have been
specifically linked to over-expression of
active pRb.
Laboratory of Biochemistry and
Molecular Biology is seeking statements
of capability or interest from parties
interested in collaborative research to
further develop, evaluate, or
commercialize the described cdk4
inhibitory peptides or equivalent
peptide mimetics. Please contact John
D. Hewes, PhD at 301–435–3121 or
hewesj@mail.nih.gov for more
information.
Applications
Pursuant to section 10(d) of the
Federal Advisory Committee Act, as
amended (5 U.S.C. Appendix 2), notice
is hereby given of a meeting of the
Board of Scientific Counselors, National
Institute of Neurological Disorders and
Stroke.
The meeting will be closed to the
public as indicated below in accordance
with the provisions set forth in section
552b(c)(6), Title 5 U.S.C., as amended
for the review, discussion, and
evaluation of individual intramural
programs and projects conducted by the
National Institute of Neurological
Disorders And Stroke, including
consideration of personnel
qualifications and performance, and the
competence of individual investigators,
the disclosure of which would
constitute a clearly unwarranted
invasion of personal privacy.
Method to treat proliferative
disorders, including cancer.
Anti-proliferative therapeutics.
Research tool to study the cell cycle.
Advantages: Expression of this
peptide either as a fusion protein with
GST or GFP results in the cessation of
cell growth.
jlentini on PROD1PC65 with NOTICES
Market
An estimated 1,444,920 new cancer
diagnoses in the U.S. in 2007.
600,000 deaths caused by cancer in
the U.S. in 2006.
Cancer is the second leading cause of
death in the United States.
It is estimated that market for cancer
drugs would double to $50 billion a year
in 2010 from $25 billion in 2006.
Development Status: The technology
is currently in the pre-clinical stage of
development.
Inventors: Bruce M. Paterson and Jianmin Zhang (NCI).
Publication: JM Zhang, et al. Coupling
of the cell cycle and myogenesis
through the cyclin D1-dependent
interaction of MyoD with cdk4. EMBO
J. 1999 Feb 15;18(4):926–933.
Patent Status: U.S. Patent Application
No. 10/018,964 filed 11 Apr 2002,
claiming priority to 18 Jun 1999 (HHS
Reference No. E–153–1998/0–US–03).
Licensing Status: Available for
exclusive or non-exclusive licensing.
Licensing Contact: Jennifer Wong;
301/435–4633; wongje@mail.nih.gov.
Collaborative Research Opportunity:
The National Cancer Institute’s
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Dated: September 6, 2007.
Steven M. Ferguson,
Director, Division of Technology Development
and Transfer, Office of Technology Transfer,
National Institutes of Health.
[FR Doc. E7–18192 Filed 9–14–07; 8:45 am]
BILLING CODE 4140–01–P
DEPARTMENT OF HEALTH AND
HUMAN SERVICES
Boulevard, Conference Room A, Rockville,
MD 20852.
Time: October 2, 2007, 8:30 a.m. to 12 p.m.
Agenda: To review and evaluate personal
qualifications and performance, and
competence of individual investigators.
Place: Hyatt Regency Bethesda, One
Bethesda Metro Center, 7400 Wisconsin
Avenue, Susquehanna/Severn Room,
Bethesda, MD 20814.
Contact Person: Alan P. Koretsky, PhD,
Scientific Director, Division of Intramural
Research. National Institute Of Neurological
Disorders & Stroke, NIH, 35 Convent Drive,
Room 6A 908, Bethesda, MD 20892, 301–
435–2232, koretskya@ninds.nih.gov.
(Catalogue of Federal Domestic Assistance
Program Nos. 93.853, Clinical Research
Related to Neurological Disorders; 93.854,
Biological Basis Research in the
Neurosciences, National Institutes of Health,
HHS).
National Institutes of Health
National Institute of Neurological
Disorders And Stroke; Notice of
Closed Meeting
Dated: September 6, 2007.
Jennifer Spaeth,
Director, Office of Federal Advisory
Committee Policy.
[FR Doc. 07–4566 Filed 9–14–07; 8:45 am]
BILLING CODE 4140–01–M
Name of Committee: Board of Scientific
Counselors, National Institute of
Neurological Disorders and Stroke.
Date: September 30–October 2, 2007.
Time: September 30, 2007, 7 p.m. to 10
p.m.
Agenda: To review and evaluate personal
qualifications and performance, and
competence of individual investigators.
Place: Hyatt Regency Bethesda, One
Bethesda Metro Center, 7400 Wisconsin
Avenue, Susquehanna/Severn Room,
Bethesda, MD 20814.
Time: October 1, 2007, 8:30 a.m. to 6:30
p.m.
Agenda: To review and evaluate personal
qualifications and performance, and
competence of individual investigators.
Place: National Institutes of Health,
Neuroscience Center, 6001 Executive
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DEPARTMENT OF HEALTH AND
HUMAN SERVICES
National Institutes of Health
National Institutes of Nursing
Research; Notice of Meeting
Pursuant to section 10(d) of the
Federal Advisory Committee Act, as
amended (5 U.S.C. Appendix 2), notice
is hereby given of a meeting of the
National Advisory Council for Nursing
Research.
The meeting will be open to the
public as indicated below, with
attendance limited to space available.
Individuals who play to attend and need
special assistance, such as sign language
interpretation or other reasonable
accommodations, should notify the
Contact Person listed below in advance
of the meeting.
The meeting will be closed to the
public in accordance with the
provisions set forth in sections
552b(c)(4) and 552b(c)(6), Title 5 U.S.C.,
as amended. The grant applications and
the discussions could disclose
confidential trade secrets or commercial
property such as patentable material,
and personal information concerning
individuals associated with the grant
applications, the disclosure of which
would constitute a clearly unwarranted
invasion of personal privacy.
Name of Committee: National Advisory
Council for Nursing Research.
Date: September 25–26, 2007.
Open: September 25, 2007, 1 p.m. to 5 p.m.
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]]>Agencies
[Federal Register Volume 72, Number 179 (Monday, September 17, 2007)]
[Notices]
[Pages 52889-52892]
From the Federal Register Online via the Government Printing Office [www.gpo.gov]
[FR Doc No: E7-18192]
-----------------------------------------------------------------------
DEPARTMENT OF HEALTH AND HUMAN SERVICES
National Institutes of Health
Government-Owned Inventions; Availability for Licensing
AGENCY: National Institutes of Health, Public Health Service, HHS.
ACTION: Notice.
-----------------------------------------------------------------------
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.
New and Improved Chemotherapy Adjuvants: Folate Based Inactivators of
O\6\-alkylguanine-DNA alkyltransferase (alkyltransferase)
Description of Technology: O6-Benzylguanine derivatives,
some O6-benzylpyrimidines, and related compounds are known
to be inactivators of the human DNA repair protein O6-
alkylguanine-DNA alkyltransferase (alkyltransferase). This repair
protein is the primary source of resistance many tumor cells develop
when exposed to chemotherapeutic agents that modify the O6-
position of DNA guanine residues. Therefore, inactivation of this
protein can bring about a significant improvement in the therapeutic
effectiveness of these chemotherapy drugs. The prototype inactivator
O6-benzylguanine is currently in clinical trials in the
United States as an adjuvant in combination with the chloroethylating
agent 1, 3-bis (2-chloroethyl)-1-nitrosourea (BCNU) and the methylating
agent temozolomide. A similar alkyltransferase inactivator,
O6-(4-bromothenyl) guanine is in clinical trials in the UK.
This technology is directed to the discovery of a new class of
potent alkyltransferase inactivators, based on folate ester derivatives
of O6-benzyl-2'-deoxyguanosine and of O6-[4-
(hydroxymethyl)benzyl] guanine. All the folate ester derivatives of
O6-benzyl-2'-deoxyguanosine were able to sensitize human
tumor cells to killing by 1, 3-bis (2-chloroethyl)-1-nitrosourea with
O6-benzyl-3'-O-[[gamma]-folyl]-2'-deoxyguanosine being the
most active. The 3' ester was found to be more potent than the 5' ester
and was more than an order of magnitude more active than O6-
[[Page 52890]]
benzylguanine, which is currently in clinical trials.
Applications
Promising candidates as chemotherapy adjuvants for the treatment of
cancer.
Therapeutic application for drug resistant tumors where acquired
resistance is caused by O6-alkylguanine-DNA
alkyltransferase.
Advantages
The folate ester derivatives are highly water soluble.
Conjugation of folic acid to an alkyltransferase inactivating
compound should allow targeting of delivery to cells that express
folate receptor as many tumor cells are known to do.
Development Status: The technology is currently in the pre-clinical
stage of development.
Inventors: Drs. Gary Pauly (NCI), Robert C. Moschel (NCI), Sahar
Javanmard (NCI), et al.
Patent Status: This technology consists of U.S. Provisional
Application No. 60/915,510 foreign equivalents, entitled ``Inactivators
of O6-Alkylguanine-DNA Alkyltransferase'' (HHS Reference No.
E-200-2007/0).
Related Technology: HHS Reference No. E-274-2003/0, entitled ``2-
Amino-O4-Substituted Pteridines and Their Use as
Inactivators of O6-Alkylguanine-DNA Alkyltransferase''.
Licensing Status: Available for exclusive and non-exclusive
licensing.
Licensing Contact: Adaku Nwachukwu, J.D.; 301/435-5560;
madua@mail.nih.gov.
Papilloma Pseudovirus for Detection and Therapy of Tumors
Description of Technology: There is extensive literature on the use
of viral vectors, particularly those based on the adenovirus and AAV,
to increase the potency of anti-tumor gene therapy. However, these
approaches have had limited success because of limited anti-tumor
effects and unacceptable toxicity. This invention describes the use of
papillomavirus pseudoviruses (PsV) as a gene transfer technology and a
tumor diagnostic method. Preliminary studies showed that PsV bind to
cells that were transplanted with human ovarian tumor (Shin-3) while
normal tissues were not affected. PsV does not infect several other
normal intact tissues but continues to selectively infect additional
cell types that are damaged. Additionally, the inventors have
constructed oligoT PsV vectors that can be engineered to express
certain cytotoxic genes to induce tumor regression and simultaneous
increase human papilloma virus' immunogenicity. This technology could
be an effective anti-tumor therapy because it has shown increased
infection of compromised cells with an inability to infect normal cells
thereby reducing potential toxicity to patients. In addition to a
potential anti-cancer therapeutic, this technology could also be used
as a diagnostic tool in the detection of tumor masses. Detection can be
achieved through the use of fluorescent dye coupled particles of PsV
that have preferential binding to tumor tissues and not normal tissues.
Applications
Method to treat and selectively target cancer with limited
toxicity.
Method to accurately diagnose cancer.
Anti-tumor therapeutic vaccines.
Anti-tumor cytoxic gene therapy constructs.
Market
An estimated 1,444,920 new cancer cases in 2007.
600,000 cancer deaths in the U.S. in 2006.
It is estimated that market for cancer drugs would double to $50
billion a year in 2010 from $25 billion in 2006.
Development Status: The technology is currently in the pre-clinical
stage of development.
Inventors: Jeffrey Roberts, John T. Schiller, Douglas R. Lowy
(NCI).
Publications
1. CB Buck, et al. Generation of HPV pseudovirions using
transfection and their use in neutralization assays. Methods Mol Med.
2005;119:445-462.
2. CB Buck, et al. Efficient intracellular assembly of
papillomaviral vectors. J Virol. 2004 Jan;78(2):751-757.
Patent Status: U.S. Provisional Application No. 60/928,495 filed 08
May 2007 (HHS Reference No. E-186-2007/0-US-01).
Licensing Status: Available for exclusive or non-exclusive
licensing.
Licensing Contact: Jennifer Wong; 301/435-4633;
wongje@mail.nih.gov.
New Synthetic Variants of 2-(4-isothiocyanatobenzyl)-6-
methyldiethylenetriamine Pentaacetic Acid (1B4M-DTPA): Novel
Macromolecular MRI Contrast Agents
Description of Technology: The present invention describes the
synthesis and use of two protected variants of the 2-(4-
isothiocyanatobenzyl)-6-methyldiethylenetriamine pentaacetic acid
(1B4M-DTPA) (also known as the commercial bifunctional chelator,
tiuxetan), bearing either an isothiocyanate or a succinimidyl ester
moiety, respectively. These molecules were synthesized for the
following uses: (1) Use in the introduction of the chelator to the N-
terminus of peptides, aptamers, PNA, etc. wherein deprotection or
cleavage from resin or solid phase support of the product is possible
and (2) introduction of the chelator to macromolecular structures such
as dendrimer wherein this is accomplished in organic solvents
eliminating the gross inefficiency of the prior aqueous methods.
In both uses, the elimination or delay of any aqueous chemistry
steps in the synthesis process obviates the possibilities of
contamination by spurious metals. Metal contaminations could compromise
latter radiolabeling or can also hinder the introduction of
paramagnetic ions such as Gd(II1) for MRI applications. The chemistry
used in this synthetic process is very flexible and provides the basis
for an extensive list of conjugation functional groups to be
introduced.
Comparative MR imaging with these dendrimer based molecules
revealed equivalent enhancement of the vessels and organs such as the
kidney and liver.
Applications
Useful in the conjugation of nearly all peptides for targeting
antigens/peptides associated with cancers.
Useful for modification of macromolecules such as dendrimer, carbon
tubes, etc., for labeling with radioactive metal ions suitable for
imaging and/or therapy and paramagnetics for MRI.
Advantages
The chemistry is very flexible and provides the basis for an
extensive list of conjugation functional groups to be introduced.
The elimination of aqueous chemistry steps obviates the
possibilities of contamination by spurious metals that could compromise
subsequent radiolabeling.
The elimination of aqueous steps aids in the introduction of
paramagnetic ions such as Gd(III) for MRI applications.
The general synthesis process provides a procedure for preparing
dendrimer-based MR agents with higher yields and efficiency while
enhancing versatility.
Benefits: In spite of advances in cancer therapeutics and
diagnostics, more than 600,000 cancer deaths are estimated to occur in
2007. Early and accurate detection is a key component of successful
clinical management of cancer. This technology can contribute to the
development of better MRI agents
[[Page 52891]]
for diagnosing cancer and thus improve overall survival and quality of
life of patients suffering from cancer.
Inventors: Drs. Martin Brechbiel and Heng Xu (NCI).
Development Status: Synthesis process and data available.
Patent Status: U.S. Provisional Application No. 60/864,503 filed 06
Nov 2006 (HHS Reference No. E-226-2006/0-US-01).
Publication: H Xu, CA Regino, M Bernardo, Y Koyama, H Kobayashi, PL
Choyke, MW Brechbiel. Toward improved syntheses of dendrimer-based
magnetic resonance imaging contrast agents: New bifunctional
diethylenetriaminepentaacetic acid ligands and nonaqueous conjugation
chemistry. J Med Chem. 2007 Jul 12;50(14):3185-3193. Epub 2007 Jun 7.
Licensing Contact: Mojdeh Bahar; 301/435-2950; baharm@mail.nih.gov.
Methods and Compositions for Treating FUS1 Related Disorders
Description of Technology: The FUS1 gene residing in the 3p21.3
chromosome region may function as a tumor suppressor gene. In animal
models, disruption of FUS1 is associated with an increased frequency of
spontaneous vascular tumors and signs of autoimmune disease. The
investigators have in vivo data that demonstrate that FUS1 null mutants
show a consistent defect in NK cell maturation that correlate with
changes in the expression of IL-15. Injection of IL-15 into FUS1
knockout mice completely rescued the NK cell maturation defect
suggesting that FUS1 plays an important role in the development and
activation of the mammalian immune system.
Applications
Method to treat cancer, autoimmune diseases, and immune disorders
such as HIV.
Method to boost immunity in conjunction with cancer and immune
disorder therapies.
Method to diagnose FUS1 related disorders.
Animal model to study anti-tumor response and autoimmunity.
Market
An estimated 1,444,920 new cancer diagnoses in the U.S. in 2007.
600,000 deaths caused by cancer in the U.S. in 2006.
Cancer is the second leading cause of death in United States.
It is estimated that market for cancer drugs would double to $50
billion a year in 2010 from $25 billion in 2006.
An estimated 8.5 million Americans are afflicted with autoimmune
diseases.
Development Status: The technology is currently in the pre-clinical
stage of development.
Inventors: Michael I. Lerman, et al. (NCI).
Publication: AV Ivanova, et al. Autoimmunity, spontaneous
tumourigenesis, and IL-15 insufficiency in mice with a targeted
disruption of the tumour suppressor gene Fus1. J Path. 2007
Apr;211(5):591-601.
Patent Status: PCT Patent Application No. PCT/US2006/026533 (HHS
Reference No. E-137-2005/0-PCT-02).
Licensing Status: Available for exclusive or non-exclusive
licensing.
Licensing Contact: Jennifer Wong; 301/435-4633;
wongje@mail.nih.gov.
Collaborative Research Opportunity: The National Cancer Institute
Basic Research Laboratory is seeking statements of capability or
interest from parties interested in collaborative research to further
develop, evaluate, or commercialize cancer and immune disorder
therapies Please contact John D. Hewes, Ph.D. at 301-435-3121 or
hewesj@mail.nih.gov for more information.
Tumor Suppressor Genes
Description of Technology: Members of the inhibitor of growth (ING)
family of tumor suppressor genes are involved in the regulation of
diverse processes including cell cycle progression, apoptosis, and DNA
repair as important cofactors of p53. ING members contain a highly
evolutionary conserved sequence common in chromatin-regulating
proteins, and there are overlapping functions between ING family
members in negative regulation of cell growth as well as a dependent
regulation between various ING members and p53.
Available for licensing are compositions for new tumor suppressor
designated p28ING5, p33ING2, and p47ING3 (pING). Overexpression of
these proteins has been shown to inhibit cell proliferation in human
cancer cells lines, and these characteristics suggest that they may
have important implications in cancer diagnosis and therapy. These
compositions include nucleic acids, polypeptides, and antibodies that
specifically bind to their respective ING members. Also claimed are
cancer diagnostic and treatment methods.
Applications
Methods to treat and diagnose cancer with pING compositions.
Methods to identify pING modulating agents.
Research tool to study cell cycle regulation and p53 pathways. pING
compositions.
Market
Cancer is the second leading cause of death in United States.
An estimated 600,000 deaths caused by cancer in 2006.
Development Status: The technology is currently in the pre-clinical
stage of development.
Inventors: Curtis C. Harris (NCI), et al.
Publications
1. T Okano, et al. Alterations in novel candidate tumor suppressor
genes, ING1 and ING2 in human lung cancer. Oncol Rep. 2006
Mar;15(3):545-549.
2. H Kataoka, et al. ING1 represses transcription by direct DNA
binding and through effects on p53. Cancer Res. 2003 Sep
15;63(18):5785-5792.
3. M Nagashima, et al. A novel PHD-finger motif protein, p47ING3,
modulates p53-mediated transcription, cell cycle control, and
apoptosis. Oncogene. 2003 Jan 23;22(3):343-350.
4. M Nagashima, et al. DNA damage-inducible gene p33ING2 negatively
regulates cell proliferation through acetylation of p53. Proc Natl Acad
Sci USA. 2001 Aug 14;98(17):9671-9676.
Patent Status
U.S. Patent No. 6,790,948 issued 14 Sep 2004 (HHS Reference No. E-272-
1998/0-US-02)
U.S. Patent Application No. 10/868,270 filed 14 Jun 2004 (HHS Reference
No. E-272-1998/0-US-03)
PCT Patent Application No. PCT/US2001/04425 filed 09 Feb 2001 (HHS
Reference No. E-254-1999/ 0-PCT-02)
U.S. Patent Application No. 10/203,532 filed 02 Aug 2002 (HHS Reference
No. E-254-1999/0-US-03)
PCT Patent Application No. PCT/US2003/02174 filed 23 Jul 2003 (HHS
Reference No. E-300-2001/0-PCT-02)
U.S. Patent Application No. 10/502,431 filed 22 Jul 2004 (HHS Reference
No. E-300-2001/0-US-03)
Licensing Status: Available for exclusive or non-exclusive
licensing.
Licensing Contact: Jennifer Wong; 301/435-4633;
wongje@mail.nih.gov.
Peptide Inhibitor of Cyclin Dependent Kinase 4 (CDK4) Derived From MyoD
Description of Technology: This invention pertains to cell cycle
regulation and the activity of the G1 cyclin-dependent kinase 4 (CDK4).
The invention describes a 15 amino acid peptide and variants thereof
derived from muscle determination factor,
[[Page 52892]]
MyoD, which is an inhibitor of the CDK4. CDK4 is one of a number of
cyclin-dependent kinases which control progression through the cell
cycle through their ability to phosphorylate particular substrates at
the correct phase of the cell cycle. CDK4 has been shown to be involved
in cell cycle control through its ability to regulate the activity of
the retinoblastoma protein, pRb, an activator of genes essential for
cell division.
Inhibitors of the cyclin-dependent kinases, such as the peptides
described in this invention, prevent cell cycle progression and induce
cells to exit the cell cycle into the Go state. The peptides described
in this invention prevent the phosphorylation of pRb by CDK4, an
obligate step for entry into the cell cycle. Osteosarcomas and
habdosarcomas are two types of tumors known to over-express pRb. The
inhibitor described in this invention may be useful in treating these
cancers or other diseases which have been specifically linked to over-
expression of active pRb.
Applications
Method to treat proliferative disorders, including cancer.
Anti-proliferative therapeutics.
Research tool to study the cell cycle.
Advantages: Expression of this peptide either as a fusion protein
with GST or GFP results in the cessation of cell growth.
Market
An estimated 1,444,920 new cancer diagnoses in the U.S. in 2007.
600,000 deaths caused by cancer in the U.S. in 2006.
Cancer is the second leading cause of death in the United States.
It is estimated that market for cancer drugs would double to $50
billion a year in 2010 from $25 billion in 2006.
Development Status: The technology is currently in the pre-clinical
stage of development.
Inventors: Bruce M. Paterson and Jian-min Zhang (NCI).
Publication: JM Zhang, et al. Coupling of the cell cycle and
myogenesis through the cyclin D1-dependent interaction of MyoD with
cdk4. EMBO J. 1999 Feb 15;18(4):926-933.
Patent Status: U.S. Patent Application No. 10/018,964 filed 11 Apr
2002, claiming priority to 18 Jun 1999 (HHS Reference No. E-153-1998/0-
US-03).
Licensing Status: Available for exclusive or non-exclusive
licensing.
Licensing Contact: Jennifer Wong; 301/435-4633;
wongje@mail.nih.gov.
Collaborative Research Opportunity: The National Cancer Institute's
Laboratory of Biochemistry and Molecular Biology is seeking statements
of capability or interest from parties interested in collaborative
research to further develop, evaluate, or commercialize the described
cdk4 inhibitory peptides or equivalent peptide mimetics. Please contact
John D. Hewes, PhD at 301-435-3121 or hewesj@mail.nih.gov for more
information.
Dated: September 6, 2007.
Steven M. Ferguson,
Director, Division of Technology Development and Transfer, Office of
Technology Transfer, National Institutes of Health.
[FR Doc. E7-18192 Filed 9-14-07; 8:45 am]
BILLING CODE 4140-01-P
