Government-Owned Inventions; Availability for Licensing, 19329-19331 [2015-08290]
Download as PDF
<![CDATA[
Federal Register / Vol. 80, No. 69 / Friday, April 10, 2015 / Notices
individuals associated with the grant
applications, the disclosure of which
would constitute a clearly unwarranted
invasion of personal privacy.
Name of Committee: National Institute of
Child Health and Human Development
Special Emphasis Panel.
Date: May 7, 2015.
Time: 8:00 a.m. to 6:00 p.m.
Agenda: To review and evaluate grant
applications.
Place: Residence Inn Bethesda, 7335
Wisconsin Avenue, Bethesda, MD 20814.
Contact Person: Peter Zelazowski, Ph.D.,
Scientific Review Officer, Scientific Review
Branch, Eunice Kennedy Shriver National
Institute of Child Health and Human
Development, NIH 6100 Executive
Boulevard, Room 5B01, Bethesda, MD
20892–9304, (301) 435–6902,
peter.zelazowski@nih.gov.
(Catalogue of Federal Domestic Assistance
Program Nos. 93.864, Population Research;
93.865, Research for Mothers and Children;
93.929, Center for Medical Rehabilitation
Research; 93.209, Contraception and
Infertility Loan Repayment Program, National
Institutes of Health, HHS)
Dated: April 7, 2015.
David Clary,
Program Analyst, Office of Federal Advisory
Committee Policy.
[FR Doc. 2015–08294 Filed 4–9–15; 8:45 am]
BILLING CODE 4140–01–P
DEPARTMENT OF HEALTH AND
HUMAN SERVICES
National Institutes of Health
National Human Genome Research
Institute; Notice of Closed Meeting
mstockstill on DSK4VPTVN1PROD with NOTICES
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: Date: Center for
Inherited Disease Research Access
Committee.
Date: April 23, 2015.
Time: 11:30 a.m. to 3:00 p.m.
Agenda: To review and evaluate grant
applications.
Place: National Institutes of Health, 5635
Fishers Lane, Bethesda, MD 20892,
(Telephone Conference Call).
VerDate Sep<11>2014
20:09 Apr 09, 2015
Jkt 235001
Contact Person: Camilla E. Day, Ph.D.,
Scientific Review Officer, CIDR, National
Human Genome Research Institute, National
Institutes of Health, 5635 Fishers Lane, Suite
4075, Bethesda, MD 20892, 301–402–8837,
camilla.day@nih.gov.
(Catalogue of Federal Domestic Assistance
Program Nos. 93.172, Human Genome
Research, National Institutes of Health, HHS)
Dated: April 6, 2015.
David Clary,
Program Analyst,
Office of Federal Advisory Committee
Policy.
[FR Doc. 2015–08213 Filed 4–9–15; 8:45 am]
BILLING CODE 4140–01–P
DEPARTMENT OF HEALTH AND
HUMAN SERVICES
National Institutes of Health
Government-Owned Inventions;
Availability for Licensing
AGENCY:
National Institutes of Health,
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. 209 and 37 CFR part 404 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.
SUPPLEMENTARY INFORMATION:
Technology descriptions follow.
SUMMARY:
Novel Immunotherapy for Cancer
Treatment: Chimeric Antigen Receptors
Targeting CD70 Antigen
Description of Technology: Scientists
at the National Institutes of Health have
developed anti-CD70 chimeric antigen
receptors (CARs) to treat cancers. CD70
is an antigen that is expressed on a
variety of human cancers such as renal
cell carcinoma, glioblastoma, nonHodgkin’s lymphoma, and chronic
lymphocytic leukemia. The anti-CD70
PO 00000
Frm 00054
Fmt 4703
Sfmt 4703
19329
CARs are hybrid proteins consisting of
a receptor portion that recognizes CD70
antigen, and intracellular T cell
signaling domains selected to optimally
activate the CAR expressing T cells.
Genetically engineered T cells that
express this CARs will bind to CD70 on
the cancer cells and will be activated to
induce an immune response that
promotes robust tumor cell elimination
when infused into cancer patients. This
technology can rapidly generate a
vigorous T-cell response from the
patient’s own blood, targeting CD70
expressing cancer cells, and potentially
induce tumor rejection.
Potential Commercial Applications:
• Immunotherapeutics to treat
cancers that overexpress CD70, such as
renal cell carcinoma, glioblastoma, nonHodgkin’s lymphoma, and chronic
lymphocytic leukemia.
• A personalized cancer treatment
strategy for patients whose tumor cells
express CD70 whereby the patient’s own
T cells are isolated, engineered to
express the anti-CD70 CARs, and reinfused into the same patient to attack
the tumor(s).
Competitive Advantages:
• CD70-specific CARs expressed on T
cells will increase the likelihood of
successful targeted therapy.
• CAR–T cells target only CD70
expressing cells and thus may generate
fewer side effects than other cancer
treatment approaches.
• With the advent of Provenge(R), and
Yervoy(R), immunotherapy is now more
widely accepted as a viable cancer
treatment option.
• T-cell transfer can provide much
larger numbers of anti-tumor immune
cells compared to other approaches
such as vaccines.
Development Stage:
• Early-stage.
• In vitro data available.
• In vivo data available (animal).
Inventors: Qiong J. Wang, Zhiya Yu,
James C. Yang (all of NCI).
Publication: Wang QJ, et al.
Distinctive features of the differentiated
phenotype and infiltration of tumorreactive lymphocytes in clear cell renal
cell carcinoma. Cancer Res. 2012 Dec 1;
72(23):6119–29. [PMID 23071066]
Intellectual Property: HHS Reference
No. E–021–2015/0—U.S. Patent
Application No. 62/088,882 filed 08 Dec
2014.
Licensing Contact: Whitney A.
Hastings, Ph.D.; 301–451–7337;
hastingw@mail.nih.gov.
Collaborative Research Opportunity:
The National Cancer Institute is seeking
statements of capability or interest from
parties interested in collaborative
research to further develop, evaluate or
E:\FR\FM\10APN1.SGM
10APN1
19330
Federal Register / Vol. 80, No. 69 / Friday, April 10, 2015 / Notices
mstockstill on DSK4VPTVN1PROD with NOTICES
commercialize chimeric antigen
receptors targeting CD70 for cancer
treatment. For collaboration
opportunities, please contact Steven A.
Rosenberg, M.D., Ph.D. at sar@nih.gov.
Novel Cancer Immunotherapy: HLA–
A11 Restricted T Cell Receptor That
Recognizes G12D Variant of Mutated
KRAS
Description of Technology: Scientists
at the National Institutes of Health have
developed T cell receptor (TCR) derived
from mouse T cells that recognize
mutated Kirsten rat sarcoma viral
oncogene homolog (KRAS), in particular
the G12D variant. Mutated KRAS, which
plays an essential driver role in
oncogenesis, is expressed by a variety of
human cancers, such as pancreatic,
colorectal, lung, endometrial, ovarian,
and prostate cancers; but not by normal,
noncancerous cells. KRAS is mutated in
nearly a third of the most lethal human
cancers and could serve as a cancerspecific therapeutic target. Most
common mutations occurred at codon
12, as glycine can be substituted with
aspartic acid (G12D), valine (G12V),
cysteine (G12C), and arginine (G12R),
and among these codon 12
substitutions, G12D is the most frequent
variant. The TCR is a protein that
specifically recognizes the most
frequent mutated KRAS G12D variant in
the context of major histocompatibility
complex (MHC) class I molecule HLA–
A11 and activates T-cells. In HLA–A11+
patients, such genetically engineered T
cells with TCRs against mutated KRAS
are expected to target and kill cancer
cells with this mutation while sparing
normal tissues after infusion into
patients.
Potential Commercial Applications:
• Immunotherapeutics to treat a
variety of human cancers that harbor
KRAS mutations, in particular, G12D
mutation, such as pancreatic,
-colorectal, lung, endometrial, ovarian,
and prostate cancers.
• T cells expressing mutated KRAS
G12D specific TCR may successfully
treat or prevent the recurrence of
mutated KRAS-positive cancers that do
not respond to other types of treatment
such as surgery, chemotherapy, and
radiation.
Competitive Advantages:
• Genetically engineered T cells with
TCRs for HLA–A11-restricted mutated
KRAS will increase the likelihood of
successful targeted therapy.
• The targeted therapy minimizes
side effect. T cells expressing antimutated KRAS TCRs target tumor cells
expressing mutated KRAS and spare
normal tissue. This therapy may have
lower tissue toxicities comparing to
VerDate Sep<11>2014
20:09 Apr 09, 2015
Jkt 235001
traditional chemotherapy and
radiotherapy.
• With the advent of Provenge(R) and
Yervoy(R), immunotherapy is now more
widely accepted as a viable cancer
treatment option.
Development Stage:
• Early-stage.
• In vitro data available.
• Ex vivo data available.
Inventors: Qiong J. Wang and James C.
Yang (NCI).
Intellectual Property: HHS Reference
No. E–028–2015/0—US Provisional
Patent Application No. 62/084,654 filed
26 Nov 2014.
Related Technologies:
• HHS Reference No. E–106–2006/3.
• HHS Reference No. E–226–2014/0.
Licensing Contact: Whitney A.
Hastings, Ph.D.; 301–451–7337;
hastingw@mail.nih.gov.
Collaborative Research Opportunity:
The National Cancer Institute is seeking
statements of capability or interest from
parties interested in collaborative
research to further develop, evaluate or
commercialize anti-mutated KRAS TCRs
for cancer treatment. For collaboration
opportunities, please contact Steven A.
Rosenberg, M.D., Ph.D. at sar@nih.gov.
Live Attenuated Japanese Encephalitis
Virus Vaccine
Description of Technology: Japanese
encephalitis virus (JEV), a member of
the genus flavivirus, is maintained in a
zoonotic cycle between Culex
mosquitoes and ardeid birds or
domestic swine and is responsible for
significant epidemics of viral
encephalitis in Asia. Three billion
people live in regions with endemic JEV
transmission resulting in an estimated
60,000 annual cases, of which 20–40%
are fatal and 45–70% of survivors have
neurologic sequelae. The live-attenuated
JEV SA14–14–2 vaccine, produced in
primary hamster kidney cells, is safe
and effective. Past attempts to adapt this
virus to replicate in cells that are more
favorable for vaccine production
resulted in mutations that significantly
reduced immunogenicity. The inventors
have isolated 10 genetically distinct
Vero cell-adapted JEV SA14–14–2
variants and a recombinant wild-type
JEV clone, modified to contain the JEV
SA14–14–2 polyprotein amino acid
sequence, was recovered in Vero cells.
Mutations were also identified that
modulated virus sensitivity to type I
interferon-stimulation in Vero cells. A
subset of JEV SA14–14–2 variants and
the recombinant clone were evaluated
in vivo and exhibited levels of
attenuation that varied significantly in
suckling mice, but were avirulent and
highly immunogenic in weanling mice
PO 00000
Frm 00055
Fmt 4703
Sfmt 4703
and are promising candidates for the
development of a second generation,
recombinant vaccine.
Potential Commercial Applications:
• JEV Vaccine.
• JEV Diagnostics.
Competitive Advantages:
• Safe and efficacious vaccine.
• Extremely low production costs.
• Positive preclinical data.
• Vero cell manufacture.
Development Stage:
• In vitro data available.
• In vivo data available (animal).
Inventors: Stephen S. Whitehead and
Gregory D. Gromowski (NIAID).
Publications:
1. Gromowski G, et al. Genetic and
phenotypic properties of vero celladapted Japanese encephalitis virus
SA14–14–2 vaccine strain variants and
a recombinant clone, which
demonstrates attenuation and
immunogenicity in mice. Am J Trop
Med Hyg. 2015 Jan; 92(1)98–107. [PMID
25311701].
2. Gromowski G, et al. Genetic
determinants of Japanese encephalitis
virus vaccine strain SA14–14–2 that
govern attenuation of virulence in mice.
J Virol. 2015, in press.
Intellectual Property: HHS Reference
No. E–231–2014/0—Research Material.
Patent protection is not being pursued
for this technology.
Licensing Contact: Peter Soukas; 301–
435–4646; ps193c@nih.gov.
IFN Gamma for Reducing Adverse
Ocular Side Effects of MEK-Inhibitor
Therapy in Cancer
Description of Technology: Use of
IFN-gamma for treating an adverse side
effect in a cancer patient being treated
by a MEK-inhibitor (MEKi) is disclosed.
MAP kinase/ERK kinase (MEK), an
oncogene or signal protein within the
P38 mitogen activated protein kinase
(MAPK) pathway, is a crucial point of
convergence that integrates a variety of
protein kinases through Ras. MEKis are
currently being tested in monotherapies
and combination therapies against a
wide variety of cancers. A number of
side effects are noticed with treatment
of cancer with MEKis, including visual
disturbances. The inventors have
discovered that MEKis decreases fluid
transport from the retina and/or
subretinal space of the retinal pigment
epithelium (RPE) resulting in the
abnormal accumulation of fluid in the
retina and subretinal space, which
causes retinal detachment and vision
loss. Their results also indicate that
apical addition of MEKis alters
transepithelial resistance in RPE. For
the first time, the inventors showed that
these effects of MEKis are almost
E:\FR\FM\10APN1.SGM
10APN1
Federal Register / Vol. 80, No. 69 / Friday, April 10, 2015 / Notices
mstockstill on DSK4VPTVN1PROD with NOTICES
completely rescued by basolateral
addition of IFN-gamma. These results
suggest that IFN-gamma can be used to
reduce adverse events (retinal edema)
associated with the therapeutic use of
MEKis.
Potential Commercial Applications:
Treatment for or prevention of adverse
side effects in cancer patients
undergoing MEK inhibitor therapy.
Competitive Advantages: A simple
and unique mode of reducing or
eliminating ocular side effects in cancer
patients undergoing treatments with
MEK inhibitors.
Development Stage:
• Early-stage.
• In vitro data available.
Inventors: Sheldon S. Miller (NEI),
Arvydas Maminishkis (NEI), Charlotte
´
E. Reme (Merck KGaA).
Intellectual Property: HHS Reference
No. E–248–2012/0—
• US Provisional Application No. 61/
721,810 filed 02 Nov 2012.
• PCT Patent Application No. PCT/
US2013/068056 filed 01 Nov 2013.
Related Technologies: HHS Reference
No. E–169–2008/0—
• US Patent No. 8,697,046 issued 15
Apr 2014 (Methods of Administering
Interferon Gamma to Absorb Fluid From
the Subretinal Space; Li R, et al.).
• US Patent Application No. 14/
252,489 filed 14 Apr 2014.
Licensing Contact: Suryanarayana
Vepa, Ph.D., J.D.; 301–435–5020;
vepas@mail.nih.gov.
Lubiprostone To Treat Retinal Diseases
Associated With Fluid Accumulation in
Retina & Subretinal Space
Description of Technology: Use of
Lubiprostone for treating age-related
macular degeneration, chronic macular
edema, diabetic retinopathy, retinal
detachment, glaucoma, or uveitis by
decreasing excess fluid accumulation in
the retina and/or subretinal space (SRS)
is described. The retinal pigment
epithelium (RPE) is a highly pigmented,
terminally differentiated monolayer of
cells at the back of the eye. The RPE
performs numerous processes that are
critical for the maintenance of
photoreceptor cell health and function.
The pathological accumulation of fluid
beneath the RPE is a symptom and a
contributing factor in the loss of vision
in a variety of ocular conditions.
Previously, the inventors have shown
that human RPE contains apical and
basolateral membrane receptors that can
be activated to increase cell cAMP or Ca
followed by basolateral membrane
activation of CFTR or Ca-activated
chloride channels resulting in a
clinically significant increase in fluid
absorption across the RPE. For the first
VerDate Sep<11>2014
20:09 Apr 09, 2015
Jkt 235001
time, using human RPE in vitro, the
inventors demonstrated that
lubiprostone can increase fluid
transport from the retinal to the
choroidal side of the RPE by activating
CLC–2 at the RPE basolateral membrane.
Further, they also showed that this
increase can be blocked by addition of
methadone, a specific CLC–2 channel
blocker. Lubiprostone added from either
the apical or basolateral side of the
epithelium. Methadone also increased
transepithelial potential (TEP) and this
increase is consistent with a
lubiprostone-induced increase in
basolateral membrane CLC–2
conductance and subsequent membrane
depolarization. These results suggest
lubiprostone can be a therapeutic in
retinal disease to increase fluid
absorption from retina and subretinal
space.
Potential Commercial Applications:
Treatment for or prevention of agerelated macular degeneration, chronic
macular edema, diabetic retinopathy,
retinal detachment, glaucoma, or uveitis
by decreasing the amount of fluid
present in the subretinal space (SRS).
Competitive Advantages: A simple
and novel therapeutic for retinal
diseases characterized by the abnormal
fluid accumulation in subretinal space.
Development Stage:
• Early-stage.
• In vitro data available.
Inventors: Sheldon S. Miller, Arvydas
Maminishkis, Jeffrey Adijanto, Tina M.
Banzon, and Qin Wan (all of NEI).
Intellectual Property: HHS Reference
No. E–283–2012/0—
• U.S. Provisional Application No.
61/777,073 filed 12 Mar 2013.
• PCT Patent Application No. PCT/
US2014/024724 filed 12 Mar 2014.
Related Technology: HHS Reference
No. E–169–2008/0—
• U.S. Patent No. 8,697,046 issued 15
Apr 2014 (Methods of Administering
Interferon Gamma to Absorb Fluid From
the Subretinal Space; Li R, et al.).
• U.S. Patent Application No. 14/
252,489 filed 14 Apr 2014.
Licensing Contact: Suryanarayana
Vepa, Ph.D., J.D.; 301–435–5020;
vepas@mail.nih.gov.
Dated: March 7, 2015.
Richard U. Rodriguez,
Acting Director, Office of Technology
Transfer, National Institutes of Health.
[FR Doc. 2015–08290 Filed 4–9–15; 8:45 am]
BILLING CODE 4140–01–P
PO 00000
Frm 00056
Fmt 4703
Sfmt 4703
19331
DEPARTMENT OF HEALTH AND
HUMAN SERVICES
Substance Abuse and Mental Health
Services Administration
Agency Information Collection
Activities: Proposed Collection;
Comment Request
In compliance with Section
3506(c)(2)(A) of the Paperwork
Reduction Act of 1995 concerning
opportunity for public comment on
proposed collections of information, the
Substance Abuse and Mental Health
Services Administration (SAMHSA)
will publish periodic summaries of
proposed projects. To request more
information on the proposed projects or
to obtain a copy of the information
collection plans, call the SAMHSA
Reports Clearance Officer on (240) 276–
1243.
Comments are invited on: (a) Whether
the proposed collections of information
are necessary for the proper
performance of the functions of the
agency, including whether the
information shall have practical utility;
(b) the accuracy of the agency’s estimate
of the burden of the proposed collection
of information; (c) ways to enhance the
quality, utility, and clarity of the
information to be collected; and (d)
ways to minimize the burden of the
collection of information on
respondents, including through the use
of automated collection techniques or
other forms of information technology.
Proposed Project: Family Treatment
Drug Court Services Evaluation (OMB
No. 0930–0330)—REINSTATEMENT
In 2010, the Substance Abuse and
Mental Health Services Administration
(SAMHSA), Center for Substance Abuse
Treatment (CSAT), provided funding to
12 existing Family Treatment Drug
Courts (FTDCs) for enhancement and/or
expansion of their FTDC’s capabilities
to provide psycho-social, emotional and
mental health services to children (0–17
years) and their families who have
methamphetamine use disorders and
involvement in child protective
services. This program was authorized
in House Report 111–220 accompanying
HR 3293 in 2010. The Committee
language stated that ‘‘these grants will
support a collaborative approach,
including treatment providers, child
welfare specialists, and judges, to
provide community-based social
services for the children of
methamphetamine-addicted parents,’’
and were to be awarded to Family
Dependency Treatment Drug Courts.
E:\FR\FM\10APN1.SGM
10APN1
]]>Agencies
[Federal Register Volume 80, Number 69 (Friday, April 10, 2015)]
[Notices]
[Pages 19329-19331]
From the Federal Register Online via the Government Printing Office [www.gpo.gov]
[FR Doc No: 2015-08290]
-----------------------------------------------------------------------
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. 209 and 37 CFR part 404 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.
SUPPLEMENTARY INFORMATION: Technology descriptions follow.
Novel Immunotherapy for Cancer Treatment: Chimeric Antigen Receptors
Targeting CD70 Antigen
Description of Technology: Scientists at the National Institutes of
Health have developed anti-CD70 chimeric antigen receptors (CARs) to
treat cancers. CD70 is an antigen that is expressed on a variety of
human cancers such as renal cell carcinoma, glioblastoma, non-Hodgkin's
lymphoma, and chronic lymphocytic leukemia. The anti-CD70 CARs are
hybrid proteins consisting of a receptor portion that recognizes CD70
antigen, and intracellular T cell signaling domains selected to
optimally activate the CAR expressing T cells. Genetically engineered T
cells that express this CARs will bind to CD70 on the cancer cells and
will be activated to induce an immune response that promotes robust
tumor cell elimination when infused into cancer patients. This
technology can rapidly generate a vigorous T-cell response from the
patient's own blood, targeting CD70 expressing cancer cells, and
potentially induce tumor rejection.
Potential Commercial Applications:
Immunotherapeutics to treat cancers that overexpress CD70,
such as renal cell carcinoma, glioblastoma, non-Hodgkin's lymphoma, and
chronic lymphocytic leukemia.
A personalized cancer treatment strategy for patients
whose tumor cells express CD70 whereby the patient's own T cells are
isolated, engineered to express the anti-CD70 CARs, and re-infused into
the same patient to attack the tumor(s).
Competitive Advantages:
CD70-specific CARs expressed on T cells will increase the
likelihood of successful targeted therapy.
CAR-T cells target only CD70 expressing cells and thus may
generate fewer side effects than other cancer treatment approaches.
With the advent of Provenge(R), and Yervoy(R),
immunotherapy is now more widely accepted as a viable cancer treatment
option.
T-cell transfer can provide much larger numbers of anti-
tumor immune cells compared to other approaches such as vaccines.
Development Stage:
Early-stage.
In vitro data available.
In vivo data available (animal).
Inventors: Qiong J. Wang, Zhiya Yu, James C. Yang (all of NCI).
Publication: Wang QJ, et al. Distinctive features of the
differentiated phenotype and infiltration of tumor-reactive lymphocytes
in clear cell renal cell carcinoma. Cancer Res. 2012 Dec 1;
72(23):6119-29. [PMID 23071066]
Intellectual Property: HHS Reference No. E-021-2015/0--U.S. Patent
Application No. 62/088,882 filed 08 Dec 2014.
Licensing Contact: Whitney A. Hastings, Ph.D.; 301-451-7337;
hastingw@mail.nih.gov.
Collaborative Research Opportunity: The National Cancer Institute
is seeking statements of capability or interest from parties interested
in collaborative research to further develop, evaluate or
[[Page 19330]]
commercialize chimeric antigen receptors targeting CD70 for cancer
treatment. For collaboration opportunities, please contact Steven A.
Rosenberg, M.D., Ph.D. at sar@nih.gov.
Novel Cancer Immunotherapy: HLA-A11 Restricted T Cell Receptor That
Recognizes G12D Variant of Mutated KRAS
Description of Technology: Scientists at the National Institutes of
Health have developed T cell receptor (TCR) derived from mouse T cells
that recognize mutated Kirsten rat sarcoma viral oncogene homolog
(KRAS), in particular the G12D variant. Mutated KRAS, which plays an
essential driver role in oncogenesis, is expressed by a variety of
human cancers, such as pancreatic, colorectal, lung, endometrial,
ovarian, and prostate cancers; but not by normal, noncancerous cells.
KRAS is mutated in nearly a third of the most lethal human cancers and
could serve as a cancer-specific therapeutic target. Most common
mutations occurred at codon 12, as glycine can be substituted with
aspartic acid (G12D), valine (G12V), cysteine (G12C), and arginine
(G12R), and among these codon 12 substitutions, G12D is the most
frequent variant. The TCR is a protein that specifically recognizes the
most frequent mutated KRAS G12D variant in the context of major
histocompatibility complex (MHC) class I molecule HLA-A11 and activates
T-cells. In HLA-A11+ patients, such genetically engineered T cells with
TCRs against mutated KRAS are expected to target and kill cancer cells
with this mutation while sparing normal tissues after infusion into
patients.
Potential Commercial Applications:
Immunotherapeutics to treat a variety of human cancers
that harbor KRAS mutations, in particular, G12D mutation, such as
pancreatic, -colorectal, lung, endometrial, ovarian, and prostate
cancers.
T cells expressing mutated KRAS G12D specific TCR may
successfully treat or prevent the recurrence of mutated KRAS-positive
cancers that do not respond to other types of treatment such as
surgery, chemotherapy, and radiation.
Competitive Advantages:
Genetically engineered T cells with TCRs for HLA-A11-
restricted mutated KRAS will increase the likelihood of successful
targeted therapy.
The targeted therapy minimizes side effect. T cells
expressing anti-mutated KRAS TCRs target tumor cells expressing mutated
KRAS and spare normal tissue. This therapy may have lower tissue
toxicities comparing to traditional chemotherapy and radiotherapy.
With the advent of Provenge(R) and Yervoy(R),
immunotherapy is now more widely accepted as a viable cancer treatment
option.
Development Stage:
Early-stage.
In vitro data available.
Ex vivo data available.
Inventors: Qiong J. Wang and James C. Yang (NCI).
Intellectual Property: HHS Reference No. E-028-2015/0--US
Provisional Patent Application No. 62/084,654 filed 26 Nov 2014.
Related Technologies:
HHS Reference No. E-106-2006/3.
HHS Reference No. E-226-2014/0.
Licensing Contact: Whitney A. Hastings, Ph.D.; 301-451-7337;
hastingw@mail.nih.gov.
Collaborative Research Opportunity: The National Cancer Institute
is seeking statements of capability or interest from parties interested
in collaborative research to further develop, evaluate or commercialize
anti-mutated KRAS TCRs for cancer treatment. For collaboration
opportunities, please contact Steven A. Rosenberg, M.D., Ph.D. at
sar@nih.gov.
Live Attenuated Japanese Encephalitis Virus Vaccine
Description of Technology: Japanese encephalitis virus (JEV), a
member of the genus flavivirus, is maintained in a zoonotic cycle
between Culex mosquitoes and ardeid birds or domestic swine and is
responsible for significant epidemics of viral encephalitis in Asia.
Three billion people live in regions with endemic JEV transmission
resulting in an estimated 60,000 annual cases, of which 20-40% are
fatal and 45-70% of survivors have neurologic sequelae. The live-
attenuated JEV SA14-14-2 vaccine, produced in primary hamster kidney
cells, is safe and effective. Past attempts to adapt this virus to
replicate in cells that are more favorable for vaccine production
resulted in mutations that significantly reduced immunogenicity. The
inventors have isolated 10 genetically distinct Vero cell-adapted JEV
SA14-14-2 variants and a recombinant wild-type JEV clone, modified to
contain the JEV SA14-14-2 polyprotein amino acid sequence, was
recovered in Vero cells. Mutations were also identified that modulated
virus sensitivity to type I interferon-stimulation in Vero cells. A
subset of JEV SA14-14-2 variants and the recombinant clone were
evaluated in vivo and exhibited levels of attenuation that varied
significantly in suckling mice, but were avirulent and highly
immunogenic in weanling mice and are promising candidates for the
development of a second generation, recombinant vaccine.
Potential Commercial Applications:
JEV Vaccine.
JEV Diagnostics.
Competitive Advantages:
Safe and efficacious vaccine.
Extremely low production costs.
Positive preclinical data.
Vero cell manufacture.
Development Stage:
In vitro data available.
In vivo data available (animal).
Inventors: Stephen S. Whitehead and Gregory D. Gromowski (NIAID).
Publications:
1. Gromowski G, et al. Genetic and phenotypic properties of vero
cell-adapted Japanese encephalitis virus SA14-14-2 vaccine strain
variants and a recombinant clone, which demonstrates attenuation and
immunogenicity in mice. Am J Trop Med Hyg. 2015 Jan; 92(1)98-107. [PMID
25311701].
2. Gromowski G, et al. Genetic determinants of Japanese
encephalitis virus vaccine strain SA14-14-2 that govern attenuation of
virulence in mice. J Virol. 2015, in press.
Intellectual Property: HHS Reference No. E-231-2014/0--Research
Material. Patent protection is not being pursued for this technology.
Licensing Contact: Peter Soukas; 301-435-4646; ps193c@nih.gov.
IFN Gamma for Reducing Adverse Ocular Side Effects of MEK-Inhibitor
Therapy in Cancer
Description of Technology: Use of IFN-gamma for treating an adverse
side effect in a cancer patient being treated by a MEK-inhibitor (MEKi)
is disclosed. MAP kinase/ERK kinase (MEK), an oncogene or signal
protein within the P38 mitogen activated protein kinase (MAPK) pathway,
is a crucial point of convergence that integrates a variety of protein
kinases through Ras. MEKis are currently being tested in monotherapies
and combination therapies against a wide variety of cancers. A number
of side effects are noticed with treatment of cancer with MEKis,
including visual disturbances. The inventors have discovered that MEKis
decreases fluid transport from the retina and/or subretinal space of
the retinal pigment epithelium (RPE) resulting in the abnormal
accumulation of fluid in the retina and subretinal space, which causes
retinal detachment and vision loss. Their results also indicate that
apical addition of MEKis alters transepithelial resistance in RPE. For
the first time, the inventors showed that these effects of MEKis are
almost
[[Page 19331]]
completely rescued by basolateral addition of IFN-gamma. These results
suggest that IFN-gamma can be used to reduce adverse events (retinal
edema) associated with the therapeutic use of MEKis.
Potential Commercial Applications: Treatment for or prevention of
adverse side effects in cancer patients undergoing MEK inhibitor
therapy.
Competitive Advantages: A simple and unique mode of reducing or
eliminating ocular side effects in cancer patients undergoing
treatments with MEK inhibitors.
Development Stage:
Early-stage.
In vitro data available.
Inventors: Sheldon S. Miller (NEI), Arvydas Maminishkis (NEI),
Charlotte E. Rem[eacute] (Merck KGaA).
Intellectual Property: HHS Reference No. E-248-2012/0--
US Provisional Application No. 61/721,810 filed 02 Nov
2012.
PCT Patent Application No. PCT/US2013/068056 filed 01 Nov
2013.
Related Technologies: HHS Reference No. E-169-2008/0--
US Patent No. 8,697,046 issued 15 Apr 2014 (Methods of
Administering Interferon Gamma to Absorb Fluid From the Subretinal
Space; Li R, et al.).
US Patent Application No. 14/252,489 filed 14 Apr 2014.
Licensing Contact: Suryanarayana Vepa, Ph.D., J.D.; 301-435-5020;
vepas@mail.nih.gov.
Lubiprostone To Treat Retinal Diseases Associated With Fluid
Accumulation in Retina & Subretinal Space
Description of Technology: Use of Lubiprostone for treating age-
related macular degeneration, chronic macular edema, diabetic
retinopathy, retinal detachment, glaucoma, or uveitis by decreasing
excess fluid accumulation in the retina and/or subretinal space (SRS)
is described. The retinal pigment epithelium (RPE) is a highly
pigmented, terminally differentiated monolayer of cells at the back of
the eye. The RPE performs numerous processes that are critical for the
maintenance of photoreceptor cell health and function. The pathological
accumulation of fluid beneath the RPE is a symptom and a contributing
factor in the loss of vision in a variety of ocular conditions.
Previously, the inventors have shown that human RPE contains apical and
basolateral membrane receptors that can be activated to increase cell
cAMP or Ca followed by basolateral membrane activation of CFTR or Ca-
activated chloride channels resulting in a clinically significant
increase in fluid absorption across the RPE. For the first time, using
human RPE in vitro, the inventors demonstrated that lubiprostone can
increase fluid transport from the retinal to the choroidal side of the
RPE by activating CLC-2 at the RPE basolateral membrane. Further, they
also showed that this increase can be blocked by addition of methadone,
a specific CLC-2 channel blocker. Lubiprostone added from either the
apical or basolateral side of the epithelium. Methadone also increased
transepithelial potential (TEP) and this increase is consistent with a
lubiprostone-induced increase in basolateral membrane CLC-2 conductance
and subsequent membrane depolarization. These results suggest
lubiprostone can be a therapeutic in retinal disease to increase fluid
absorption from retina and subretinal space.
Potential Commercial Applications: Treatment for or prevention of
age-related macular degeneration, chronic macular edema, diabetic
retinopathy, retinal detachment, glaucoma, or uveitis by decreasing the
amount of fluid present in the subretinal space (SRS).
Competitive Advantages: A simple and novel therapeutic for retinal
diseases characterized by the abnormal fluid accumulation in subretinal
space.
Development Stage:
Early-stage.
In vitro data available.
Inventors: Sheldon S. Miller, Arvydas Maminishkis, Jeffrey
Adijanto, Tina M. Banzon, and Qin Wan (all of NEI).
Intellectual Property: HHS Reference No. E-283-2012/0--
U.S. Provisional Application No. 61/777,073 filed 12 Mar
2013.
PCT Patent Application No. PCT/US2014/024724 filed 12 Mar
2014.
Related Technology: HHS Reference No. E-169-2008/0--
U.S. Patent No. 8,697,046 issued 15 Apr 2014 (Methods of
Administering Interferon Gamma to Absorb Fluid From the Subretinal
Space; Li R, et al.).
U.S. Patent Application No. 14/252,489 filed 14 Apr 2014.
Licensing Contact: Suryanarayana Vepa, Ph.D., J.D.; 301-435-5020;
vepas@mail.nih.gov.
Dated: March 7, 2015.
Richard U. Rodriguez,
Acting Director, Office of Technology Transfer, National Institutes of
Health.
[FR Doc. 2015-08290 Filed 4-9-15; 8:45 am]
BILLING CODE 4140-01-P
