Government-Owned Inventions; Availability for Licensing, 26404-26406 [E7-8894]
Download as PDF
<![CDATA[
26404
Federal Register / Vol. 72, No. 89 / Wednesday, May 9, 2007 / Notices
Aug 2006 (HHS Ref. No. E–110–2004/0–
US–06).
Licensing Status: Available for
exclusive and non-exclusive licensing.
Licensing Contact: Adaku
Nwachukwu, J.D.; 301/435–5560;
madua@mail.nih.gov.
Leu574 of HIF–1alpha as a Molecular
Basis for Therapeutic Application
sroberts on PROD1PC70 with NOTICES
Description of Technology: The
hypoxia-inducible factor 1 (HIF–1) is a
transcription factor that plays a pivotal
role in cellular adaptation to oxygen
availability. HIF–1alpha protein is a
subunit of HIF–1. Although the gene for
HIF–1alpha is constitutively expressed,
it is an extremely short-lived protein
under normoxic conditions and is
targeted for destruction via the
proteosome pathway by an E3 ubiquitin
ligase involving the VHL protein.
The invention relates to the discovery
that mutations or deletions of Leu574
result in a more stable and more active
form of HIF–1alpha. Therefore, the
invention relates to methods and
compositions for modulating oxygen
homeostasis for therapeutic application.
In one aspect, the inventors contemplate
the use of a more stable form of HIF–
1alpha protein for therapeutic
angiogenesis purposes such as may be
useful in ischemic vascular disease. In
another aspect, the inventors
contemplate the use of this particular
site in a screen for targeted drugs that
modulates HIF–1alpha activity. The
inventors also suggest that Leu574 could
be used for developing drugs targeted to
HIF hydroxylase binding, thereby
altering HIF–1alpha stability.
Inventor: L. Eric Huang (NCI).
Patent Status: U.S. Patent No.
7,193,053 issued 20 Mar 2007 (HHS
Reference No. E–281–2002/0–US–02).
Licensing Status: This technology is
available for licensing on an exclusive
or a non-exclusive basis.
Licensing Contact: Jesse S. Kindra,
J.D.; 301/435–5559;
kindraj@mail.nih.gov.
Dated: April 30, 3007.
Steven M. Ferguson,
Director, Division of Technology Development
and Transfer,Office of Technology Transfer,
National Institutes of Health.
[FR Doc. E7–8893 Filed 5–8–07; 8:45 am]
BILLING CODE 4140–01–P
VerDate Aug<31>2005
18:12 May 08, 2007
Jkt 211001
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.
New Compounds and Methods for the
Treatment of Spinal Muscular Atrophy
and Other Diseases
Description of Technology: Spinal
muscular atrophy (SMA) is caused by
mutations in the SMN1 gene that result
in reduced expression of the survival
motor neuron (SMN) protein and a loss
of spinal motor neurons. An SMN2 gene
paralog that differs from SMN by a
single base pair has inadequate
expression of SMN to support motor
neuron survival. Alternative splicing
caused by the single base substitution in
the SMN2 gene results in a slightly
truncated and highly unstable SMN
protein. Drugs that allow translational
read through of the stop codons
introduced by the alternative splice
event have been shown to stabilize the
mutant protein, resulting in increased
levels of SMN.
A chemical library screen identified
indoprofen, a nonsteroidal antiinflammatory drug, as an inducer of
SMN expression in cultured cells.
However, indoprofen cannot enter the
brain in satisfactory amounts, has a
relatively low level of activity and can
cause substantial side-effects in part due
to its cyclooxygenase inhibitory activity.
NIH inventors designed indoprofen
derivatives without cyclooxygenase
PO 00000
Frm 00072
Fmt 4703
Sfmt 4703
activity that can enter the CNS and
increase expression of a SMN protein
from the SMN2 gene with increased
potency and efficacy. The mechanism of
action of these indoprofen analogs
appears to be translational readthrough
of stop codons introduced by the
alternative SMN2 splicing event. In
addition to treating SMA, novel drugs
that allow read through of stop codons
could potentially treat many other
diseases caused by such mutations such
as cystic fibrosis and muscular
dystrophy.
Available for licensing are
compounds and methods useful for the
treatment of spinal muscular atrophy by
increasing SMN expression and
increasing the expression from any
nucleic acid that encodes a translational
stop codon.
Applications: Efficacious treatment
for SMA, utilizing indoprofen analogs
that increase SMN protein expression;
Treatment of any genetic disease caused
by premature termination of protein
translation.
Market: SMA is a rare genetic disease
that affects approximately 1 in 6,000
live births, and is the leading genetic
cause of death in infants and toddlers.
The projected market size for SMA is
between $250 million and $750 million.
Development Status: Clinical
candidate selection scheduled for June
2007.
Inventors: Jill Heemskerk (NINDS), et
al.
Publication: MR Lunn, DE Root, AM
Martino, SP Flaherty, BP Kelley, DD
Coovert, AH Burghes, NT Man, GE
Morris, J Zhou, EJ Androphy, CJ
Sumner, BR Stockwell. Indoprofen
upregulates the survival motor neuron
protein through a cyclooxygenaseindependent mechanism. Chem. Biol.
2004 Nov;11(11):1489–1493.
Patent Status: U.S. Provisional
Application No. 60/783,292 filed 17 Mar
2006 (HHS Reference No. E–133–2006/
0-US–01); PCT Application No. PCT/
2007/006772 filed 16 Mar 2007 (HHS
Reference No. E–133–2006/1–PCT–01)
Licensing Availability: Available for
exclusive and non-exclusive licensing.
Licensing Contact: Norbert Pontzer,
J.D., Ph.D.; 301/435–5502;
pontzern@mail.nih.gov.
STAMP, a Novel Cofactor and Possible
Steroid Sparing Agent, Modulates
Steroid-Induced Induction or
Repression of Steroid Receptors
Description of Technology: Steroid
hormones such as androgens,
glucocorticoids, and estrogens are used
in the treatments of many diseases.
They act to regulate many physiological
responses by binding to steroid
E:\FR\FM\09MYN1.SGM
09MYN1
Federal Register / Vol. 72, No. 89 / Wednesday, May 9, 2007 / Notices
receptors. However, because steroid
receptors are expressed in many tissues,
efforts to therapeutically modify the
effects of steroid hormones on a specific
tissue or on a specific receptor of the
steroid receptor family often cause
undesirable effects in other tissues or on
other receptors. STAMP (SRC–1 and
TIF–2 Associated Modulatory Protein), a
novel protein that acts to lower the
concentration of steroid hormone
needed to induce (or repress) selected
target genes by regulating steroid
receptor synthesis, offers an novel
approach for reducing the severity of
unwanted side-effects, thereby
increasing the ability to use steroid
hormone therapies.
sroberts on PROD1PC70 with NOTICES
Applications
1. Diseases requiring chronic steroid
treatment such as rheumatoid arthritis,
psoriatic arthritis, asthma, inflammatory
and auto-immune diseases;
2. Diseases characterized by excess or
deficiency of glucocorticoids such as
obesity, diabetes, hypertension,
Cushing’s Syndrome, Parkinson’s
Disease, Addison’s Disease;
3. Diseases in which glucocorticoidresponsive gene expression is deranged,
so deranging carbohydrate, protein or
lipid metabolism;
4. Cancers responsive to androgen or
estrogen, such as breast cancer or
prostate cancer;
5. Therapeutic applications related to
male or female hormone replacement,
symptoms related to menopause, birth
control, menstrual cycle/amenorrhea,
fertility or endometriosis.
Advantages
1. STAMP reduces the severity of
unwanted side-effects of steroid
hormone therapies;
2. STAMP modulates the gene
induction properties of androgen and
progesterone receptors;
3. STAMP modulates both induction
and repression properties of
glucocorticoid receptors;
4. STAMP is inactive toward alpha
and beta estrogen receptors, thyroid
receptor beta, PPAR gamma 2, retinoid
receptor alpha or RXR alpha;
5. The siRNAs could be useful as
therapeutics.
Market: The protein, STAMP, offers a
novel approach for reducing the severity
of unwanted side-effects of steroid
hormone therapies. Therefore, STAMP
would be helpful in the treatment of
diseases requiring chronic steroid
treatments, those characterized by
excess or deficiency of glucocorticoid
response, therapies related to male or
female hormone replacement or cancers
responsive to androgen or estrogen.
VerDate Aug<31>2005
18:12 May 08, 2007
Jkt 211001
Development Status
1. STAMP, a protein which is a novel
nuclear receptor cofactor, has been
identified;
2. STAMP siRNAs have been shown
to change the dose response curve of
endogenous glucocorticoid receptor
induced genes;
3. A STAMP antibody has been
prepared.
Further Research & Development
Required
1. Further in-vivo studies into the role
of STAMP in glucocorticoid receptormediated repression;
2. Further study into the activity of
STAMP in androgen receptor-mediated
responses;
3. Investigation into the mechanism of
action of STAMP;
4. Development of STAMP knockout
mouse.
Inventors: Drs. S. Stoney Simons Jr
(NIDDK) and Yuanzheng He (NIDDK)
Publication: Y He and SS Simons Jr.
STAMP: A Novel Predicted Factor
Assisting TIF2 Actions in
Glucocorticoid Receptor-mediated
Induction and Repression. Mol Cell
Biol. 2007 Feb;27(4);1467–1485.
Patent Status: PCT International No.
PCT/US2005/006393 filed 25 Feb 2005
(priority date 26 Feb 2004), which
published as WO 2005/082935 on 09
Sep 2005, entitled ‘‘A Novel Cofactor
that Modulates Steroid Receptor
Activities’’; National Stage U.S., Europe,
Canada, Australia (HHS Reference No.
E–056–2004/0).
Related Technologies: HHS Reference
No. E–015–2000/0, ‘‘Antiprogestins
with Partial Agonist Activity.’’ Global IP
pending: US, Europe, Australia, Canada,
Japan.
Licensing Status: Available for
exclusive and non-exclusive licensing.
Licensing Contact: Dr. Susan Carson;
301/435–5020; carsonsu@mail.nih.gov.
Collaborative Research Opportunity:
The National Institute of Diabetes,
Digestive and Kidney Diseases,
Laboratory of Molecular and Cellular
Biology is seeking statements of
capability or interest from parties
interested in collaborative research to
further develop, evaluate or
commercialize this technology. Please
contact Dr. Stoney Simons, Chief,
Steroid Hormones Section (NIDDK) at
steroids@helix.nih.gov; Tel: 301–4960–
6796 for more information.
TMC1, a Deafness-Related Gene
Description of Technology: Hearing
loss is a common communication
disorder affecting nearly 1 in 1,000
children in the United States alone, and
PO 00000
Frm 00073
Fmt 4703
Sfmt 4703
26405
nearly 50% of adults by the age of
eighty. Hearing loss can be caused by
environmental and disease-related
factors; however, hearing loss due to
genetic factors accounts for
approximately 50% of cases.
The NIH announces the isolation of
two novel genes involved in hearing;
TMC1, short for transmembrane
channel-like gene 1. The inventors have
discovered that dominant and recessive
mutations in TMC1 underlie two forms
of hereditary deafness, known as
DFNA36 and DFNB7/11. TMC1 encodes
a protein required for normal function
of the mammalian hair cell, which plays
a critical role within the hearing
pathway that detects sound in the inner
ear.
The invention discloses TMC1
nucleic acids, vectors, and cells. Also
disclosed are methods of detecting
hearing loss, or a predisposition to
hearing loss, due to a mutation in
TMC1, as well as methods for
identifying agents that interact with the
TMC1 gene in a cell. Nucleic acids and
methods of use for TMC2, a gene closely
related to TMC1, are also disclosed.
Applications: Development of a
genetic diagnostic test for hearing loss;
Development of pharmaceuticals to treat
hearing loss.
Market: Hearing loss with a genetic
component accounts for 50% of all
cases of hearing loss.
Development Status: Early stage.
Inventors: Andrew J. Griffith et al.
(NIDCD).
Publication: K Kurima et al. Dominant
and recessive deafness caused by
mutations of a novel gene, TMC1,
required for cochlear hair-cell function.
Nat Genet. 2002 Mar;30(3):277–284.
Patent Status
1. HHS Reference No. E–168–2001/0:
a. U.S. Provisional Application No.
60/323,275 filed 19 Sep 2001.
b. PCT Application No. PCT/US02/
29614 filed 19 Sep 2002, which
published as WO 03/025140 on 27 Mar
2003.
c. U.S. Patent No. 7,192,705 issued 20
Mar 2007.
d. U.S. Patent Application No. 11/
615,250 filed 22 Dec 2006.
e. Foreign counterparts in Australia,
Canada, Europe, and Japan.
2. HHS Reference No. E–168–2001/1:
a. U.S. Patent No. 7,116,433 issued 23
Jan 2007.
b. Foreign counterparts in Australia
and Canada.
Licensing Status: Available for nonexclusive licensing.
Licensing Contact: Tara L. Kirby,
Ph.D.; 301/435–4426;
tarak@mail.nih.gov.
E:\FR\FM\09MYN1.SGM
09MYN1
26406
Federal Register / Vol. 72, No. 89 / Wednesday, May 9, 2007 / Notices
Collaborative Research Opportunity:
The NIDCD Otolaryngology Branch is
seeking statements of capability or
interest from parties interested in
collaborative research to further
develop, evaluate, or commercialize this
technology as well as collaborate on
further pre-clinical and clinical studies
with the TMC2 gene mutations. Please
contact Ms. Marianne Lynch at 301–
402–5579 or via e-mail at
lynchm@nhlbi.nih.gov for more
information.
Dated: April 30, 2007.
Steven M. Ferguson,
Director, Division of Technology Development
and Transfer, Office of Technology Transfer,
National Institutes of Health.
[FR Doc. E7–8894 Filed 5–8–07; 8:45 am]
BILLING CODE 4140–01–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:
sroberts on PROD1PC70 with NOTICES
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.
Influenza Vaccines and Antiviral
Agents
Description of Technology: The
subject invention offers candidate DNA
vaccines to target H5N1, H1N1, H3N2
and other subtypes of influenza. These
candidates are designed primarily to
elicit neutralizing antibodies. The
candidate vaccines express
hemagglutinin (H/HA) or neuramidase
VerDate Aug<31>2005
18:12 May 08, 2007
Jkt 211001
(N/NA) protein that has been codon
optimized and/or modified at the
protease cleavage site. The modified
genes could be used in DNA vaccines,
in viral vectors, recombinant proteins/
particles or combination. The studies
use proprietary expression systems that
increase protein expression relative to
commonly used alternatives. This
invention potentially provides a vaccine
strategy for controlling influenza
epidemics, including avian flu, should
it cross over to humans; the 1918 strain
of flu; and seasonal flu strains. In
addition, this invention is designed to
lead to a combination vaccine to
provide a broadly protective vaccine.
The incorporation of specific cleavage
site types to facilitate preparation of
pseudotypes from a variety of strains is
an important aspect of this invention.
In addition, HA pseudotyped
lentiviral vectors are being tested to
screen for neutralizing abs in patients
and to screen for diagnostic and
therapeutic monoclonal abs.
Applications and Advantages:
Influenza vaccine for pandemic or
epidemic application; Potential for
combination vaccine for broad
protection, removing need for seasonal
strain monitoring; DNA vaccines are
easy to produce and store; No risk of
reversion to pathogenic strain as with
live-attenuated virus vaccines.
Development Status Highlights: Phase
I clinical trials planned for select
candidates; DNA vaccine encoding 1918
influenza virus HA protein protects
mice against lethal viral challenge;
Codon optimized for expression in
human cells.
Inventors: Gary J. Nabel (VRC/NIAID),
Wing-pui Kong (VRC/NIAID), Zhi-yong
Yang (VRC, NIAID), et al.
Publication: Certain aspects of this
technology were published in WP Kong
et al. Protective immunity to lethal
challenge of the 1918 pandemic
influenza virus by vaccination. Proc
Natl Acad Sci USA. 2006 Oct
24;103(43):15987–15991. Epub 2006 Oct
16, doi: 10.1073/pnas.0607564103.
Patent Status: U.S. Provisional
Application No. 60/774,923 filed 16 Feb
2006 (HHS Reference No. E–116–2006/
0–US–01) and PCT Application No.
PCT/US2007/004506 filed 16 Feb 2007
(influenza) (HHS Reference No. E–116–
2006/1–PCT–01); U.S. Patent No.
7,094,598 issued 22 Aug 2006 (CMV/R)
(HHS Reference No. E–241–2001/1–US–
01) and associated foreign rights.
Licensing Status: Available for
exclusive or non-exclusive licensing.
Licensing Contact: Susan Ano, Ph.D.;
301/435–5515; anos@mail.nih.gov.
PO 00000
Frm 00074
Fmt 4703
Sfmt 4703
Enhanced, Targeted Delivery for DNA
Vaccines
Description of Technology: Available
for licensing from the NIH is a fusion
protein for enhanced gene delivery.
Exemplary proteins for achieving this
improvement comprise an adenovirus
serotype 5 fiber, penton base and core
protein V fused to the DNA binding
domain of HMG. In vitro studies have
shown the effectiveness of the chimeric
protein-DNA vaccine co-administration
by an increase in uptake of ten to twenty
fold. In particular, the plasmid with the
chimeric core protein V was delivered
efficiently to dendritic cells (DC) as well
as 293T cells. The utilization of this
chimeric protein could further enhance
the immune response elicited by DNA
vaccines.
Potential Applications: Improved
DNA vaccine delivery and uptake.
Inventors: Gary J. Nabel and Wataru
Akahata (VRC/NIAID).
Patent Status: U.S. Provisional
Application No. 60/737,896 filed 18
Nov 2005 (HHS Reference No. E–043–
2006/0–US–01); U.S. Provisional
Application No. 60/795,529 filed 26 Apr
2006 (HHS Reference No. E–043–2006/
1–US–01); PCT Application No. PCT/
US2006/044525 filed 20 Nov 2006 (HHS
Reference No. E–043–2006/3–PCT–01)
Licensing Status: Available for nonexclusive or exclusive licensing.
Licensing Contact: Susan Ano, Ph.D.;
301/435–5515; anos@mail.nih.gov.
Dated: April 30, 2007.
Steven M. Ferguson,
Director, Division of Technology Development
and Transfer, Office of Technology Transfer,
National Institutes of Health.
[FR Doc. E7–8895 Filed 5–8–07; 8:45 am]
BILLING CODE 4140–01–P
DEPARTMENT OF HEALTH AND
HUMAN SERVICES
National Institutes of Health
National Cancer Institute; Notice of
Meeting
Pursuant to section 10(a) of the
Federal Advisory Committee Act, as
amended (5 U.S.C. Appendix 2), notice
is hereby given of a meeting of the
National Cancer Institute Director’s
Consumer Liaison Group.
The meeting will be open to the
public, with attendance limited to space
available. Individuals who plan 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.
E:\FR\FM\09MYN1.SGM
09MYN1
]]>Agencies
[Federal Register Volume 72, Number 89 (Wednesday, May 9, 2007)]
[Notices]
[Pages 26404-26406]
From the Federal Register Online via the Government Printing Office [www.gpo.gov]
[FR Doc No: E7-8894]
-----------------------------------------------------------------------
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 Compounds and Methods for the Treatment of Spinal Muscular Atrophy
and Other Diseases
Description of Technology: Spinal muscular atrophy (SMA) is caused
by mutations in the SMN1 gene that result in reduced expression of the
survival motor neuron (SMN) protein and a loss of spinal motor neurons.
An SMN2 gene paralog that differs from SMN by a single base pair has
inadequate expression of SMN to support motor neuron survival.
Alternative splicing caused by the single base substitution in the SMN2
gene results in a slightly truncated and highly unstable SMN protein.
Drugs that allow translational read through of the stop codons
introduced by the alternative splice event have been shown to stabilize
the mutant protein, resulting in increased levels of SMN.
A chemical library screen identified indoprofen, a nonsteroidal
anti-inflammatory drug, as an inducer of SMN expression in cultured
cells. However, indoprofen cannot enter the brain in satisfactory
amounts, has a relatively low level of activity and can cause
substantial side-effects in part due to its cyclooxygenase inhibitory
activity. NIH inventors designed indoprofen derivatives without
cyclooxygenase activity that can enter the CNS and increase expression
of a SMN protein from the SMN2 gene with increased potency and
efficacy. The mechanism of action of these indoprofen analogs appears
to be translational readthrough of stop codons introduced by the
alternative SMN2 splicing event. In addition to treating SMA, novel
drugs that allow read through of stop codons could potentially treat
many other diseases caused by such mutations such as cystic fibrosis
and muscular dystrophy.
Available for licensing are compounds and methods useful for the
treatment of spinal muscular atrophy by increasing SMN expression and
increasing the expression from any nucleic acid that encodes a
translational stop codon.
Applications: Efficacious treatment for SMA, utilizing indoprofen
analogs that increase SMN protein expression; Treatment of any genetic
disease caused by premature termination of protein translation.
Market: SMA is a rare genetic disease that affects approximately 1
in 6,000 live births, and is the leading genetic cause of death in
infants and toddlers. The projected market size for SMA is between $250
million and $750 million.
Development Status: Clinical candidate selection scheduled for June
2007.
Inventors: Jill Heemskerk (NINDS), et al.
Publication: MR Lunn, DE Root, AM Martino, SP Flaherty, BP Kelley,
DD Coovert, AH Burghes, NT Man, GE Morris, J Zhou, EJ Androphy, CJ
Sumner, BR Stockwell. Indoprofen upregulates the survival motor neuron
protein through a cyclooxygenase-independent mechanism. Chem. Biol.
2004 Nov;11(11):1489-1493.
Patent Status: U.S. Provisional Application No. 60/783,292 filed 17
Mar 2006 (HHS Reference No. E-133-2006/0-US-01); PCT Application No.
PCT/2007/006772 filed 16 Mar 2007 (HHS Reference No. E-133-2006/1-PCT-
01)
Licensing Availability: Available for exclusive and non-exclusive
licensing.
Licensing Contact: Norbert Pontzer, J.D., Ph.D.; 301/435-5502;
pontzern@mail.nih.gov.
STAMP, a Novel Cofactor and Possible Steroid Sparing Agent, Modulates
Steroid-Induced Induction or Repression of Steroid Receptors
Description of Technology: Steroid hormones such as androgens,
glucocorticoids, and estrogens are used in the treatments of many
diseases. They act to regulate many physiological responses by binding
to steroid
[[Page 26405]]
receptors. However, because steroid receptors are expressed in many
tissues, efforts to therapeutically modify the effects of steroid
hormones on a specific tissue or on a specific receptor of the steroid
receptor family often cause undesirable effects in other tissues or on
other receptors. STAMP (SRC-1 and TIF-2 Associated Modulatory Protein),
a novel protein that acts to lower the concentration of steroid hormone
needed to induce (or repress) selected target genes by regulating
steroid receptor synthesis, offers an novel approach for reducing the
severity of unwanted side-effects, thereby increasing the ability to
use steroid hormone therapies.
Applications
1. Diseases requiring chronic steroid treatment such as rheumatoid
arthritis, psoriatic arthritis, asthma, inflammatory and auto-immune
diseases;
2. Diseases characterized by excess or deficiency of
glucocorticoids such as obesity, diabetes, hypertension, Cushing's
Syndrome, Parkinson's Disease, Addison's Disease;
3. Diseases in which glucocorticoid-responsive gene expression is
deranged, so deranging carbohydrate, protein or lipid metabolism;
4. Cancers responsive to androgen or estrogen, such as breast
cancer or prostate cancer;
5. Therapeutic applications related to male or female hormone
replacement, symptoms related to menopause, birth control, menstrual
cycle/amenorrhea, fertility or endometriosis.
Advantages
1. STAMP reduces the severity of unwanted side-effects of steroid
hormone therapies;
2. STAMP modulates the gene induction properties of androgen and
progesterone receptors;
3. STAMP modulates both induction and repression properties of
glucocorticoid receptors;
4. STAMP is inactive toward alpha and beta estrogen receptors,
thyroid receptor beta, PPAR gamma 2, retinoid receptor alpha or RXR
alpha;
5. The siRNAs could be useful as therapeutics.
Market: The protein, STAMP, offers a novel approach for reducing
the severity of unwanted side-effects of steroid hormone therapies.
Therefore, STAMP would be helpful in the treatment of diseases
requiring chronic steroid treatments, those characterized by excess or
deficiency of glucocorticoid response, therapies related to male or
female hormone replacement or cancers responsive to androgen or
estrogen.
Development Status
1. STAMP, a protein which is a novel nuclear receptor cofactor, has
been identified;
2. STAMP siRNAs have been shown to change the dose response curve
of endogenous glucocorticoid receptor induced genes;
3. A STAMP antibody has been prepared.
Further Research & Development Required
1. Further in-vivo studies into the role of STAMP in glucocorticoid
receptor-mediated repression;
2. Further study into the activity of STAMP in androgen receptor-
mediated responses;
3. Investigation into the mechanism of action of STAMP;
4. Development of STAMP knockout mouse.
Inventors: Drs. S. Stoney Simons Jr (NIDDK) and Yuanzheng He
(NIDDK)
Publication: Y He and SS Simons Jr. STAMP: A Novel Predicted Factor
Assisting TIF2 Actions in Glucocorticoid Receptor-mediated Induction
and Repression. Mol Cell Biol. 2007 Feb;27(4);1467-1485.
Patent Status: PCT International No. PCT/US2005/006393 filed 25 Feb
2005 (priority date 26 Feb 2004), which published as WO 2005/082935 on
09 Sep 2005, entitled ``A Novel Cofactor that Modulates Steroid
Receptor Activities''; National Stage U.S., Europe, Canada, Australia
(HHS Reference No. E-056-2004/0).
Related Technologies: HHS Reference No. E-015-2000/0,
``Antiprogestins with Partial Agonist Activity.'' Global IP pending:
US, Europe, Australia, Canada, Japan.
Licensing Status: Available for exclusive and non-exclusive
licensing.
Licensing Contact: Dr. Susan Carson; 301/435-5020;
carsonsu@mail.nih.gov.
Collaborative Research Opportunity: The National Institute of
Diabetes, Digestive and Kidney Diseases, Laboratory of Molecular and
Cellular Biology is seeking statements of capability or interest from
parties interested in collaborative research to further develop,
evaluate or commercialize this technology. Please contact Dr. Stoney
Simons, Chief, Steroid Hormones Section (NIDDK) at
steroids@helix.nih.gov; Tel: 301-4960-6796 for more information.
TMC1, a Deafness-Related Gene
Description of Technology: Hearing loss is a common communication
disorder affecting nearly 1 in 1,000 children in the United States
alone, and nearly 50% of adults by the age of eighty. Hearing loss can
be caused by environmental and disease-related factors; however,
hearing loss due to genetic factors accounts for approximately 50% of
cases.
The NIH announces the isolation of two novel genes involved in
hearing; TMC1, short for transmembrane channel-like gene 1. The
inventors have discovered that dominant and recessive mutations in TMC1
underlie two forms of hereditary deafness, known as DFNA36 and DFNB7/
11. TMC1 encodes a protein required for normal function of the
mammalian hair cell, which plays a critical role within the hearing
pathway that detects sound in the inner ear.
The invention discloses TMC1 nucleic acids, vectors, and cells.
Also disclosed are methods of detecting hearing loss, or a
predisposition to hearing loss, due to a mutation in TMC1, as well as
methods for identifying agents that interact with the TMC1 gene in a
cell. Nucleic acids and methods of use for TMC2, a gene closely related
to TMC1, are also disclosed.
Applications: Development of a genetic diagnostic test for hearing
loss; Development of pharmaceuticals to treat hearing loss.
Market: Hearing loss with a genetic component accounts for 50% of
all cases of hearing loss.
Development Status: Early stage.
Inventors: Andrew J. Griffith et al. (NIDCD).
Publication: K Kurima et al. Dominant and recessive deafness caused
by mutations of a novel gene, TMC1, required for cochlear hair-cell
function. Nat Genet. 2002 Mar;30(3):277-284.
Patent Status
1. HHS Reference No. E-168-2001/0:
a. U.S. Provisional Application No. 60/323,275 filed 19 Sep 2001.
b. PCT Application No. PCT/US02/29614 filed 19 Sep 2002, which
published as WO 03/025140 on 27 Mar 2003.
c. U.S. Patent No. 7,192,705 issued 20 Mar 2007.
d. U.S. Patent Application No. 11/615,250 filed 22 Dec 2006.
e. Foreign counterparts in Australia, Canada, Europe, and Japan.
2. HHS Reference No. E-168-2001/1:
a. U.S. Patent No. 7,116,433 issued 23 Jan 2007.
b. Foreign counterparts in Australia and Canada.
Licensing Status: Available for non-exclusive licensing.
Licensing Contact: Tara L. Kirby, Ph.D.; 301/435-4426;
tarak@mail.nih.gov.
[[Page 26406]]
Collaborative Research Opportunity: The NIDCD Otolaryngology Branch
is seeking statements of capability or interest from parties interested
in collaborative research to further develop, evaluate, or
commercialize this technology as well as collaborate on further pre-
clinical and clinical studies with the TMC2 gene mutations. Please
contact Ms. Marianne Lynch at 301-402-5579 or via e-mail at
lynchm@nhlbi.nih.gov for more information.
Dated: April 30, 2007.
Steven M. Ferguson,
Director, Division of Technology Development and Transfer, Office of
Technology Transfer, National Institutes of Health.
[FR Doc. E7-8894 Filed 5-8-07; 8:45 am]
BILLING CODE 4140-01-P
