Government-Owned Inventions; Availability for Licensing, 37554-37556 [2013-14821]
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Federal Register / Vol. 78, No. 120 / Friday, June 21, 2013 / Notices
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Dated: June 14, 2013.
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Coordination.
[FR Doc. 2013–14837 Filed 6–20–13; 8:45 am]
BILLING CODE 4165–15–P
DEPARTMENT OF HEALTH AND
HUMAN SERVICES
National Institutes of Health
Government-Owned Inventions;
Availability for Licensing
AGENCY:
National Institutes of Health,
HHS.
ACTION:
Notice.
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.
SUMMARY:
TKELLEY on DSK3SPTVN1PROD with NOTICES
FOR FURTHER INFORMATION CONTACT:
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.
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GPR116 Knockout and Conditional
Knockout Mice
Description of Technology:
Pulmonary surfactant plays a critical
role in preventing alveolar collapse by
decreasing surface tension at the
alveolar air-liquid interface. Surfactant
deficiency contributes to the
pathogenesis of acute lung injury (ALI)
and acute respiratory distress syndrome
(ARDS), common disorders that can
afflict patients of all ages and carry a
mortality rate greater than 25%. Excess
surfactant leads to pulmonary alveolar
proteinosis. The NCI investigators
created a G-protein coupled receptor
GPR116 mutant mouse model and
showed that GPR116 plays a previously
unexpected, essential role in
maintaining normal surfactant levels in
the lung.
The mouse model could aid in the
development of drug screens to identify
agents that can modulate surfactant
levels. Alveolar type II cells have also
been isolated from the GPR116 wildtype
and knockout mice that could be
directly used in such assays. The
identification of surfactant modulating
agents could be important to a number
of lung surfactant disorders.
Potential Commercial Applications:
Research materials to study lung
surfactant homeostasis and disorders.
Competitive Advantages: Not
available elsewhere.
Development Stage:
• Prototype.
• Pre-clinical.
• In vitro data available.
• In vivo data available (animal).
Inventors: Bradley Dean St. Croix and
Mi Young Yang (NCI).
Publication: Yang MY, et al. Essential
Regulation of Lung Surfactant
Homeostasis by the Orphan G ProteinCoupled Receptor GPR116. Cell Rep.
2013 May 30;3(5):1457–64. [PMID
23684610]
Intellectual Property: HHS Reference
No. E–269–2012/0—Research Tool.
Patent prosecution is not being pursued
for this technology.
Licensing Contact: Betty B. Tong,
Ph.D.; 301–594–6565;
tongb@mail.nih.gov.
Collaborative Research Opportunity:
The Center for Cancer Research Mouse
Cancer Genetics Program is seeking
statements of capability or interest from
parties interested in collaborative
research to further develop, evaluate or
commercialize GPR116 Knockout and
Conditional Knockout Mice. For
collaboration opportunities, please
contact John Hewes, Ph.D. at
hewesj@mail.nih.gov.
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Engineered Anthrax Toxin Variants
That Target Cancer
Description of Technology: This
technology describes the use of novel
mutated anthrax protective antigen (PA)
protein variants to target tumor cells
and tumor vasculature. NIH scientists
have engineered two PA variants that
selectively complement one another and
combine to form active octamers that
target tumor cells. This controlled
oligomeric activation of the PA proteins
makes the likelihood of toxicity to nontumor cells very low since non-tumor
tissue does not express certain cellsurface proteases required to activate
the PA variants. Using proteases that are
highly expressed in tumor cells, e.g.,
matrix metalloproteases (MMP) and
urokinase plasminogen activator (uPA),
the scientists have shown significant
tumor growth suppression with the
oligomer in a mouse model.
Furthermore, other tumor-specific
proteases could also be used to control
formation of the targeted octameric
anthrax toxin structures. Moreover, the
structures can be expanded to include
several PA variants. In summary, this
technology provides a unique,
expandable platform that reduces
toxicity to normal tissues compared to
other systems and can be used to treat
cancers more effectively.
Potential Commercial Applications:
Therapeutic treatment for solid tumors,
cancers, and infectious diseases.
Competitive Advantages:
• Specificity in targeting tumors
while eliminating side effects associated
with non-specific targeting of normal
cells.
• Method can be expanded to include
different proteases and up to eight PA
variants.
Development Stage:
• Pre-clinical.
• In vitro data available.
• In vivo data available (animal).
Inventors: Clinton E. Leysath, Stephen
H. Leppla, Damilola D. Phillips (NIAID).
Publication: Phillips DD, et al.
Engineering anthrax toxin variants that
exclusively form octamers and their
application to targeting tumors. J Biol
Chem. 2013 Mar 29;288(13):9058–65.
[PMID 23393143]
Intellectual Property: HHS Reference
No. E–246–2012/0—U.S. Provisional
Application No. 61/692,143 filed 22
Aug 2012.
Related Technologies:
• HHS Reference No. E–293–1999—
Mutated Anthrax Toxin Protective
Antigen Proteins That Specifically
Target Cells Containing High Amounts
of Cell-Surface Metalloproteinases or
Plasminogen Activator Receptors
(Leppla/NIAID).
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Federal Register / Vol. 78, No. 120 / Friday, June 21, 2013 / Notices
• HHS Reference No. E–070–2007—
Human Cancer Therapy Using
Engineered Metalloproteinase-Activated
Anthrax Lethal Toxin That Target
Tumor Vasculature (Leppla/NIAID).
• HHS Reference No. E–059–2004—
Multimeric Protein Toxins to Target
Cells Having Multiple Identifying
Characteristics (Leppla/NIAID).
Licensing Contact: Whitney Hastings;
301–451–7337; hastingw@mail.nih.gov.
TKELLEY on DSK3SPTVN1PROD with NOTICES
Intra-Bone Drug Delivery Device and
Method
Description of Technology: The
invention pertains to devices for
directly infusing cellular therapeutics
into patient bone. The device monitors
intra-bone pressure using pressure
sensors disposed at its proximal end
and adjusts infusion pressures during
infusion such that intra-bone pressure
does not exceed levels of systemic blood
pressure. Such devices, apparatus and
methods are particularly suitable for use
in performing bone marrow transplants,
particularly transplants that utilize cord
blood as a stem cell source.
Potential Commercial Applications:
Drug delivery to bones.
Competitive Advantages:
• Therapeutic uptake efficiency.
• Drug delivery efficiency.
• Target specificity.
Development Stage:
• Prototype.
• In vitro data available.
Inventors: Robert Hoyt (NHLBI),
Jeremy Pantin (NHLBI), Timothy Hunt
(NHLBI), Randall Clevenger (NHLBI),
Omer Aras (NIHCC), Richard Childs
(NHLBI), Peter Choyke (NCI).
Publication: Pantin JM, et al.
‘‘Optimization of an Intra-Bone
Hematopoietic Stem Cell Delivery
Technique in a Swine Model.’’ Poster
abstract presented at the 54th ASH
Annual Meeting and Exposition,
Atlanta, Georgia, December 8–11, 2012.
[https://ash.confex.com/ash/2012/
webprogram/Paper53150.html]
Intellectual Property: HHS Reference
No. E–165–2012/0—U.S. Provisional
Patent Application No. 61/771,463 filed
01 Mar 2013.
Related Technology: HHS Reference
No. E–196–1998/2—U.S. Patent No.
8,409,166 issued 02 Apr 2013.
Licensing Contact: Michael
Shmilovich; 301–435–5019;
shmilovm@mail.nih.gov.
Collaborative Research Opportunity:
The National Heart, Lung, and Blood
Institute is seeking statements of
capability or interest from parties
interested in collaborative research to
further develop, evaluate or
commercialize Intra-bone Drug Delivery
Device and Method. For collaboration
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opportunities, please contact Denise
Crooks at crooksd@nhlbi.nih.gov.
Method of Inducing Pluripotent or
Multipotent Stem Cells by Blocking
CD47 Receptor Signaling
Description of Technology: NIH
researchers have discovered that
blockade of the signaling activity of a
single cell-surface receptor, CD47,
without transfection or introduction of
potentially transforming viral vectors,
results in high frequency, spontaneous
generation of self-renewing cells with a
high proliferative capacity. Induced
pluripotent stem cells (iPS cells) are
currently produced by transforming
cells with viral or other constitutive
expression vectors encoding four stem
cell transcription factors (c-Myc, Sox2,
Klf4, and Oct4), but this method
presents challenges such as overexpression of c-Myc, which can result in
malignant transformation. The present
invention relates to a method of using
CD47-modulating compounds to induce
multipotent stem cells without the
concomitant risk of malignant
transformation and without requiring
the use of feeder cells. The cellular
phenotypes are associated with
increased expression of the hallmark
stem cell-inducing transcription factors,
c-Myc, Sox2, Klf4, and Oct4. The
current invention builds on the NIH’s
previous discoveries of antibodies,
antisense morpholino oligonucleotides,
peptide compounds and other small
molecules that modulate CD47.
Potential Commercial Applications:
Regenerative medicine and stem cell
therapy.
Competitive Advantages:
• Does not require use of viral
vectors.
• Eliminates risk of malignant
transformation for clinical applications.
• Eliminates need for feeder cells.
• Allows generation and maintenance
of a ready supply of iPS cells using a
single defined agent.
• Avoids loss of differentiated
phenotype associated with telomerase
or T antigen transfection.
Development Stage:
• In vitro data available.
• In vivo data available (animal).
Inventors: David D. Roberts, Sukhbir
Kaur, Jeff S. Isenberg (NCI)
Publications:
1. Kaur S, et al. Thrombospondin-1
signaling through CD47 inhibits selfrenewal by regulating c-Myc and other
stem cell transcription factors. Sci Rep.
2013;3:1673. [PMID 23591719]
2. NCI News Note: A drug target that
stimulates development of healthy stem
cells. 2013 Apr 17. [https://
www.cancer.gov/newscenter/
newsfromnci/2013/cd47stemcell]
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Intellectual Property:
• HHS Reference No. E–086–2012/
0—U.S. Application No. 61/621,994
filed 09 Apr 2012.
• HHS Reference No. E–086–2012/
1—U.S. Application No. 61/735,701
filed 11 Dec 2012.
• HHS Reference No. E–086–2012/
2—International Application PCT/
US2013/035838 filed 09 Apr 2013.
Related Technologies: HHS Reference
No. E–227–2006/5—
• U.S. Application No. 12/444,364
filed 3 Apr 09.
• CA Application No. 2,665,287 filed
5 Oct 07.
• EP Application No. 07868382.8
filed 27 Mar 09.
• U.S. Application No. 13/546,941
filed 11 Jul 12.
Licensing Contact: Charlene Sydnor,
Ph.D.; 301–435–4689;
sydnorc@mail.nih.gov.
Collaborative Research Opportunity:
The National Cancer Institute, Center for
Cancer Research, Laboratory of
Pathology, is seeking statements of
capability or interest from parties
interested in collaborative research to
further develop, evaluate or
commercialize CD47 modulators for
regenerative medicine and stem cell
therapy applications. For collaboration
opportunities, please contact John
Hewes, Ph.D. at hewesj@mail.nih.gov.
Human Monoclonal Antibodies to
Glypican-3 Protein and Heparan
Sulfate for Treatment of Cancer
Description of Technology:
Hepatocellular carcinoma (HCC) is the
most common form of liver cancer, and
is among the more deadly cancers in the
world due to its late detection and poor
prognosis. No effective treatment is
available for liver cancer therapy.
Glypican-3 (GPC3) is a cell surface
protein that is preferentially expressed
on HCC cells, making it an attractive
potential target for developing a
therapeutic. This invention concerns
human monoclonal antibodies against
GPC3 and their use for the treatment of
GPC3-expressing cancers such as HCC.
Specifically, the inventors have
generated two distinct human
monoclonal antibodies to GPC3. The
first antibody (HN3) binds to a
conformational epitope on the cell
surface domain of GPC3. The second
antibody (HS20) binds specifically to
heparan sulfate chains on GPC3. These
antibodies can inhibit the growth of
HCC cells, thereby decreasing the ability
of tumors to grow and metastasize.
Furthermore, by using the antibodies to
target a toxic moiety to only those cells
that express GPC3, cancer cells can be
eliminated while allowing healthy,
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TKELLEY on DSK3SPTVN1PROD with NOTICES
37556
Federal Register / Vol. 78, No. 120 / Friday, June 21, 2013 / Notices
essential cells to remain unharmed.
Thus, monoclonal antibodies to GPC3
(and corresponding immunotoxins)
represent a novel therapeutic candidate
for treatment of HCC, as well as other
cancers associated with the differential
expression of GPC3.
Potential Commercial Applications:
• Therapeutic antibodies against
cancers that overexpress GPC3.
• Therapeutic immunotoxins or
antibody-drug conjugates for killing
cancer cells that overexpress GPC3.
• Diagnostics for detecting cancers
associated with GPC3 overexpression.
• Specific cancers include
hepatocellular cancer (HCC), melanoma,
ovarian cancer, thyroid cancer, lung
squamous cell carcinoma, Wilms’
tumor, neuroblastoma, hepatoblastoma,
and testicular germ-cell tumors.
Competitive Advantages:
• Monoclonal antibodies create a
level of specificity that can reduce
deleterious side-effects.
• Multiple treatment strategies
available including the killing of cancer
cells with a toxic agent or by inhibiting
cell signaling.
• Non-invasive and potentially nonliver toxic alternative to current HCC
treatment strategies.
Development Stage:
• Pre-clinical.
• In vitro data available.
• In vivo data available (animal).
Inventors: Mitchell Ho (NCI) et al.
Publications:
1. Feng M, et al. Therapeutically
targeting glypican-3 via a conformationspecific single-domain antibody in
hepatocellular carcinoma. Proc Natl
Acad Sci U S A. 2013 Mar
19;110(12):E1083–91. [PMID 23471984]
2. Feng M, et al. Recombinant soluble
glypican 3 protein inhibits the growth of
hepatocellular carcinoma in vitro. Int J
Cancer 2011 May1;128(9):2246–7.
[PMID: 20617511]
3. Zitterman SI, et al. Soluble glypican
3 inhibits the growth of hepatocellular
carcinoma in vitro and in vivo. Int J
Cancer 2010 Mar 15;126(6):1291–1301.
[PMID: 19816934]
Intellectual Property: HHS Reference
No. E–130–2011/0—U.S. Provisional
Application No. 61/477,020 filed 19 Apr
2011; PCT Application No. PCT/
US2012/034186 filed 19 Apr 2012.
Related Technology: HHS Reference
No. E–136–2012/0—U.S. Provisional
Application No. 61/654,232 filed 01 Jun
2012.
Licensing Contact: David A.
Lambertson, Ph.D.; 301–435–4632;
lambertsond@mail.nih.gov.
Collaborative Research Opportunity:
The National Cancer Institute, Center for
Cancer Research, Laboratory of
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Molecular Biology, is seeking statements
of capability or interest from parties
interested in collaborative research to
further develop, evaluate, or
commercialize novel antibody or
antibody-drug conjugate therapies for
the treatment of liver cancer. For
collaboration opportunities, please
contact John Hewes, Ph.D. at
hewesj@mail.nih.gov.
Dated: June 14, 2013.
Richard U. Rodriguez,
Director, Division of Technology Development
and Transfer, Office of Technology Transfer,
National Institutes of Health.
[FR Doc. 2013–14821 Filed 6–20–13; 8:45 am]
BILLING CODE 4140–01–P
Extramural Research, National Eye Institute,
National Institutes of Health, 5635 Fishers
Lane, Suite 1300, MSC 9300, 301–451–2020,
hoshawb@mail.nih.gov.
(Catalogue of Federal Domestic Assistance
Program Nos. 93.867, Vision Research,
National Institutes of Health, HHS)
Dated: June 17, 2013.
Melanie J. Gray,
Program Analyst, Office of Federal Advisory
Committee Policy.
[FR Doc. 2013–14816 Filed 6–20–13; 8:45 am]
BILLING CODE 4140–01–P
DEPARTMENT OF HEALTH AND
HUMAN SERVICES
National Institutes of Health
DEPARTMENT OF HEALTH AND
HUMAN SERVICES
National Institutes of Health
National Eye Institute; Notice of Closed
Meeting
Pursuant to section 10(d) of the
Federal Advisory Committee Act, as
amended (5 U.S.C. App.), 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 Eye Institute
Special Emphasis Panel; NEI Epidemiology
and Genetics.
Date: July 10, 2013.
Time: 11:30 a.m. to 2:30 p.m.
Agenda: To review and evaluate grant
applications.
Place: National Institutes of Health, 5635
Fishers Lane, Bethesda, MD 20892
(Telephone Conference Call).
Contact Person: Anne E. Schaffner, Ph.D.,
Chief, Scientific Review Officer, Division of
Extramural Research, National Eye Institute,
National Institutes of Health, 5635 Fishers
Lane, Suite 1300, MSC 9300, 301–451–2020,
aes@nei.nih.gov.
Name of Committee: National Eye Institute
Special Emphasis Panel; NEI Institutional
Training Grants and Conference Grants.
Date: July 30, 2013.
Time: 8:00 a.m. to 5:00 p.m.
Agenda: To review and evaluate grant
applications.
Place: National Institutes of Health,
Terrace Level Conference Center, 5635
Fishers Lane, Bethesda, MD 20892.
Contact Person: Brian Hoshaw, Ph.D.,
Scientific Review Branch, Division of
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Center for Scientific Review; Notice of
Closed Meeting
Pursuant to section 10(d) of the
Federal Advisory Committee Act, as
amended (5 U.S.C. App.), notice is
hereby given of the following meeting.
The meeting will be closed to the
public in accordance with the
provisions set forth in sections
552b(c)(4) and 552b(c)(6), Title 5 U.S.C.,
as amended. The grant applications and
the discussions could disclose
confidential trade secrets or commercial
property such as patentable material,
and personal information concerning
individuals associated with the grant
applications, the disclosure of which
would constitute a clearly unwarranted
invasion of personal privacy.
Name of Committee: Center for Scientific
Review Special Emphasis Panel; RFA Panel:
Molecular and Cellular Substrates of
Complex Brain Disorders.
Date: July 19, 2013.
Time: 8:00 a.m. to 5:30 p.m.
Agenda: To review and evaluate grant
applications.
Place: Embassy Suites at the Chevy Chase
Pavilion, 4300 Military Road NW.,
Washington, DC 20015.
Contact Person: Deborah L Lewis, Ph.D.,
Scientific Review Officer, Center for
Scientific Review, National Institutes of
Health, 6701 Rockledge Drive, Room 4183,
MSC 7850, Bethesda, MD 20892, 301–408–
9129, lewisdeb@csr.nih.gov.
(Catalogue of Federal Domestic Assistance
Program Nos. 93.306, Comparative Medicine;
93.333, Clinical Research, 93.306, 93.333,
93.337, 93.393–93.396, 93.837–93.844,
93.846–93.878, 93.892, 93.893, National
Institutes of Health, HHS)
Dated: June 14, 2013.
Anna Snouffer,
Deputy Director, Office of Federal Advisory
Committee Policy.
[FR Doc. 2013–14815 Filed 6–20–13; 8:45 am]
BILLING CODE 4140–01–P
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]]>Agencies
[Federal Register Volume 78, Number 120 (Friday, June 21, 2013)]
[Notices]
[Pages 37554-37556]
From the Federal Register Online via the Government Printing Office [www.gpo.gov]
[FR Doc No: 2013-14821]
-----------------------------------------------------------------------
DEPARTMENT OF HEALTH AND HUMAN SERVICES
National Institutes of Health
Government-Owned Inventions; Availability for Licensing
AGENCY: National Institutes of Health, 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.
FOR FURTHER INFORMATION CONTACT: 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.
GPR116 Knockout and Conditional Knockout Mice
Description of Technology: Pulmonary surfactant plays a critical
role in preventing alveolar collapse by decreasing surface tension at
the alveolar air-liquid interface. Surfactant deficiency contributes to
the pathogenesis of acute lung injury (ALI) and acute respiratory
distress syndrome (ARDS), common disorders that can afflict patients of
all ages and carry a mortality rate greater than 25%. Excess surfactant
leads to pulmonary alveolar proteinosis. The NCI investigators created
a G-protein coupled receptor GPR116 mutant mouse model and showed that
GPR116 plays a previously unexpected, essential role in maintaining
normal surfactant levels in the lung.
The mouse model could aid in the development of drug screens to
identify agents that can modulate surfactant levels. Alveolar type II
cells have also been isolated from the GPR116 wildtype and knockout
mice that could be directly used in such assays. The identification of
surfactant modulating agents could be important to a number of lung
surfactant disorders.
Potential Commercial Applications: Research materials to study lung
surfactant homeostasis and disorders.
Competitive Advantages: Not available elsewhere.
Development Stage:
Prototype.
Pre-clinical.
In vitro data available.
In vivo data available (animal).
Inventors: Bradley Dean St. Croix and Mi Young Yang (NCI).
Publication: Yang MY, et al. Essential Regulation of Lung
Surfactant Homeostasis by the Orphan G Protein-Coupled Receptor GPR116.
Cell Rep. 2013 May 30;3(5):1457-64. [PMID 23684610]
Intellectual Property: HHS Reference No. E-269-2012/0--Research
Tool. Patent prosecution is not being pursued for this technology.
Licensing Contact: Betty B. Tong, Ph.D.; 301-594-6565;
tongb@mail.nih.gov.
Collaborative Research Opportunity: The Center for Cancer Research
Mouse Cancer Genetics Program is seeking statements of capability or
interest from parties interested in collaborative research to further
develop, evaluate or commercialize GPR116 Knockout and Conditional
Knockout Mice. For collaboration opportunities, please contact John
Hewes, Ph.D. at hewesj@mail.nih.gov.
Engineered Anthrax Toxin Variants That Target Cancer
Description of Technology: This technology describes the use of
novel mutated anthrax protective antigen (PA) protein variants to
target tumor cells and tumor vasculature. NIH scientists have
engineered two PA variants that selectively complement one another and
combine to form active octamers that target tumor cells. This
controlled oligomeric activation of the PA proteins makes the
likelihood of toxicity to non-tumor cells very low since non-tumor
tissue does not express certain cell-surface proteases required to
activate the PA variants. Using proteases that are highly expressed in
tumor cells, e.g., matrix metalloproteases (MMP) and urokinase
plasminogen activator (uPA), the scientists have shown significant
tumor growth suppression with the oligomer in a mouse model.
Furthermore, other tumor-specific proteases could also be used to
control formation of the targeted octameric anthrax toxin structures.
Moreover, the structures can be expanded to include several PA
variants. In summary, this technology provides a unique, expandable
platform that reduces toxicity to normal tissues compared to other
systems and can be used to treat cancers more effectively.
Potential Commercial Applications: Therapeutic treatment for solid
tumors, cancers, and infectious diseases.
Competitive Advantages:
Specificity in targeting tumors while eliminating side
effects associated with non-specific targeting of normal cells.
Method can be expanded to include different proteases and
up to eight PA variants.
Development Stage:
Pre-clinical.
In vitro data available.
In vivo data available (animal).
Inventors: Clinton E. Leysath, Stephen H. Leppla, Damilola D.
Phillips (NIAID).
Publication: Phillips DD, et al. Engineering anthrax toxin variants
that exclusively form octamers and their application to targeting
tumors. J Biol Chem. 2013 Mar 29;288(13):9058-65. [PMID 23393143]
Intellectual Property: HHS Reference No. E-246-2012/0--U.S.
Provisional Application No. 61/692,143 filed 22 Aug 2012.
Related Technologies:
HHS Reference No. E-293-1999--Mutated Anthrax Toxin
Protective Antigen Proteins That Specifically Target Cells Containing
High Amounts of Cell-Surface Metalloproteinases or Plasminogen
Activator Receptors (Leppla/NIAID).
[[Page 37555]]
HHS Reference No. E-070-2007--Human Cancer Therapy Using
Engineered Metalloproteinase-Activated Anthrax Lethal Toxin That Target
Tumor Vasculature (Leppla/NIAID).
HHS Reference No. E-059-2004--Multimeric Protein Toxins to
Target Cells Having Multiple Identifying Characteristics (Leppla/
NIAID).
Licensing Contact: Whitney Hastings; 301-451-7337;
hastingw@mail.nih.gov.
Intra-Bone Drug Delivery Device and Method
Description of Technology: The invention pertains to devices for
directly infusing cellular therapeutics into patient bone. The device
monitors intra-bone pressure using pressure sensors disposed at its
proximal end and adjusts infusion pressures during infusion such that
intra-bone pressure does not exceed levels of systemic blood pressure.
Such devices, apparatus and methods are particularly suitable for use
in performing bone marrow transplants, particularly transplants that
utilize cord blood as a stem cell source.
Potential Commercial Applications: Drug delivery to bones.
Competitive Advantages:
Therapeutic uptake efficiency.
Drug delivery efficiency.
Target specificity.
Development Stage:
Prototype.
In vitro data available.
Inventors: Robert Hoyt (NHLBI), Jeremy Pantin (NHLBI), Timothy Hunt
(NHLBI), Randall Clevenger (NHLBI), Omer Aras (NIHCC), Richard Childs
(NHLBI), Peter Choyke (NCI).
Publication: Pantin JM, et al. ``Optimization of an Intra-Bone
Hematopoietic Stem Cell Delivery Technique in a Swine Model.'' Poster
abstract presented at the 54th ASH Annual Meeting and Exposition,
Atlanta, Georgia, December 8-11, 2012. [https://ash.confex.com/ash/2012/webprogram/Paper53150.html]
Intellectual Property: HHS Reference No. E-165-2012/0--U.S.
Provisional Patent Application No. 61/771,463 filed 01 Mar 2013.
Related Technology: HHS Reference No. E-196-1998/2--U.S. Patent No.
8,409,166 issued 02 Apr 2013.
Licensing Contact: Michael Shmilovich; 301-435-5019;
shmilovm@mail.nih.gov.
Collaborative Research Opportunity: The National Heart, Lung, and
Blood Institute is seeking statements of capability or interest from
parties interested in collaborative research to further develop,
evaluate or commercialize Intra-bone Drug Delivery Device and Method.
For collaboration opportunities, please contact Denise Crooks at
crooksd@nhlbi.nih.gov.
Method of Inducing Pluripotent or Multipotent Stem Cells by Blocking
CD47 Receptor Signaling
Description of Technology: NIH researchers have discovered that
blockade of the signaling activity of a single cell-surface receptor,
CD47, without transfection or introduction of potentially transforming
viral vectors, results in high frequency, spontaneous generation of
self-renewing cells with a high proliferative capacity. Induced
pluripotent stem cells (iPS cells) are currently produced by
transforming cells with viral or other constitutive expression vectors
encoding four stem cell transcription factors (c-Myc, Sox2, Klf4, and
Oct4), but this method presents challenges such as over-expression of
c-Myc, which can result in malignant transformation. The present
invention relates to a method of using CD47-modulating compounds to
induce multipotent stem cells without the concomitant risk of malignant
transformation and without requiring the use of feeder cells. The
cellular phenotypes are associated with increased expression of the
hallmark stem cell-inducing transcription factors, c-Myc, Sox2, Klf4,
and Oct4. The current invention builds on the NIH's previous
discoveries of antibodies, antisense morpholino oligonucleotides,
peptide compounds and other small molecules that modulate CD47.
Potential Commercial Applications: Regenerative medicine and stem
cell therapy.
Competitive Advantages:
Does not require use of viral vectors.
Eliminates risk of malignant transformation for clinical
applications.
Eliminates need for feeder cells.
Allows generation and maintenance of a ready supply of iPS
cells using a single defined agent.
Avoids loss of differentiated phenotype associated with
telomerase or T antigen transfection.
Development Stage:
In vitro data available.
In vivo data available (animal).
Inventors: David D. Roberts, Sukhbir Kaur, Jeff S. Isenberg (NCI)
Publications:
1. Kaur S, et al. Thrombospondin-1 signaling through CD47 inhibits
self-renewal by regulating c-Myc and other stem cell transcription
factors. Sci Rep. 2013;3:1673. [PMID 23591719]
2. NCI News Note: A drug target that stimulates development of
healthy stem cells. 2013 Apr 17. [https://www.cancer.gov/newscenter/newsfromnci/2013/cd47stemcell]
Intellectual Property:
HHS Reference No. E-086-2012/0--U.S. Application No. 61/
621,994 filed 09 Apr 2012.
HHS Reference No. E-086-2012/1--U.S. Application No. 61/
735,701 filed 11 Dec 2012.
HHS Reference No. E-086-2012/2--International Application
PCT/US2013/035838 filed 09 Apr 2013.
Related Technologies: HHS Reference No. E-227-2006/5--
U.S. Application No. 12/444,364 filed 3 Apr 09.
CA Application No. 2,665,287 filed 5 Oct 07.
EP Application No. 07868382.8 filed 27 Mar 09.
U.S. Application No. 13/546,941 filed 11 Jul 12.
Licensing Contact: Charlene Sydnor, Ph.D.; 301-435-4689;
sydnorc@mail.nih.gov.
Collaborative Research Opportunity: The National Cancer Institute,
Center for Cancer Research, Laboratory of Pathology, is seeking
statements of capability or interest from parties interested in
collaborative research to further develop, evaluate or commercialize
CD47 modulators for regenerative medicine and stem cell therapy
applications. For collaboration opportunities, please contact John
Hewes, Ph.D. at hewesj@mail.nih.gov.
Human Monoclonal Antibodies to Glypican-3 Protein and Heparan Sulfate
for Treatment of Cancer
Description of Technology: Hepatocellular carcinoma (HCC) is the
most common form of liver cancer, and is among the more deadly cancers
in the world due to its late detection and poor prognosis. No effective
treatment is available for liver cancer therapy.
Glypican-3 (GPC3) is a cell surface protein that is preferentially
expressed on HCC cells, making it an attractive potential target for
developing a therapeutic. This invention concerns human monoclonal
antibodies against GPC3 and their use for the treatment of GPC3-
expressing cancers such as HCC.
Specifically, the inventors have generated two distinct human
monoclonal antibodies to GPC3. The first antibody (HN3) binds to a
conformational epitope on the cell surface domain of GPC3. The second
antibody (HS20) binds specifically to heparan sulfate chains on GPC3.
These antibodies can inhibit the growth of HCC cells, thereby
decreasing the ability of tumors to grow and metastasize. Furthermore,
by using the antibodies to target a toxic moiety to only those cells
that express GPC3, cancer cells can be eliminated while allowing
healthy,
[[Page 37556]]
essential cells to remain unharmed. Thus, monoclonal antibodies to GPC3
(and corresponding immunotoxins) represent a novel therapeutic
candidate for treatment of HCC, as well as other cancers associated
with the differential expression of GPC3.
Potential Commercial Applications:
Therapeutic antibodies against cancers that overexpress
GPC3.
Therapeutic immunotoxins or antibody-drug conjugates for
killing cancer cells that overexpress GPC3.
Diagnostics for detecting cancers associated with GPC3
overexpression.
Specific cancers include hepatocellular cancer (HCC),
melanoma, ovarian cancer, thyroid cancer, lung squamous cell carcinoma,
Wilms' tumor, neuroblastoma, hepatoblastoma, and testicular germ-cell
tumors.
Competitive Advantages:
Monoclonal antibodies create a level of specificity that
can reduce deleterious side-effects.
Multiple treatment strategies available including the
killing of cancer cells with a toxic agent or by inhibiting cell
signaling.
Non-invasive and potentially non-liver toxic alternative
to current HCC treatment strategies.
Development Stage:
Pre-clinical.
In vitro data available.
In vivo data available (animal).
Inventors: Mitchell Ho (NCI) et al.
Publications:
1. Feng M, et al. Therapeutically targeting glypican-3 via a
conformation-specific single-domain antibody in hepatocellular
carcinoma. Proc Natl Acad Sci U S A. 2013 Mar 19;110(12):E1083-91.
[PMID 23471984]
2. Feng M, et al. Recombinant soluble glypican 3 protein inhibits
the growth of hepatocellular carcinoma in vitro. Int J Cancer 2011
May1;128(9):2246-7. [PMID: 20617511]
3. Zitterman SI, et al. Soluble glypican 3 inhibits the growth of
hepatocellular carcinoma in vitro and in vivo. Int J Cancer 2010 Mar
15;126(6):1291-1301. [PMID: 19816934]
Intellectual Property: HHS Reference No. E-130-2011/0--U.S.
Provisional Application No. 61/477,020 filed 19 Apr 2011; PCT
Application No. PCT/US2012/034186 filed 19 Apr 2012.
Related Technology: HHS Reference No. E-136-2012/0--U.S.
Provisional Application No. 61/654,232 filed 01 Jun 2012.
Licensing Contact: David A. Lambertson, Ph.D.; 301-435-4632;
lambertsond@mail.nih.gov.
Collaborative Research Opportunity: The National Cancer Institute,
Center for Cancer Research, Laboratory of Molecular Biology, is seeking
statements of capability or interest from parties interested in
collaborative research to further develop, evaluate, or commercialize
novel antibody or antibody-drug conjugate therapies for the treatment
of liver cancer. For collaboration opportunities, please contact John
Hewes, Ph.D. at hewesj@mail.nih.gov.
Dated: June 14, 2013.
Richard U. Rodriguez,
Director, Division of Technology Development and Transfer, Office of
Technology Transfer, National Institutes of Health.
[FR Doc. 2013-14821 Filed 6-20-13; 8:45 am]
BILLING CODE 4140-01-P
