Government-Owned Inventions; Availability for Licensing, 38440-38442 [E9-18504]
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38440
Federal Register / Vol. 74, No. 147 / Monday, August 3, 2009 / Notices
sroberts on DSKD5P82C1PROD with NOTICES
sale to the consumer. The term ‘‘leafy
greens’’ as used in this draft guidance
includes raw agricultural commodities
and fresh-cut/value-added products.
Examples of leafy greens include iceberg
lettuce, romaine lettuce, leaf lettuce,
butter lettuce, baby leaf lettuce
(immature lettuce or leafy greens),
escarole, endive, spring mix, spinach,
cabbage, kale, arugula, and chard. Leafy
greens do not include herbs such as
cilantro and parsley.
This draft guidance is based primarily
on leafy greens industry guidelines
issued in 2006 (Ref. 1), along with
agency experience and information from
other recent public and private
programs. The leafy greens industry has
since updated and supplemented its
2006 guidelines with additional
recommendations on the production
and harvest of leafy greens that include
quantitative metrics and measures to
assist industry in implementing the
guidelines (Ref. 2). This draft guidance
does not include these more specific
and quantitative metrics and measures.
We are considering the extent to which
more specific measures, including
metrics, should be utilized to help
verify the implementation and efficacy
of the Federal recommendations and
industry practices. We are also
evaluating the extent to which metrics
can be applied to diverse geographic
areas within the United States and
internationally. FDA invites comment
on whether such information should be
incorporated into the guidance, when
finalized.
FDA is issuing this draft guidance as
Level 1 draft guidance consistent with
FDA’s good guidance practices
regulation (21 CFR 10.115). The draft
guidance, when finalized, will represent
the agency’s current thinking on the
microbiological hazards presented by
fresh and fresh-cut leafy greens products
and the recommended control measures
for such hazards in production and
harvesting, postharvest operations,
processing, distribution, and retail and
food service handling of such produce.
It does not create or confer any rights for
or on any person and does not operate
to bind FDA or the public. An
alternative approach may be used if
such approach satisfies the
requirements of the applicable statutes
and regulations.
II. Paperwork Reduction Act of 1995
Under the Paperwork Reduction Act
of 1995 (the PRA) (44 U.S.C. 3501–
3520), Federal agencies must obtain
approval from the Office of Management
and Budget (OMB) for each collection of
information they conduct or sponsor.
‘‘Collection of information’’ is defined
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16:05 Jul 31, 2009
Jkt 217001
in 44 U.S.C. 3502(3) and 5 CFR
1320.3(c) and includes agency requests
or requirements that members of the
public submit reports, keep records, or
provide information to a third party.
Section 3506(c)(2)(A) of the PRA (44
U.S.C. 3506(c)(2)(A)) requires Federal
agencies to publish notice in the
Federal Register soliciting public
comment on each proposed collection of
information before submitting the
collection to OMB for approval. To
comply with this requirement, FDA will
publish a 60-day notice on the proposed
collection of information in a future
issue of the Federal Register.
III. Comments
Interested persons may submit to the
Division of Dockets Management (see
ADDRESSES) written or electronic
comments regarding this document.
Submit a single copy of electronic
comments or two paper copies of any
mailed comments, except that
individuals may submit one paper copy.
Comments are to be identified with the
docket number found in brackets in the
heading of this document. The draft
guidance and received comments may
be seen in the Division of Dockets
Management between 9 a.m. and 4 p.m.,
Monday through Friday.
IV. Electronic Access
Persons with access to the Internet
may obtain the draft guidance at either
https://www.fda.gov/FoodGuidances or
https://www.regulations.gov.
V. References
The following references have been
placed on display in the Division of
Dockets Management, 5630 Fishers
Lane, rm. 1061, Rockville, MD 20852
and may be seen by interested persons
between 9 a.m. and 4 p.m., Monday
through Friday.
1. Gorny, J., et al., editors, ‘‘Commodity
Specific Food Safety Guidelines for the
Lettuce and Leafy Greens Supply Chain’’ (1st
ed.); International Fresh-cut Produce
Association, Produce Marketing Association,
United Fresh Fruit and Vegetable
Association, Western Growers Association;
April 25, 2006. Accessed online at https://
www.fda.gov/Food/FoodSafety/ProductSpecificInformation/FruitsVegetablesJuices/
GuidanceComplianceRegulatoryInformation/
ucm168630.htm.
2. See ‘‘Commodity Specific Food Safety
Guidelines for the Production and Harvest of
Lettuce and Leafy Greens’’; Produce
Marketing Association, United Fresh Fruit
and Vegetable Association, and Western
Growers Association; last revised June 13,
2008. Accessed online at https://
www.caleafygreens.ca.gov/trade/documents/
LGMAAcceptedGAPs06.13.08.pdf. (FDA has
verified the Web site address, but FDA is not
responsible for any subsequent changes to
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the Web site after this document publishes in
the Federal Register.)
Dated: July 28, 2009.
Jeffrey Shuren,
Associate Commissioner for Policy and
Planning.
[FR Doc. E9–18451 Filed 7–31–09; 8:45 am]
BILLING CODE 4160–01–S
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.
Treatment of Cancer Using Metal
Coordinating Compounds That Kill
Multi-Drug Resistant Cancer Cells
Description of Invention: One of the
major hindrances to successful cancer
chemotherapy is the development of
multi-drug resistance (MDR) in cancer
cells. MDR is frequently caused by the
increased expression or activity of ABC
transporter proteins in response to the
toxic agents used in chemotherapy.
Research has generally been directed to
overcoming MDR by inhibiting the
activity of ABC transporters. However,
compounds that inhibit ABC transporter
activity often elicit strong and
undesirable side-effects, restricting their
usefulness as therapeutics.
In an alternative approach to reducing
the debilitating effects of MDR during
cancer therapy, scientists at the NIH
have identified a family of compounds
E:\FR\FM\03AUN1.SGM
03AUN1
Federal Register / Vol. 74, No. 147 / Monday, August 3, 2009 / Notices
whose activities are enhanced, rather
than decreased, in MDR cancer cells.
Particular embodiments of these ‘‘MDRselective compounds’’ include certain
metal coordinating compounds. Recent
evidence suggests that these MDRselective compounds can be used to kill
cancer cells that overexpress ABC
transporters or to re-sensitize multi-drug
resistant cancer cells to
chemotherapeutics. Furthermore, the
effectiveness of these compositions in
killing MDR cancer cells correlates
directly with the level of ABC
transporter expression. Importantly,
MDR-selective compounds are not
inhibitors of ABC transporters, thereby
reducing the likelihood of undesirable
side-effects during treatment. Thus,
MDR-selective compounds represent a
powerful strategy for treating multi-drug
resistant cancers as a direct
chemotherapeutic and as agents that can
re-sensitize MDR cancer cells for
treatment with additional
chemotherapeutic agents.
Applications
• Treatment of cancers associated
with multi-drug resistance, either alone
or in combination with other
therapeutics.
• Re-sensitization of multi-drug
resistant cancer cells to
chemotherapeutic agents.
sroberts on DSKD5P82C1PROD with NOTICES
Advantages
• MDR-selective compounds
capitalize on one of the most common
drawbacks to cancer therapies (MDR) by
using it as an advantage for treating
cancer.
• The compositions do not inhibit the
function of ABC transporters, reducing
the chance of side-effects during
treatment.
• The effects of MDR-selective
compounds correlate with the level of
ABC transporter expression, allowing
healthy cells which do not express high
levels of ABC transporters to better
survive treatment.
Development Status: Preclinical stage
of development.
Patent Status: U.S. Provisional
Application No. 61/182,511 (HHS
Reference No. E–157–2009/0–US–01).
Inventors: Gergely Szakacs et al.
(NCI).
For More Information, See
• C Hegedus et al. Interaction of ABC
multidrug transporters with anticancer
protein kinase inhibitors: substrates
and/or inhibitors? Curr Cancer Drug
Targets. 2009 May;9(3):252–272.
• MD Hall et al. Synthesis, activity,
and pharmacophore development for
isatin-beta-thiosemicarbazones with
VerDate Nov<24>2008
16:05 Jul 31, 2009
Jkt 217001
selective activity toward multidrugresistant cells. J Med Chem. 2009 May
28;52(10):3191–3204.
• U.S. Patent Application Publication
20080214606 A1 (U.S. Patent
Application 11/629,233).
Licensing Status: Available for
licensing.
Licensing Contact: David A.
Lambertson, Ph.D.; 301–435–4632;
lambertsond@mail.nih.gov.
Collaborative Research Opportunity:
The Institute of Enzymology is seeking
statements of capability or interest from
parties interested in collaborative
research to further develop, evaluate, or
commercialize MDR-selective
compounds. Please contact John D.
Hewes, Ph.D. at 301–435–3121 or
hewesj@mail.nih.gov for more
information.
Non Toxic Peptide Treatment for
Dyslipidemic and Vascular Disorders
Description of Invention:
Dyslipidemia and vascular disorders
such as hyperlipidemia,
hypercholesterolemia, HDL deficiency,
coronary heart disease, atherosclerosis,
or thrombic stroke, have become major
health concerns in recent years. Various
approaches to treating these diseases
have led to mixed success with some
undesirable side effects. Long term
administration of some regimens aimed
at reducing cholesterol levels in cells
can lead to persistent
hypertriglyceridemia; a condition that is
characterized by chronically high
triglycerides in the blood. Other
approaches, such as using peptides to
stimulate the efflux of lipids from cells,
are also associated with high toxicity,
which has limited their use.
This technology uses peptide and
peptide analogues with multiple
amphipathic alpha helical domains that
have the dual ability to promote lipid
efflux from cells and stimulate
lipoprotein lipase activity, without
inducing toxicity. It consists of motifs
that mimick apolipoprotein A–I (apoA–
I), the most abundant protein
constituent of high density lipoproteins
(HDLs) that is capable of inducing
cellular lipid efflux, and motif
resembling apolipoprotein C–II (apoC–
II), a known activator of lipoprotein
lipase. Peptides constructed with these
structural domains are capable of
stimulating lipid efflux and activating
lipoprotein lipase, leading to a reduced
incidence of hypertriglyceridemia.
Unlike previous methods, some
amphipathic peptides cause transient
hypertriglyceridema in mice that lasts
for less than 8 hours. Mice treated with
these modified peptides have shown
preserved liver function as they have
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38441
failed to express increased levels of
biomarkers for liver damage and prevent
hypertriglyceridemia. Furthermore,
treated mice show a reduced level of
pro-atherogenic lipoproteins. This
technology demonstrates specific
control of lipid efflux and transport; a
desirable property that gives it a
significant advantage for treating or
preventing a vast range of vascular
diseases and their dyslipidemic
precursors.
This technology also encompasses a
method for identifying non-cytotoxic
peptides that promote lipid efflux from
cells and activates lipoprotein lipase.
Applications and Advantages
• Peptide treatment of dyslipidemic
and vascular disorders.
• Transient hypertriglyceridemia
with no reported toxicity.
• Method of identifying therapeutic
non-cytotoxic peptides.
Development Status: Pre-clinical.
Inventor: Alan T. Remaley and
Marcelo Amar (NHLBI).
Publication: AT Remaley, F Thomas,
JA Stonik, SJ Demosky, SE Bark, EB
Neufeld, AV Bocharov, TG
Vishnyakova, AP Patterson, TL
Eggerman, S Santamarina-Fojo, HB
Brewer. Synthetic amphipathic helical
peptides promote lipid efflux from cells
by an ABCA1-dependent and an
ABCA1-independent pathway. J Lipid
Res. 2003 Apr;44(4):828–836.
Patent Status: U.S. Provisional
Application No. 60/045,213 filed 15 Apr
2008 (HHS Reference No. E–138–2008/
0–US–01); PCT Application No. PCT/
US2009/040560 filed 14 Apr 2009 (HHS
Reference No. E–138–2008/0–PCT–02).
Licensing Status: Available for
licensing.
Licensing Contact: Fatima Sayyid,
M.H.P.M.; 301–435–4521;
sayyidf@mail.nih.gov.
Methods for Treating or Ameliorating
Fibrosis by Inhibiting the Interaction
Between IL–21 Receptor (IL–21R) and
IL–21
Description of Invention: This
invention includes methods for treating
or ameliorating fibrosis by inhibiting the
interaction between IL–21 Receptor (IL–
21R) and IL–21 using either anti-IL21R
monoclonal antibodies (or binding
fragments of anti-IL–21R mAbs), antiIL21 monoclonal antibodies (or binding
fragments of anti-IL–21 mAbs) or
soluble IL–21R (or binding fragments of
IL–21R). It is believed that the TH2
immune response, induced by IL–21,
plays a major role in the pathogenesis of
tissue fibrosis. Antagonism of IL–21R by
anti-IL–21R monoclonal antibodies or
the sequestration of IL–21 by soluble IL–
E:\FR\FM\03AUN1.SGM
03AUN1
38442
Federal Register / Vol. 74, No. 147 / Monday, August 3, 2009 / Notices
sroberts on DSKD5P82C1PROD with NOTICES
21R or anti-IL–21 monoclonal
antibodies has been demonstrated to
reduce TH2 immune responses
associated with fibrosis in animal
models.
The causes of chronic tissue fibrosis
are diverse and the market for a
therapeutic that targets fibrosis is large.
Fibrosis is associated with diverse
causes which include: genetic diseases
(such as cystic fibrosis); autoimmune
diseases (such as scleroderma); chronic
viral infections (such as hepatitis),
parasitic infections (such as
schistosomiasis); and occupational
exposures to causative agents (such as
asbestosis). Additionally, many cases of
tissue fibrosis are idiopathic.
Application: The treatment or
amelioration of tissue fibrosis.
Inventors: Thomas A. Wynn (NIAID);
Deborah A Young; Mary Collins; and
Michael J. Grusby.
Relevant Publication: J Pesce et al.
The IL–21 receptor augments Th2
effector function and alternative
macrophage activation. J Clin Invest
2006 Jul;116(7):2044–2055.
Patent Status: U.S. patent application
no. 11/402,885 (priority date April 14,
2005) and international patent
applications including European patent
application No. EP06/0750009 (HHS
Reference No. E–250–2005).
Licensing Status: Available for nonexclusive licensing.
Licensing Contact: Surekha Vathyam,
Ph.D.; 301–435–4076;
vathyams@mail.nih.gov.
Collaborative Research Opportunity:
The National Institute of Allergy and
Infectious Diseases is seeking statements
of capability or interest from parties
interested in collaborative research to
further develop, evaluate, or
commercialize this invention. Please
contact Nicole Mahoney at 301–435–
9017 or mahoneyn@niaid.nih.gov for
more information.
Use of Discoidin Domain Receptor 1
(DDR1) and Agents That Affect the
DDR1/Collagen Pathway
Description of Invention: Dendritic
cells (DCs) are pivotal antigenpresenting cells for initiation of an
immune response. Indeed, dendritic
cells provide the basis for the
production of an effective immune
response to a vaccine, particularly for
antigens wherein conventional
vaccination is inadequate. DCs are also
important in the production on an
immune response to tumor antigens.
The present invention discloses
methods of using the receptor tyrosine
kinase discoidin domain receptor 1
(DDR1) to facilitate the maturation/
differentiation of DCs or macrophages.
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Activating agents of DDR1 may be
useful in the induction of highly potent,
mature DCs or highly differentiated
macrophages from DC precursors, such
as monocytes. Use of this method may
enhance the antigen presenting
capabilities of the immune system,
leading to a more effective overall
immune response.
Inventor: Teizo Yoshimura (NCI).
Relevant Publications
1. H Kamohara et al. Discoidin
domain receptor 1 isoform-a (DDR1a)
promotes migration of leukocytes in
three-dimensional collagen lattices.
FASEB J. 2001 Dec;15(14):2724–2726.
2. W Matsuyama et al. Interaction of
discoidin domain receptor 1 isoform b
(DDR1b) with collagen activates p38
mitogen-activated protein kinase and
promotes differentiation of
macrophages. FASEB J. 2003
Jul;17(10):1286–1288.
Patent Status: U.S. Application No.
10/507,385 filed 09 Sep 2004 (HHS
Reference No. E–083–2002/2–US–02).
Licensing Status: Available for
licensing.
Licensing Contact: Betty B. Tong,
Ph.D.; 301–594–6565;
tongb@mail.nih.gov.
Dated: July 28, 2009.
Richard U. Rodriguez,
Director, Division of Technology Development
and Transfer, Office of Technology Transfer,
National Institutes of Health.
[FR Doc. E9–18504 Filed 7–31–09; 8:45 am]
BILLING CODE 4140–01–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.
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
PO 00000
Frm 00052
Fmt 4703
Sfmt 4703
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.
A Tumorigenic MEF/3T3 Tet-Off Mouse
Fibroblast Cell Line Stably Transfected
With a T7–Tagged Srp20 Expression
Construct (pJR17)
Description of Technology:
Alternative RNA splicing is a means by
which the human genome can produce
many more proteins from the genes
available. It is emerging that aberrations
in alternative RNA splicing contributes
to the development of cancers. SRp20 is
a cellular splicing factor that is involved
in the process of alternative splicing of
RNA. Investigators at the National
Cancer Institute (NCI), National
Institutes of Health (NIH) have
discovered that SRp20 is overexpressed
in many types of cancer and
furthermore promotes the induction and
maintenance of tumor cell growth. This
was demonstrated in part by
engineering a non-tumorigenic cell to
become tumorigenic in mice by
overexpressing SRp20.
Research Material available for
licensing is a tumorigenic MEF/3T3 tetoff mouse fibroblast cell line stably
transfected with a T7-tagged SRp20
expression construct (pJR17) that is
under the transcriptional control of
tetracycline.
Applications: Use in pre-clinical
development of therapeutic approaches
to cancer that target aberrant alternative
RNA splicing.
Advantages: Transcriptional control
of expression using Tet-off system;
Availability of stably transfected cell
line saves time and effort for other
investigators.
Market: Research Tool.
Development Status: Ready to use.
Inventors: Zhi-Ming Zheng and Rong
Jia (NCI).
Publications: Manuscript in
preparation.
Patent Status: HHS Reference No. E–
229–2009/0—Research Material. Patent
protection is not being sought for this
technology.
Licensing Status: Available for
licensing.
Licensing Contact: Sabarni Chatterjee,
Ph.D.; 301–435–5587;
chatterjeesa@mail.nih.gov.
Collaborative Research Opportunity:
The National Cancer Institute, Center for
Cancer Research, HIV and AIDS
Malignancy Branch, is seeking
statements of capability or interest from
E:\FR\FM\03AUN1.SGM
03AUN1
Agencies
[Federal Register Volume 74, Number 147 (Monday, August 3, 2009)]
[Notices]
[Pages 38440-38442]
From the Federal Register Online via the Government Printing Office [www.gpo.gov]
[FR Doc No: E9-18504]
-----------------------------------------------------------------------
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.
Treatment of Cancer Using Metal Coordinating Compounds That Kill Multi-
Drug Resistant Cancer Cells
Description of Invention: One of the major hindrances to successful
cancer chemotherapy is the development of multi-drug resistance (MDR)
in cancer cells. MDR is frequently caused by the increased expression
or activity of ABC transporter proteins in response to the toxic agents
used in chemotherapy. Research has generally been directed to
overcoming MDR by inhibiting the activity of ABC transporters. However,
compounds that inhibit ABC transporter activity often elicit strong and
undesirable side-effects, restricting their usefulness as therapeutics.
In an alternative approach to reducing the debilitating effects of
MDR during cancer therapy, scientists at the NIH have identified a
family of compounds
[[Page 38441]]
whose activities are enhanced, rather than decreased, in MDR cancer
cells. Particular embodiments of these ``MDR-selective compounds''
include certain metal coordinating compounds. Recent evidence suggests
that these MDR-selective compounds can be used to kill cancer cells
that overexpress ABC transporters or to re-sensitize multi-drug
resistant cancer cells to chemotherapeutics. Furthermore, the
effectiveness of these compositions in killing MDR cancer cells
correlates directly with the level of ABC transporter expression.
Importantly, MDR-selective compounds are not inhibitors of ABC
transporters, thereby reducing the likelihood of undesirable side-
effects during treatment. Thus, MDR-selective compounds represent a
powerful strategy for treating multi-drug resistant cancers as a direct
chemotherapeutic and as agents that can re-sensitize MDR cancer cells
for treatment with additional chemotherapeutic agents.
Applications
Treatment of cancers associated with multi-drug
resistance, either alone or in combination with other therapeutics.
Re-sensitization of multi-drug resistant cancer cells to
chemotherapeutic agents.
Advantages
MDR-selective compounds capitalize on one of the most
common drawbacks to cancer therapies (MDR) by using it as an advantage
for treating cancer.
The compositions do not inhibit the function of ABC
transporters, reducing the chance of side-effects during treatment.
The effects of MDR-selective compounds correlate with the
level of ABC transporter expression, allowing healthy cells which do
not express high levels of ABC transporters to better survive
treatment.
Development Status: Preclinical stage of development.
Patent Status: U.S. Provisional Application No. 61/182,511 (HHS
Reference No. E-157-2009/0-US-01).
Inventors: Gergely Szakacs et al. (NCI).
For More Information, See
C Hegedus et al. Interaction of ABC multidrug transporters
with anticancer protein kinase inhibitors: substrates and/or
inhibitors? Curr Cancer Drug Targets. 2009 May;9(3):252-272.
MD Hall et al. Synthesis, activity, and pharmacophore
development for isatin-beta-thiosemicarbazones with selective activity
toward multidrug-resistant cells. J Med Chem. 2009 May 28;52(10):3191-
3204.
U.S. Patent Application Publication 20080214606 A1 (U.S.
Patent Application 11/629,233).
Licensing Status: Available for licensing.
Licensing Contact: David A. Lambertson, Ph.D.; 301-435-4632;
lambertsond@mail.nih.gov.
Collaborative Research Opportunity: The Institute of Enzymology is
seeking statements of capability or interest from parties interested in
collaborative research to further develop, evaluate, or commercialize
MDR-selective compounds. Please contact John D. Hewes, Ph.D. at 301-
435-3121 or hewesj@mail.nih.gov for more information.
Non Toxic Peptide Treatment for Dyslipidemic and Vascular Disorders
Description of Invention: Dyslipidemia and vascular disorders such
as hyperlipidemia, hypercholesterolemia, HDL deficiency, coronary heart
disease, atherosclerosis, or thrombic stroke, have become major health
concerns in recent years. Various approaches to treating these diseases
have led to mixed success with some undesirable side effects. Long term
administration of some regimens aimed at reducing cholesterol levels in
cells can lead to persistent hypertriglyceridemia; a condition that is
characterized by chronically high triglycerides in the blood. Other
approaches, such as using peptides to stimulate the efflux of lipids
from cells, are also associated with high toxicity, which has limited
their use.
This technology uses peptide and peptide analogues with multiple
amphipathic alpha helical domains that have the dual ability to promote
lipid efflux from cells and stimulate lipoprotein lipase activity,
without inducing toxicity. It consists of motifs that mimick
apolipoprotein A-I (apoA-I), the most abundant protein constituent of
high density lipoproteins (HDLs) that is capable of inducing cellular
lipid efflux, and motif resembling apolipoprotein C-II (apoC-II), a
known activator of lipoprotein lipase. Peptides constructed with these
structural domains are capable of stimulating lipid efflux and
activating lipoprotein lipase, leading to a reduced incidence of
hypertriglyceridemia. Unlike previous methods, some amphipathic
peptides cause transient hypertriglyceridema in mice that lasts for
less than 8 hours. Mice treated with these modified peptides have shown
preserved liver function as they have failed to express increased
levels of biomarkers for liver damage and prevent hypertriglyceridemia.
Furthermore, treated mice show a reduced level of pro-atherogenic
lipoproteins. This technology demonstrates specific control of lipid
efflux and transport; a desirable property that gives it a significant
advantage for treating or preventing a vast range of vascular diseases
and their dyslipidemic precursors.
This technology also encompasses a method for identifying non-
cytotoxic peptides that promote lipid efflux from cells and activates
lipoprotein lipase.
Applications and Advantages
Peptide treatment of dyslipidemic and vascular disorders.
Transient hypertriglyceridemia with no reported toxicity.
Method of identifying therapeutic non-cytotoxic peptides.
Development Status: Pre-clinical.
Inventor: Alan T. Remaley and Marcelo Amar (NHLBI).
Publication: AT Remaley, F Thomas, JA Stonik, SJ Demosky, SE Bark,
EB Neufeld, AV Bocharov, TG Vishnyakova, AP Patterson, TL Eggerman, S
Santamarina-Fojo, HB Brewer. Synthetic amphipathic helical peptides
promote lipid efflux from cells by an ABCA1-dependent and an ABCA1-
independent pathway. J Lipid Res. 2003 Apr;44(4):828-836.
Patent Status: U.S. Provisional Application No. 60/045,213 filed 15
Apr 2008 (HHS Reference No. E-138-2008/0-US-01); PCT Application No.
PCT/US2009/040560 filed 14 Apr 2009 (HHS Reference No. E-138-2008/0-
PCT-02).
Licensing Status: Available for licensing.
Licensing Contact: Fatima Sayyid, M.H.P.M.; 301-435-4521;
sayyidf@mail.nih.gov.
Methods for Treating or Ameliorating Fibrosis by Inhibiting the
Interaction Between IL-21 Receptor (IL-21R) and IL-21
Description of Invention: This invention includes methods for
treating or ameliorating fibrosis by inhibiting the interaction between
IL-21 Receptor (IL-21R) and IL-21 using either anti-IL21R monoclonal
antibodies (or binding fragments of anti-IL-21R mAbs), anti-IL21
monoclonal antibodies (or binding fragments of anti-IL-21 mAbs) or
soluble IL-21R (or binding fragments of IL-21R). It is believed that
the TH2 immune response, induced by IL-21, plays a major role in the
pathogenesis of tissue fibrosis. Antagonism of IL-21R by anti-IL-21R
monoclonal antibodies or the sequestration of IL-21 by soluble IL-
[[Page 38442]]
21R or anti-IL-21 monoclonal antibodies has been demonstrated to reduce
TH2 immune responses associated with fibrosis in animal models.
The causes of chronic tissue fibrosis are diverse and the market
for a therapeutic that targets fibrosis is large. Fibrosis is
associated with diverse causes which include: genetic diseases (such as
cystic fibrosis); autoimmune diseases (such as scleroderma); chronic
viral infections (such as hepatitis), parasitic infections (such as
schistosomiasis); and occupational exposures to causative agents (such
as asbestosis). Additionally, many cases of tissue fibrosis are
idiopathic.
Application: The treatment or amelioration of tissue fibrosis.
Inventors: Thomas A. Wynn (NIAID); Deborah A Young; Mary Collins;
and Michael J. Grusby.
Relevant Publication: J Pesce et al. The IL-21 receptor augments
Th2 effector function and alternative macrophage activation. J Clin
Invest 2006 Jul;116(7):2044-2055.
Patent Status: U.S. patent application no. 11/402,885 (priority
date April 14, 2005) and international patent applications including
European patent application No. EP06/0750009 (HHS Reference No. E-250-
2005).
Licensing Status: Available for non-exclusive licensing.
Licensing Contact: Surekha Vathyam, Ph.D.; 301-435-4076;
vathyams@mail.nih.gov.
Collaborative Research Opportunity: The National Institute of
Allergy and Infectious Diseases is seeking statements of capability or
interest from parties interested in collaborative research to further
develop, evaluate, or commercialize this invention. Please contact
Nicole Mahoney at 301-435-9017 or mahoneyn@niaid.nih.gov for more
information.
Use of Discoidin Domain Receptor 1 (DDR1) and Agents That Affect the
DDR1/Collagen Pathway
Description of Invention: Dendritic cells (DCs) are pivotal
antigen-presenting cells for initiation of an immune response. Indeed,
dendritic cells provide the basis for the production of an effective
immune response to a vaccine, particularly for antigens wherein
conventional vaccination is inadequate. DCs are also important in the
production on an immune response to tumor antigens.
The present invention discloses methods of using the receptor
tyrosine kinase discoidin domain receptor 1 (DDR1) to facilitate the
maturation/differentiation of DCs or macrophages. Activating agents of
DDR1 may be useful in the induction of highly potent, mature DCs or
highly differentiated macrophages from DC precursors, such as
monocytes. Use of this method may enhance the antigen presenting
capabilities of the immune system, leading to a more effective overall
immune response.
Inventor: Teizo Yoshimura (NCI).
Relevant Publications
1. H Kamohara et al. Discoidin domain receptor 1 isoform-a (DDR1a)
promotes migration of leukocytes in three-dimensional collagen
lattices. FASEB J. 2001 Dec;15(14):2724-2726.
2. W Matsuyama et al. Interaction of discoidin domain receptor 1
isoform b (DDR1b) with collagen activates p38 mitogen-activated protein
kinase and promotes differentiation of macrophages. FASEB J. 2003
Jul;17(10):1286-1288.
Patent Status: U.S. Application No. 10/507,385 filed 09 Sep 2004
(HHS Reference No. E-083-2002/2-US-02).
Licensing Status: Available for licensing.
Licensing Contact: Betty B. Tong, Ph.D.; 301-594-6565;
tongb@mail.nih.gov.
Dated: July 28, 2009.
Richard U. Rodriguez,
Director, Division of Technology Development and Transfer, Office of
Technology Transfer, National Institutes of Health.
[FR Doc. E9-18504 Filed 7-31-09; 8:45 am]
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