Government-Owned Inventions; Availability for Licensing, 5726-5728 [E7-1931]
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5726
sroberts on PROD1PC70 with NOTICES
Inventors: Martin Wade Brechbiel and
Thomas Clifford (NCI).
Publications:
1. T Clifford et al. Validation of a
novel CHX-A’’ derivative suitable for
peptide conjugation: small animal PET/
CT imaging using yttrium–86–CHX–A’’–
octreotide. J Med Chem. 2006 Jul
13;49(14):4297–4304.
2. HS Chong et al. Synthesis and
evaluation of novel macrocyclic and
acyclic ligands as contrast enhancement
agents for magnetic resonance imaging.
J Med Chem. 2006 Mar 23;49(6):2055–
2062.
Licensing Status: Available for
exclusive or non-exclusive licensing or
collaborative research opportunity.
Patent Status: U.S. Provisional
Application No. 60/603,781 filed 23
Aug 2004 (HHS Reference No. E–317–
2004/1–US–01); International Patent
Application PCT/US2005/028125 filed
09 Aug 2005 (HHS Reference No. E–
317–2004/1–PCT–02).
Licensing Contact: Michael A.
Shmilovich, Esq.; 301/435–5019;
shmilovm@mail.nih.gov.
Dated: January 30, 2007.
Steven M. Ferguson,
Director, Division of Technology Development
and Transfer, Office of Technology Transfer,
National Institutes of Health.
[FR Doc. 07–526 Filed 2–6–07; 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:
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.
Extended Transgene Expression for a
Non-Integrating Adenoviral Vector
Containing Retroviral Elements
Description of Technology: Anthrax
lethal toxin (LeTx) consists of two
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components: The protective antigen
(PrAg) and the lethal factor (LF). PrAg
binds to the cell surface where it is
activated by furin protease, followed by
the formation of a PrAg heptamer. LF is
then translocated into the cytosol of a
cell via this heptamer, where it acts as
a metalloprotease on all but one
mitogen-activated protein kinase kinase
(MAPKK). Approximately 70% of
human melanomas contain a mutation
(B–RAF V600E) that constitutively
activates a MAPKK pathway, and LeTx
has been shown to have significant
toxicity towards cells which have this
mutation. This suggested a potential use
for LeTx in cancer therapy.
Unfortunately, native LeTx is toxic to
normal cells, detracting from its in vivo
applicability.
PrAg has been engineered to be
activated by a matrix metalloprotease
(MMP), instead of by furin protease.
Because MMPs are highly expressed in
tumor cells, this modification increases
selectivity towards cancer cells.
Surprisingly, mouse data shows that the
modified LeTx (denoted PrAg-L1/LF) is
less cytotoxic to ‘‘normal’’ cells in vivo,
when compared to wild-type LeTx.
Significantly, PrAg-L1/LF maintained
its high toxicity toward human tumors
in mouse xenograft models of human
tumors, including melanomas. However,
this toxicity applied not only to tumors
having mutations that constitutively
activate MAPKKs, but also to other
tumor types such as lung and colon
carcinomas. The absence of toxicity to
‘‘normal’’ cells coupled to its
effectiveness on a wide range of cancer
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Federal Register / Vol. 72, No. 25 / Wednesday, February 7, 2007 / Notices
Federal Register / Vol. 72, No. 25 / Wednesday, February 7, 2007 / Notices
cell types suggests that PrAg-L1/LF may
represent a novel cancer therapeutic.
Applications: PrAg-L1/LF has
applications as a human cancer
therapeutic; Applicability extends
beyond melanomas, including lung and
colon carcinomas.
Market: The worldwide market for
melanoma therapeutics is
approximately $437M, and is predicted
to reach $680M by the year 2009.
Approximately 2.4 million people are
afflicted with melanoma, with around
150,000 new cases each year.
Demonstration of effectiveness in vivo
for lung and colon carcinomas will
increase the market for this technology.
Development Status: The technology
is at the preclinical stage.
Inventors: Stephen H. Leppla (NIAID),
Shi-hui Liu (NIAID), Thomas H. Bugge
(NIDCR), John R. Basile (NIDCR), Brooke
Currie (NIDCR).
Related Publications:
1. S Liu et al. Intermolecular
complementation achieves highspecificity tumor targeting by anthrax
toxin. Nat Biotechnol. 2005
Jun;23(6):725–730.
2. RJ Abi-Habib et al. A urokinaseactivated recombinant anthrax toxin is
selectively cytotoxic to many human
tumor cell types. Mol Cancer Ther. 2006
Oct;5(10):2556–2562.
Patent Status: U.S. Provisional
Application No. 60/870,050 filed 14 Dec
2006 (HHS Reference E–070–2007/0–
US–01).
Licensing Status: Available for
exclusive or non-exclusive licensing.
Licensing Contact: David A.
Lambertson, Ph.D.; 301/435–4632;
lambertsond@od.nih.gov.
Collaborative Research Opportunity:
The NIAID Laboratory of Bacterial
Diseases is seeking statements of
capability or interest from parties
interested in collaborative research to
further develop, evaluate, or
commercialize PrAg-L1/LF as a novel
cancer therapeutic. Please contact
Stephen H. Leppla, Ph.D. at 301/594–
2865 and/or sleppla@niaid.nih.gov for
more information.
sroberts on PROD1PC70 with NOTICES
A Novel Combination of CXCR–4
Antagonist T22 With Conventional
Immunotherapy Improves Treatment
Efficacy in Established Tumors
Description of Technology:
Immunotherapy for cancer rarely results
in complete responses, possibly due to
chemokine receptor mediated activation
of prosurvival pathways in cancer cells.
CXCR4, is one such receptor that is
expressed in a variety of cancers,
including melanoma. Inhibiting these
chemokine receptors may circumvent
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Jkt 211001
the ability of cancer to protect
themselves from immunological attack.
This invention provides a method of
treating cancers that expresses the
chemokine receptor CXCR4 by a novel
combination therapeutic approach.
More specifically, the invention claims
methods and compositions for the
improved treatment of metastatic
tumors by using a CXCR4 antagonist in
conjunction with conventional
monoclonal antibody based
immunotherapy (e.g., anti-CTLA4 mAb)
or immunostimulatory
chemotherapeutics (e.g.,
cyclophosphamide). The invention
clearly demonstrates that treatment of in
vivo experimental lung cancer models
with T22, a CXCR4 antagonist, followed
by anti-Cytotoxic lymphocyte antigen
(CTLA)-4 monoclonal antibody (or
cyclophosphamide) treatment
synergistically reduced the total tumor
burden compared with the reduction of
tumor burden when either agent is used
alone. T22 treatment alone is not
cytotoxic and has no demonstrated
ability to increase non-specific host
autoimmunity when used in
combination with anti-CTLA4 mAb or
cyclophosphamide. This invention has
significant potential as a new, effective
combination immunotherapy.
Applications and Modality: (1) A new
method of combination therapy for
cancer based on immunotherapeutics,
including adoptive transfer of antitumor lymphocytes and treatment with
immunostimulatory agents (monoclonal
antibodies or chemotherapy); (2) A new
therapeutic method for the treatment of
CXCR4 chemokine receptor expressing
cancers; (3) A new therapeutic method
exploiting the role of chemokine
receptor CXCR4 that potentially renders
immunotherapy more effective without
further increasing risks of patient
autoimmunity.
Market: Chemokine receptor CXCR4
has a proven role in cancer metastasis
in several cancers. The anti-cancer
market is projected to reach sales of $60
billion by 2010.
Development Status: The technology
is currently in the pre-clinical stage of
development. Animal data is available.
Inventor: Sam T. Hwang (NCI).
Publications:
1. CH Lee et al. Sensitization of B16
tumor cells with a CXCR4 antagonist
increases the efficacy of immunotherapy
for established lung metastases. Mol
Cancer Ther. 2006 Oct;5(10):2592–2599.
2. T Kakinuma and ST Hwang.
Chemokines, chemokine receptors, and
cancer metastasis. J Leukoc Biol. 2006
Apr;79(4): 639–651.
3. T Murakami et al. Expression of
CXC chemokine receptor-4 enhances the
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5727
pulmonary metastatic potential of
murine B16 melanoma cells. Cancer
Res. 2002 Dec 15;62(24):7328–7334.
Patent Status: U.S. Provisional
Application No. 60/840,216 filed 25
Aug 2006, entitled ‘‘Combination
Therapy for the Treatment of Cancer’’
(HHS Reference No. E–267–2006/0–US–
01).
Licensing Status: Available for
exclusive and non-exclusive licensing.
Licensing Contact: John Stansberry,
Ph.D.; 301/435–5236;
stansbej@mail.nih.gov.
Lentivirus Based Vector System for
Gene Therapy Delivery
Description of Technology: Gene
therapy is a technique based on the idea
that a genetic disorder can be treated by
replacing a dysfunctional gene with a
functional copy of that gene. Currently,
retroviral vectors and adenoviral vectors
are most frequently used for gene
therapy clinical trials. Retroviral vectors
provide long term gene expression and
are capable of transferring genes into
non-dividing cells, unlike their
adenoviral counterparts. However,
retroviral vectors often suffer from weak
viral titers and inefficient encapsidation
of the therapeutic gene, detracting from
their therapeutic value. Thus, there is a
need in the art for improved retroviral
gene therapy vectors.
This technology family is directed to
a retroviral vector system comprising a
packaging vector and a transfer vector,
and a method of using the vectors for
gene therapy. The packaging vector is
the result of an HIV-2 lentiviral vector
containing mutations in sequences
surrounding a splice donor site within
the packaging signal. The transfer vector
comprises mutations that render a splice
donor site non-functional. These
mutations increase the viral titer and
expression/encapsidation of the
transgene, but without a corresponding
increase in the packaging of viral RNA.
Thus, these vectors may address some of
the pressing concerns with current gene
therapy vectors systems.
Applications: Improved lentivirus
based vector system with practical
application in gene therapy/gene
transfer; Two vector system minimizes
possibility of HIV infection; Packaging
vector is a result of HIV-2 Lentivirus
vector; Improved packaging and
expression ability addresses current low
viral titer problem.
Market: The only gene therapy
product currently in the market was
approved in China in 2004; The R&D
market of gene therapy is projected to
grow to several billion dollars in the
next 5 years.
E:\FR\FM\07FEN1.SGM
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Federal Register / Vol. 72, No. 25 / Wednesday, February 7, 2007 / Notices
Inventors: Larry Kwak (NCI) and Arya
Biragyn (NIA).
Patent Status: U.S. Patent No.
6,562,347 issued 13 May 2003 (HHS
Reference No. E–107–1998–0-US–03).
Licensing Status: Available for
exclusive and non-exclusive licensing.
Licensing Contact: Jennifer Wong;
301/435–4633; wongje@mail.nih.gov.
Methods and Compositions of
Chemokine-Tumor Antigen Fusion
Proteins as Cancer Vaccines
sroberts on PROD1PC70 with NOTICES
Development Status: The technology
is currently in the pre-clinical stage of
development.
Inventors: Suresh K. Arya (NCI).
Publication: SK Arya et al. Human
immunodeficiency virus type 2
lentivirus vectors for gene transfer:
expression and potential for helper
virus-free packaging. Hum Gene Ther.
1998 Jun 10;9(9):1371–1380.
Patent Status: U.S. Patent No.
6,790,657 issued 14 Sep 2004, entitled
‘‘Lentivirus Vector System’’ (HHS
Reference No. E–231–1998/0-US–03);
U.S. Patent Application No. 10/731,988
filed 09 Dec 2003, now allowed, entitled
‘‘Lentivirus Vector System’’ (HHS
Reference No. E–231–1998/0-US–04).
Licensing Status: Available for
exclusive or non-exclusive licensing.
Licensing Contact: David Lambertson,
Ph.D.; 301/435–4632;
lambertsond@od.nih.gov.
National Cancer Institute; Notice of
Meeting
Description of Technology: Tumor
cells are known to express tumor
specific antigens on the cell surface.
These antigens are believed to be poorly
immunogenic, largely because they
represent gene products of oncogenes or
other cellular genes which are normally
present in the host. As a result, poor
immunogenicity of relevant cancer
antigens has proven to be a major
obstacle to successful immunotherapy
with tumor vaccines. Thus, there is a
need for a more potent vaccine to elicit
an immune response effective in the
treatment or prevention of cancer.
The current invention embodies a
fusion protein comprising of a
chemokine and tumor antigen. The
inventors reported in several peerreviewed manuscripts that these fusion
proteins represent potential vaccines for
use against cancer. More specifically,
the inventors have developed a vaccine
construct that expresses fusion protein
comprising human monocyte
chemotactic protein-3 fused with tumor
antigens, such as lymphoma-derived Id
or breast cancer Muc-1. Administration
of the fusion protein, or a nucleic acid
encoding the fusion protein, elicits a
specific immune response directed
against the tumor antigen or protein,
thereby inhibiting the growth of cells
expressing this antigen or protein.
Applications and Modality: Potential
immunotherapy for cancer.
Market: 600,000 deaths from cancer
related diseases estimated in 2006.
Development Status: This technology
is currently in the pre-clinical stage of
development.
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Dated: January 31, 2007.
Steven M. Ferguson,
Director, Division of Technology Development
and Transfer, Office of Technology Transfer,
National Institutes of Health.
[FR Doc. E7–1931 Filed 2–6–07; 8:45 am]
BILLING CODE 4140–01–P
DEPARTMENT OF HEALTH AND
HUMAN SERVICES
National Institutes of Health
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 Board of
Scientific Advisors.
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.
Name of Committee: National Cancer
Institute Board of Scientific Advisors.
Date: March 5–6, 2007.
Time: March 5, 2007, 8 a.m. to 6 p.m.
Agenda: Director’s Report: Ongoing and
New Business; Reports of Program Review
Group(s); and Budget Presentation; Reports of
Special Initiatives; RFA and RFP Concept
Reviews; and Scientific Presentations.
Place: National Institutes of Health,
Building 31, 31 Center Drive, Conference
Room 10, Bethesda, MD 20892.
Time: March 6, 2007, 8 a.m. to 1 p.m.
Agenda: Reports of Special Initiatives; RFA
and RFP Concept Reviews; and Scientific
Presentations.
Place: National Institutes of Health,
Building 31, 31 Center Drive, Conference
Room 10, Bethesda, MD 20892.
Contact Person: Paulette S. Gray, PhD,
Executive Secretary, Director, Division of
Extramural Activities, National Cancer
Institute, National Institutes of Health, 6116
Executive Boulevard, 8th Floor, Rm. 8001,
Bethesda, MD 20892, 301–496–5147,
grayp@mail.nih.gov.
Any interested person may file written
comments with the committee by forwarding
the statement to the Contact Person listed on
this notice. The statement should include the
name, address, telephone number and when
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applicable, the business or professional
affiliation of the interested person.
In the interest of security, NIH as instituted
stringent procedures for entrance onto the
NIH campus. All visitor vehicles, including
taxicabs, hotel, and airport shuttles will be
inspected before being allowed on campus.
Visitors will be asked to show one form of
identification (for example, a governmentissued photo ID, driver’s license, or passport)
and to state the purpose of their visit.
Information is also available on the
Institute’s/Center’s home page:
deainfo.nci.nih.gov/advisory/bsa.htm, where
an agenda and any additional information for
the meeting will be posted when available.
(Catalogue of Federal Domestic Assistance
Program Nos. 93.392, Cancer Construction;
93.393, Cancer Cause and Prevention
Research; 93.394, Cancer Detection and
Diagnosis Research; 93.395, Cancer
Treatment Research; 93.396, Cancer Biology
Research; 93.397, Cancer Centers Support;
93.398, Cancer Research Manpower; 93.399,
Cancer Control, National Institutes of Health,
HHS)
Dated: January 31, 2007.
Anna Snouffer,
Acting Director, Office of Federal Advisory
Committee Policy.
[FR Doc. 07–519 Filed 2–6–07; 8:45 am]
BILLING CODE 4140–01–M
DEPARTMENT OF HEALTH AND
HUMAN SERVICES
National Institutes of Health
National Heart, Lung, and Blood
Institute; Notice of Closed Meetings
Pursuant to section 10(d) of the
Federal Advisory Committee Act, as
amended (5 U.S.C. Appendix 2), notice
is hereby given of the following
meetings.
The meetings will be closed to the
public in accordance with the
provisions set forth in sections
552b(c)(4) and 552b(c)(6), Title 5 U.S.C.,
as amended. The grant applications and
the discussions could disclose
confidential trade secrets or commercial
property such as patentable material,
and personal information concerning
individuals associated with the grant
applications, the disclosure of which
would constitute a clearly unwarranted
invasion of personal privacy.
Name of Committee: National Heart, Lung,
and Blood Institute Special Emphasis Panel,
Research Project in Cardiothoracic Surgery.
Date: March 7–8, 2007.
Time: 8 a.m. to 5 p.m.
Agenda: To review and evaluate grant
applications.
Place: Holiday Inn Georgetown, 2101
Wisconsin Avenue, NW., Washington, DC
20007.
Contact Person: Shelly S. Sehnert, PhD.,
Scientific Review Administrator, Review
E:\FR\FM\07FEN1.SGM
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]]>Agencies
[Federal Register Volume 72, Number 25 (Wednesday, February 7, 2007)]
[Notices]
[Pages 5726-5728]
From the Federal Register Online via the Government Printing Office [www.gpo.gov]
[FR Doc No: E7-1931]
-----------------------------------------------------------------------
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.
Extended Transgene Expression for a Non-Integrating Adenoviral Vector
Containing Retroviral Elements
Description of Technology: Anthrax lethal toxin (LeTx) consists of
two components: The protective antigen (PrAg) and the lethal factor
(LF). PrAg binds to the cell surface where it is activated by furin
protease, followed by the formation of a PrAg heptamer. LF is then
translocated into the cytosol of a cell via this heptamer, where it
acts as a metalloprotease on all but one mitogen-activated protein
kinase kinase (MAPKK). Approximately 70% of human melanomas contain a
mutation (B-RAF V600E) that constitutively activates a MAPKK pathway,
and LeTx has been shown to have significant toxicity towards cells
which have this mutation. This suggested a potential use for LeTx in
cancer therapy. Unfortunately, native LeTx is toxic to normal cells,
detracting from its in vivo applicability.
PrAg has been engineered to be activated by a matrix
metalloprotease (MMP), instead of by furin protease. Because MMPs are
highly expressed in tumor cells, this modification increases
selectivity towards cancer cells. Surprisingly, mouse data shows that
the modified LeTx (denoted PrAg-L1/LF) is less cytotoxic to ``normal''
cells in vivo, when compared to wild-type LeTx. Significantly, PrAg-L1/
LF maintained its high toxicity toward human tumors in mouse xenograft
models of human tumors, including melanomas. However, this toxicity
applied not only to tumors having mutations that constitutively
activate MAPKKs, but also to other tumor types such as lung and colon
carcinomas. The absence of toxicity to ``normal'' cells coupled to its
effectiveness on a wide range of cancer
[[Page 5727]]
cell types suggests that PrAg-L1/LF may represent a novel cancer
therapeutic.
Applications: PrAg-L1/LF has applications as a human cancer
therapeutic; Applicability extends beyond melanomas, including lung and
colon carcinomas.
Market: The worldwide market for melanoma therapeutics is
approximately $437M, and is predicted to reach $680M by the year 2009.
Approximately 2.4 million people are afflicted with melanoma, with
around 150,000 new cases each year. Demonstration of effectiveness in
vivo for lung and colon carcinomas will increase the market for this
technology.
Development Status: The technology is at the preclinical stage.
Inventors: Stephen H. Leppla (NIAID), Shi-hui Liu (NIAID), Thomas
H. Bugge (NIDCR), John R. Basile (NIDCR), Brooke Currie (NIDCR).
Related Publications:
1. S Liu et al. Intermolecular complementation achieves high-
specificity tumor targeting by anthrax toxin. Nat Biotechnol. 2005
Jun;23(6):725-730.
2. RJ Abi-Habib et al. A urokinase-activated recombinant anthrax
toxin is selectively cytotoxic to many human tumor cell types. Mol
Cancer Ther. 2006 Oct;5(10):2556-2562.
Patent Status: U.S. Provisional Application No. 60/870,050 filed 14
Dec 2006 (HHS Reference E-070-2007/0-US-01).
Licensing Status: Available for exclusive or non-exclusive
licensing.
Licensing Contact: David A. Lambertson, Ph.D.; 301/435-4632;
lambertsond@od.nih.gov.
Collaborative Research Opportunity: The NIAID Laboratory of
Bacterial Diseases is seeking statements of capability or interest from
parties interested in collaborative research to further develop,
evaluate, or commercialize PrAg-L1/LF as a novel cancer therapeutic.
Please contact Stephen H. Leppla, Ph.D. at 301/594-2865 and/or
sleppla@niaid.nih.gov for more information.
A Novel Combination of CXCR-4 Antagonist T22 With Conventional
Immunotherapy Improves Treatment Efficacy in Established Tumors
Description of Technology: Immunotherapy for cancer rarely results
in complete responses, possibly due to chemokine receptor mediated
activation of prosurvival pathways in cancer cells. CXCR4, is one such
receptor that is expressed in a variety of cancers, including melanoma.
Inhibiting these chemokine receptors may circumvent the ability of
cancer to protect themselves from immunological attack.
This invention provides a method of treating cancers that expresses
the chemokine receptor CXCR4 by a novel combination therapeutic
approach. More specifically, the invention claims methods and
compositions for the improved treatment of metastatic tumors by using a
CXCR4 antagonist in conjunction with conventional monoclonal antibody
based immunotherapy (e.g., anti-CTLA4 mAb) or immunostimulatory
chemotherapeutics (e.g., cyclophosphamide). The invention clearly
demonstrates that treatment of in vivo experimental lung cancer models
with T22, a CXCR4 antagonist, followed by anti-Cytotoxic lymphocyte
antigen (CTLA)-4 monoclonal antibody (or cyclophosphamide) treatment
synergistically reduced the total tumor burden compared with the
reduction of tumor burden when either agent is used alone. T22
treatment alone is not cytotoxic and has no demonstrated ability to
increase non-specific host autoimmunity when used in combination with
anti-CTLA4 mAb or cyclophosphamide. This invention has significant
potential as a new, effective combination immunotherapy.
Applications and Modality: (1) A new method of combination therapy
for cancer based on immunotherapeutics, including adoptive transfer of
anti-tumor lymphocytes and treatment with immunostimulatory agents
(monoclonal antibodies or chemotherapy); (2) A new therapeutic method
for the treatment of CXCR4 chemokine receptor expressing cancers; (3) A
new therapeutic method exploiting the role of chemokine receptor CXCR4
that potentially renders immunotherapy more effective without further
increasing risks of patient autoimmunity.
Market: Chemokine receptor CXCR4 has a proven role in cancer
metastasis in several cancers. The anti-cancer market is projected to
reach sales of $60 billion by 2010.
Development Status: The technology is currently in the pre-clinical
stage of development. Animal data is available.
Inventor: Sam T. Hwang (NCI).
Publications:
1. CH Lee et al. Sensitization of B16 tumor cells with a CXCR4
antagonist increases the efficacy of immunotherapy for established lung
metastases. Mol Cancer Ther. 2006 Oct;5(10):2592-2599.
2. T Kakinuma and ST Hwang. Chemokines, chemokine receptors, and
cancer metastasis. J Leukoc Biol. 2006 Apr;79(4): 639-651.
3. T Murakami et al. Expression of CXC chemokine receptor-4
enhances the pulmonary metastatic potential of murine B16 melanoma
cells. Cancer Res. 2002 Dec 15;62(24):7328-7334.
Patent Status: U.S. Provisional Application No. 60/840,216 filed 25
Aug 2006, entitled ``Combination Therapy for the Treatment of Cancer''
(HHS Reference No. E-267-2006/0-US-01).
Licensing Status: Available for exclusive and non-exclusive
licensing.
Licensing Contact: John Stansberry, Ph.D.; 301/435-5236;
stansbej@mail.nih.gov.
Lentivirus Based Vector System for Gene Therapy Delivery
Description of Technology: Gene therapy is a technique based on the
idea that a genetic disorder can be treated by replacing a
dysfunctional gene with a functional copy of that gene. Currently,
retroviral vectors and adenoviral vectors are most frequently used for
gene therapy clinical trials. Retroviral vectors provide long term gene
expression and are capable of transferring genes into non-dividing
cells, unlike their adenoviral counterparts. However, retroviral
vectors often suffer from weak viral titers and inefficient
encapsidation of the therapeutic gene, detracting from their
therapeutic value. Thus, there is a need in the art for improved
retroviral gene therapy vectors.
This technology family is directed to a retroviral vector system
comprising a packaging vector and a transfer vector, and a method of
using the vectors for gene therapy. The packaging vector is the result
of an HIV-2 lentiviral vector containing mutations in sequences
surrounding a splice donor site within the packaging signal. The
transfer vector comprises mutations that render a splice donor site
non-functional. These mutations increase the viral titer and
expression/encapsidation of the transgene, but without a corresponding
increase in the packaging of viral RNA. Thus, these vectors may address
some of the pressing concerns with current gene therapy vectors
systems.
Applications: Improved lentivirus based vector system with
practical application in gene therapy/gene transfer; Two vector system
minimizes possibility of HIV infection; Packaging vector is a result of
HIV-2 Lentivirus vector; Improved packaging and expression ability
addresses current low viral titer problem.
Market: The only gene therapy product currently in the market was
approved in China in 2004; The R&D market of gene therapy is projected
to grow to several billion dollars in the next 5 years.
[[Page 5728]]
Development Status: The technology is currently in the pre-clinical
stage of development.
Inventors: Suresh K. Arya (NCI).
Publication: SK Arya et al. Human immunodeficiency virus type 2
lentivirus vectors for gene transfer: expression and potential for
helper virus-free packaging. Hum Gene Ther. 1998 Jun 10;9(9):1371-1380.
Patent Status: U.S. Patent No. 6,790,657 issued 14 Sep 2004,
entitled ``Lentivirus Vector System'' (HHS Reference No. E-231-1998/0-
US-03); U.S. Patent Application No. 10/731,988 filed 09 Dec 2003, now
allowed, entitled ``Lentivirus Vector System'' (HHS Reference No. E-
231-1998/0-US-04).
Licensing Status: Available for exclusive or non-exclusive
licensing.
Licensing Contact: David Lambertson, Ph.D.; 301/435-4632;
lambertsond@od.nih.gov.
Methods and Compositions of Chemokine-Tumor Antigen Fusion Proteins as
Cancer Vaccines
Description of Technology: Tumor cells are known to express tumor
specific antigens on the cell surface. These antigens are believed to
be poorly immunogenic, largely because they represent gene products of
oncogenes or other cellular genes which are normally present in the
host. As a result, poor immunogenicity of relevant cancer antigens has
proven to be a major obstacle to successful immunotherapy with tumor
vaccines. Thus, there is a need for a more potent vaccine to elicit an
immune response effective in the treatment or prevention of cancer.
The current invention embodies a fusion protein comprising of a
chemokine and tumor antigen. The inventors reported in several peer-
reviewed manuscripts that these fusion proteins represent potential
vaccines for use against cancer. More specifically, the inventors have
developed a vaccine construct that expresses fusion protein comprising
human monocyte chemotactic protein-3 fused with tumor antigens, such as
lymphoma-derived Id or breast cancer Muc-1. Administration of the
fusion protein, or a nucleic acid encoding the fusion protein, elicits
a specific immune response directed against the tumor antigen or
protein, thereby inhibiting the growth of cells expressing this antigen
or protein.
Applications and Modality: Potential immunotherapy for cancer.
Market: 600,000 deaths from cancer related diseases estimated in
2006.
Development Status: This technology is currently in the pre-
clinical stage of development.
Inventors: Larry Kwak (NCI) and Arya Biragyn (NIA).
Patent Status: U.S. Patent No. 6,562,347 issued 13 May 2003 (HHS
Reference No. E-107-1998-0-US-03).
Licensing Status: Available for exclusive and non-exclusive
licensing.
Licensing Contact: Jennifer Wong; 301/435-4633;
wongje@mail.nih.gov.
Dated: January 31, 2007.
Steven M. Ferguson,
Director, Division of Technology Development and Transfer, Office of
Technology Transfer, National Institutes of Health.
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