Government-Owned Inventions; Availability for Licensing, 52054-52057 [E8-20651]
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Federal Register / Vol. 73, No. 174 / Monday, September 8, 2008 / Notices
attitudes towards substance abuse. In
order to test the effectiveness of the
interactive multimedia module, data
will be collected in the form of pre and
post test surveys from 10th and 11th
grade high school students utilizing the
developed module. The findings will
provide valuable information regarding
information pertaining to the use of
interactive multimedia educational
modules in high school science
classrooms and their ability to increase
knowledge and change attitudes and
perceptions.
Frequency of Response: 4. Affected
Public: High school students engaged
with the ArchieMD: The Science of
Drugs program. Type of Respondent:
Participants will include high school
students enrolled in the tenth and
eleventh grade. Estimated Total Annual
Number of Respondents: 360. Estimated
Number of
respondents
Type of respondents
Number of Responses per Respondent:
4. Average Burden Hours per Response:
One high school period lasting 50
minutes. Estimated Total Annual
Burden Hours Requested: 1199.95.
There are no Capital Costs to report.
There are no Operating or Maintenance
Costs to report. The estimated
annualized burden is summarized
below.
Average
burden hours
per response
Frequency
of response
Estimated total
burden hours
requested
Participants—High School Students ................................................................
360
4
.8333
1199.95
Total ..........................................................................................................
360
4
.8333
1199.95
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Request for Comments: Written
comments and/or suggestions from the
public and affected agencies are invited
on one or more of the following points:
(1) Whether the proposed collection of
information is necessary for the proper
performance of the functions of the
agency, including whether the
information shall have practical utility;
(2) the accuracy of the agency’s estimate
of the burden of the proposed collection
of information; (3) ways to enhance the
quality, utility, and clarity of the
information to be collected; and (4)
ways to minimize the burden of the
collection of information on
respondents, including through the use
of automated collection techniques or
other forms of information technology.
Comments Due Date: Comments
regarding this information collection are
best assured of having their full effect if
received within 30-days of the date of
this publication.
FOR FURTHER INFORMATION CONTACT: To
request more information on the
proposed project or to obtain a copy of
the information collection plans, please
contact Dr. Cathrine Sasek, Coordinator,
Science Education Program, Office of
Science Policy and Communications,
National Institute on Drug Abuse, 6001
Executive Blvd, Room 5237, Bethesda,
MD 20892, or call non-toll-free number
(301) 443–6071; fax (301) 443–6277; or
by e-mail to csasek@nida.nih.gov.
Comments Due Date: Comments
regarding this information collection are
best assured of having their full effect if
received within 60-days of the date of
this publication.
Dated: August 25, 2008.
Mary Affeldt,
Associate Director for Management, National
Institute on Drug Abuse, National Institutes
of Health.
[FR Doc. E8–20778 Filed 9–5–08; 8:45 am]
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DEPARTMENT OF HEALTH AND
HUMAN SERVICES
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.
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.
Over-Expression and Mutation of a
Tyrosine Kinase Receptor FGFR4 in
Tumors
Description of Technology:
Rhabdomyosarcoma (RMS) is the most
common type of pediatric soft tissue
sarcoma. Most children (>70%) with the
disease die at higher stage (metastatic
disease).
Researchers at NIH have identified
mutations in fibroblast growth factor
receptor 4 (FGFR4) that are associated
with RMS tumors. It is proposed that
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individuals with FGFR4 mutations may
have an increased risk for tumor
metastasis. The identified FGFR4
variants can be used to identify
individuals who may benefit most from
treatment with an FGFR4 inhibitor as an
adjuvant to standard anticancer
therapeutics to decrease the risk of
tumor metastasis.
Available for licensing are methods
for identifying candidates for treatment
with an inhibitor of FGFR4 by
determining the presence of at least one
FGFR4 variant, kits for identifying said
candidates, and methods for identifying
compounds that induce tumor cell
death or that inhibit tumor growth or
metastasis.
Applications:
• Potential new method for treatment
of Rhabdomyosarcomas (RMS).
• Potential new method to prepare
kits to diagnose activating mutations in
FGFR4.
• These mutations can be used in
laboratory settings to screen thousands
of compounds for more specific FGFR4
gene inhibitors.
• FGFR4 is also a potential target for
lung and breast cancer.
• FGFR4 monoclonal can be
developed to target RMS tumors.
Market:
• In the United States, approximately
12,000 new cases of cancer are
diagnosed in children each year.
Childhood cancer remains the leading
disease-related cause of death in
children and adolescents in North
America, with about 2,300 deaths each
year.
• Rhabdomyosarcoma accounts for
about 3 percent of childhood cancers. In
the U.S., about 350 children are
diagnosed with Rhabdomyosarcoma
each year.
Development Status: Early-stage of
development.
Inventors: Javed Khan et al. (NCI).
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Patent Status: U.S. Provisional
Application No. 61/044,875 filed 14 Apr
2008 (HHS Reference No. E–175–2008/
0–US–01).
Licensing Status: Available for
exclusive and non-exclusive licensing.
Licensing Contact: Betty B. Tong,
Ph.D.; 301–594–6565;
tongb@mail.nih.gov.
Collaborative Research Opportunity:
The National Cancer Institute, Pediatric
Oncology Branch, is seeking statements
of capability or interest from parties
interested in collaborative research to
further develop, evaluate, or
commercialize Over-expression and
Mutation of a Tyrosine Kinase Receptor
FGFR4 in Tumors. Please contact John
D. Hewes, Ph.D. at 301–435–3121 or
hewesj@mail.nih.gov for more
information.
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Small Molecule Inhibitors of c-Met
Description of Technology: Aberrant c
Met signaling is documented in a wide
variety of malignancies and occurs via
several mechanisms including
amplification of c-Met (increased gene
copy number), point mutations in the
gene encoding c-Met, receptor overexpression, and ligand dependent
autocrine/paracrine receptor activation.
This application describes novel small
molecule inhibitors of c-Met signaling.
The small molecules selectively bind to
c-Met and have an IC50 in the
micromolar range. The small molecules
belong to two different families. One
family of small molecules reduces the
level of c Met expression via receptor
down-regulation and blocks ATP
binding. The other family of small
molecules block ATP binding without
inducing receptor down-regulation.
Evidence suggests that the second
family of compounds bind to both active
and inactive conformations of c-Met.
Applications: Therapy for cancers
associated with aberrant c-Met
signaling, for example bladder, breast,
cervical, colorectal, endometrial,
esophageal, gastric, head and neck,
kidney, liver, lung, nasopharyngeal,
ovarian, pancreatic, prostate and thyroid
cancers, as well as cholangiocarconoma,
osteosarcoma, rhabdomyosarcoma,
synovial sarcoma, Kaposi’s sarcoma,
leiomyosarcomas and MFH/
fibrosarcoma. In addition to these
malignancies, aberrant c Met signaling
is associated with hematological
malignancies such as acute
myelogenous leukemia, adult T cell
leukemia, chronic myeloid leukemia,
lymphomas and multiple myeloma as
well as other tumors like melanoma,
mesothelioma, Wilms’ tumor,
glioblastomata and astrocytomas.
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Market: Although the percentage of
cancers associated with aberrant c Met
signaling is not yet well established, the
wide variety of cancers associated with
aberrant c Met signaling are indicative
of a potentially large market for these
compounds. For example, worldwide
over 1 million persons per year are
diagnosed with colorectal cancer and it
is the most common gastrointestinal
cancer in industrialized countries. In
one study of colorectal cancer 69% of
the patients had at least a two-fold
elevation of cMet mRNA and 48% of the
patients had at least a ten fold elevation
of c Met mRNA. In a study of breast
cancer, 22% of patients with invasive
ductal breast tumor specimens exhibited
strong expression of c Met and patients
exhibiting c Met expression had only a
52% 5 year survival rate compared with
an 89% 5 year survival rate in patients
with normal c Met levels.
Development Status: The technology
is currently in the pre-clinical stage of
development.
Inventors: Donald P. Bottaro, Terrence
Burke, Jr., et al. (NCI).
Patent Status: U.S. Provisional
Application No. 61/041,523 filed 01 Apr
2008 (HHS Reference No. E–332–2007/
0–US–01).
Publications: The patent application
has not been published. There are no
journal articles available related to this
work.
Licensing Status: Available for
licensing on an exclusive or nonexclusive basis.
Licensing Contact: Susan S. Rucker;
301–435–4478;
Susan.Rucker@nih.hhs.gov.
Collaborative Research Opportunity:
The National Cancer Institute, Urologic
Oncology Branch, is seeking statements
of capability or interest from parties
interested in collaborative research to
further develop, evaluate, or
commercialize small molecule
inhibitors of the HGF/c-Met signaling
pathway. Please contact John D. Hewes,
Ph.D. at 301–435–3121 or
hewesj@mail.nih.gov for more
information.
Quantitative Immunoassays for
Measurement of Topoisomerase I as a
Pharmacodynamic Marker for the
Effect of Anti-Cancer Drugs
Description of Technology:
Topoisomerase I (TopoI) is an enzyme
that catalyses DNA unwinding which is
necessary for many cellular functions.
Recent data from the Fluorouracil,
Oxaliplatin, CPT–11: Use and
Sequencing (FOCUS) trial demonstrates
that nuclear staining of TopoI correlates
with chemotherapy efficacy [J Clin
Oncol (2008) 26, 2690–8]. This enzyme
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covalently binds with the DNA substrate
and introduces a single strand break.
Some anti-cancer drugs, including those
in clinical trials target this cleavage site
and prevent re-ligation of the unwound
DNA, trapping the TopoI/DNA covalent
complex. TopoI trapped by Topo I
inhibitor compounds such as Topotecan
is degraded by the ubiquitin/proteosome
pathway. This change in intracellular
TopoI levels makes total TopoI and the
TopoI/DNA covalent complex potential
pharmacodynamic biomarkers for
monitoring TopoI inhibiting agents,
used in cancer therapy.
The technology involves a validated,
enzyme linked immunosorbent assay
(ELISA) with a chemiluminescence
readout, using commercially available
antibodies to quantitate total TopoI from
cell and tumor extracts.
This technology has been used in a
high throughput assay for measurement
of estrogen and estrogen metabolites in
serum. A similar ELISA assay has also
been used in NCI Phase 0 and Phase I
clinical trials of a PARP inhibitor
Applications:
• Anti-cancer drug testing.
• Patient selection for anti-cancer
drug treatment.
Advantages:
• Simple, quantitative, sensitive (LLQ
∼40pg/well LLOD= (LOD 220 pg/ml as
formulated), range 200 pg/ml to 50ng/
ml).
• Uses commercially available
antibodies.
• Excludes the use of radioisotopes.
• Validated Assay.
• SOP available.
• In vitro data support use in anticancer drug treated melanoma cell lines.
• Mouse model data support use in
anti-cancer drug treated melanoma and
colon cancer xenografts.
Developmental Status: ELISA was
developed in support of Phase I clinical
trial on experimental TopoI inhibiting
drugs.
Publication: Thomas D. Pfister, Ralph
E. Parchment, Joseph Tomaszewski,
James Doroshow and Robert J. Kinders.
‘‘Development of a quantitative
immunoassay for measurement of
topoisomerase I covalent complex as a
pharmacodynamic marker for the effect
of anti-cancer drugs.’’ AACR Annual
Meeting, Los Angeles, CA April 14–18,
2007.
Inventors: Thomas D. Pfister and
Robert J. Kinders (SAIC/NCI).
Patent Status: HHS Reference No. E–
100–2007/0—Research Tool. Patent
protection is not being pursued for this
technology.
Licensing Status: Available for nonexclusive licensing of biological
material.
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Licensing Contact: John Stansberry,
Ph.D.; 301–435–5236;
stansbej@mail.nih.gov.
Collaborative Research Opportunity:
The National Cancer Institute’s
Laboratory of Human Toxicology and
Pharmacology is seeking statements of
capability or interest from parties
interested in collaborative research to
further develop, evaluate, or
commercialize Quantitative
Immunoassays for Measurement of
Topoisomerase I as a Pharmacodynamic
Marker for the Effect of Anti-Cancer
Drugs. Please contact John D. Hewes,
Ph.D. at 301–435–3121 or
hewesj@mail.nih.gov for more
information.
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New Tumor Endothelial Markers:
Genes That Distinguish Physiological
and Pathological Angiogenesis
Description of Technology:
Angiogenesis, the formation of new
blood vessels, is associated with normal
physiological processes such as wound
healing, ovulation or menstruation as
well as with many diseases. Presently,
it is thought to be required for the
progressive growth of solid tumors and
age-related macular degeneration. Lack
of disease-specific endothelial markers
has hindered the development of cancer
therapies targeted against angiogenesis.
This invention describes specific
markers that can be used to identify
tumor angiogenesis, separate from
normal physiological angiogenesis.
Several markers have been identified
which may serve as potential targets for
tumor vessels by using comparative
gene expression analysis on various
normal and tumor endothelial cells.
Furthermore, the invention describes
several organ-specific endothelial
markers that can aid in the selective
delivery of molecular medicine to
specific sites. For example, brain
endothelial markers (BEMs) and liver
endothelial markers (LEMs) described
herein could potentially be used to
direct molecular medicine specifically
to these tissues.
The novel tumor endothelial markers
(TEMs) described in this invention also
have potential diagnostic ability. These
markers can be used to distinguish
between normal and tumor tissues.
Some of the secreted TEMs can serve as
surrogate markers in the determination
of the optimum biological dose (OBD)
for the current anti-angiogenic drugs in
clinical trials.
Applications and Modality:
• Novel therapeutic targets associated
with tumor vessels.
• New agents can be developed
against these novel targets.
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• Novel endothelial markers that
distinguish pathological angiogenesis
from normal physiological angiogenesis.
• Surrogate tumor endothelial
markers that can be used to determine
optimal biological dose (OBD) of antiangiogenic drugs.
Market:
• Sales of the first FDA approved
anti-angiogenic drug AvastinTM has
reached $600 million.
• Another promising anti-angiogenic
molecule, ThalidomideTM, has been
approved as an anti-cancer agent and for
other use in Europe and Australia.
Development Status: The technology
is currently in the pre-clinical stage of
development.
Inventors: Brad St. Croix and Steven
Seaman (NCI).
Relevant Publication: A Nanda and B
St. Croix. Tumor endothelial markers:
new targets for cancer therapy. Curr
Opin Oncol. 2004 Jan;16(1):44–49.
Patent Status:
• U.S. Provisional Application No.
60/858,068 filed 09 Nov 2006 (HHS
Reference No. E–285–2006/0–US–01).
• U.S. Provisional Application No.
60/879,457 filed 08 Jan 2007 (HHS
Reference No. E–285–2006/1–US–01).
• PCT Application No. PCT/US2007/
072395 filed 28 Jun 2007, which
published as WO 2008/057632 on 15
May 2008 (HHS Reference No. E–285–
2006/2–PCT–01).
Licensing Status: Available for
exclusive and non-exclusive licensing.
Licensing Contact: Adaku
Nwachukwu, J.D.; 301–435–5560;
madua@mail.nih.gov.
Collaborative Research Opportunity:
The NIH National Cancer Institute,
Tumor Angiogenesis Section, is seeking
statements of capability or interest from
parties interested in collaborative
research to further develop, evaluate, or
commercialize specific biomarkers that
can be used to identify tumor
angiogenesis. Please contact John D.
Hewes, PhD at 301/435–3121 or
hewesj@mail.nih.gov for more
information.
Methods of Treating and Preventing
Renal Cancer Using a Dimethane
Sulfonate Compound
Description of Technology: Currently
only a few small molecule inhibitors are
effective in patients with renal cell
carcinoma. Approximately 30,000
patients per year are diagnosed with this
disease but many of them are
untreatable because of intrinsic drug
resistance, and efficient drug transport
and detoxification mechanisms. This
invention described and claimed in the
patent application describes a series of
dimethane sulfonate compounds based
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on NSC 281612 that are suitable for the
treatment of renal cancer. Compositions
comprising a pharmaceuticallyacceptable carrier and a compound, or
a salt suitable for use in the treatment
or prevention of renal cancer are also
described. The anti-tumor activity of
NSC 281612 has been established in
vivo against human renal tumor
xenografts in mice. Suitable dosing and
administration schedules for treatment
of renal tumors have also been
determined in this study.
Applications: For treatment or
prevention of renal cancer.
Development Status: The technology
is currently in the pre-clinical stage of
development. Phase I clinical trials will
begin this fall.
Inventors: Susan D. Mertins, Susan E.
Bates, David G. Covell, Geoffrey W.
Patton, Melinda G. Hollingshead, B. Rao
Vishnuvajjala (NCI).
Patent Status: U.S. Patent Application
No. 12/083,583 filed 14 Apr 2008,
claiming priority to 14 Oct 2005 (HHS
Reference No. E–249–2005/0–US–04).
Licensing Status: Available for
exclusive or non-exclusive licensing.
Licensing Contact: Adaku
Nwachukwu, J.D.; 301–435–5560;
madua@mail.nih.gov.
Collaborative Research Opportunity:
The National Cancer Institute, Screening
Technologies Branch, is seeking
statements of capability or interest from
parties interested in collaborative
research to further develop, evaluate, or
commercialize biomarker assays for
clinical utility (potential molecular
targets have been identified). Please
contact John D. Hewes, Ph.D. at 301–
435–3121 or hewesj@mail.nih.gov for
more information.
2-Amino-O4-Substituted Pteridines:
Improved Chemotherapy Adjuvants
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
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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, 2-aminoO4-benzylpteridine derivatives targeted
for use in cancer treatment in
combination with chemotherapeutic
agents such as 1, 3-bis (2-chloroethyl)1-nitrosurea (BCNU) or temozolomide.
The derivatives of the present invention
inactivate the O6-alkylguanine-DNAalkyltransferase repair protein and thus
enhance activity of such
chemotherapeutic agents. Some of the
derivatives are water soluble and
possess tumor cell selectivity in
particular by inactivating
alkyltransferase in tumor cells that
overexpress folic acid receptors. The 2amino-O4-benzylpteridine derivatives
represent a promising new class of
alkyltransferase inactivator with
representatives that may be great
candidates as chemotherapy adjuvants.
Applications and Modality:
• New small molecules as
alkyltransferase inactivators based on 2amino-O4-benzylpteridine compounds.
• 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.
Market:
• 600,000 deaths from cancer related
diseases estimated in 2006.
• This technology involving small
molecule therapeutics for the treatment
of several cancers has a potential market
of several billion U.S. dollars.
Development Status: The technology
is currently in the pre-clinical stage of
development.
Inventors: Robert C. Moschel (NCI) et
al.
Publication: ME Nelson, NA
Loktionova, AE Pegg, RC Moschel. 2amino-O4-benzylpteridine derivatives:
Potent inactivators of O6-alkylguanineDNA alkyltransferase. J Med Chem.
2004 Jul 15;47(15):3887–3891.
Patent Status:
• U.S. Patent Application No. 10/
585,566 filed 29 Aug 2006, claiming
priority to 06 Jan 2004 (HHS Reference
No. E–274–2003/0–US–03).
• Foreign equivalents
Licensing Status: Available for
exclusive or non-exclusive licensing.
Licensing Contact: Adaku
Nwachukwu, J.D.; 301–435–5560;
madua@mail.nih.gov.
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Dated: August 26, 2008.
Richard U. Rodriguez,
Director, Division of Technology Development
and Transfer, Office of Technology Transfer,
National Institutes of Health.
[FR Doc. E8–20651 Filed 9–5–08; 8:45 am]
BILLING CODE 4140–01–P
DEPARTMENT OF HEALTH AND
HUMAN SERVICES
National Institutes of Health
Eunice Kennedy Shriver National
Institute of Child Health & Human
Development; Notice of Closed
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 the following
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 Institute of
Child Health and Human Development
Special Emphasis Panel EARDA.
Date: October 3, 2008.
Time: 9 a.m. to 3 p.m.
Agenda: To review and evaluate grant
applications.
Place: National Institutes of Health, 6100
Executive Boulevard, 4B01 CRMC, Rockville,
MD 20852.
Contact Person: Michele C. HindiAlexander, PhD, Division of Scientific
Review, National Institutes of Health, Eunice
Kennedy Shriver National Institute for Child
Health & Development, 1600 Executive
Boulevard, 5B01, Bethesda, MD 20812–7510,
(301) 435–8382, hindialm@mail.nih.gov.
(Catalogue of Federal Domestic Assistance
Program Nos. 93.864, Population Research;
93.865, Research for Mothers and Children;
93.929, Center for Medical Rehabilitation
Research; 93.209, Contraception and
Infertility Loan Repayment Program, National
Institutes of Health, HHS)
DEPARTMENT OF HEALTH AND
HUMAN SERVICES
National Institutes of Health
Eunice Kennedy Shriver National
Institute of Child Health & Human
Development; Notice of Closed
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 the following
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 Institute of
Child Health and Human Development
Special Emphasis Panel; The Role of Human
Milk in Infant Nutrition and Health.
Date: October 7, 2008.
Time: 2 a.m. to 5 p.m.
Agenda: To review and evaluate grant
applications.
Place: National Institutes of Health, 6100
Executive Boulevard, 5B01, Rockville, MD
20852 (Telephone Conference Call).
Contact Person: Rita Anand, PhD,
Scientific Review Administrator, Division of
Scientific Review, National Institute of Child
Health and Human Development, NIH, 6100
Executive Blvd, Room 5B01, Bethesda, MD
20892, (301) 496–1487,
anandr@mail.nih.gov.
(Catalogue of Federal Domestic Assistance
Program Nos. 93.864, Population Research;
93.865, Research for Mothers and Children;
93.929, Center for Medical Rehabilitation
Research; 93.209, Contraception and
Infertility Loan Repayment Program, National
Institutes of Health, HHS)
Dated: August 28, 2008.
Jennifer Spaeth,
Director, Office of Federal Advisory
Committee Policy.
[FR Doc. E8–20646 Filed 9–5–08; 8:45 am]
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Dated: August 28, 2008.
Jennifer Spaeth,
Director, Office of Federal Advisory
Committee Policy.
[FR Doc. E8–20644 Filed 9–5–08; 8:45 am]
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]]>Agencies
[Federal Register Volume 73, Number 174 (Monday, September 8, 2008)]
[Notices]
[Pages 52054-52057]
From the Federal Register Online via the Government Printing Office [www.gpo.gov]
[FR Doc No: E8-20651]
-----------------------------------------------------------------------
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.
Over-Expression and Mutation of a Tyrosine Kinase Receptor FGFR4 in
Tumors
Description of Technology: Rhabdomyosarcoma (RMS) is the most
common type of pediatric soft tissue sarcoma. Most children (>70%) with
the disease die at higher stage (metastatic disease).
Researchers at NIH have identified mutations in fibroblast growth
factor receptor 4 (FGFR4) that are associated with RMS tumors. It is
proposed that individuals with FGFR4 mutations may have an increased
risk for tumor metastasis. The identified FGFR4 variants can be used to
identify individuals who may benefit most from treatment with an FGFR4
inhibitor as an adjuvant to standard anticancer therapeutics to
decrease the risk of tumor metastasis.
Available for licensing are methods for identifying candidates for
treatment with an inhibitor of FGFR4 by determining the presence of at
least one FGFR4 variant, kits for identifying said candidates, and
methods for identifying compounds that induce tumor cell death or that
inhibit tumor growth or metastasis.
Applications:
Potential new method for treatment of Rhabdomyosarcomas
(RMS).
Potential new method to prepare kits to diagnose
activating mutations in FGFR4.
These mutations can be used in laboratory settings to
screen thousands of compounds for more specific FGFR4 gene inhibitors.
FGFR4 is also a potential target for lung and breast
cancer.
FGFR4 monoclonal can be developed to target RMS tumors.
Market:
In the United States, approximately 12,000 new cases of
cancer are diagnosed in children each year. Childhood cancer remains
the leading disease-related cause of death in children and adolescents
in North America, with about 2,300 deaths each year.
Rhabdomyosarcoma accounts for about 3 percent of childhood
cancers. In the U.S., about 350 children are diagnosed with
Rhabdomyosarcoma each year.
Development Status: Early-stage of development.
Inventors: Javed Khan et al. (NCI).
[[Page 52055]]
Patent Status: U.S. Provisional Application No. 61/044,875 filed 14
Apr 2008 (HHS Reference No. E-175-2008/0-US-01).
Licensing Status: Available for exclusive and non-exclusive
licensing.
Licensing Contact: Betty B. Tong, Ph.D.; 301-594-6565;
tongb@mail.nih.gov.
Collaborative Research Opportunity: The National Cancer Institute,
Pediatric Oncology Branch, is seeking statements of capability or
interest from parties interested in collaborative research to further
develop, evaluate, or commercialize Over-expression and Mutation of a
Tyrosine Kinase Receptor FGFR4 in Tumors. Please contact John D. Hewes,
Ph.D. at 301-435-3121 or hewesj@mail.nih.gov for more information.
Small Molecule Inhibitors of c-Met
Description of Technology: Aberrant c Met signaling is documented
in a wide variety of malignancies and occurs via several mechanisms
including amplification of c-Met (increased gene copy number), point
mutations in the gene encoding c-Met, receptor over-expression, and
ligand dependent autocrine/paracrine receptor activation. This
application describes novel small molecule inhibitors of c-Met
signaling. The small molecules selectively bind to c-Met and have an
IC50 in the micromolar range. The small molecules belong to two
different families. One family of small molecules reduces the level of
c Met expression via receptor down-regulation and blocks ATP binding.
The other family of small molecules block ATP binding without inducing
receptor down-regulation. Evidence suggests that the second family of
compounds bind to both active and inactive conformations of c-Met.
Applications: Therapy for cancers associated with aberrant c-Met
signaling, for example bladder, breast, cervical, colorectal,
endometrial, esophageal, gastric, head and neck, kidney, liver, lung,
nasopharyngeal, ovarian, pancreatic, prostate and thyroid cancers, as
well as cholangiocarconoma, osteosarcoma, rhabdomyosarcoma, synovial
sarcoma, Kaposi's sarcoma, leiomyosarcomas and MFH/fibrosarcoma. In
addition to these malignancies, aberrant c Met signaling is associated
with hematological malignancies such as acute myelogenous leukemia,
adult T cell leukemia, chronic myeloid leukemia, lymphomas and multiple
myeloma as well as other tumors like melanoma, mesothelioma, Wilms'
tumor, glioblastomata and astrocytomas.
Market: Although the percentage of cancers associated with aberrant
c Met signaling is not yet well established, the wide variety of
cancers associated with aberrant c Met signaling are indicative of a
potentially large market for these compounds. For example, worldwide
over 1 million persons per year are diagnosed with colorectal cancer
and it is the most common gastrointestinal cancer in industrialized
countries. In one study of colorectal cancer 69% of the patients had at
least a two-fold elevation of cMet mRNA and 48% of the patients had at
least a ten fold elevation of c Met mRNA. In a study of breast cancer,
22% of patients with invasive ductal breast tumor specimens exhibited
strong expression of c Met and patients exhibiting c Met expression had
only a 52% 5 year survival rate compared with an 89% 5 year survival
rate in patients with normal c Met levels.
Development Status: The technology is currently in the pre-clinical
stage of development.
Inventors: Donald P. Bottaro, Terrence Burke, Jr., et al. (NCI).
Patent Status: U.S. Provisional Application No. 61/041,523 filed 01
Apr 2008 (HHS Reference No. E-332-2007/0-US-01).
Publications: The patent application has not been published. There
are no journal articles available related to this work.
Licensing Status: Available for licensing on an exclusive or non-
exclusive basis.
Licensing Contact: Susan S. Rucker; 301-435-4478;
Susan.Rucker@nih.hhs.gov.
Collaborative Research Opportunity: The National Cancer Institute,
Urologic Oncology Branch, is seeking statements of capability or
interest from parties interested in collaborative research to further
develop, evaluate, or commercialize small molecule inhibitors of the
HGF/c-Met signaling pathway. Please contact John D. Hewes, Ph.D. at
301-435-3121 or hewesj@mail.nih.gov for more information.
Quantitative Immunoassays for Measurement of Topoisomerase I as a
Pharmacodynamic Marker for the Effect of Anti-Cancer Drugs
Description of Technology: Topoisomerase I (TopoI) is an enzyme
that catalyses DNA unwinding which is necessary for many cellular
functions. Recent data from the Fluorouracil, Oxaliplatin, CPT-11: Use
and Sequencing (FOCUS) trial demonstrates that nuclear staining of
TopoI correlates with chemotherapy efficacy [J Clin Oncol (2008) 26,
2690-8]. This enzyme covalently binds with the DNA substrate and
introduces a single strand break. Some anti-cancer drugs, including
those in clinical trials target this cleavage site and prevent re-
ligation of the unwound DNA, trapping the TopoI/DNA covalent complex.
TopoI trapped by Topo I inhibitor compounds such as Topotecan is
degraded by the ubiquitin/proteosome pathway. This change in
intracellular TopoI levels makes total TopoI and the TopoI/DNA covalent
complex potential pharmacodynamic biomarkers for monitoring TopoI
inhibiting agents, used in cancer therapy.
The technology involves a validated, enzyme linked immunosorbent
assay (ELISA) with a chemiluminescence readout, using commercially
available antibodies to quantitate total TopoI from cell and tumor
extracts.
This technology has been used in a high throughput assay for
measurement of estrogen and estrogen metabolites in serum. A similar
ELISA assay has also been used in NCI Phase 0 and Phase I clinical
trials of a PARP inhibitor
Applications:
Anti-cancer drug testing.
Patient selection for anti-cancer drug treatment.
Advantages:
Simple, quantitative, sensitive (LLQ ~40pg/well LLOD= (LOD
220 pg/ml as formulated), range 200 pg/ml to 50ng/ml).
Uses commercially available antibodies.
Excludes the use of radioisotopes.
Validated Assay.
SOP available.
In vitro data support use in anti-cancer drug treated
melanoma cell lines.
Mouse model data support use in anti-cancer drug treated
melanoma and colon cancer xenografts.
Developmental Status: ELISA was developed in support of Phase I
clinical trial on experimental TopoI inhibiting drugs.
Publication: Thomas D. Pfister, Ralph E. Parchment, Joseph
Tomaszewski, James Doroshow and Robert J. Kinders. ``Development of a
quantitative immunoassay for measurement of topoisomerase I covalent
complex as a pharmacodynamic marker for the effect of anti-cancer
drugs.'' AACR Annual Meeting, Los Angeles, CA April 14-18, 2007.
Inventors: Thomas D. Pfister and Robert J. Kinders (SAIC/NCI).
Patent Status: HHS Reference No. E-100-2007/0--Research Tool.
Patent protection is not being pursued for this technology.
Licensing Status: Available for non-exclusive licensing of
biological material.
[[Page 52056]]
Licensing Contact: John Stansberry, Ph.D.; 301-435-5236;
stansbej@mail.nih.gov.
Collaborative Research Opportunity: The National Cancer Institute's
Laboratory of Human Toxicology and Pharmacology is seeking statements
of capability or interest from parties interested in collaborative
research to further develop, evaluate, or commercialize Quantitative
Immunoassays for Measurement of Topoisomerase I as a Pharmacodynamic
Marker for the Effect of Anti-Cancer Drugs. Please contact John D.
Hewes, Ph.D. at 301-435-3121 or hewesj@mail.nih.gov for more
information.
New Tumor Endothelial Markers: Genes That Distinguish Physiological and
Pathological Angiogenesis
Description of Technology: Angiogenesis, the formation of new blood
vessels, is associated with normal physiological processes such as
wound healing, ovulation or menstruation as well as with many diseases.
Presently, it is thought to be required for the progressive growth of
solid tumors and age-related macular degeneration. Lack of disease-
specific endothelial markers has hindered the development of cancer
therapies targeted against angiogenesis.
This invention describes specific markers that can be used to
identify tumor angiogenesis, separate from normal physiological
angiogenesis. Several markers have been identified which may serve as
potential targets for tumor vessels by using comparative gene
expression analysis on various normal and tumor endothelial cells.
Furthermore, the invention describes several organ-specific endothelial
markers that can aid in the selective delivery of molecular medicine to
specific sites. For example, brain endothelial markers (BEMs) and liver
endothelial markers (LEMs) described herein could potentially be used
to direct molecular medicine specifically to these tissues.
The novel tumor endothelial markers (TEMs) described in this
invention also have potential diagnostic ability. These markers can be
used to distinguish between normal and tumor tissues. Some of the
secreted TEMs can serve as surrogate markers in the determination of
the optimum biological dose (OBD) for the current anti-angiogenic drugs
in clinical trials.
Applications and Modality:
Novel therapeutic targets associated with tumor vessels.
New agents can be developed against these novel targets.
Novel endothelial markers that distinguish pathological
angiogenesis from normal physiological angiogenesis.
Surrogate tumor endothelial markers that can be used to
determine optimal biological dose (OBD) of anti-angiogenic drugs.
Market:
Sales of the first FDA approved anti-angiogenic drug
AvastinTM has reached $600 million.
Another promising anti-angiogenic molecule,
ThalidomideTM, has been approved as an anti-cancer agent and
for other use in Europe and Australia.
Development Status: The technology is currently in the pre-clinical
stage of development.
Inventors: Brad St. Croix and Steven Seaman (NCI).
Relevant Publication: A Nanda and B St. Croix. Tumor endothelial
markers: new targets for cancer therapy. Curr Opin Oncol. 2004
Jan;16(1):44-49.
Patent Status:
U.S. Provisional Application No. 60/858,068 filed 09 Nov
2006 (HHS Reference No. E-285-2006/0-US-01).
U.S. Provisional Application No. 60/879,457 filed 08 Jan
2007 (HHS Reference No. E-285-2006/1-US-01).
PCT Application No. PCT/US2007/072395 filed 28 Jun 2007,
which published as WO 2008/057632 on 15 May 2008 (HHS Reference No. E-
285-2006/2-PCT-01).
Licensing Status: Available for exclusive and non-exclusive
licensing.
Licensing Contact: Adaku Nwachukwu, J.D.; 301-435-5560;
madua@mail.nih.gov.
Collaborative Research Opportunity: The NIH National Cancer
Institute, Tumor Angiogenesis Section, is seeking statements of
capability or interest from parties interested in collaborative
research to further develop, evaluate, or commercialize specific
biomarkers that can be used to identify tumor angiogenesis. Please
contact John D. Hewes, PhD at 301/435-3121 or hewesj@mail.nih.gov for
more information.
Methods of Treating and Preventing Renal Cancer Using a Dimethane
Sulfonate Compound
Description of Technology: Currently only a few small molecule
inhibitors are effective in patients with renal cell carcinoma.
Approximately 30,000 patients per year are diagnosed with this disease
but many of them are untreatable because of intrinsic drug resistance,
and efficient drug transport and detoxification mechanisms. This
invention described and claimed in the patent application describes a
series of dimethane sulfonate compounds based on NSC 281612 that are
suitable for the treatment of renal cancer. Compositions comprising a
pharmaceutically-acceptable carrier and a compound, or a salt suitable
for use in the treatment or prevention of renal cancer are also
described. The anti-tumor activity of NSC 281612 has been established
in vivo against human renal tumor xenografts in mice. Suitable dosing
and administration schedules for treatment of renal tumors have also
been determined in this study.
Applications: For treatment or prevention of renal cancer.
Development Status: The technology is currently in the pre-clinical
stage of development. Phase I clinical trials will begin this fall.
Inventors: Susan D. Mertins, Susan E. Bates, David G. Covell,
Geoffrey W. Patton, Melinda G. Hollingshead, B. Rao Vishnuvajjala
(NCI).
Patent Status: U.S. Patent Application No. 12/083,583 filed 14 Apr
2008, claiming priority to 14 Oct 2005 (HHS Reference No. E-249-2005/0-
US-04).
Licensing Status: Available for exclusive or non-exclusive
licensing.
Licensing Contact: Adaku Nwachukwu, J.D.; 301-435-5560;
madua@mail.nih.gov.
Collaborative Research Opportunity: The National Cancer Institute,
Screening Technologies Branch, is seeking statements of capability or
interest from parties interested in collaborative research to further
develop, evaluate, or commercialize biomarker assays for clinical
utility (potential molecular targets have been identified). Please
contact John D. Hewes, Ph.D. at 301-435-3121 or hewesj@mail.nih.gov for
more information.
2-Amino-O\4\-Substituted Pteridines: Improved Chemotherapy Adjuvants
Description of Technology: O\6\-Benzylguanine derivatives, some
O\6\-benzylpyrimidines, and related compounds are known to be
inactivators of the human DNA repair protein O\6\-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 O\6\-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 O\6\-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
[[Page 52057]]
similar alkyltransferase inactivator, O\6\-(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, 2-amino-O\4\-benzylpteridine
derivatives targeted for use in cancer treatment in combination with
chemotherapeutic agents such as 1, 3-bis (2-chloroethyl)-1-nitrosurea
(BCNU) or temozolomide. The derivatives of the present invention
inactivate the O\6\-alkylguanine-DNA-alkyltransferase repair protein
and thus enhance activity of such chemotherapeutic agents. Some of the
derivatives are water soluble and possess tumor cell selectivity in
particular by inactivating alkyltransferase in tumor cells that
overexpress folic acid receptors. The 2-amino-O\4\-benzylpteridine
derivatives represent a promising new class of alkyltransferase
inactivator with representatives that may be great candidates as
chemotherapy adjuvants.
Applications and Modality:
New small molecules as alkyltransferase inactivators based
on 2-amino-O\4\-benzylpteridine compounds.
Promising candidates as chemotherapy adjuvants for the
treatment of cancer.
Therapeutic application for drug resistant tumors where
acquired resistance is caused by O\6\-alkylguanine-DNA
alkyltransferase.
Market:
600,000 deaths from cancer related diseases estimated in
2006.
This technology involving small molecule therapeutics for
the treatment of several cancers has a potential market of several
billion U.S. dollars.
Development Status: The technology is currently in the pre-clinical
stage of development.
Inventors: Robert C. Moschel (NCI) et al.
Publication: ME Nelson, NA Loktionova, AE Pegg, RC Moschel. 2-
amino-O\4\-benzylpteridine derivatives: Potent inactivators of O\6\-
alkylguanine-DNA alkyltransferase. J Med Chem. 2004 Jul 15;47(15):3887-
3891.
Patent Status:
U.S. Patent Application No. 10/585,566 filed 29 Aug 2006,
claiming priority to 06 Jan 2004 (HHS Reference No. E-274-2003/0-US-
03).
Foreign equivalents
Licensing Status: Available for exclusive or non-exclusive
licensing.
Licensing Contact: Adaku Nwachukwu, J.D.; 301-435-5560;
madua@mail.nih.gov.
Dated: August 26, 2008.
Richard U. Rodriguez,
Director, Division of Technology Development and Transfer, Office of
Technology Transfer, National Institutes of Health.
[FR Doc. E8-20651 Filed 9-5-08; 8:45 am]
BILLING CODE 4140-01-P
