Government-Owned Inventions; Availability for Licensing, 9252-9253 [E9-4477]
Download as PDF
<![CDATA[
9252
Federal Register / Vol. 74, No. 40 / Tuesday, March 3, 2009 / Notices
status, the reasons they seek care at
health centers, their diagnoses, the
services they utilize at health centers
and elsewhere, the quality of those
services, and their satisfaction with the
care they receive, through personal
interviews of a stratified random sample
of health center patients. Interviews are
planned to take approximately 1 hour
and six minutes each.
The Patient Survey builds on previous
periodic User-Visit Surveys which were
conducted to learn about the process
and outcomes of care in CHCs and HCH
projects. The original survey questions
were derived from the National Health
Interview Survey (NHIS) and the
National Hospital Ambulatory Medical
Care Survey (NHAMCS) conducted by
the National Center for Health Statistics
(NCHS). Conformance with the NHIS
and NHAMCS allowed comparisons
between these NCHS surveys and the
previous CHC and HCH User-Visit
Surveys. The new Patient Survey was
developed using a questionnaire
methodology similar to that used in the
past, and will also allow some
longitudinal comparisons for CHCs and
HCH projects with the previous UserVisit survey data, including monitoring
of process outcomes over time. In
addition, this survey will include
interviews of patients drawn from
migrant populations and from residents
of public housing; these populations
were not included in the previous
surveys.
The annual estimate of burden is as
follows:
The estimated response burden for the
survey is as follows:
SURVEY
Number of
respondents
Responses
per
respondent
Grantee/Site Recruitment and Site Training ..........................................
Patient Recruitment ...............................................................................
Patient Survey .......................................................................................
115
5,658
4,526
3
1
1
345
5,658
4,526
3.75
.167
1.1
1,294
945
4,979
Total ................................................................................................
5,773
....................
10,529
......................
7,218
Type of respondent; activity involved
Written comments and
recommendations concerning the
proposed information collection should
be sent within 30 days of this notice to
the desk officer for HRSA, either by email to OIRA_submission@omb.eop.gov
or by fax to 202–395–6974. Please direct
all correspondence to the ‘‘attention of
the desk officer for HRSA.’’
Dated: February 24, 2009.
Alexandra Huttinger,
Director, Division of Policy Review and
Coordination.
[FR Doc. E9–4460 Filed 3–2–09; 8:45 am]
Prevention of Head and Neck Cancer
Using Rapamycin and Its Analogs
BILLING CODE 4165–15–P
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.
mstockstill on PROD1PC66 with NOTICES
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.
VerDate Nov<24>2008
16:42 Mar 02, 2009
Jkt 217001
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:
Description of Technology: It is
frequently observed in head and neck
squamous cell carcinoma (HNSCC), a
cancer occurring mostly in the mouth,
that the Akt/mTOR pathway is
abnormally activated. Therefore,
inhibiting this signaling pathway may
help in treating this disease. Rapamycin
and its analogs are known to inhibit the
activity of mTOR so in principle they
could serve as therapeutics for treating
HNSCC.
Researchers at the NIH have
developed a method of potentially
preventing or treating HNSCC through
the inhibition of mTOR activity. The
proof of this principle was
demonstrated by rapid regression of
mouth tumors in mice afflicted with
Cowden syndrome with the
administration of rapamycin. Like
HNSCC, development of this disease is
linked to over activation of the Akt/
mTOR pathway. Furthermore, the
therapeutic potential of rapamycin was
demonstrated using mice in
PO 00000
Frm 00042
Fmt 4703
Sfmt 4703
Total
number of
responses
Burden per
response
(hours)
Total hour
burden
experiments that model chronic
exposure to tobacco, which promotes
the development of HNSCC. Therefore,
inhibitors of mTOR have considerable
potential in the prevention and
treatment of HNSCC.
Applications: Preventing the
development of oral cancer using mTOR
inhibitors to halt progression of precancerous lesions.
Market: Approximately 500,000 new
cases of squamous cell carcinomas of
the head and neck arise every year
making it the 6th most common cancer
in the world.
Frequently, prognosis is poor due to
late detection of cancer.
Development Status: Pre-clinical
proof of principle.
Inventors: J. Silvio Gutkind et al.
(NIDCR).
Publications: 1. CH Squarize, RM
Castilho, JS Gutkind. Chemoprevention
and treatment of experimental Cowden’s
disease by mTOR inhibition with
rapamycin. Cancer Res. 2008 Sep
1;68(17):7066–7072.
2. R Czerninski, P Amornphimoltham,
V Patel, AA Molinolo, JS Gutkind.
Targeting mTOR by rapamycin prevents
tumor progression in an oral-specific
chemical carcinogenesis model. Cancer
Prevention Res. 2009 Jan;2(1):27–36.
Patent Status: U.S. Patent Application
No. 61/090/414 filed 20 Aug 2008 (HHS
Reference No. E–302–2008/0-US–01).
Licensing Status: Available for
licensing.
Licensing Contact: Whitney Hastings;
301–451–7337; hastingw@mail.nih.gov.
Collaborative Research Opportunity:
The National Institute of Dental and
E:\FR\FM\03MRN1.SGM
03MRN1
Federal Register / Vol. 74, No. 40 / Tuesday, March 3, 2009 / Notices
mstockstill on PROD1PC66 with NOTICES
Craniofacial Research, Oral and
Pharyngeal Cancer Branch, is seeking
statements of capability or interest from
parties interested in collaborative
research to further develop, evaluate, or
commercialize this technology. Please
contact David W. Bradley, PhD at
bradleyda@nidcr.nih.gov for more
information.
Use of Tetracyclines as Anti-Cancer
Agents
Description of Technology: The
invention describes compositions of
tetracycline compounds and their
derivatives as having anti-cancer
activity, as well as methods of treating
cancer. Tetracyclines are commonly
used as antibiotics; however, testing of
these compounds in a high throughput
screening system revealed certain
derivatives to be potent inhibitors of
tyrosyl-DNA-phosphodiesterase (Tdp1).
Camptothecins are effective
Topoisomerase I (Top1) inhibitors, and
two derivatives (Topotecan® and
Camptosar®) are currently approved for
treatment of ovarian and colorectal
cancer. Camptothecins damage DNA by
trapping covalent complexes between
the Top1 catalytic tyrosine and the 3=end of the broken DNA. Tdp1 repairs
Top1-DNA covalent complexes by
hydrolyzing the tyrosyl-DNA bond. This
can reduce the effectiveness of
camptothecins as anti-cancer agents. In
addition, Tdp1 repairs free-radicalmediated DNA breaks.
As disclosed in the instant
technology, tetracyclines have the
potential to enhance the anti-neoplastic
activity of Top1 inhibitors by reducing
repair of Top1-DNA lesions through
inhibition of Tdp1. Inhibition of Tdp1
may also reduce repair of DNA breaks
and increase the rate of apoptosis in
cancer cells, making them potential
anti-cancer agents on their own.
Development Status: Pre-clinical
stage.
Inventors: Yves Pommier, Christophe
Marchand, Laurent Thibaut (NCI).
Publications: 1. Z Liao et al.
Inhibition of human tyrosyl-DNA
phosphodiesterase (Tdp1) by
aminoglycoside antibiotics and
ribosome inhibitors. Mol Pharmacol.
2006 Jul;70(1):366–372.
2. Y Pommier. Camptothecins and
topoisomerase I: A foot in the door.
Targeting the genome beyond
topoisomerase I with camptothecins and
novel anticancer drugs: Importance of
DNA replication, repair and cell cycle
checkpoints. Curr Med Chem
Anticancer Agents. 2004 Sep;4(5):429–
434. Review.
3. Y Pommier et al. Repair of and
checkpoint response to topoisomerase I
VerDate Nov<24>2008
16:42 Mar 02, 2009
Jkt 217001
mediated DNA damage. Mutat Res. 2003
Nov 27;532(1–2):173–203. Review.
Patent Status: U.S. Provisional
Application No. 60/786,746 filed 27 Mar
2006 (HHS Reference No. E–097–2006/
0–US–01).
International Application No. PCT/
US2007/007724 filed 27 Mar 2007 (HHS
Reference No. E–097–2006/0–PCT–02).
U.S. Patent Application No. 12/
241,011 filed 29 Sep 2008 (HHS
Reference No. E–097–2006/1–US–01).
Licensing Status: Available for
licensing.
Licensing Contact: Betty Tong, PhD;
301–594–6565; tongb@mail.nih.gov.
Collaborative Research Opportunity:
The Laboratory of Molecular
Pharmacology at the National Cancer
Institute is seeking statements of
capability or interest from parties
interested in collaborative research to
further develop, evaluate, or
commercialize tetracycline derivatives,
particularly optimizing them for
therapeutic use. Please contact John D.
Hewes, PhD at 301–435–3121 or
hewesj@mail.nih.gov for more
information.
Glutathione S-transferase Clones for
Members of the Ubiquitin-Dependent
Protein Degradation Pathway
Description of Technology: Scientists
at the National Institutes of Health have
developed cDNA for glutathione Stransferase (GST) clones for the
following factors: Nedd4, XIAP,
UBCH5B, and CBL–B. These proteins
are involved in the ubiquitin-dependent
pathway of protein degradation in cells,
the major cellular system for protein
degradation. The ubiquitin-proteosome
pathway regulates several cancer
regulated proteins. Defects in this
pathway can lead to cancer
development. The GST clones can be
used to produce corresponding GST
fusion proteins in order to isolate each
protein from the pathway for further
analysis. These constructs can also be
incorporated into assays/kits to detect
proteins in the ubiquitin-dependent
pathway.
Applications: Research tools for
detection and isolation of ubiquitindependent pathway members in order to
understand the pathway defects that
lead to cancer and develop preventions
and treatments to overcome these
defects.
Research tools for generating fusion
proteins of Nedd4, XIAP, UBCH5B, and
CBL–B to further analyze their functions
in vivo and in vitro.
Controls for screening inhibitors of
the ubiquitin-dependent pathway in
order to better understand the different
PO 00000
Frm 00043
Fmt 4703
Sfmt 4703
9253
mechanisms of ubiquitin-dependent
protein degradation.
Inventors: Allan M. Weissman et al.
(NCI).
Patent Status: HHS Reference No. E–
245–2003/0—Research Tool. Patent
protection is not being pursued for this
technology.
Licensing Status: Available for
licensing under a Biological Materials
License Agreement.
Licensing Contact: Samuel E. Bish,
Ph.D.; 301–435–5282;
bishse@mail.nih.gov.
Dated: February 24, 2009.
Richard U. Rodriguez,
Director, Division of Technology Development
and Transfer, Office of Technology Transfer,
National Institutes of Health.
[FR Doc. E9–4477 Filed 3–2–09; 8:45 am]
BILLING CODE 4140–01–P
DEPARTMENT OF HEALTH AND
HUMAN SERVICES
National Institutes of Health
National Institute of Allergy and
Infectious Diseases; Notice of Closed
Meetings
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
meetings.
The meetings 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: Microbiology,
Infectious Diseases and AIDS Initial Review
Group; Acquired Immunodeficiency
Syndrome Research Review Committee.
Date: March 30–31, 2009.
Time: 8 a.m. to 12 p.m.
Agenda: To review and evaluate grant
applications.
Place: Hilton Washington/Rockville, 1750
Rockville Pike, Rockville, MD 20852.
Contact Person: Erica L. Brown, PhD,
Scientific Review Officer, Scientific Review
Program, Division of Extramural Activities,
National Institutes of Health/NIAID, 6700B
Rockledge Drive, MSC 7616, Bethesda, MD
20892–7616, 301–451–2639,
ebrown@niaid.nih.gov.
Name of Committee: National Institute of
Allergy and Infectious Diseases Special
Emphasis Panel; Pandemic Flu.
Date: April 1, 2009.
E:\FR\FM\03MRN1.SGM
03MRN1
]]>Agencies
[Federal Register Volume 74, Number 40 (Tuesday, March 3, 2009)]
[Notices]
[Pages 9252-9253]
From the Federal Register Online via the Government Printing Office [www.gpo.gov]
[FR Doc No: E9-4477]
-----------------------------------------------------------------------
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.
Prevention of Head and Neck Cancer Using Rapamycin and Its Analogs
Description of Technology: It is frequently observed in head and
neck squamous cell carcinoma (HNSCC), a cancer occurring mostly in the
mouth, that the Akt/mTOR pathway is abnormally activated. Therefore,
inhibiting this signaling pathway may help in treating this disease.
Rapamycin and its analogs are known to inhibit the activity of mTOR so
in principle they could serve as therapeutics for treating HNSCC.
Researchers at the NIH have developed a method of potentially
preventing or treating HNSCC through the inhibition of mTOR activity.
The proof of this principle was demonstrated by rapid regression of
mouth tumors in mice afflicted with Cowden syndrome with the
administration of rapamycin. Like HNSCC, development of this disease is
linked to over activation of the Akt/mTOR pathway. Furthermore, the
therapeutic potential of rapamycin was demonstrated using mice in
experiments that model chronic exposure to tobacco, which promotes the
development of HNSCC. Therefore, inhibitors of mTOR have considerable
potential in the prevention and treatment of HNSCC.
Applications: Preventing the development of oral cancer using mTOR
inhibitors to halt progression of pre-cancerous lesions.
Market: Approximately 500,000 new cases of squamous cell carcinomas
of the head and neck arise every year making it the 6th most common
cancer in the world.
Frequently, prognosis is poor due to late detection of cancer.
Development Status: Pre-clinical proof of principle.
Inventors: J. Silvio Gutkind et al. (NIDCR).
Publications: 1. CH Squarize, RM Castilho, JS Gutkind.
Chemoprevention and treatment of experimental Cowden's disease by mTOR
inhibition with rapamycin. Cancer Res. 2008 Sep 1;68(17):7066-7072.
2. R Czerninski, P Amornphimoltham, V Patel, AA Molinolo, JS
Gutkind. Targeting mTOR by rapamycin prevents tumor progression in an
oral-specific chemical carcinogenesis model. Cancer Prevention Res.
2009 Jan;2(1):27-36.
Patent Status: U.S. Patent Application No. 61/090/414 filed 20 Aug
2008 (HHS Reference No. E-302-2008/0-US-01).
Licensing Status: Available for licensing.
Licensing Contact: Whitney Hastings; 301-451-7337;
hastingw@mail.nih.gov.
Collaborative Research Opportunity: The National Institute of
Dental and
[[Page 9253]]
Craniofacial Research, Oral and Pharyngeal Cancer Branch, is seeking
statements of capability or interest from parties interested in
collaborative research to further develop, evaluate, or commercialize
this technology. Please contact David W. Bradley, PhD at
bradleyda@nidcr.nih.gov for more information.
Use of Tetracyclines as Anti-Cancer Agents
Description of Technology: The invention describes compositions of
tetracycline compounds and their derivatives as having anti-cancer
activity, as well as methods of treating cancer. Tetracyclines are
commonly used as antibiotics; however, testing of these compounds in a
high throughput screening system revealed certain derivatives to be
potent inhibitors of tyrosyl-DNA-phosphodiesterase (Tdp1).
Camptothecins are effective Topoisomerase I (Top1) inhibitors, and
two derivatives (Topotecan[supreg] and Camptosar[supreg]) are currently
approved for treatment of ovarian and colorectal cancer. Camptothecins
damage DNA by trapping covalent complexes between the Top1 catalytic
tyrosine and the 3=-end of the broken DNA. Tdp1 repairs Top1-DNA
covalent complexes by hydrolyzing the tyrosyl-DNA bond. This can reduce
the effectiveness of camptothecins as anti-cancer agents. In addition,
Tdp1 repairs free-radical-mediated DNA breaks.
As disclosed in the instant technology, tetracyclines have the
potential to enhance the anti-neoplastic activity of Top1 inhibitors by
reducing repair of Top1-DNA lesions through inhibition of Tdp1.
Inhibition of Tdp1 may also reduce repair of DNA breaks and increase
the rate of apoptosis in cancer cells, making them potential anti-
cancer agents on their own.
Development Status: Pre-clinical stage.
Inventors: Yves Pommier, Christophe Marchand, Laurent Thibaut
(NCI).
Publications: 1. Z Liao et al. Inhibition of human tyrosyl-DNA
phosphodiesterase (Tdp1) by aminoglycoside antibiotics and ribosome
inhibitors. Mol Pharmacol. 2006 Jul;70(1):366-372.
2. Y Pommier. Camptothecins and topoisomerase I: A foot in the
door. Targeting the genome beyond topoisomerase I with camptothecins
and novel anticancer drugs: Importance of DNA replication, repair and
cell cycle checkpoints. Curr Med Chem Anticancer Agents. 2004
Sep;4(5):429-434. Review.
3. Y Pommier et al. Repair of and checkpoint response to
topoisomerase I mediated DNA damage. Mutat Res. 2003 Nov 27;532(1-
2):173-203. Review.
Patent Status: U.S. Provisional Application No. 60/786,746 filed 27
Mar 2006 (HHS Reference No. E-097-2006/0-US-01).
International Application No. PCT/US2007/007724 filed 27 Mar 2007
(HHS Reference No. E-097-2006/0-PCT-02).
U.S. Patent Application No. 12/241,011 filed 29 Sep 2008 (HHS
Reference No. E-097-2006/1-US-01).
Licensing Status: Available for licensing.
Licensing Contact: Betty Tong, PhD; 301-594-6565;
tongb@mail.nih.gov.
Collaborative Research Opportunity: The Laboratory of Molecular
Pharmacology at the National Cancer Institute is seeking statements of
capability or interest from parties interested in collaborative
research to further develop, evaluate, or commercialize tetracycline
derivatives, particularly optimizing them for therapeutic use. Please
contact John D. Hewes, PhD at 301-435-3121 or hewesj@mail.nih.gov for
more information.
Glutathione S-transferase Clones for Members of the Ubiquitin-Dependent
Protein Degradation Pathway
Description of Technology: Scientists at the National Institutes of
Health have developed cDNA for glutathione S-transferase (GST) clones
for the following factors: Nedd4, XIAP, UBCH5B, and CBL-B. These
proteins are involved in the ubiquitin-dependent pathway of protein
degradation in cells, the major cellular system for protein
degradation. The ubiquitin-proteosome pathway regulates several cancer
regulated proteins. Defects in this pathway can lead to cancer
development. The GST clones can be used to produce corresponding GST
fusion proteins in order to isolate each protein from the pathway for
further analysis. These constructs can also be incorporated into
assays/kits to detect proteins in the ubiquitin-dependent pathway.
Applications: Research tools for detection and isolation of
ubiquitin-dependent pathway members in order to understand the pathway
defects that lead to cancer and develop preventions and treatments to
overcome these defects.
Research tools for generating fusion proteins of Nedd4, XIAP,
UBCH5B, and CBL-B to further analyze their functions in vivo and in
vitro.
Controls for screening inhibitors of the ubiquitin-dependent
pathway in order to better understand the different mechanisms of
ubiquitin-dependent protein degradation.
Inventors: Allan M. Weissman et al. (NCI).
Patent Status: HHS Reference No. E-245-2003/0--Research Tool.
Patent protection is not being pursued for this technology.
Licensing Status: Available for licensing under a Biological
Materials License Agreement.
Licensing Contact: Samuel E. Bish, Ph.D.; 301-435-5282;
bishse@mail.nih.gov.
Dated: February 24, 2009.
Richard U. Rodriguez,
Director, Division of Technology Development and Transfer, Office of
Technology Transfer, National Institutes of Health.
[FR Doc. E9-4477 Filed 3-2-09; 8:45 am]
BILLING CODE 4140-01-P
