Government-Owned Inventions; Availability for Licensing, 57635-57637 [E8-23436]
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57635
Federal Register / Vol. 73, No. 193 / Friday, October 3, 2008 / Notices
DEPARTMENT OF HEALTH AND
HUMAN SERVICES
National Institutes of Health
Submission for OMB Review;
Comment Request: The National
Survey of Physicians Attitudes
Regarding the Care of Cancer
Survivors (SPARCCS) (NCI)
SUMMARY: Under the provisions of
Section 3507(a)(1)(D) of the Paperwork
Reduction Act of 1995, the National
Cancer Institute (NCI), the National
Institutes of Health (NIH), has submitted
to the Office of Management and Budget
(OMB) a request to review and approve
the information collection listed below.
This proposed information collection
was previously published in the Federal
Register on July 31, 2008 (Vol. 73, No.
148, p. 44751) and allowed 60-days for
public comment. There were no public
comments received. The purpose of this
notice is to allow an additional 30 days
for public comment. The National
Institutes of Health may not conduct or
sponsor, and the respondent is not
required to respond to, an information
collection that has been extended,
revised, or implemented on or after
October 1, 1995, unless it displays a
currently valid OMB control number.
Proposed Collection: Title: NIH–
Survey of Physicians Attitudes
Regarding the Care of Cancer Survivors
(SPARCCS). Type of Information
Collection Request: New. Need and Use
of Information Collection: The purpose
of this study is to identify the beliefs,
knowledge, attitudes, and practices of
primary care physicians and cancer
specialists regarding the components
described by the IOM. These data will
inform the process of standardization of
survivorship care practices; augment the
data collected in other cancer
survivorship studies and monitor the
progress being made toward achieving
NCI strategic goals of improving the
quality of cancer care across the cancer
control continuum. This questionnaire
adheres to The Public Health Service
Act, Section 412 (42 U.S.C. 285a–1) and
Section 413 (42 U.S.C. 285a–2), which
authorizes the Division of Cancer
Control and Population Sciences of the
National Cancer Institute (NCI) to
establish and support programs for the
detection, diagnosis, prevention and
treatment of cancer; and to collect,
identify, analyze and disseminate
information on cancer research,
diagnosis, prevention and treatment.
Frequency of Response: Once. Affected
Public: Individuals and Businesses.
Type of Respondents: Primary care and
medical oncology physicians practicing
in a non-federal facility. The annual
reporting burden is estimated at 904
hours as shown in Table 1. The total
burden hours is estimated at 1808 hours
over the two year field period of the
study. There is no capital, operating or
maintenance costs to report.
TABLE 1—ESTIMATES OF ANNUAL BURDEN HOURS
Receptionists .............................................
Family Practice ..........................................
General Internists ......................................
OB/GYNs ...................................................
Oncologists ................................................
Receptionists & Administrators ..................
Screener ..................
PCP Instrument .......
PCP Instrument .......
PCP Instrument .......
Oncology Instrument
Follow-Up Phone
Calls.
2,033
250
250
50
550
1,103
1
1
1
1
1
4
5/60
20/60
20/60
20/60
20/60
5/60
169
83
83
17
183
368
Total ....................................................
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Survey
..................................
4,236
............................
............................
904
Request for Comments: Written
comments and/or suggestions from the
public and affected agencies are invited
on one or more of the following points:
(1) Whether the proposed collection of
information is necessary for the proper
performance of the function of the
agency, including whether the
information will have practical utility;
(2) The accuracy of the agency’s
estimate of the burden of the proposed
collection of information, including the
validity of the methodology and
assumptions used; (3) Ways to enhance
the quality, utility, and clarity of the
information to be collected; and (4)
Ways to minimize the burden of the
collection of information on those who
are to respond, including the use of
appropriate automated, electronic,
mechanical, or other technological
collection techniques or other forms of
information technology.
Direct Comments To OMB: Written
comments and/or suggestions regarding
the item(s) contained in this notice,
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Jkt 217001
Number of
respondents
Average time
per response
(minutes/hour)
Type of
respondents
Frequency of
response
especially regarding the estimated
public burden and associated response
time, should be directed to the
Attention: NIH Desk Officer, Office of
Management and Budget, at
OIRA_submission@omb.eop.gov or by
fax to 202–395–6974. To request more
information on the proposed project or
to obtain a copy of the data collection
plans and instruments, contact Arnie
Potosky, Ph.D., Task Order Monitor,
Applied Research Branch, Division of
Cancer Control and Population
Sciences, National Cancer Institute,
National Institutes of Health, Bethesda,
Maryland, 20892–7344, or call non-tollfree number (301)402–3362 or e-mail
your request, including your address to:
potoskya@mail.nih.gov.
Comments Due Date: Comments
regarding this information collection are
best assured of having their full effect if
received within 30 days of the date of
this publication.
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Annual burden
hours
Dated: August 23, 2008.
Vivian Horovitch-Kelley,
NCI Project Clearance Liaison Office,
National Institutes of Health.
[FR Doc. E8–23443 Filed 10–2–08; 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.
AGENCY:
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
E:\FR\FM\03OCN1.SGM
03OCN1
57636
Federal Register / Vol. 73, No. 193 / Friday, October 3, 2008 / Notices
Licensing Status: Available for nonexclusive licensing under a Biological
Materials License Agreement.
Licensing Contact: Adaku
Nwachukwu, J.D.; 301–435–5560;
madua@mail.nih.gov.
Collaborative Research Opportunity:
The National Institute of Dental and
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, Ph.D. at 301–
402–0540 or bradleyda@nidcr.nih.gov
for more information.
Matriptase Hypomorphic Mouse Model
of a Human Ichthyosis
mstockstill on PROD1PC66 with NOTICES
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.
Prostatic Adenocarcinoma Cells
Expressing or Lacking the Tumor
Suppressor Gene PTEN
Description of Technology: PTEN is a
tumor suppressor gene that is frequently
deleted or mutated in a variety of
human cancers, including prostate,
breast, endometrial, lung, and ovarian
cancers. In prostate cancer cells, PTEN
deletion is the most common event
observed. The loss of PTEN is thought
to play and important role in tumor cell
proliferation and metastasis due to a
lack of control of the signaling pathways
that mediate cellular processes such as
apoptosis and migration. Previously
PTEN had been shown to downregulate
cyclin D1 expression as well as regulate
p53 protein levels and transcriptional
activity, and recently the inventors of
this technology have shown that PTEN
decreases surface IGF–IR protein levels
in prostate cancer cell lines in an Aktindependent manner.
PC3 cells are prostate cancer cells that
lack PTEN gene. This technology
describes PC3 cells that overexpress the
PTEN gene. These cell lines can be used
to study the role of the PTEN gene in
cancer growth and metastasis.
Market:
• Prostate cancer is the most common
type of cancer found in American men,
and it has been estimated that there
were more than 230,000 new cases in
the U.S. in 2007. Prostate cancer is also
the second leading cause of cancer
death in men.
• In the U.S. over 2 million women
have been treated for breast cancer, with
more than 200,000 women diagnosed in
the year 2007 alone. Breast cancer is the
second leading cause of cancer death in
women.
Development Status: The technology
is currently in the pre-clinical stage of
development.
Inventors: Derek LeRoith and Michael
Quon (NIDDK).
Publication: H Zhao et al. PTEN
inhibits cell proliferation and induces
Description of Technology: Available
for licensing are mice with greatly
reduced levels of matriptase, a
membrane protease involved in
epithelial development, immune
function, and carcinogenesis. These
mice were created to study autosomal
recessive ichthyosis with hypotricosis
(ARIH), an inherited human disease that
has been linked to a mutation in the
ST14 gene that encodes matriptase.
These mice manifest the same defects
seen in people afflicted by ARIH, so it
can be an effective model for studying
the role of matriptase in disorders that
affect skin development.
Applications:
• Research tool for skin development
research.
• Model to develop and test
therapeutics for treating skin disorders,
including skin cancer.
• Model immunity and allergy.
Advantages: Well characterized
animal model closely related to a
human genetic disorder.
Market: Ichthyosis is a series of
genetic skin diseases characterized by
dry, thickened, scaling skin that affects
more than one million Americans.
Presently, there is no cure for
ichthyosis, only treatments to help
manage symptoms.
Development Status: Well
characterized mouse model of human
ARIH.
Inventors: Thomas H. Bugge (NIDCR)
et al.
Publication: K List et al. Autosomal
ichthyosis with hypotrichosis syndrome
displays low matriptase proteolytic
activity and is phenocopied in ST14
hypomorphic mice. J Biol Chem. 2007
Dec 14;282(50):36714–36723.
Patent Status: HHS Reference No. E–
323–2008/0—Biological Material. Patent
protection is not being pursued for this
technology.
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23:33 Oct 02, 2008
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PO 00000
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apoptosis by downregulating cell
surface IGF–IR expression in prostate
cancer cells. Oncogene 2004 Jan
22;23(3):786–794.
Patent Status: HHS Reference No. E–
292–2008/0—Research Tool. Patent
protection is not being pursued for this
technology.
Licensing Status: Available for
licensing.
Licensing Contact: Whitney A.
Hastings; 301–451–7337;
hastingw@mail.nih.gov.
Fully Human Anti-Human NKG2D
Monoclonal Antibody
Description of Technology: Available
for licensing is a fully human
monoclonal antibody (KYK–2.0 IgG1)
with high specificity and affinity to
human NKG2D, a stimulatory or
costimulatory receptor located on the
cell surface of natural killer (NK) cells
and CD8+ T cells. NKG2D plays a role
in mediating immune responses in
autoimmune and infectious diseases
and cancer and it makes NKG2D an
attractive target for therapeutic
intervention. Nonetheless, monoclonal
antibodies to NKG2D that are suitable
for clinical investigations have not been
available. In solution, KYK–2.0 IgG1
interferes with the cytolytic activity of
human NK cells. When immobilized,
KYK–2.0 IgG1 induces human NK cell
activation. The dual antagonistic and
agonistic activity promises a broad
range of therapeutic applications.
Application: Therapeutic fully human
monoclonal antibody for a variety of
indications including autoimmune and
infectious diseases, cancer, and
transplantation.
Advantage: The dual antagonistic and
agonistic activity in concert with low
immunogenicity suggests broad and
potent therapeutic utility of KYK–2.0
IgG1 and its derivatives.
Development Status: The technology
is currently in the pre-clinical stage of
development.
Market:
• Monoclonal antibody market is one
of the fastest growing and most lucrative
sectors of the pharmaceutical industry
with a 48.1% growth between 2003 and
2004.
• Monoclonal antibody market is
estimated to be worth $30.3 billion in
2010.
Inventors: Christoph Rader and Ka
Yin Kwong (NCI)
Related Publication: KY Kwong, S
Baskar, H Zhang, CL Mackall, C Rader.
Generation, affinity maturation, and
characterization of a human anti-human
NKG2D monoclonal antibody with dual
antagonistic and agonistic activity. J Mol
E:\FR\FM\03OCN1.SGM
03OCN1
Federal Register / Vol. 73, No. 193 / Friday, October 3, 2008 / Notices
mstockstill on PROD1PC66 with NOTICES
Biol., in press (available online 2008
Sep 16, doi:10.1016/j.jmb.2008.09.008).
Patent Status: U.S. Provisional
Application No. 61/086,027 filed 04
Aug 2008 (HHS Reference No. E–211–
2008/0–US–01).
Licensing Status: Available for
exclusive or non-exclusive licensing.
Licensing Contact: Jennifer Wong;
301–435–4633; wongje@mail.nih.gov.
Collaborative Research Opportunity:
The Experimental Transplantation and
Immunology Branch, Center for Cancer
Research, National Cancer Institute is
seeking statements of capability or
interest from parties interested in
collaborative research to further
develop, evaluate, or commercialize the
fully human anti-human NKG2D
monoclonal antibody KYK–2.0 IgG1.
Please contact John D. Hewes, Ph.D. at
301–435–3121 or hewesj@mail.nih.gov
for more information.
Methods for the Detection and
Treatment of Lung Cancer
Description of Technology: Lung
cancer is the third most common
malignant disease and the first leading
cause of cancer death in the western
world. Non-small cell lung cancer
(NSCLC) is one of the leading causes of
death accounting for nearly 30% of all
cancer deaths. Despite considerable
research, lung cancer remains difficult
to diagnose and treat effectively. Current
chemotherapeutic regimens provide
poor survival benefits and the unmet
clinical need among lung cancer
patients is very high. The prognosis is
very bleak since most patients are
diagnosed with lung cancer at a late
stage.
The inventors have discovered that
approximately 20% of common adult
NSCLC have an aberrant activation of
CRTC gene members with marked
induction of CRTC regulated genes.
CRTC activation is linked with the loss
of LKB1/STK11 kinases which results in
CRTC underphosphorylation and
enhanced nuclear localization. As the
LKB1/STK11 signaling pathways has
been exploited in potential cancer
therapeutic treatments, this novel
unrecognized consequence the loss of
LKB1/STK11 function associated with
aberrant CRTC activation in cancer
offers new candidate diagnostic and
therapeutic targets for NSCLC.
Applications:
• Novel cancer diagnostics and
therapeutic treatments.
• Method to detect and treat lung
cancer.
Development Status: The technology
is currently in the pre-clinical stage of
development.
Market:
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23:33 Oct 02, 2008
Jkt 217001
• Lung cancer is the leading cause of
cancer deaths among both men and
women in the U.S.
• The NSCLC market was estimated
to be worth US$3.7 billion in 2006 and
will increase by 17% by 2012.
Inventors: Frederic Kaye and Amy
Coxon (NCI).
Patent Status: U.S. Provisional
Application No.61/036,830 filed 13 Mar
2008 (HHS Reference No. E–069–2008/
0–US–01).
Licensing Status: Available for
exclusive or non-exclusive licensing.
Licensing Contact: Jennifer Wong;
301–435–4633; wongje@mail.nih.gov.
Human Perilipin Proteins
Description of Technology: Perilipins
are important regulators of lipid storage
in fat cells. These proteins stabilize fat
droplets and control their breakdown by
controlling access of lipid-degrading
enzymes. Since these proteins are
central to the storage and breakdown of
body fat it very likely that they are
crucial for the regulation of body
weight. Perilipin expression is elevated
in obese animals and humans.
Mutations in the perilipin gene are
associated with increased risk of obesity
in women. Importantly, when the
perilipin gene is inactivated the obesity
of model mice is reversed. Therefore,
perilipin could be a good candidate for
therapeutic targeting to treat obesity in
humans.
This NIH invention claims DNA
sequences of splice variants that code
for human perilipin protein isoforms
and methods of expressing the
recombinant protein in bacteria or
mammalian cells. It also claims
substantially purified perilipin proteins
and methods for detecting their
presence in a biological sample.
Applications:
• Drug development for obesity.
• Diagnostics for detection of
perilipins.
• Antigens for antibody production.
• Markers for identifying true
adipocytes.
Advantages:
• Cloned DNA sequences ready for
protein expression.
• Isoforms allow greater flexibility in
designing therapeutics.
Development Status: Pre-clinical.
Inventors: Constantine Londos,
Andrew S. Greenberg, Alan R. Kimmel,
John J. Egan (NIDDK).
Related Publication: AS Greenberg et
al. Perilipin, a major hormonally
regulated adipocyte-specific
phosphoprotein associated with the
periphery of lipid storage droplets. J
Biol Chem. 1991 Jun 15;266(17):11341–
11346.
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57637
Patent Status:
• U.S. Patent No. 6,074,842 issued 13
Jun 2000 (HHS Reference No. E–111–
1991/0–US–03).
• U.S. Patent No. 5,585,462 issued 17
Dec 1996 (HHS Reference No. E–111–
1991/1–US–01).
Licensing Status: Available for
exclusive or non-exclusive licensing.
Licensing Contact: Surekha Vathyam,
PhD; 301–435–4076;
vathyams@mail.nih.gov.
Dated: September 29, 2008.
Richard U. Rodriguez,
Director, Division of Technology Development
and Transfer, Office of Technology Transfer,
National Institutes of Health.
[FR Doc. E8–23436 Filed 10–2–08; 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:
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.
Murine Monoclonal Antibodies
Effective To Treat Respiratory
Syncytial Virus
Description of Technology: Available
for licensing through a Biological
Materials License Agreement are the
murine MAbs described in Beeler et al,
‘‘Neutralization epitopes of the F
glycoprotein of respiratory syncytial
virus: effect of mutation upon fusion
function,’’ J Virol. 1989 Jul;63(7):2941–
E:\FR\FM\03OCN1.SGM
03OCN1
]]>Agencies
[Federal Register Volume 73, Number 193 (Friday, October 3, 2008)]
[Notices]
[Pages 57635-57637]
From the Federal Register Online via the Government Printing Office [www.gpo.gov]
[FR Doc No: E8-23436]
-----------------------------------------------------------------------
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
[[Page 57636]]
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.
Matriptase Hypomorphic Mouse Model of a Human Ichthyosis
Description of Technology: Available for licensing are mice with
greatly reduced levels of matriptase, a membrane protease involved in
epithelial development, immune function, and carcinogenesis. These mice
were created to study autosomal recessive ichthyosis with hypotricosis
(ARIH), an inherited human disease that has been linked to a mutation
in the ST14 gene that encodes matriptase. These mice manifest the same
defects seen in people afflicted by ARIH, so it can be an effective
model for studying the role of matriptase in disorders that affect skin
development.
Applications:
Research tool for skin development research.
Model to develop and test therapeutics for treating skin
disorders, including skin cancer.
Model immunity and allergy.
Advantages: Well characterized animal model closely related to a
human genetic disorder.
Market: Ichthyosis is a series of genetic skin diseases
characterized by dry, thickened, scaling skin that affects more than
one million Americans. Presently, there is no cure for ichthyosis, only
treatments to help manage symptoms.
Development Status: Well characterized mouse model of human ARIH.
Inventors: Thomas H. Bugge (NIDCR) et al.
Publication: K List et al. Autosomal ichthyosis with hypotrichosis
syndrome displays low matriptase proteolytic activity and is
phenocopied in ST14 hypomorphic mice. J Biol Chem. 2007 Dec
14;282(50):36714-36723.
Patent Status: HHS Reference No. E-323-2008/0--Biological Material.
Patent protection is not being pursued for this technology.
Licensing Status: Available for non-exclusive licensing under a
Biological Materials License Agreement.
Licensing Contact: Adaku Nwachukwu, J.D.; 301-435-5560;
madua@mail.nih.gov.
Collaborative Research Opportunity: The National Institute of
Dental and 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, Ph.D. at 301-402-0540
or bradleyda@nidcr.nih.gov for more information.
Prostatic Adenocarcinoma Cells Expressing or Lacking the Tumor
Suppressor Gene PTEN
Description of Technology: PTEN is a tumor suppressor gene that is
frequently deleted or mutated in a variety of human cancers, including
prostate, breast, endometrial, lung, and ovarian cancers. In prostate
cancer cells, PTEN deletion is the most common event observed. The loss
of PTEN is thought to play and important role in tumor cell
proliferation and metastasis due to a lack of control of the signaling
pathways that mediate cellular processes such as apoptosis and
migration. Previously PTEN had been shown to downregulate cyclin D1
expression as well as regulate p53 protein levels and transcriptional
activity, and recently the inventors of this technology have shown that
PTEN decreases surface IGF-IR protein levels in prostate cancer cell
lines in an Akt-independent manner.
PC3 cells are prostate cancer cells that lack PTEN gene. This
technology describes PC3 cells that overexpress the PTEN gene. These
cell lines can be used to study the role of the PTEN gene in cancer
growth and metastasis.
Market:
Prostate cancer is the most common type of cancer found in
American men, and it has been estimated that there were more than
230,000 new cases in the U.S. in 2007. Prostate cancer is also the
second leading cause of cancer death in men.
In the U.S. over 2 million women have been treated for
breast cancer, with more than 200,000 women diagnosed in the year 2007
alone. Breast cancer is the second leading cause of cancer death in
women.
Development Status: The technology is currently in the pre-clinical
stage of development.
Inventors: Derek LeRoith and Michael Quon (NIDDK).
Publication: H Zhao et al. PTEN inhibits cell proliferation and
induces apoptosis by downregulating cell surface IGF-IR expression in
prostate cancer cells. Oncogene 2004 Jan 22;23(3):786-794.
Patent Status: HHS Reference No. E-292-2008/0--Research Tool.
Patent protection is not being pursued for this technology.
Licensing Status: Available for licensing.
Licensing Contact: Whitney A. Hastings; 301-451-7337;
hastingw@mail.nih.gov.
Fully Human Anti-Human NKG2D Monoclonal Antibody
Description of Technology: Available for licensing is a fully human
monoclonal antibody (KYK-2.0 IgG1) with high specificity and affinity
to human NKG2D, a stimulatory or costimulatory receptor located on the
cell surface of natural killer (NK) cells and CD8+ T cells. NKG2D plays
a role in mediating immune responses in autoimmune and infectious
diseases and cancer and it makes NKG2D an attractive target for
therapeutic intervention. Nonetheless, monoclonal antibodies to NKG2D
that are suitable for clinical investigations have not been available.
In solution, KYK-2.0 IgG1 interferes with the cytolytic activity of
human NK cells. When immobilized, KYK-2.0 IgG1 induces human NK cell
activation. The dual antagonistic and agonistic activity promises a
broad range of therapeutic applications.
Application: Therapeutic fully human monoclonal antibody for a
variety of indications including autoimmune and infectious diseases,
cancer, and transplantation.
Advantage: The dual antagonistic and agonistic activity in concert
with low immunogenicity suggests broad and potent therapeutic utility
of KYK-2.0 IgG1 and its derivatives.
Development Status: The technology is currently in the pre-clinical
stage of development.
Market:
Monoclonal antibody market is one of the fastest growing
and most lucrative sectors of the pharmaceutical industry with a 48.1%
growth between 2003 and 2004.
Monoclonal antibody market is estimated to be worth $30.3
billion in 2010.
Inventors: Christoph Rader and Ka Yin Kwong (NCI)
Related Publication: KY Kwong, S Baskar, H Zhang, CL Mackall, C
Rader. Generation, affinity maturation, and characterization of a human
anti-human NKG2D monoclonal antibody with dual antagonistic and
agonistic activity. J Mol
[[Page 57637]]
Biol., in press (available online 2008 Sep 16, doi:10.1016/
j.jmb.2008.09.008).
Patent Status: U.S. Provisional Application No. 61/086,027 filed 04
Aug 2008 (HHS Reference No. E-211-2008/0-US-01).
Licensing Status: Available for exclusive or non-exclusive
licensing.
Licensing Contact: Jennifer Wong; 301-435-4633;
wongje@mail.nih.gov.
Collaborative Research Opportunity: The Experimental
Transplantation and Immunology Branch, Center for Cancer Research,
National Cancer Institute is seeking statements of capability or
interest from parties interested in collaborative research to further
develop, evaluate, or commercialize the fully human anti-human NKG2D
monoclonal antibody KYK-2.0 IgG1. Please contact John D. Hewes, Ph.D.
at 301-435-3121 or hewesj@mail.nih.gov for more information.
Methods for the Detection and Treatment of Lung Cancer
Description of Technology: Lung cancer is the third most common
malignant disease and the first leading cause of cancer death in the
western world. Non-small cell lung cancer (NSCLC) is one of the leading
causes of death accounting for nearly 30% of all cancer deaths. Despite
considerable research, lung cancer remains difficult to diagnose and
treat effectively. Current chemotherapeutic regimens provide poor
survival benefits and the unmet clinical need among lung cancer
patients is very high. The prognosis is very bleak since most patients
are diagnosed with lung cancer at a late stage.
The inventors have discovered that approximately 20% of common
adult NSCLC have an aberrant activation of CRTC gene members with
marked induction of CRTC regulated genes. CRTC activation is linked
with the loss of LKB1/STK11 kinases which results in CRTC
underphosphorylation and enhanced nuclear localization. As the LKB1/
STK11 signaling pathways has been exploited in potential cancer
therapeutic treatments, this novel unrecognized consequence the loss of
LKB1/STK11 function associated with aberrant CRTC activation in cancer
offers new candidate diagnostic and therapeutic targets for NSCLC.
Applications:
Novel cancer diagnostics and therapeutic treatments.
Method to detect and treat lung cancer.
Development Status: The technology is currently in the pre-clinical
stage of development.
Market:
Lung cancer is the leading cause of cancer deaths among
both men and women in the U.S.
The NSCLC market was estimated to be worth US$3.7 billion
in 2006 and will increase by 17% by 2012.
Inventors: Frederic Kaye and Amy Coxon (NCI).
Patent Status: U.S. Provisional Application No.61/036,830 filed 13
Mar 2008 (HHS Reference No. E-069-2008/0-US-01).
Licensing Status: Available for exclusive or non-exclusive
licensing.
Licensing Contact: Jennifer Wong; 301-435-4633;
wongje@mail.nih.gov.
Human Perilipin Proteins
Description of Technology: Perilipins are important regulators of
lipid storage in fat cells. These proteins stabilize fat droplets and
control their breakdown by controlling access of lipid-degrading
enzymes. Since these proteins are central to the storage and breakdown
of body fat it very likely that they are crucial for the regulation of
body weight. Perilipin expression is elevated in obese animals and
humans. Mutations in the perilipin gene are associated with increased
risk of obesity in women. Importantly, when the perilipin gene is
inactivated the obesity of model mice is reversed. Therefore, perilipin
could be a good candidate for therapeutic targeting to treat obesity in
humans.
This NIH invention claims DNA sequences of splice variants that
code for human perilipin protein isoforms and methods of expressing the
recombinant protein in bacteria or mammalian cells. It also claims
substantially purified perilipin proteins and methods for detecting
their presence in a biological sample.
Applications:
Drug development for obesity.
Diagnostics for detection of perilipins.
Antigens for antibody production.
Markers for identifying true adipocytes.
Advantages:
Cloned DNA sequences ready for protein expression.
Isoforms allow greater flexibility in designing
therapeutics.
Development Status: Pre-clinical.
Inventors: Constantine Londos, Andrew S. Greenberg, Alan R. Kimmel,
John J. Egan (NIDDK).
Related Publication: AS Greenberg et al. Perilipin, a major
hormonally regulated adipocyte-specific phosphoprotein associated with
the periphery of lipid storage droplets. J Biol Chem. 1991 Jun
15;266(17):11341-11346.
Patent Status:
U.S. Patent No. 6,074,842 issued 13 Jun 2000 (HHS
Reference No. E-111-1991/0-US-03).
U.S. Patent No. 5,585,462 issued 17 Dec 1996 (HHS
Reference No. E-111-1991/1-US-01).
Licensing Status: Available for exclusive or non-exclusive
licensing.
Licensing Contact: Surekha Vathyam, PhD; 301-435-4076;
vathyams@mail.nih.gov.
Dated: September 29, 2008.
Richard U. Rodriguez,
Director, Division of Technology Development and Transfer, Office of
Technology Transfer, National Institutes of Health.
[FR Doc. E8-23436 Filed 10-2-08; 8:45 am]
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