Government-Owned Inventions; Availability for Licensing, 39824-39825 [E7-14031]
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39824
Federal Register / Vol. 72, No. 139 / Friday, July 20, 2007 / Notices
of the grant, the terms and conditions of
the award, the effective date of the
award, and the budget/project period.
2. Administrative Requirements
Grants are administered in accordance
with the following documents:
• This Program Announcement.
• 45 CFR Part 74, ‘‘Uniform
Administrative Requirements for
Awards to Institutions of Higher
Education, Hospitals, Other Non-Profit
Organizations, and Commercial
Organizations.’’
• Grants Policy Guidance: HHS
Grants Policy Statement, January 2007.
• ‘‘Non-Profit Organizations’’ (Title 2
Part 230).
• Audit Requirements: OMB Circular
A–133, ‘‘Audits of States, Local
Governments, and Non-Profit
Organizations.’’
3. Indirect Costs
This section applies to indirect costs
in accordance with HHS Grants Policy
Statement, Part II–27, IHS requires
applicants to have a current indirect
cost rate agreement in place prior to
award. The rate agreement must be
prepared in accordance with the
applicable cost principles and guidance
as provided by the cognizant agency or
office. A current rate means the rate
covering the applicable activities and
the award budget period. If the current
rate is not on file with the awarding
office, the award shall include funds for
reimbursement of indirect costs.
However, the indirect costs portion will
remain restricted until the current rate
is provided to DGO.
If an Urban Indian organization has
questions regarding the indirect costs
policy, please contact the DGO at (301)
443–5204.
mstockstill on PROD1PC66 with NOTICES
4. Reporting
A. Progress Report. Program progress
reports are required semi-annually.
These reports will include a brief
comparison of actual accomplishments
to the goals established for the period,
reasons for slippage (if applicable), and
other pertinent information as required.
A final report must be submitted within
90 days of expiration of the budget/
project period.
B. Financial Status Report. Semiannual financial status reports must be
submitted within 30 days of the end of
the half year. Final financial status
reports are due within 90 days of
expiration of the budget period.
Standard Form 269 (long form) will be
used for financial reporting.
Failure to submit required reports
within the time allowed may result in
suspension or termination of an active
VerDate Aug<31>2005
16:19 Jul 19, 2007
Jkt 211001
agreement, withholding of additional
awards for the project, or other
enforcement actions such as
withholding of payments or converting
to the reimbursement method of
payment. Continued failure to submit
required reports may result in one or
both of the following: (1) The
imposition of special award provisions;
and (2) the non-funding or non-award of
other eligible projects or activities. This
applies whether the delinquency is
attributable to the failure of the
organization or the individual
responsible for preparation of the
reports.
Telecommunication for the hearing
impaired is available at: TTY 301–443–
6394.
VII. Agency Contacts
For program-related information:
Phyllis S. Wolfe, Director, Office of
Urban Indian Health Programs, 801
Thompson Avenue, Suite 200,
Rockville, Maryland 20852, (301) 443–
4680 or phyllis.wolfe@ihs.gov.
For general information regarding this
announcement: Danielle Steward,
Health Systems Specialist, Office of
Urban Indian Health Programs, 801
Thompson Road, Room 200, Rockville,
MD 20852, (301) 443–4680 or
danielle.steward@ihs.gov.
For specific grant-related and
business management information:
Denise Clark, Senior Grants
Management Specialist, 801 Thompson
Avenue, TMP 360, Rockville, MD
20852, 301–443–5204 or
denise.clark@ihs.gov.
VIII. Other Information
None.
Dated: July 16, 2007.
Robert G. McSwain,
Deputy Director, Indian Health Service.
[FR Doc. E7–14033 Filed 7–19–07; 8:45 am]
BILLING CODE 4165–16–P
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
PO 00000
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Fmt 4703
Sfmt 4703
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.
Photosensitization by Nuclear
Receptor-Ligand Complexes and Cell
Ablation Uses Thereof
Description of Technology: Androgen
receptors (AR) mediate the effects of
male steroid hormones and contribute to
a wide variety of physiological and
pathophysiological conditions. Prostate
cancer development and progression are
mediated through AR, a liganddependent transcription factor, and it is
present in all stages of prostate
carcinoma. Increased levels of PSA, an
AR-induced prostate tumor-specific
protein, are indicative of prostate
cancer. Benign, non-cancerous
conditions are also AR-dependent and
can be therapeutic targets as well.
This technology is a method to cause
AR-induced cell death (apoptosis)
through photoactivation of a nonsteroidal androgen receptor antagonist
1,2,3,4-tetrahydro-2,2-dimethyl-6(trifluoromethyl)-8-pyridono[5,6-g]
quinoline (TDPQ). Upon TDPQ binding
to AR, a highly potent photocytoxic
reaction induced once the TDPQ–AR
complex is exposed to visible light
irradiation of a specific wavelength. The
inventors have cell-culture results
demonstrating that cell death is a
function of TDPQ, AR and light
irradiation. This treatment method can
potentially target AR-containing
cancerous cells, while sparing nearby
cells that lack AR.
The process has been extended to
other nuclear receptors by choice of
other photoactivatable ligands for these
receptors. Certain suitable ligands are
marketed drugs.
Applications: Therapeutic
compounds to treat AR related
conditions such as prostate cancer,
baldness, hirsutism, and acne; Potential
therapeutics for progesterone and
glucorticoid receptor ligand related
conditions such as breast and brain
cancers, lymphoma, leukemia and
arthritis; Method to treat androgen,
E:\FR\FM\20JYN1.SGM
20JYN1
Federal Register / Vol. 72, No. 139 / Friday, July 20, 2007 / Notices
mstockstill on PROD1PC66 with NOTICES
progesterone, and glucorticoid receptor
related conditions.
Market: Prostate cancer is the second
most common type of cancer among
men, wherein one in six men will be
diagnosed with prostate cancer; An
estimated 218,890 new cases of prostate
cancer and 27,050 deaths due to
prostate cancer in the U.S. in 2007;
Hirsutism affects approximately 5% of
adult women in the United States; Hair
loss and acne industries are worth
several billions of dollars.
Development Status: The technology
is currently in the pre-clinical stage of
development.
Inventors: William T. Schrader et al.
(NIEHS).
Publications:
1. B Risek et al. Androgen ReceptorMediated Apoptosis is Regulated by
Photoactivatable AR Ligands. Abstract
submitted to the Endocrine Society; To
be presented at the Annual Meeting of
the Endocrine Society in Toronto,
Canada in June 2007.
2. B Risek et al. Photocytotoxic
Properties of the Non-Steroidal
Androgen Receptor Antagonist TDPQ.
Presented at the Annual Meeting of the
Endocrine Society in Boston, MA in
June 2006.
Patent Status: U.S. Provisional
Application No. 60/926,218 filed 24 Apr
2007 (HHS Reference No. E–108–2007/
0–US–01).
Licensing Status: Available for
exclusive or non-exclusive licensing.
Licensing Contact: Jennifer Wong;
301/435–4633; wongje@mail.nih.gov.
Method of Treating or Preventing
Oxidative Stress-Related Diseases
(Stroke and Neurodegenerative
Diseases, Wound Healing and
Cardiovascular Diseases)
Description of Technology: Reactive
oxygen species (ROS) and reactive
nitrogen species (RNS) produce
oxidative stress to DNA, lipids and
proteins thus causing cellular and tissue
damage. A number of diseases are
associated with oxidative stress
including Alzheimer’s disease, ischemic
stroke, heart disease, cancer, hepatitis,
and autoimmune disease. Uric acid is a
natural antioxidant effective in reducing
ROS and research has shown that uric
acid contributes approximately twothirds of all free radical scavenging
capacity in plasma. Because uric oxide
is too insoluble to be used as a
therapeutic agent, scientists at the NIH
developed uric acid analogs with
improved anti-oxidative and solubility
properties for use as free radical
scavengers or antioxidants. These
analogs increased survival of PC12 and
hippocampal neurons after challenge by
VerDate Aug<31>2005
16:19 Jul 19, 2007
Jkt 211001
Fe, MPP and Glutamate. When
administered to a mouse model of focal
ischemic stroke, these compounds
protect neuronal cells from ROS and
reduce brain damage and ameliorate
neurological deficits. Other studies
show a single application of these
analogs on skin lacerations in mice
decreased the time for wound repair.
Available for licensing are methods of
treating ischemic stroke and wound
healing, and for the prevention or
treatment of other oxidative stressrelated diseases, such as epilepsy,
Parkinson’s disease and dementia.
Applications: Novel uric acid analogs
for use as antioxidants to help reduce
the risk of stroke, neurological diseases
and assisting with wound repair.
Market: Stroke is the third-leading
cause of death and the leading cause of
severe neurological disability
worldwide; Americans will pay
approximately $62.7 billion dollars in
2007 for stroke-related medical costs
and disability.
Development Status: Pre-clinical data.
Inventors: Nigel H. Greig (NIA), Mark
P. Mattson (NIA), et al.
Patent Status: U.S. Provisional
Application No. 60/839,800 filed 23
Aug 2006 (HHS Reference No. E–059–
2006/0–US–01).
Licensing Status: Available for
licensing.
Licensing Contact: Norbert Pontzer,
PhD, J.D.; 301/435–5502;
pontzern@mail.nih.gov.
Collaborative Research Opportunity:
The National Institute on Aging,
Laboratory of Neurosciences, is seeking
statements of capability or interest from
parties interested in collaborative
research to further develop, evaluate, or
commercialize the described uric acid
analogue technology in the treatment of
neurodegenerative diseases, wound
healing and cardiovascular disease.
Please contact John D. Hewes, PhD at
301–435–3121 or hewesj@mail.nih.gov
for more information.
Thiazepine Inhibitors of HIV–1
Integrase
Description of Technology: The
human immunodeficiency virus (HIV) is
the causative agent of acquired
immunodeficiency syndrome (AIDS).
Drug resistance is a critical factor
contributing to the gradual loss of
clinical benefit of treatments for HIV
infection. Accordingly, combination
therapies have further evolved to
address the mutating resistance of HIV.
However, there has been great concern
regarding the apparent growing
resistance of HIV strains to current
therapies.
PO 00000
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Fmt 4703
Sfmt 4703
39825
It has been found that a certain class
of compounds including thiazepines
and analogs and derivatives thereof are
effective and selective anti-integrase
inhibitors. These compounds have been
found to inhibit both viral replication
and the activity of purified HIV–1
integrase. The subject invention
provides for such compounds and for
methods of inhibiting HIV integrase.
Inventors: Yves Pommier et al. (NCI).
Patent Status: U.S. Patent No.
7,015,212 issued 21 Mar 2006 (HHS
Reference No. E–036–1999/0–US–03).
Licensing Status: Available for
exclusive or non-exclusive licensing.
Licensing Contact: Sally Hu, PhD,
MBA; 301/435–5606; hus@mail.nih.gov.
Collaborative Research Opportunity:
The Laboratory of Molecular
Pharmacology of the National Cancer
Institute is seeking statements of
capability or interest from parties
interested in collaborative research to
further develop, evaluate, or
commercialize anti-integrase inhibitors.
Please contact John D. Hewes, PhD at
301–435–3121 or hewesj@mail.nih.gov
for more information.
Dated: July 13, 2007.
Steven M. Ferguson,
Director, Division of Technology Development
and Transfer, Office of Technology Transfer,
National Institutes of Health.
[FR Doc. E7–14031 Filed 7–19–07; 8:45 am]
BILLING CODE 4140–01–P
DEPARTMENT OF HEALTH AND
HUMAN SERVICES
National Institutes of Health
National Eye Institute; 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 Eye Institute
Special Emphasis Panel, NEI Clinical
Applications II.
Date: July 25, 2007.
Time: 10:30 a.m. to 11:15 a.m.
E:\FR\FM\20JYN1.SGM
20JYN1
Agencies
[Federal Register Volume 72, Number 139 (Friday, July 20, 2007)]
[Notices]
[Pages 39824-39825]
From the Federal Register Online via the Government Printing Office [www.gpo.gov]
[FR Doc No: E7-14031]
-----------------------------------------------------------------------
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.
Photosensitization by Nuclear Receptor-Ligand Complexes and Cell
Ablation Uses Thereof
Description of Technology: Androgen receptors (AR) mediate the
effects of male steroid hormones and contribute to a wide variety of
physiological and pathophysiological conditions. Prostate cancer
development and progression are mediated through AR, a ligand-dependent
transcription factor, and it is present in all stages of prostate
carcinoma. Increased levels of PSA, an AR-induced prostate tumor-
specific protein, are indicative of prostate cancer. Benign, non-
cancerous conditions are also AR-dependent and can be therapeutic
targets as well.
This technology is a method to cause AR-induced cell death
(apoptosis) through photoactivation of a non-steroidal androgen
receptor antagonist 1,2,3,4-tetrahydro-2,2-dimethyl-6-
(trifluoromethyl)-8-pyridono[5,6-g] quinoline (TDPQ). Upon TDPQ binding
to AR, a highly potent photocytoxic reaction induced once the TDPQ-AR
complex is exposed to visible light irradiation of a specific
wavelength. The inventors have cell-culture results demonstrating that
cell death is a function of TDPQ, AR and light irradiation. This
treatment method can potentially target AR-containing cancerous cells,
while sparing nearby cells that lack AR.
The process has been extended to other nuclear receptors by choice
of other photoactivatable ligands for these receptors. Certain suitable
ligands are marketed drugs.
Applications: Therapeutic compounds to treat AR related conditions
such as prostate cancer, baldness, hirsutism, and acne; Potential
therapeutics for progesterone and glucorticoid receptor ligand related
conditions such as breast and brain cancers, lymphoma, leukemia and
arthritis; Method to treat androgen,
[[Page 39825]]
progesterone, and glucorticoid receptor related conditions.
Market: Prostate cancer is the second most common type of cancer
among men, wherein one in six men will be diagnosed with prostate
cancer; An estimated 218,890 new cases of prostate cancer and 27,050
deaths due to prostate cancer in the U.S. in 2007; Hirsutism affects
approximately 5% of adult women in the United States; Hair loss and
acne industries are worth several billions of dollars.
Development Status: The technology is currently in the pre-clinical
stage of development.
Inventors: William T. Schrader et al. (NIEHS).
Publications:
1. B Risek et al. Androgen Receptor-Mediated Apoptosis is Regulated
by Photoactivatable AR Ligands. Abstract submitted to the Endocrine
Society; To be presented at the Annual Meeting of the Endocrine Society
in Toronto, Canada in June 2007.
2. B Risek et al. Photocytotoxic Properties of the Non-Steroidal
Androgen Receptor Antagonist TDPQ. Presented at the Annual Meeting of
the Endocrine Society in Boston, MA in June 2006.
Patent Status: U.S. Provisional Application No. 60/926,218 filed 24
Apr 2007 (HHS Reference No. E-108-2007/0-US-01).
Licensing Status: Available for exclusive or non-exclusive
licensing.
Licensing Contact: Jennifer Wong; 301/435-4633;
wongje@mail.nih.gov.
Method of Treating or Preventing Oxidative Stress-Related Diseases
(Stroke and Neurodegenerative Diseases, Wound Healing and
Cardiovascular Diseases)
Description of Technology: Reactive oxygen species (ROS) and
reactive nitrogen species (RNS) produce oxidative stress to DNA, lipids
and proteins thus causing cellular and tissue damage. A number of
diseases are associated with oxidative stress including Alzheimer's
disease, ischemic stroke, heart disease, cancer, hepatitis, and
autoimmune disease. Uric acid is a natural antioxidant effective in
reducing ROS and research has shown that uric acid contributes
approximately two-thirds of all free radical scavenging capacity in
plasma. Because uric oxide is too insoluble to be used as a therapeutic
agent, scientists at the NIH developed uric acid analogs with improved
anti-oxidative and solubility properties for use as free radical
scavengers or antioxidants. These analogs increased survival of PC12
and hippocampal neurons after challenge by Fe, MPP and Glutamate. When
administered to a mouse model of focal ischemic stroke, these compounds
protect neuronal cells from ROS and reduce brain damage and ameliorate
neurological deficits. Other studies show a single application of these
analogs on skin lacerations in mice decreased the time for wound
repair. Available for licensing are methods of treating ischemic stroke
and wound healing, and for the prevention or treatment of other
oxidative stress-related diseases, such as epilepsy, Parkinson's
disease and dementia.
Applications: Novel uric acid analogs for use as antioxidants to
help reduce the risk of stroke, neurological diseases and assisting
with wound repair.
Market: Stroke is the third-leading cause of death and the leading
cause of severe neurological disability worldwide; Americans will pay
approximately $62.7 billion dollars in 2007 for stroke-related medical
costs and disability.
Development Status: Pre-clinical data.
Inventors: Nigel H. Greig (NIA), Mark P. Mattson (NIA), et al.
Patent Status: U.S. Provisional Application No. 60/839,800 filed 23
Aug 2006 (HHS Reference No. E-059-2006/0-US-01).
Licensing Status: Available for licensing.
Licensing Contact: Norbert Pontzer, PhD, J.D.; 301/435-5502;
pontzern@mail.nih.gov.
Collaborative Research Opportunity: The National Institute on
Aging, Laboratory of Neurosciences, is seeking statements of capability
or interest from parties interested in collaborative research to
further develop, evaluate, or commercialize the described uric acid
analogue technology in the treatment of neurodegenerative diseases,
wound healing and cardiovascular disease. Please contact John D. Hewes,
PhD at 301-435-3121 or hewesj@mail.nih.gov for more information.
Thiazepine Inhibitors of HIV-1 Integrase
Description of Technology: The human immunodeficiency virus (HIV)
is the causative agent of acquired immunodeficiency syndrome (AIDS).
Drug resistance is a critical factor contributing to the gradual loss
of clinical benefit of treatments for HIV infection. Accordingly,
combination therapies have further evolved to address the mutating
resistance of HIV. However, there has been great concern regarding the
apparent growing resistance of HIV strains to current therapies.
It has been found that a certain class of compounds including
thiazepines and analogs and derivatives thereof are effective and
selective anti-integrase inhibitors. These compounds have been found to
inhibit both viral replication and the activity of purified HIV-1
integrase. The subject invention provides for such compounds and for
methods of inhibiting HIV integrase.
Inventors: Yves Pommier et al. (NCI).
Patent Status: U.S. Patent No. 7,015,212 issued 21 Mar 2006 (HHS
Reference No. E-036-1999/0-US-03).
Licensing Status: Available for exclusive or non-exclusive
licensing.
Licensing Contact: Sally Hu, PhD, MBA; 301/435-5606;
hus@mail.nih.gov.
Collaborative Research Opportunity: The Laboratory of Molecular
Pharmacology of the National Cancer Institute is seeking statements of
capability or interest from parties interested in collaborative
research to further develop, evaluate, or commercialize anti-integrase
inhibitors. Please contact John D. Hewes, PhD at 301-435-3121 or
hewesj@mail.nih.gov for more information.
Dated: July 13, 2007.
Steven M. Ferguson,
Director, Division of Technology Development and Transfer, Office of
Technology Transfer, National Institutes of Health.
[FR Doc. E7-14031 Filed 7-19-07; 8:45 am]
BILLING CODE 4140-01-P