Government-Owned Inventions; Availability for Licensing, 69866-69869 [2012-28276]
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Federal Register / Vol. 77, No. 225 / Wednesday, November 21, 2012 / Notices
Estimated
number of
respondents
Data collection instrument(s)
Responses
per
respondent
Average burden hour per
response *
Total annual
burden hours
IHS 843–1A .....................................................................................................
7,977
52
3/60
20,740
Total ..........................................................................................................
........................
........................
........................
20,740
* For ease of understanding, burden hours are also provided in actual minutes.
The total estimated burden for this
collection is 20,740 hours.
There are no Capital Costs, Operating
Costs, and/or Maintenance Costs to
report.
Request for Comments: Your written
comments and/or suggestions are
invited on one or more of the following
points: (a) Whether the information
collection activity is necessary to carry
out an agency function; (b) whether the
IHS processes the information collected
in a useful and timely fashion; (c) the
accuracy of the public burden estimate
(this is the amount of time needed for
individual respondents to provide the
requested information); (d) whether the
methodology and assumptions used to
determine the estimate are logical; (e)
ways to enhance the quality, utility, and
clarity of the information being
collected; and (f) ways to minimize the
public burden through the use of
automated, electronic, mechanical, or
other technological collection
techniques or other forms of information
technology.
Send Comments and Requests for
Further Information: Send your written
comments and requests for more
information on the proposed collection
or requests to obtain a copy of the data
collection instrument(s) and
instructions to: Tamara Clay, IHS
Reports Clearance Officer, 801
Thompson Avenue, TMP, Suite 450,
Rockville, MD 20852; call non-toll free
(301) 443–1611; send via facsimile to
(301) 443–2316, or send your email
requests, comments, and return address
to tamara.clay@ihs.gov.
Comment Due Date: Your comments
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best assured of having their full effect if
received within 60-days of the date of
this publication.
srobinson on DSK4SPTVN1PROD with
Dated: November 9, 2012.
Yvette Roubideaux,
Director, Indian Health Service.
[FR Doc. 2012–28236 Filed 11–20–12; 8:45 am]
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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:
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.
SUMMARY:
A New Class, Now in Session: the First
HLA Class II Restricted T Cell Receptor
That Recognizes the Cancer Testis
Antigen, MAGE–A3, Developed for
Cancer Immunotherapy
Description of Technology: NIH
scientists have developed T cell
receptors (TCRs) against the melanoma
antigen family A3 (MAGE–A3) tumor
antigen in the context of major
histocompatibility complex (MHC) class
II molecule HLA–DP-beta1*04. They are
the first HLA class II restricted MAGE–
A3 TCRs developed for use in adoptive
immunotherapy. Previously developed
MAGE–A3 TCRs are HLA class I
restricted and generate CD8+ T cell
responses to mediate tumor regression
in some patients with MAGE–A3+
tumors. Other patients may not respond
due to a lack of CD4+ T cells
participation. Cancer immunotherapy
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with these new HLA class II TCRs could
yield a robust and effective CD4+ T cell
immune response that selectively targets
MAGE–A3 expressing tumors without
generating toxicity against healthy cells.
MAGE–A3 is a cancer testis antigen
expressed on many types of cancer cells
that blocks the functions of tumor
suppressor proteins to mediate tumor
growth and spreading. MAGE–A3 is not
expressed on normal cells other than
non-MHC expressing germ cells of the
testis, which do not generate an immune
response. Thus, MAGE–A3 represents
an ideal target for cancer
immunotherapies that are predicted to
generate fewer toxic side effects than
current standard cancer treatments.
Potential Commercial Applications:
• A personalized immunotherapy to
mediate regression of many types of
cancers using human T cells expressing
a HLA class II TCR.
• An adoptive immunotherapy
combining T cells engineered to express
a HLA class I restricted TCR with HLA
class II TCR-expressing T cells to
enhance the antitumor response by
eliciting CD8+ and CD4+ T cell immune
responses in patients.
• A research tool to investigate
signaling pathways in MAGE–A3
antigen expressing cancer cells.
• An in vitro diagnostic tool to screen
for cells expressing the MAGE–A3
tumor antigen.
Competitive Advantages:
• Class I restricted TCRs can only
treat a subset of patients, but since
∼80% of patients express the HLA–DPbeta1*04 class II HLA allele, this TCR
expands the population pool treatable
with MAGE–A3 TCRs to include the
majority of patients.
• MAGE–A3 is a highly expressed
tumor target on many cancer cells, so
MAGE–A3 TCR therapy should be a
viable treatment option for many cancer
cases.
• MAGE–A3 is only expressed on
tumor cells and non-MHC expressing
cells so these TCRs should target
MAGE–A3 expressing tumor cells with
little or no side effects/toxicity to
normal cells.
Development Stage:
• Early-stage.
• Pre-clinical.
• In vitro data available.
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Inventors: Paul Robbins, Xin Yao,
Steven Rosenberg (NCI).
Intellectual Property: HHS Reference
No. E–230–2012/0 — U.S. Patent
Application No. 61/701,056 filed 14 Sep
2012.
Related Technologies:
• HHS Reference No. E–236–2010/
0—PCT Patent Application No. PCT/
US2011/057272.
• HHS Reference No. E–266–2011/
0—PCT Patent Application No. PCT/
US2012/054623.
Licensing Contact: Samuel E. Bish,
Ph.D.; 301–435–5282; bishse@mail.nih.
gov.
srobinson on DSK4SPTVN1PROD with
Novel Small Molecule Agonists of the
Relaxin Receptor as Potential Therapy
for Heart Failure and Fibrosis
2. Additional manuscript is under
revision.
Intellectual Property: HHS Reference
No. E–072–2012/0—U.S. Provisional
Application No. 61/642,986 filed 04
May 2012.
Licensing Contact: Lauren NguyenAntczak, Ph.D., J.D.; 301–435–4074;
nguyenantczakla@mail.nih.gov.
Collaborative Research Opportunity:
The National Center for Advancing
Translational Sciences is seeking
statements of capability or interest from
parties interested in collaborative
research to further develop, evaluate, or
commercialize small molecule agonists
of RXFP1. For collaboration
opportunities, please contact Krishna
(Balki) Balakrishnan, Ph.D. at 301–217–
2336 or balki@nih.gov.
Description of Technology: The
present invention is directed to novel
small molecule agonists of the
mammalian relaxin family receptor 1
(RXFP1), including human RXFP1.
Activation of RXFP1 induces: (1)
Vasodilation due to up-regulation of the
endothelin system; (2) extracellular
matrix remodeling; (3) moderation of
inflammation by reducing levels of
inflammatory cytokines; and (4)
angiogenesis. Small molecule agonists
of RXFP1 may be useful in treating
acute heart failure (AHF), scleroderma,
fibrosis, other conditions associated
with the biology of relaxin, and in
improving reproductive health and
wound healing. These compounds are
the first and only small molecule
agonists of RXFP1.
Potential Commercial Applications:
Therapeutics for:
• Cardiovascular diseases.
• Ischemia.
• Fibrosis.
• Inflammation.
• Acute heart failure.
• Human and animal reproductive
health.
Competitive Advantages:
• First and only small molecule
agonists of RXFP1.
• Potent and highly selective.
• Bioavailable with excellent
exposure.
• Easy to synthesize and scale-up.
Development Stage:
• Early-stage.
• In vitro data available.
• In vivo data available (animal).
Inventors: Juan J. Marugan (NCATS),
et al.
Publications:
1. Chen ZC, et al. Identification of
small-molecule agonists of human
relaxin family receptor 1 (RXFP1) by
utilizing a homogeneous cell-based
cAMP assay. J. Biomol. Screen. 2012,
accepted.
Treatment of Tuberculosis—Adjuvant
Therapies To Increase the Efficiency of
Antibiotic Treatments
Description of Technology: There is
growing evidence that resistance to
Mycobacterium tuberculosis infection is
governed in large part by the regulation
of host cell death. Lipid mediators
called eicosanoids are thought to play a
central role in this process. The subject
invention is a novel method of
enhancing the efficacy of antibiotic
treatments for Mycobacterium
tuberculosis infection by coadministering an inhibitor of 5lipoxygenase and a COX–2 dependent
prostaglandin. Inhibition of 5lipoxygenase and treatment with
prostaglandin E2 results in alteration of
the eicosanoid balance. The synergistic
effects of altering the eicosanoid balance
and treatment with antibiotics is
believed to result in more efficient
reduction of the bacterial burden and
thus, the period of antibiotic
administration and antibiotic dosage
could potentially be reduced. In vivo
data from mouse models can be
provided upon request.
Potential Commercial Applications:
The subject invention can be used as an
adjuvant therapy for existing antibiotic
treatment regiments against
tuberculosis.
Competitive Advantages: The
disclosed method can be applied to
increase the efficacy of existing
antibiotic treatments for tuberculosis,
potentially reducing both the duration
and dosage of the antibiotic treatment.
Development State:
• Early-stage.
• Pre-clinical.
• In vitro data available.
• In vivo data available (animal).
Inventors: Katrin D. Mayer, Bruno
Bezerril D. Andrade, F. Alan Sher, and
Daniel L. Barber (NIAID).
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Intellectual Property:
• HHS Reference No. E–189–2011/
0—U.S. Provisional Patent Application
No. 61/515,229 filed 04 Aug 2011.
• HHS Reference No. E–189–2011/
1—U.S. Provisional Patent Application
No. 61/515,237 filed 04 Aug 2011.
• HHS Reference No. E–189–2011/
2—International Application No. PCT/
US2012/049280 filed 02 Aug 2012.
Licensing Contact: Kevin W. Chang,
Ph.D.; 301–435–5018; changke@mail.
nih.gov.
Collaborative Research Opportunity:
The National Institute of Allergy and
Infectious Diseases is seeking statements
of capability or interest from parties
interested in collaborative research to
further develop, evaluate or
commercialize adjuvant therapy for
antibiotic treatment regiments against
tuberculosis. For collaboration
opportunities, please contact Katrin
Mayer, Ph.D. at mayerk@niaid.nih.gov
or 301–594–8061.
Adeno-Associated Virus Gene Therapy
for Diabetes and Obesity
Description of Technology: This
invention is directed to adenoassociated virus (AAV) vector delivery
of exendin-4 (Ex-4) to salivary glands as
treatment for diabetes and obesity. Ex4 is a potent and long-acting agonist of
the receptor for glucagon-like peptide 1
(GLP–1). Scientists at NIDCR have
shown that AAV-mediated delivery of
Ex-4 resulted in improved glucose
homeostasis and weight profile in two
rat models of obesity and type 2
diabetes. Further, AAV-mediated
delivery of Ex-4 to rat salivary glands
resulted in localized and sustained
expression of Ex-4 that was biologically
active and well tolerated.
AAV-mediated delivery of Ex-4 is
superior to administering GLP–1
analogs in that AAV-Ex-4 expression is
more stable and longer acting. Like
GLP–1 analogs, Ex-4 expression also
potentially provides beneficial effects
like reduced hypoglycemia, appetite
suppression, and potential weight loss.
Potential Commercial Applications:
Therapy for diabetes or obesity.
Competitive Advantages:
• Potential for potent glucose
homeostasis therapy with longer
duration than current drugs.
• More convenient than daily or
weekly injections.
Development Stage:
• Early-stage.
• In vitro data available.
• In vivo data available (animal).
Inventors: John A. Chiorini (NIDCR),
Giovanni DiPasquale (NIDCR), Edoardo
Mannucci (Careggi Teaching Hospital).
Publication: Di Pasquale G, et al.
Sustained exendin-4 secretion through
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srobinson on DSK4SPTVN1PROD with
gene therapy targeting salivary glands in
two different rodent models of obesity/
type 2 diabetes. PLoS One.
2012;7(7):e40074. [PMID 22808093]
Intellectual Property: HHS Reference
No. E–142–2011/0—
• U.S. Application No. 61/477,523
filed 20 May 2011.
• PCT Application No. PCT/US2012/
34268 filed 19 Apr 2012.
Licensing Contact: Lauren NguyenAntczak, Ph.D., J.D.; 301–435–4074;
nguyenantczakla@mail.nih.gov.
Collaborative Research Opportunity:
The NIDCR is seeking statements of
capability or interest from parties
interested in collaborative research to
further develop, evaluate, or
commercialize treatment of diabetes by
expression NGF-extendin 4 protein. For
collaboration opportunities, please
contact David Bradley, Ph.D. at 301–
402–9242 or bradleyda@nidcr.nih.gov.
Small Molecule MRS5474 With
Anticonvulsant Activity for Treatment
of Epilepsy
Description of Technology: Adenosine
modulates many physiological
processes by activating specific
adenosine receptors. These adenosine
receptors play a critical role in the
regulation of cellular signaling and are
broadly distributed throughout the
body. Thus, the ability to modulate
adenosine receptor-mediated signaling
is an attractive therapeutic strategy for
a broad range of diseases. This
technology relates to a group of
compounds that display high affinity
and specificity for the A1 adenosine
receptor subtype.
One of the compounds, MRS5474,
displays anticonvulsant activity in the 6
Hz animal model of clonic seizures. In
the minimal behavioral toxicity test
using the rotarod, no toxicity (zero out
of eight mice) was observed at all doses
tested up to 30 mg/kg, the highest dose
tested, which was nearly completely
protective (seven out of eight animals)
in the 6 Hz model. MRS 5474 also tested
well in the corneal kindled mouse
model to examine its effect on focal
seizures.
Potential Commercial Applications:
• Oral anticonvulsant drug.
• Provides a means to mimic A1AR
mediated signaling in vitro and in vivo.
Competitive Advantages:
• These small molecules display
increased specificity for the A1 type of
adenosine receptors, which may reduce
unwanted side effects previously seen
in A1AR agonist therapies.
• The physical properties of these
molecules are drug-like, which makes
them attractive for pre-clinical
development.
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Development Stage:
• Early-stage.
• In vitro data available.
• In vivo data available (animal).
Inventor: Kenneth A. Jacobson
(NIDDK).
Publication: Tosh DK, et al. Truncated
(N)-Methanocarba Nucleosides as A1
Adenosine Receptor Agonists and
Partial Agonists: Receptor Docking and
Potent Anticonvulsant Activity. In
preparation.
Intellectual Property:
• HHS Reference No. E–285–2008/
0—International Application No. PCT/
US2009/52439 filed 31 Jul 2009.
• HHS Reference No. E–285–2008/
1—U.S. Patent Application No. 13/
479,973 filed 24 May 2012.
Licensing Contact: Betty B. Tong,
Ph.D.; 301–594–6565; tongb@mail.nih.
gov.
Collaborative Research Opportunity:
The NIDDK is seeking statements of
capability or interest from parties
interested in collaborative research to
further develop, evaluate, or
commercialize MRS5474, A1 adenosine
receptor agonist for treatment of
seizures. For collaboration
opportunities, please contact Marguerite
Miller at millermarg@mail.nih.gov.
Glucocorticoid-Induced TNFR FamilyRelated Receptor Ligand (GITRL)
Antibodies for Diagnosis and Treatment
of Immune System Disorders
Description of Technology: This
technology provides novel antibodies
and methods for diagnostics and
treatment of disorders arising from
dysregulation of the immune system
using antibodies directed against
glucocorticoid-induced tumor necrosis
factor receptor family-related receptor
ligand (GITRL). Also available are
hybridomas producing anti-mouse
GITRL monoclonal antibodies (clone
5F1).
Glucocorticoid-induced TNFR familyrelated receptor (GITR, also known as
TNFRSF18) is expressed on the surface
of responder T cells (CD4+CD25- or
CD8+CD25- T cells). Upon activation of
the immune response, GITR is upregulated and binds to its ligand, GITRL
(also known as TNFSF18), which
enhances the immune response. The
inventors have developed anti-GITRL
monoclonal antibodies that block the
interaction between GITR and GITRL,
and have demonstrated in in vitro
experiments that administration of these
blocking antibodies can suppress the
immune response. These antibodies
may be useful for treatment of immune
system disorders such as multiple
sclerosis, rheumatoid arthritis, and
other inflammatory diseases.
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Potential Commercial Applications:
• Development of therapeutic agents
for autoimmune diseases, including
autoimmune and inflammatory diseases,
allergy and transplant rejection.
• Tool for investigating the role of
GITRL in enhancement of the T-cell
mediated immune response.
Competitive Advantages: The GITR/
GITRL pathway is a novel target for the
treatment of autoimmune diseases.
Development Stage:
• In vitro data available.
• In vivo data available (animal).
Inventors: Ethan Shevach et al.
(NIAID).
Publication: Stephens GL, et al.
Engagement of glucocorticoid-induced
TNFR family-related receptor on effector
T cells by its ligand mediates resistance
to suppression by CD4+CD25+ T cells.
J Immunol. 2004 Oct 15;173(8):5008–20.
[PMID 15470044].
Intellectual Property: HHS Reference
No. E–229–2003/2—
• U.S. Patent No. 7,618,632 issued 17
Nov 2009.
• JP Patent No. 4638876 issued 03
Dec 2010.
Licensing Contact: Tara L. Kirby.
Ph.D.; 301–435–4426; tarak@mail.nih.
gov.
Treatment for Ichthyosiform Skin
Diseases
Description of Technology: A
synthetic composition that contains the
transglutaminase 1 (TGase I) enzyme
and a lipid vesicle, which can be used
to provide ameliorative therapy for
inherited autosomal recessive
ichthyoses (ARI). Icthyoses are rare
inherited skin disorders that result in
extensive scaling of the skin. Because
this abnormality can affect heat and
fluid transfer through the skin,
individuals with this disease may have
an increased risk for dehydration and
skin infections. Each year, more than
16,000 babies are born with some form
of ichthyosis. Ichthyosis affects people
of all ages, races and gender. Currently,
there is no cure for this disease and the
only treatments available alleviate
symptoms without affecting the disease
itself. ARI are often caused by defects in
lipid barrier function in the skin and are
the result of genetic errors of either
protein or lipid synthesis. One such
disease, termed lamellar ichthyosis, is
caused by genetic inactivation of the
(TGase I) gene. The TGase I enzyme is
essential for maintaining proper skin
cornification, which protects skin cells
against water loss and infection. Rather
than simply treating the disease
symptoms superficially, this technology
provides a platform for treating the
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Federal Register / Vol. 77, No. 225 / Wednesday, November 21, 2012 / Notices
underlying cause of disease, namely the
absence of TGase I function.
Potential Commercial Applications:
• Treatment for ichthyosiform skin
diseases.
• Method for correcting defects in
skin cell cornification.
Competitive Advantages: Targets
underlying cause of skin disorder rather
than just treating the resulting
symptoms.
Development Stage:
• Early-stage.
• In vitro data available.
Inventors: Peter M Steinert, Nemes
Zoltan, Lyuben N Marckov (NIAMS).
Publications:
1. Candi E, et al. Transglutaminase 1
mutations in lamellar ichthyosis. Loss of
activity due to failure of activation by
proteolytic processing. J Biol Chem.
1998 May 29;273(22):13693–702. [PMID
9593710]
2. Yang YM, et al. Novel mutations of
the transglutaminase 1 gene in lamellar
ichthyosis. J Invest Dermatol. 2001
Aug;117(2):214–8. [PMID 11511296]
Intellectual Property: HHS Reference
No. E–149–1999/0—U.S. Patent No.
6,852,686 issued 08 Feb 2005.
Licensing Contact: Suryanarayana
Vepa, Ph.D., J.D.; 301–435–5020;
vepas@mail.nih.gov.
Special Emphasis Panel, PAR 12–151:
Centers of Excellence for Research on
Complementary Alternative Medicine (CAM).
Date: January 16–18, 2013.
Time: 5 p.m. to 5 p.m..
Agenda: To review and evaluate grant
applications.
Place: Bethesda North Marriott Hotel &
Conference Center, 5701 Marinelli Road,
Bethesda, MD 20852.
Contact Person: Martina Schmidt, Ph.D.
Scientific Review Officer, Office of Scientific
Review, National Center for Complementary,
& Alternative Medicine, NIH, 6707
Democracy Blvd., Suite 401, Bethesda, MD
20892, 301–594–3456,
schmidma@mail.nih.gov.
(Catalogue of Federal Domestic Assistance
Program Nos. 93.213, Research and Training
in Complementary and Alternative Medicine,
National Institutes of Health, HHS)
Dated: November 16, 2012.
Richard U. Rodriguez,
Director, Division of Technology Development
and Transfer, Office of Technology Transfer,
National Institutes of Health.
National Advisory Council on Alcohol
Abuse and Alcoholism, National
Advisory Council on Drug Abuse, and
National Cancer Advisory Board;
Notice of Joint Meeting
Dated: November 15, 2012.
Michelle Trout,
Program Analyst, Office of Federal Advisory
Committee Policy.
[FR Doc. 2012–28278 Filed 11–20–12; 8:45 am]
BILLING CODE 4140–01–P
DEPARTMENT OF HEALTH AND
HUMAN SERVICES
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[FR Doc. 2012–28276 Filed 11–20–12; 8:45 am]
Pursuant to section 10(a) of the
Federal Advisory Committee Act, as
amended (5 U.S.C. App.), notice is
hereby given of a joint teleconference
and Web cast meeting of the National
Advisory Council on Alcohol Abuse and
Alcoholism, National Advisory Council
on Drug Abuse, and National Cancer
Advisory Board. The meeting will be
open to the public as indicated below.
BILLING CODE 4140–01–P
DEPARTMENT OF HEALTH AND
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National Institutes of Health
srobinson on DSK4SPTVN1PROD with
National Center for Complementary
and Alternative Medicine; 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: National Center for
Complementary and Alternative Medicine
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Name of Committee: National Advisory
Council on Alcohol Abuse and Alcoholism,
National Advisory Council on Drug Abuse,
and National Cancer Advisory Board.
Date: December 13, 2012.
Time: 11:30 a.m. to 1:00 p.m. EST.
Agenda: NIH report on the functional
integration of substance use, abuse and
addiction-related research and discussion
with the NIH Principal Deputy Director and
Members of NIAAA and NIDA Councils, and
the NCAB.
Teleconference Line: 1–888–324–8014
(toll-free); Passcode: 4418818.
Webcast Site: https://webmeeting.nih.gov/
suaa/.
Contact Persons: Abraham Bautista, Ph.D.,
Office of Extramural Activities, National
Institute on Alcohol Abuse and Alcoholism,
National Institutes of Health, 5635 Fishers
Lane, RM 2085, Rockville, MD 20892, 301–
443–9737, bautista@mail.nih.gov.
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Teresa Levitin, Ph.D., Office of Extramural
Affairs, National Institute on Drug Abuse,
National Institutes of Health, 6001 Executive
Blvd., RM 4243, Rockville, MD 20852, 301–
443–2755, tlevitin@nida.nih.gov. Paulette S.
Gray, Ph.D., 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(s) by
forwarding the statement to a Contact Person
listed on this notice. The statement should
include the name, address, telephone number
and when applicable, the business or
professional affiliation of the interested
person.
Information will also be available on the
Institute’s/Center’s home pages: https://
www.niaaa.nih.gov/AboutNIAAA/
AdvisoryCouncil/Pages/default.aspx, https://
www.drugabuse.gov/about/organization/
nacda/NACDAHome.html, and https://
deainfo.nci.nih.gov/advisory/ncab/ncab.htm,
as well as NIH’s Feedback page: https://
feedback.nih.gov, where an agenda and any
additional information for the meeting will
be posted when available.
(Catalogue of Federal Domestic Assistance
Program Nos.: 93.271, Alcohol Research
Career Development Awards for Scientists
and Clinicians; 93.272, Alcohol National
Research Service Awards for Research
Training; 93.273, Alcohol Research Programs;
93.891, Alcohol Research Center Grants;
93.701, ARRA Related Biomedical Research
and Research Support Awards, National
Institutes of Health, HHS)
Dated: November 16, 2012.
Jennifer S. Spaeth,
Director, Office of Federal Advisory
Committee Policy.
[FR Doc. 2012–28277 Filed 11–20–12; 8:45 am]
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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. 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.
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]]>Agencies
[Federal Register Volume 77, Number 225 (Wednesday, November 21, 2012)]
[Notices]
[Pages 69866-69869]
From the Federal Register Online via the Government Printing Office [www.gpo.gov]
[FR Doc No: 2012-28276]
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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.
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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.
A New Class, Now in Session: the First HLA Class II Restricted T Cell
Receptor That Recognizes the Cancer Testis Antigen, MAGE-A3, Developed
for Cancer Immunotherapy
Description of Technology: NIH scientists have developed T cell
receptors (TCRs) against the melanoma antigen family A3 (MAGE-A3) tumor
antigen in the context of major histocompatibility complex (MHC) class
II molecule HLA-DP-beta1*04. They are the first HLA class II restricted
MAGE-A3 TCRs developed for use in adoptive immunotherapy. Previously
developed MAGE-A3 TCRs are HLA class I restricted and generate CD8+ T
cell responses to mediate tumor regression in some patients with MAGE-
A3+ tumors. Other patients may not respond due to a lack of CD4+ T
cells participation. Cancer immunotherapy with these new HLA class II
TCRs could yield a robust and effective CD4+ T cell immune response
that selectively targets MAGE-A3 expressing tumors without generating
toxicity against healthy cells.
MAGE-A3 is a cancer testis antigen expressed on many types of
cancer cells that blocks the functions of tumor suppressor proteins to
mediate tumor growth and spreading. MAGE-A3 is not expressed on normal
cells other than non-MHC expressing germ cells of the testis, which do
not generate an immune response. Thus, MAGE-A3 represents an ideal
target for cancer immunotherapies that are predicted to generate fewer
toxic side effects than current standard cancer treatments.
Potential Commercial Applications:
A personalized immunotherapy to mediate regression of many
types of cancers using human T cells expressing a HLA class II TCR.
An adoptive immunotherapy combining T cells engineered to
express a HLA class I restricted TCR with HLA class II TCR-expressing T
cells to enhance the antitumor response by eliciting CD8+ and CD4+ T
cell immune responses in patients.
A research tool to investigate signaling pathways in MAGE-
A3 antigen expressing cancer cells.
An in vitro diagnostic tool to screen for cells expressing
the MAGE-A3 tumor antigen.
Competitive Advantages:
Class I restricted TCRs can only treat a subset of
patients, but since ~80% of patients express the HLA-DP-beta1*04 class
II HLA allele, this TCR expands the population pool treatable with
MAGE-A3 TCRs to include the majority of patients.
MAGE-A3 is a highly expressed tumor target on many cancer
cells, so MAGE-A3 TCR therapy should be a viable treatment option for
many cancer cases.
MAGE-A3 is only expressed on tumor cells and non-MHC
expressing cells so these TCRs should target MAGE-A3 expressing tumor
cells with little or no side effects/toxicity to normal cells.
Development Stage:
Early-stage.
Pre-clinical.
In vitro data available.
[[Page 69867]]
Inventors: Paul Robbins, Xin Yao, Steven Rosenberg (NCI).
Intellectual Property: HHS Reference No. E-230-2012/0 -- U.S.
Patent Application No. 61/701,056 filed 14 Sep 2012.
Related Technologies:
HHS Reference No. E-236-2010/0--PCT Patent Application No.
PCT/US2011/057272.
HHS Reference No. E-266-2011/0--PCT Patent Application No.
PCT/US2012/054623.
Licensing Contact: Samuel E. Bish, Ph.D.; 301-435-5282;
bishse@mail.nih.gov.
Novel Small Molecule Agonists of the Relaxin Receptor as Potential
Therapy for Heart Failure and Fibrosis
Description of Technology: The present invention is directed to
novel small molecule agonists of the mammalian relaxin family receptor
1 (RXFP1), including human RXFP1. Activation of RXFP1 induces: (1)
Vasodilation due to up-regulation of the endothelin system; (2)
extracellular matrix remodeling; (3) moderation of inflammation by
reducing levels of inflammatory cytokines; and (4) angiogenesis. Small
molecule agonists of RXFP1 may be useful in treating acute heart
failure (AHF), scleroderma, fibrosis, other conditions associated with
the biology of relaxin, and in improving reproductive health and wound
healing. These compounds are the first and only small molecule agonists
of RXFP1.
Potential Commercial Applications: Therapeutics for:
Cardiovascular diseases.
Ischemia.
Fibrosis.
Inflammation.
Acute heart failure.
Human and animal reproductive health.
Competitive Advantages:
First and only small molecule agonists of RXFP1.
Potent and highly selective.
Bioavailable with excellent exposure.
Easy to synthesize and scale-up.
Development Stage:
Early-stage.
In vitro data available.
In vivo data available (animal).
Inventors: Juan J. Marugan (NCATS), et al.
Publications:
1. Chen ZC, et al. Identification of small-molecule agonists of
human relaxin family receptor 1 (RXFP1) by utilizing a homogeneous
cell-based cAMP assay. J. Biomol. Screen. 2012, accepted.
2. Additional manuscript is under revision.
Intellectual Property: HHS Reference No. E-072-2012/0--U.S.
Provisional Application No. 61/642,986 filed 04 May 2012.
Licensing Contact: Lauren Nguyen-Antczak, Ph.D., J.D.; 301-435-
4074; nguyenantczakla@mail.nih.gov.
Collaborative Research Opportunity: The National Center for
Advancing Translational Sciences is seeking statements of capability or
interest from parties interested in collaborative research to further
develop, evaluate, or commercialize small molecule agonists of RXFP1.
For collaboration opportunities, please contact Krishna (Balki)
Balakrishnan, Ph.D. at 301-217-2336 or balki@nih.gov.
Treatment of Tuberculosis--Adjuvant Therapies To Increase the
Efficiency of Antibiotic Treatments
Description of Technology: There is growing evidence that
resistance to Mycobacterium tuberculosis infection is governed in large
part by the regulation of host cell death. Lipid mediators called
eicosanoids are thought to play a central role in this process. The
subject invention is a novel method of enhancing the efficacy of
antibiotic treatments for Mycobacterium tuberculosis infection by co-
administering an inhibitor of 5-lipoxygenase and a COX-2 dependent
prostaglandin. Inhibition of 5-lipoxygenase and treatment with
prostaglandin E2 results in alteration of the eicosanoid balance. The
synergistic effects of altering the eicosanoid balance and treatment
with antibiotics is believed to result in more efficient reduction of
the bacterial burden and thus, the period of antibiotic administration
and antibiotic dosage could potentially be reduced. In vivo data from
mouse models can be provided upon request.
Potential Commercial Applications: The subject invention can be
used as an adjuvant therapy for existing antibiotic treatment regiments
against tuberculosis.
Competitive Advantages: The disclosed method can be applied to
increase the efficacy of existing antibiotic treatments for
tuberculosis, potentially reducing both the duration and dosage of the
antibiotic treatment.
Development State:
Early-stage.
Pre-clinical.
In vitro data available.
In vivo data available (animal).
Inventors: Katrin D. Mayer, Bruno Bezerril D. Andrade, F. Alan
Sher, and Daniel L. Barber (NIAID).
Intellectual Property:
HHS Reference No. E-189-2011/0--U.S. Provisional Patent
Application No. 61/515,229 filed 04 Aug 2011.
HHS Reference No. E-189-2011/1--U.S. Provisional Patent
Application No. 61/515,237 filed 04 Aug 2011.
HHS Reference No. E-189-2011/2--International Application
No. PCT/US2012/049280 filed 02 Aug 2012.
Licensing Contact: Kevin W. Chang, Ph.D.; 301-435-5018;
changke@mail.nih.gov.
Collaborative Research Opportunity: The National Institute of
Allergy and Infectious Diseases is seeking statements of capability or
interest from parties interested in collaborative research to further
develop, evaluate or commercialize adjuvant therapy for antibiotic
treatment regiments against tuberculosis. For collaboration
opportunities, please contact Katrin Mayer, Ph.D. at
mayerk@niaid.nih.gov or 301-594-8061.
Adeno-Associated Virus Gene Therapy for Diabetes and Obesity
Description of Technology: This invention is directed to adeno-
associated virus (AAV) vector delivery of exendin-4 (Ex-4) to salivary
glands as treatment for diabetes and obesity. Ex-4 is a potent and
long-acting agonist of the receptor for glucagon-like peptide 1 (GLP-
1). Scientists at NIDCR have shown that AAV-mediated delivery of Ex-4
resulted in improved glucose homeostasis and weight profile in two rat
models of obesity and type 2 diabetes. Further, AAV-mediated delivery
of Ex-4 to rat salivary glands resulted in localized and sustained
expression of Ex-4 that was biologically active and well tolerated.
AAV-mediated delivery of Ex-4 is superior to administering GLP-1
analogs in that AAV-Ex-4 expression is more stable and longer acting.
Like GLP-1 analogs, Ex-4 expression also potentially provides
beneficial effects like reduced hypoglycemia, appetite suppression, and
potential weight loss.
Potential Commercial Applications: Therapy for diabetes or obesity.
Competitive Advantages:
Potential for potent glucose homeostasis therapy with
longer duration than current drugs.
More convenient than daily or weekly injections.
Development Stage:
Early-stage.
In vitro data available.
In vivo data available (animal).
Inventors: John A. Chiorini (NIDCR), Giovanni DiPasquale (NIDCR),
Edoardo Mannucci (Careggi Teaching Hospital).
Publication: Di Pasquale G, et al. Sustained exendin-4 secretion
through
[[Page 69868]]
gene therapy targeting salivary glands in two different rodent models
of obesity/type 2 diabetes. PLoS One. 2012;7(7):e40074. [PMID 22808093]
Intellectual Property: HHS Reference No. E-142-2011/0--
U.S. Application No. 61/477,523 filed 20 May 2011.
PCT Application No. PCT/US2012/34268 filed 19 Apr 2012.
Licensing Contact: Lauren Nguyen-Antczak, Ph.D., J.D.; 301-435-
4074; nguyenantczakla@mail.nih.gov.
Collaborative Research Opportunity: The NIDCR is seeking statements
of capability or interest from parties interested in collaborative
research to further develop, evaluate, or commercialize treatment of
diabetes by expression NGF-extendin 4 protein. For collaboration
opportunities, please contact David Bradley, Ph.D. at 301-402-9242 or
bradleyda@nidcr.nih.gov.
Small Molecule MRS5474 With Anticonvulsant Activity for Treatment of
Epilepsy
Description of Technology: Adenosine modulates many physiological
processes by activating specific adenosine receptors. These adenosine
receptors play a critical role in the regulation of cellular signaling
and are broadly distributed throughout the body. Thus, the ability to
modulate adenosine receptor-mediated signaling is an attractive
therapeutic strategy for a broad range of diseases. This technology
relates to a group of compounds that display high affinity and
specificity for the A1 adenosine receptor subtype.
One of the compounds, MRS5474, displays anticonvulsant activity in
the 6 Hz animal model of clonic seizures. In the minimal behavioral
toxicity test using the rotarod, no toxicity (zero out of eight mice)
was observed at all doses tested up to 30 mg/kg, the highest dose
tested, which was nearly completely protective (seven out of eight
animals) in the 6 Hz model. MRS 5474 also tested well in the corneal
kindled mouse model to examine its effect on focal seizures.
Potential Commercial Applications:
Oral anticonvulsant drug.
Provides a means to mimic A1AR mediated signaling in vitro
and in vivo.
Competitive Advantages:
These small molecules display increased specificity for
the A1 type of adenosine receptors, which may reduce unwanted side
effects previously seen in A1AR agonist therapies.
The physical properties of these molecules are drug-like,
which makes them attractive for pre-clinical development.
Development Stage:
Early-stage.
In vitro data available.
In vivo data available (animal).
Inventor: Kenneth A. Jacobson (NIDDK).
Publication: Tosh DK, et al. Truncated (N)-Methanocarba Nucleosides
as A1 Adenosine Receptor Agonists and Partial Agonists: Receptor
Docking and Potent Anticonvulsant Activity. In preparation.
Intellectual Property:
HHS Reference No. E-285-2008/0--International Application
No. PCT/US2009/52439 filed 31 Jul 2009.
HHS Reference No. E-285-2008/1--U.S. Patent Application
No. 13/479,973 filed 24 May 2012.
Licensing Contact: Betty B. Tong, Ph.D.; 301-594-6565;
tongb@mail.nih.gov.
Collaborative Research Opportunity: The NIDDK is seeking statements
of capability or interest from parties interested in collaborative
research to further develop, evaluate, or commercialize MRS5474, A1
adenosine receptor agonist for treatment of seizures. For collaboration
opportunities, please contact Marguerite Miller at
millermarg@mail.nih.gov.
Glucocorticoid-Induced TNFR Family-Related Receptor Ligand (GITRL)
Antibodies for Diagnosis and Treatment of Immune System Disorders
Description of Technology: This technology provides novel
antibodies and methods for diagnostics and treatment of disorders
arising from dysregulation of the immune system using antibodies
directed against glucocorticoid-induced tumor necrosis factor receptor
family-related receptor ligand (GITRL). Also available are hybridomas
producing anti-mouse GITRL monoclonal antibodies (clone 5F1).
Glucocorticoid-induced TNFR family-related receptor (GITR, also
known as TNFRSF18) is expressed on the surface of responder T cells
(CD4+CD25- or CD8+CD25- T cells). Upon activation of the immune
response, GITR is up-regulated and binds to its ligand, GITRL (also
known as TNFSF18), which enhances the immune response. The inventors
have developed anti-GITRL monoclonal antibodies that block the
interaction between GITR and GITRL, and have demonstrated in in vitro
experiments that administration of these blocking antibodies can
suppress the immune response. These antibodies may be useful for
treatment of immune system disorders such as multiple sclerosis,
rheumatoid arthritis, and other inflammatory diseases.
Potential Commercial Applications:
Development of therapeutic agents for autoimmune diseases,
including autoimmune and inflammatory diseases, allergy and transplant
rejection.
Tool for investigating the role of GITRL in enhancement of
the T-cell mediated immune response.
Competitive Advantages: The GITR/GITRL pathway is a novel target
for the treatment of autoimmune diseases.
Development Stage:
In vitro data available.
In vivo data available (animal).
Inventors: Ethan Shevach et al. (NIAID).
Publication: Stephens GL, et al. Engagement of glucocorticoid-
induced TNFR family-related receptor on effector T cells by its ligand
mediates resistance to suppression by CD4+CD25+ T cells. J Immunol.
2004 Oct 15;173(8):5008-20. [PMID 15470044].
Intellectual Property: HHS Reference No. E-229-2003/2--
U.S. Patent No. 7,618,632 issued 17 Nov 2009.
JP Patent No. 4638876 issued 03 Dec 2010.
Licensing Contact: Tara L. Kirby. Ph.D.; 301-435-4426;
tarak@mail.nih.gov.
Treatment for Ichthyosiform Skin Diseases
Description of Technology: A synthetic composition that contains
the transglutaminase 1 (TGase I) enzyme and a lipid vesicle, which can
be used to provide ameliorative therapy for inherited autosomal
recessive ichthyoses (ARI). Icthyoses are rare inherited skin disorders
that result in extensive scaling of the skin. Because this abnormality
can affect heat and fluid transfer through the skin, individuals with
this disease may have an increased risk for dehydration and skin
infections. Each year, more than 16,000 babies are born with some form
of ichthyosis. Ichthyosis affects people of all ages, races and gender.
Currently, there is no cure for this disease and the only treatments
available alleviate symptoms without affecting the disease itself. ARI
are often caused by defects in lipid barrier function in the skin and
are the result of genetic errors of either protein or lipid synthesis.
One such disease, termed lamellar ichthyosis, is caused by genetic
inactivation of the (TGase I) gene. The TGase I enzyme is essential for
maintaining proper skin cornification, which protects skin cells
against water loss and infection. Rather than simply treating the
disease symptoms superficially, this technology provides a platform for
treating the
[[Page 69869]]
underlying cause of disease, namely the absence of TGase I function.
Potential Commercial Applications:
Treatment for ichthyosiform skin diseases.
Method for correcting defects in skin cell cornification.
Competitive Advantages: Targets underlying cause of skin disorder
rather than just treating the resulting symptoms.
Development Stage:
Early-stage.
In vitro data available.
Inventors: Peter M Steinert, Nemes Zoltan, Lyuben N Marckov
(NIAMS).
Publications:
1. Candi E, et al. Transglutaminase 1 mutations in lamellar
ichthyosis. Loss of activity due to failure of activation by
proteolytic processing. J Biol Chem. 1998 May 29;273(22):13693-702.
[PMID 9593710]
2. Yang YM, et al. Novel mutations of the transglutaminase 1 gene
in lamellar ichthyosis. J Invest Dermatol. 2001 Aug;117(2):214-8. [PMID
11511296]
Intellectual Property: HHS Reference No. E-149-1999/0--U.S. Patent
No. 6,852,686 issued 08 Feb 2005.
Licensing Contact: Suryanarayana Vepa, Ph.D., J.D.; 301-435-5020;
vepas@mail.nih.gov.
Dated: November 16, 2012.
Richard U. Rodriguez,
Director, Division of Technology Development and Transfer, Office of
Technology Transfer, National Institutes of Health.
[FR Doc. 2012-28276 Filed 11-20-12; 8:45 am]
BILLING CODE 4140-01-P
