Government-Owned Inventions; Availability for Licensing, 10286-10289 [2010-4757]
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• U.S. Provisional Application No.
61/004,940 filed 30 Nov 2007 (HHS
Reference No. E–042–2007/0–US–01).
• PCT Application No. PCT/US2008/
012064 filed 22 Oct 2008, which
published as WO 2009/073068 on 11
Jun 2009 (HHS Reference No. E–042–
2007/0–PCT–02).
Licensing Status: Available for
licensing.
Licensing Contact: Charlene Sydnor,
PhD; 301–435–4689;
sydnorc@mail.nih.gov.
Collaborative Research Opportunity:
The National Institute of Dental and
Craniofacial Research, Craniofacial and
Skeletal Diseases Branch, is seeking
statements of capability or interest from
parties interested in collaborative
research to further develop, evaluate, or
commercialize this technology. Please
contact David W. Bradley, PhD at 301–
402–0540 or bradleyda@nidcr.nih.gov
for more information.
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Gamma Substituted Peptide Nucleic
Acids
Description of Invention: PNAs are
nuclease/protease resistant synthetic
nucleic acid analogs capable of forming
very stable and highly sequence-specific
complexes with DNA. Scientists at the
NIH have developed novel peptide
nucleic acids (PNAs) that contain a
unique sidechain that can attach any
small ligand, peptide, or carbohydrate to
complementary DNA for rapid
optimization. This invention could
revolutionize the way in which
multivalent display is used in research
as well as help develop new
medications.
Applications:
• Controlled interactions ensure only
a single stoichiometry is attained.
• Simple access to a wide range of
multivalent platforms.
Development Status: Early stage.
Inventors: Daniel Appella (NIDDK)
Patent Status: U.S. Provisional
Application No. 61/162,175 filed 20 Mar
2009 (HHS Reference No. E–151–2009/
0–US–01).
Licensing Status: Available for
licensing.
Licensing Contact: Charlene Sydnor,
PhD; 301–435–4689;
sydnorc@mail.nih.gov.
Collaborative Research Opportunity:
The National Institute of Diabetes and
Digestive and Kidney Diseases,
Laboratory of Bioorganic Chemistry,
Drug-Receptor Interactions Section, is
seeking statements of capability or
interest from parties interested in
collaborative research to further
develop, evaluate, or commercialize this
technology. Please contact Dr. Daniel
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Appella at appellad@niddk.nih.gov for
more information.
Appella at appellad@niddk.nih.gov for
more information.
Use of Modified Peptide Nucleic Acids
for Visualizing DNA
Dated: March 1, 2010.
Richard U. Rodriguez,
Director, Division of Technology Development
and Transfer, Office of Technology Transfer,
National Institutes of Health.
Description of Technology: The
compounds described in this technology
may be useful in the development of
nucleic acid detection kits for various
pathogens.
Technologies for genomic detection
most commonly use DNA probes to
hybridize to target sequences, and
require the use of Polymerase Chain
Reaction (PCR) to amplify target
sequences. Replacing the DNA probe
with peptide nucleic acid (PNA) can
greatly eliminate the need for PCR
because the binding strength of PNAs to
complementary DNA is stronger than
DNA binding to complementary DNA.
In addition, PNAs are nuclease and
protease resistant, and form very stable
and highly sequence-specific complexes
with DNA.
This technology describes a method of
making pure enantiomers of trans-tertbutyl-2-aminocyclopentylcarbamate
(tcycp) and methods of modifying PNAs
by incorporating tcycp compounds into
the PNA. This technology may also be
practical for detecting infectious agents
such as anthrax, avian flu, tuberculosis
(TB), severe acute respiratory syndrome
(SARS), human papilloma virus (HPV)
and human immunodeficiency virus
(HIV).
Applications:
• Very stable diagnostic method to
detect nucleic acids without using
Polymerase Chain Reaction (PCR).
• Binding to complementary DNA
can be seen by eye.
• Visual detection of anthrax has
been shown.
• Useful for outside of a laboratory
environment.
Development Status: Early stage.
Inventors: Daniel Appella et al.
(NIDDK).
Patent Status: U.S. Patent Application
No. 12/441,925 filed 19 Mar 2009 (HHS
Reference No. E–308–2006/2–US–02).
Licensing Status: Available for
licensing.
Licensing Contact: Charlene Sydnor,
PhD; 301–435–4689;
sydnorc@mail.nih.gov.
Collaborative Research Opportunity:
The National Institute of Diabetes and
Digestive and Kidney Diseases,
Laboratory of Bioorganic Chemistry,
Drug-Receptor Interactions Section, is
seeking statements of capability or
interest from parties interested in
collaborative research to further
develop, evaluate, or commercialize this
technology. Please contact Dr. Daniel
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[FR Doc. 2010–4759 Filed 3–4–10; 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,
Public Health Service, HHS.
ACTION: Notice.
SUMMARY: The inventions listed below
are owned by an agency of the U.S.
Government and are available for
licensing in the U.S. in accordance with
35 U.S.C. 207 to achieve expeditious
commercialization of results of
federally-funded research and
development. Foreign patent
applications are filed on selected
inventions to extend market coverage
for companies and may also be available
for licensing.
ADDRESSES: Licensing information and
copies of the U.S. patent applications
listed below may be obtained by writing
to the indicated licensing contact at the
Office of Technology Transfer, National
Institutes of Health, 6011 Executive
Boulevard, Suite 325, Rockville,
Maryland 20852–3804; telephone: 301/
496–7057; fax: 301/402–0220. A signed
Confidential Disclosure Agreement will
be required to receive copies of the
patent applications.
Methods To Increase Stability of
Recombinant Vaccinia-Vectored
Vaccines and Increase Expression of a
Foreign Gene Inserted in Such Vaccines
Description of Invention: The
technology offered for licensing is in the
field of vaccinia-based recombinant
vaccines. In particular the invention
relates to methods of stabilizing the
recombinant virus, thus resulting in
efficient production of the vaccine and
efficient expression of the inserted gene.
Stabilization of the recombinant virus is
achieved by the insertion of the
exogenous gene into an intergenic
region (IGR) of the viral genome (i.e.
Modified Vaccinia Ankara, MVA),
where the IGR is flanked by open
reading frames of conserved poxvirus
genes. Furthermore, the invention
relates to plasmids vectors useful to
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Federal Register / Vol. 75, No. 43 / Friday, March 5, 2010 / Notices
insert the exogenous DNA into the
genome of a vaccinia virus. Stability can
be further enhanced by incorporating
silent mutations that decrease the
lengths of homopolynucleotide runs in
the foreign gene.
Applications:
• Efficient production of vacciniavectored vaccines for infectious diseases
and other diseases such as cancer.
• Efficient production of therapeutic
proteins from vaccinia-vectored
exogenous genes.
Advantages:
• Enhancing stability of foreign genes
in vaccinia-vectored constructs.
• Increasing efficiency of vaccine
production and gene expression.
Development Status: The invention is
fully developed.
Market: Vaccines development based
on vaccinia (e.g. MVA) vector inserted
with foreign gene of immunologic or
therapeutic interest has become one of
the most promising approaches for
vaccine development. Several
companies established vaccine
development programs based on this
approach and many research
laboratories around the world conduct
research in the area. Improvements in
the production process and in
production yields, such as provided by
the subject invention, are therefore of
great significance for successful
accomplishments in this area.
Commercial products for veterinary use
already exist. Many applications for
human use are now in various stages of
clinical trials, in particular applications
for HIV, HPV in the infectious disease
area and as therapeutic vaccine in the
cancer field. The market potential for
the subject technology is therefore vast.
Inventors: Bernard Moss et al.
(NIAID).
Related Publication: LS Wyatt, PL
Earl, W Xiao, J Americo, C Cotter, J
Vogt, B Moss. Elucidating and
minimizing the loss by recombinant
vaccinia virus of human
immunodeficiency virus gene
expression resulting from spontaneous
mutations and positive selections. J
Virol. 2009 Jul;83(14):7176–7184.
[PubMed: 19420086].
Patent Status: U.S. Provisional
Application No. 61/252,326 filed
October 16, 2009, entitled ‘‘Plasmid
Shuttle Vector for Insertion of Foreign
Genes into Del III Site of Modified
Vaccinia Ankara (MVA) to Increase
Stability of Foreign Gene Expression in
This Site’’ (HHS Reference No. E–018–
2010/0–US–01).
Related Technologies:
• WO 2008/142479 A2 (PCT/IB2007/
004575)—‘‘Intergenic Sites between
Conserved Genes In The Genome of
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Modified Vaccinia Ankara (MVA)
Vaccinia Virus,’’ Bernard Moss et al.
• US Patent 6,998,252; US Patent
7,015,024; US Patent 7,045,136; US
Patent 7,045,313—‘‘Recombinant
Vaccinia Virus Containing a Chimeric
Gene Having Foreign DNA Flanked by
Vaccinia Regulatory DNA,’’ Bernard
Moss et al.
Licensing Status: Available for
licensing.
Licensing Contacts: Uri Reichman,
PhD, MBA; 301–435–4616;
UR7a@nih.gov; or John Stansberry,
Ph.D.; 301–435–5236;
stansbej@mail.nih.gov.
Compounds That Interfere With the
Androgen Receptor Complex: Use in
Treating Prostate Cancer or
Enlargements, Diabetes, and as
Contraceptives
Description of Invention: Investigators
at the National Institutes of Health (NIH)
have discovered compounds that have
potential as novel anti-androgen
therapeutics. The immunophilin protein
FKBP52 is part of a protein complex
that helps fold the androgen receptor
(AR) protein, a target for treating
prostate cancer, and enhances its
activity. Disruption of the FKPB52–AR
interaction greatly reduces the activity
of the AR. With the goal of finding
potential therapeutic compounds that
inhibit the FKBP52-mediated activation
of AR, several small molecules were
tested and found to be antagonists of
FKBP52 and to inhibit AR activity in
prostate cells. These compounds can
serve as therapeutics for the treatment of
prostate cancer and benign prostate
enlargement. Moreover, FKBP52 is also
implicated in the regulation of other
hormone receptors so these compounds
could be used to treat other hormonedependent diseases such as diabetes or
even used as contraceptives.
One of the standard treatments for
prostate cancer makes use of antiandrogens, like bicalutamide, which
compete for binding with the natural
male hormones to AR and inhibit their
proliferative activity. The problem with
available anti-androgen drugs is that
prostate tumors eventually become drug
resistant resulting in so-called
androgen-resistant prostate cancer. One
cause of this is an increase in the levels
of AR produced by the prostate cancer
cells. A solution to this problem may lie
in disrupting the protein folding of AR
by interfering with its interaction with
FKBP52 using these compounds.
Applications:
• Use of the compounds for treatment
of prostate cancer and benign prostate
enlargement
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• Use of the compounds in treating
insulin-independent diabetes
• Use of the compounds as male or
female contraceptives
• Use in screening for compounds
that inhibit of FKBP52-enhanced AR
activity
Advantages:
• The compounds do not compete
with androgens and specifically inhibit
FKBP52-enhanced AR function
• Potential for synergistic use with
conventional anti-androgens for
treatment of androgen resistant prostate
cancer
Development Status: Pre-clinical.
Market: Prostate cancer is the second
most common type of cancer among
men in the United States and is the
second leading cause of cancer death in
men. It was estimated that in 2009 there
would be 192,280 new cases and 27,360
deaths from prostate cancer in the U.S.
The prevalence of benign prostate
enlargement is much greater as 50%
men age 50 are affected and continues
to increase with age.
Diabetes is a growing health problem
in the U.S. and the world. The most
recent estimate (2007 National Diabetes
Fact Sheet) in the U.S. was that 7.8% of
the population had diabetes and 1.6
million new cases per year would be
diagnosed. In the population of people
over 60 the prevalence of diabetes is
even higher (23%).
Among the 64 million women of
reproductive age in the U.S., the leading
contraceptive method is hormonal
contraceptives. Presently, there are no
hormonal contraceptives to reversibly
block fertility in men and there is a need
for safe and effective hormonal methods
as exist for women.
Inventors: Leonard M. Neckers (NCI),
Marc Cox (UTEP) et al.
Relevant Publication: J Cheung-Flynn
et al. Physiological role for the
cochaperone FKBP52 in androgen
receptor signaling. Mol Endocrinol.
2005 Jun;19(6):1654–1666. [PubMed:
15831525].
Patent Status: U.S. Provisional
Application No. 61/242,541 filed 15 Sep
2009 (HHS Reference No. E–162–2009/
0–US–01).
Licensing Status: Available for
licensing.
Licensing Contact: Sabarni Chatterjee,
Ph.D.; 301–435–5587;
chatterjeesa@mail.nih.gov.
Collaborative Research Opportunity:
The Center for Cancer Research,
Urologic Oncology Branch, is seeking
statements of capability or interest from
parties interested in collaborative
research to further develop, evaluate, or
commercialize antagonists of FKBP52dependent remodeling of the androgen
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receptor. Please contact John D. Hewes,
Ph.D. at 301–435–3121 or
hewesj@mail.nih.gov for more
information.
Radioprotectants and Tumor
Radiosensitizers Targeting
Thrombospondin-1 and CD47
Description of Invention: Radiation
therapy not only damages cancer cells,
but it also damages healthy cells and
can cause serious side effects for
patients. One effort to enhance the
therapeutic potential of radiotherapy,
while reducing its detrimental effects on
normal tissue and maintaining tumor
sensitivity, is centered upon the
development of radioprotective agents.
NIH inventors previously discovered
that when the secreted protein,
thrombospondin-1 (TSP1) binds to its
receptor CD47, this signaling pathway
prevents nitric oxide from dilating
blood vessels and increasing blood flow
to organs and tissues. They found that
blocking TSP1–CD47 interaction
through the use of antisense morpholino
oligonucleotides, peptides or antibodies
has several therapeutic benefits; one of
them being increased blood flow to
ischemic tissues.
In the present technology, the
inventors discovered that hindlimb
irradiated TSP1 and CD47 null mice
have less hair loss, and decreased cell
death in muscle and bone marrow than
untreated TSP1 and CD47 null mice.
They also discovered that when
irradiated human vascular cells are
treated with antibodies towards TSP1 or
CD47, viability and proliferative
capacity are preserved. Furthermore, the
inventors determined that irradiation of
wild type mice following treatment with
CD47 antisense morpholino resulted in
decreased apoptosis in irradiated tissues
at 24 hours, preservation of
hematopoietic stem cell proliferative
capacity in irradiated bone marrow, and
less alopecia, ulceration, and
desquamation at the end of eight weeks.
These results led the inventors to
propose that antagonists of TSP1 and/or
CD47 preserve cell viability and tissue
function following radiation treatment,
and these antagonists may be useful as
radioprotective agents to reduce side
effects associated with radiation
therapy. Remarkably, the same
treatment dramatically enhanced the
delay in melanoma and squamous
carcinoma tumor regrowth following
irradiation. Thus, these agents are
radioprotective agents for normal tissue
but radiosensitizers for tumor tissue.
The present technology describes the
use of morpholinos, peptides and
antibodies that block the TSP1/CD47
signaling pathway as radioprotectants
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for normal tissue, radioenhancers for
tumor tissue, and methods of selectively
protecting normal tissue from damage
caused by radiation exposure by
contacting the tissue with these agents.
Applications:
• Protect normal tissue from damage
following radiation therapy.
• Enhance tumor responses to
radiotherapy.
• Enable use of higher therapeutic
doses for radiotherapy of cancer.
• Protect personnel from radiation
injuries resulting from occupational
exposure to ionizing radiation, military
exposure, or terrorist acts.
Development Status: Mouse data
available. In vitro data available in
mouse, bovine, porcine, and human
cells.
Inventors: Jeffery S. Isenberg, David D.
Roberts, Justin B. Maxhimer (NCI)
Related Publications:
1. JB Maxhimer, DR Soto-Pantoja, LA
Ridnour, HB Shih, WG DeGraff, M
Tsokos, DA Wink, JS Isenberg, DD
Roberts. Radioprotection in normal
tissue and delayed tumor growth by
blockade of CD47 signaling. Sci Transl
Med. 21 October 2009; Vol 1, Issue 3,
pg. 3ra7; DOI:10.1126/
scitranslmed.3000139.
2. JS Isenberg, G Martin-Manso, JB
Maxhimer, DD Roberts. Regulation of
nitric oxide signaling by
thrombospondin-1: implications for
anti-angiogenic therapies. Nat Rev
Cancer. 2009 Mar;9(3):182–194.
[PubMed: 19194382]
3. JS Isenberg, JB Maxhimer, F Hyodo,
ML Pendrak, LA Ridnour, WG DeGraff,
M Tsokos, DA Wink, DD Roberts.
Thrombospondin-1 and CD47 limit cell
and tissue survival of radiation injury.
Am J Pathol. 2008;173(4):1100–1112.
[PubMed: 18787106]
Patent Status: PCT/US2009/052902
filed 05 Aug 2009 (HHS Reference No.
E–153–2008/0–PCT–02).
Licensing Status: Available for
licensing.
Licensing Contact: Charlene A.
Sydnor, Ph.D.; 301–435–4689;
sydnorc@mail.nih.gov.
Collaborative Research Opportunity:
The 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-targeting agents as
radioprotectants and tumor sensitizers.
Please contact John D. Hewes, Ph.D. at
301–435–3121 or hewesj@mail.nih.gov
for more information.
Mouse Lacking the Chemokine
Receptor CX3CR1
Description of Invention: This mouse
has been generated by targeted gene
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disruption. The mouse provides a model
to investigate the function of the
chemokine receptor CX3CR1, which is a
proinflammatory receptor for the
leukocyte chemoattractant CX3CL1 (aka
fractalkine). As an example, the mouse
is in use in the study of atherosclerosis.
Further, the mouse may serve as a
model study the role of the immune
system during infection with pathogens
as well as other immunologically
mediated diseases and responses to
tumors.
Inventors: Philip Murphy, Christopher
`
Combadiere, Ji-liang Gao (NIAID).
`
Related Publication: C Combadiere et
al. Decreased atheroscelerotic lesion
formation in CX3R1/ApoE double
knockout mice. Circulation 2003 Feb
25;107(7):1009–1016. [PubMed:
12600915].
Patent Status: HHS Reference No. E–
216–2003/0—Research Tool. Patent
protection is not being pursued for this
technology.
Licensing Status: Available for
licensing under a biological materials
license.
Licensing Contact: Susan Ano, Ph.D.;
301–435–5515; anos@mail.nih.gov.
Oligonucleotides Which Specifically
Bind Retroviral Nucleocapsid Proteins
Description of Invention: The human
immunodeficiency virus (HIV) is the
causative agent of acquired
immunodeficiency syndrome (AIDS). A
retroviral protein species, the gag
polyprotein, is involved in the assembly
of retrovirus particles and capable of
specific interactions with nucleic acids.
After the virion is released from the cell,
the polyprotein is cleaved by the virusencoded protease. One of the cleaved
products, the nucleocapsid (NC)
protein, then binds to genomic RNA,
forming the ribonucleoprotein core of
the mature particle. The interaction
between gag and genomic RNA is
known to involve the NC domain of the
polyprotein. In addition, the NC protein
plays crucial roles in both the reverse
transcription and integration steps in
the viral life cycle.
The present invention relates to
retroviral nucleocapsid proteins, such as
NC and the gag precursor, and their
ability to bind to specific nucleic acid
sequences with high affinity. The high
affinity of this interaction has potential
applications in the design of new
antiviral approaches and in sensitive
detection of HIV particles. Accordingly,
the invention provides for
oligonucleotides which bind to
nucleocapsid proteins with high
affinity, molecular decoys for retroviral
nucleocapsid proteins which inhibit
viral replication, targeted molecules
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comprising high affinity
oligonucleotides, assays for selecting
test compounds, and related kits.
Inventors: Alan R. Rein et al. (NCI).
Patent Status: U.S. Patent No.
6,316,190 issued 13 Nov 2001 (HHS
Reference No. E–107–1996/0–US–06).
Licensing Status: Available for
licensing.
Licensing Contact: Sally Hu, PhD;
301–435–5606; hus@mail.nih.gov.
Dated: March 1, 2010.
Richard U. Rodriguez,
Director, Division of Technology Development
and Transfer, Office of Technology Transfer,
National Institutes of Health.
[FR Doc. 2010–4757 Filed 3–4–10; 8:45 am]
BILLING CODE 4140–01–P
DEPARTMENT OF HEALTH AND
HUMAN SERVICES
Centers for Medicare & Medicaid
Services
Notice of Opportunity for a Hearing on
Compliance of Missouri State Plan
Provisions Concerning Payments for
Home Health Services With Title XIX
(Medicaid) of the Social Security Act
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AGENCY: Centers for Medicare &
Medicaid Services (CMS), HHS.
ACTION: Notice of Opportunity for a
Hearing; Compliance of Missouri
Medicaid State Plan Home Health
Benefit.
SUMMARY: This notice announces the
opportunity for an administrative
hearing to be held no later than 60 days
following publication in the Federal
Register at the CMS Kansas City
Regional Office, 601 E. 12th Street,
Kansas City, Missouri 64106, to
consider whether Missouri State plan
provisions concerning payments for
home health services comply with the
requirements of the Social Security Act
as discussed in the February 26, 2010
letter sent to the State and published
herein.
Closing Date: Requests to participate
in the hearing as a party must be
received by the presiding officer by
April 5, 2010.
FOR FURTHER INFORMATION CONTACT:
Benjamin R. Cohen, Presiding Officer,
CMS, 2520 Lord Baltimore Drive, Suite
L, Baltimore, Maryland 21244,
Telephone: (410) 786–3169.
SUPPLEMENTARY INFORMATION: This
notice announces the opportunity for an
administrative hearing concerning the
finding of the Administrator of the
Centers for Medicare & Medicaid
Services (CMS) that the approved State
plan under title XIX (Medicaid) of the
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Social Security Act (the Act) for the
State of Missouri is not in compliance
with the provisions of sections 1902(a)
of the Act and the proposed
withholding of Federal financial
participation for a portion of Missouri’s
expenditures for home health services.
In particular, CMS has found that the
State plan does not provide for home
health services for Medicaid
beneficiaries who are not ‘‘confined to
the home.’’ As a result of this
‘‘homebound’’ requirement, certain
Medicaid beneficiaries are not receiving
the full benefit package required under
the Act and applicable regulations.
Consequently, Federal payments for a
portion of the Federal funding for home
health services will be withheld, subject
to the opportunity for a hearing
described below. This notice is being
provided pursuant to the requirements
of section 1904 of the Act, as
implemented at 42 CFR 430.35 and 42
CFR part 430, subpart D.
Section 1902(a)(10)(D) requires that
State plans provide for the coverage of
home health services for any individual
who, under the State plan, is entitled to
nursing facility services. Nursing facility
services are a required service for
categorically needy populations under
section 1902(a)(10)(A), as defined in
section 1905(a)(4)(A). Under CMS
regulations, a service included as a
covered benefit under a State plan must
be ‘‘sufficient in amount, duration and
scope to reasonably achieve its purpose’’
(42 CFR 440.230(b)) and, for required
services, cannot be denied or reduced to
an eligible beneficiary ‘‘solely because of
the diagnosis, type of illness, or
condition’’ (42 CFR 440.230(c)). It is not
consistent with these requirements to
deny home health services to eligible
individuals who need such services on
the basis that they are not ‘‘homebound.’’
The CMS provided interpretive
guidance indicating that these statutory
requirements preclude denial of home
health services to eligible individuals
because they are not ‘‘homebound.’’ On
July 25, 2000, CMS, then the Health
Care Financing Administration, issued
Olmstead Update #3 which clarified
that the Medicare rule for home health
services requiring an individual to be
‘‘homebound’’ did not apply to the
receipt of Medicaid home health
services. Specifically, Olmstead Update
#3 states that the ‘‘homebound’’
requirement violates Federal regulatory
requirements at 42 CFR section
440.230(c) and section 440.240(b).
The ‘‘homebound’’ requirement in
Missouri was raised during the review
of Missouri State plan amendment
(SPA) 05–09. At that time, Missouri
chose to withdraw the page containing
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the ‘‘homebound’’ language but did not
reverse the policy. Since that time, there
have been numerous discussions
between CMS and Missouri regarding
this issue. On October 30, 2009, CMS
provided Missouri with notice of the
preliminary determination that it
appeared to be out of compliance with
Federal Medicaid requirements. In
addition, CMS requested that Missouri
submit a SPA to remove the
‘‘homebound’’ requirement.
In its response dated December 31,
2009, Missouri indicated that it was
operating under its approved State plan
and that the requirements of Missouri’s
home health program are the same as
those of the Federal Medicare program.
The State did not submit a SPA. CMS
believes that Missouri has had
numerous opportunities to come into
compliance with Federal requirements.
The notice to Missouri, dated
February 26, 2010, containing the
details concerning the compliance issue,
the proposed withhold, and the
opportunity for an administrative
hearing reads as follows:
CERTIFIED MAIL—RETURN RECEIPT
REQUESTED
Mr. Ronald J. Levy, Director,
Department of Social Services,
Broadway State Office Building,
Jefferson City, MO 65102.
Dear Mr. Levy: This letter provides
notice that the Centers for Medicare &
Medicaid Services (CMS) has found that
Missouri is not providing all Medicaid
beneficiaries with home health benefits
that are required under title XIX of the
Social Security Act (the Act) and that
until this deficiency is corrected (by
making home health services available
to all beneficiaries entitled to such
services), a portion of the Federal
funding for home health services will be
withheld, subject to the opportunity for
a hearing. The details of the finding,
proposed withholding, and opportunity
for a hearing are described in detail
below.
Specifically, CMS has found that the
approved Missouri State plan under title
XIX (Medicaid) of the Act is not in
compliance with the provisions of
section 1902(a) of the Act with respect
to the home health benefit. In particular,
CMS has found that the State plan does
not provide for home health services for
Medicaid beneficiaries who are not
‘‘confined to the home.’’ As a result of
this ‘‘homebound’’ requirement, certain
Medicaid beneficiaries are not receiving
the full benefit package required under
section 1902(a)(10) of the Act, which in
subparagraph (D) provides for the
inclusion of home health services in the
standard Medicaid benefit package.
E:\FR\FM\05MRN1.SGM
05MRN1
]]>Agencies
[Federal Register Volume 75, Number 43 (Friday, March 5, 2010)]
[Notices]
[Pages 10286-10289]
From the Federal Register Online via the Government Printing Office [www.gpo.gov]
[FR Doc No: 2010-4757]
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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.
ADDRESSES: Licensing information and copies of the U.S. patent
applications listed below may be obtained by writing to the indicated
licensing contact at the Office of Technology Transfer, National
Institutes of Health, 6011 Executive Boulevard, Suite 325, Rockville,
Maryland 20852-3804; telephone: 301/496-7057; fax: 301/402-0220. A
signed Confidential Disclosure Agreement will be required to receive
copies of the patent applications.
Methods To Increase Stability of Recombinant Vaccinia-Vectored Vaccines
and Increase Expression of a Foreign Gene Inserted in Such Vaccines
Description of Invention: The technology offered for licensing is
in the field of vaccinia-based recombinant vaccines. In particular the
invention relates to methods of stabilizing the recombinant virus, thus
resulting in efficient production of the vaccine and efficient
expression of the inserted gene. Stabilization of the recombinant virus
is achieved by the insertion of the exogenous gene into an intergenic
region (IGR) of the viral genome (i.e. Modified Vaccinia Ankara, MVA),
where the IGR is flanked by open reading frames of conserved poxvirus
genes. Furthermore, the invention relates to plasmids vectors useful to
[[Page 10287]]
insert the exogenous DNA into the genome of a vaccinia virus. Stability
can be further enhanced by incorporating silent mutations that decrease
the lengths of homopolynucleotide runs in the foreign gene.
Applications:
Efficient production of vaccinia-vectored vaccines for
infectious diseases and other diseases such as cancer.
Efficient production of therapeutic proteins from
vaccinia-vectored exogenous genes.
Advantages:
Enhancing stability of foreign genes in vaccinia-vectored
constructs.
Increasing efficiency of vaccine production and gene
expression.
Development Status: The invention is fully developed.
Market: Vaccines development based on vaccinia (e.g. MVA) vector
inserted with foreign gene of immunologic or therapeutic interest has
become one of the most promising approaches for vaccine development.
Several companies established vaccine development programs based on
this approach and many research laboratories around the world conduct
research in the area. Improvements in the production process and in
production yields, such as provided by the subject invention, are
therefore of great significance for successful accomplishments in this
area. Commercial products for veterinary use already exist. Many
applications for human use are now in various stages of clinical
trials, in particular applications for HIV, HPV in the infectious
disease area and as therapeutic vaccine in the cancer field. The market
potential for the subject technology is therefore vast.
Inventors: Bernard Moss et al. (NIAID).
Related Publication: LS Wyatt, PL Earl, W Xiao, J Americo, C
Cotter, J Vogt, B Moss. Elucidating and minimizing the loss by
recombinant vaccinia virus of human immunodeficiency virus gene
expression resulting from spontaneous mutations and positive
selections. J Virol. 2009 Jul;83(14):7176-7184. [PubMed: 19420086].
Patent Status: U.S. Provisional Application No. 61/252,326 filed
October 16, 2009, entitled ``Plasmid Shuttle Vector for Insertion of
Foreign Genes into Del III Site of Modified Vaccinia Ankara (MVA) to
Increase Stability of Foreign Gene Expression in This Site'' (HHS
Reference No. E-018-2010/0-US-01).
Related Technologies:
WO 2008/142479 A2 (PCT/IB2007/004575)--``Intergenic Sites
between Conserved Genes In The Genome of Modified Vaccinia Ankara (MVA)
Vaccinia Virus,'' Bernard Moss et al.
US Patent 6,998,252; US Patent 7,015,024; US Patent
7,045,136; US Patent 7,045,313--``Recombinant Vaccinia Virus Containing
a Chimeric Gene Having Foreign DNA Flanked by Vaccinia Regulatory
DNA,'' Bernard Moss et al.
Licensing Status: Available for licensing.
Licensing Contacts: Uri Reichman, PhD, MBA; 301-435-4616;
UR7a@nih.gov; or John Stansberry, Ph.D.; 301-435-5236;
stansbej@mail.nih.gov.
Compounds That Interfere With the Androgen Receptor Complex: Use in
Treating Prostate Cancer or Enlargements, Diabetes, and as
Contraceptives
Description of Invention: Investigators at the National Institutes
of Health (NIH) have discovered compounds that have potential as novel
anti-androgen therapeutics. The immunophilin protein FKBP52 is part of
a protein complex that helps fold the androgen receptor (AR) protein, a
target for treating prostate cancer, and enhances its activity.
Disruption of the FKPB52-AR interaction greatly reduces the activity of
the AR. With the goal of finding potential therapeutic compounds that
inhibit the FKBP52-mediated activation of AR, several small molecules
were tested and found to be antagonists of FKBP52 and to inhibit AR
activity in prostate cells. These compounds can serve as therapeutics
for the treatment of prostate cancer and benign prostate enlargement.
Moreover, FKBP52 is also implicated in the regulation of other hormone
receptors so these compounds could be used to treat other hormone-
dependent diseases such as diabetes or even used as contraceptives.
One of the standard treatments for prostate cancer makes use of
anti-androgens, like bicalutamide, which compete for binding with the
natural male hormones to AR and inhibit their proliferative activity.
The problem with available anti-androgen drugs is that prostate tumors
eventually become drug resistant resulting in so-called androgen-
resistant prostate cancer. One cause of this is an increase in the
levels of AR produced by the prostate cancer cells. A solution to this
problem may lie in disrupting the protein folding of AR by interfering
with its interaction with FKBP52 using these compounds.
Applications:
Use of the compounds for treatment of prostate cancer and
benign prostate enlargement
Use of the compounds in treating insulin-independent
diabetes
Use of the compounds as male or female contraceptives
Use in screening for compounds that inhibit of FKBP52-
enhanced AR activity
Advantages:
The compounds do not compete with androgens and
specifically inhibit FKBP52-enhanced AR function
Potential for synergistic use with conventional anti-
androgens for treatment of androgen resistant prostate cancer
Development Status: Pre-clinical.
Market: Prostate cancer is the second most common type of cancer
among men in the United States and is the second leading cause of
cancer death in men. It was estimated that in 2009 there would be
192,280 new cases and 27,360 deaths from prostate cancer in the U.S.
The prevalence of benign prostate enlargement is much greater as 50%
men age 50 are affected and continues to increase with age.
Diabetes is a growing health problem in the U.S. and the world. The
most recent estimate (2007 National Diabetes Fact Sheet) in the U.S.
was that 7.8% of the population had diabetes and 1.6 million new cases
per year would be diagnosed. In the population of people over 60 the
prevalence of diabetes is even higher (23%).
Among the 64 million women of reproductive age in the U.S., the
leading contraceptive method is hormonal contraceptives. Presently,
there are no hormonal contraceptives to reversibly block fertility in
men and there is a need for safe and effective hormonal methods as
exist for women.
Inventors: Leonard M. Neckers (NCI), Marc Cox (UTEP) et al.
Relevant Publication: J Cheung-Flynn et al. Physiological role for
the cochaperone FKBP52 in androgen receptor signaling. Mol Endocrinol.
2005 Jun;19(6):1654-1666. [PubMed: 15831525].
Patent Status: U.S. Provisional Application No. 61/242,541 filed 15
Sep 2009 (HHS Reference No. E-162-2009/0-US-01).
Licensing Status: Available for licensing.
Licensing Contact: Sabarni Chatterjee, Ph.D.; 301-435-5587;
chatterjeesa@mail.nih.gov.
Collaborative Research Opportunity: The Center for Cancer Research,
Urologic Oncology Branch, is seeking statements of capability or
interest from parties interested in collaborative research to further
develop, evaluate, or commercialize antagonists of FKBP52-dependent
remodeling of the androgen
[[Page 10288]]
receptor. Please contact John D. Hewes, Ph.D. at 301-435-3121 or
hewesj@mail.nih.gov for more information.
Radioprotectants and Tumor Radiosensitizers Targeting Thrombospondin-1
and CD47
Description of Invention: Radiation therapy not only damages cancer
cells, but it also damages healthy cells and can cause serious side
effects for patients. One effort to enhance the therapeutic potential
of radiotherapy, while reducing its detrimental effects on normal
tissue and maintaining tumor sensitivity, is centered upon the
development of radioprotective agents.
NIH inventors previously discovered that when the secreted protein,
thrombospondin-1 (TSP1) binds to its receptor CD47, this signaling
pathway prevents nitric oxide from dilating blood vessels and
increasing blood flow to organs and tissues. They found that blocking
TSP1-CD47 interaction through the use of antisense morpholino
oligonucleotides, peptides or antibodies has several therapeutic
benefits; one of them being increased blood flow to ischemic tissues.
In the present technology, the inventors discovered that hindlimb
irradiated TSP1 and CD47 null mice have less hair loss, and decreased
cell death in muscle and bone marrow than untreated TSP1 and CD47 null
mice. They also discovered that when irradiated human vascular cells
are treated with antibodies towards TSP1 or CD47, viability and
proliferative capacity are preserved. Furthermore, the inventors
determined that irradiation of wild type mice following treatment with
CD47 antisense morpholino resulted in decreased apoptosis in irradiated
tissues at 24 hours, preservation of hematopoietic stem cell
proliferative capacity in irradiated bone marrow, and less alopecia,
ulceration, and desquamation at the end of eight weeks. These results
led the inventors to propose that antagonists of TSP1 and/or CD47
preserve cell viability and tissue function following radiation
treatment, and these antagonists may be useful as radioprotective
agents to reduce side effects associated with radiation therapy.
Remarkably, the same treatment dramatically enhanced the delay in
melanoma and squamous carcinoma tumor regrowth following irradiation.
Thus, these agents are radioprotective agents for normal tissue but
radiosensitizers for tumor tissue.
The present technology describes the use of morpholinos, peptides
and antibodies that block the TSP1/CD47 signaling pathway as
radioprotectants for normal tissue, radioenhancers for tumor tissue,
and methods of selectively protecting normal tissue from damage caused
by radiation exposure by contacting the tissue with these agents.
Applications:
Protect normal tissue from damage following radiation
therapy.
Enhance tumor responses to radiotherapy.
Enable use of higher therapeutic doses for radiotherapy of
cancer.
Protect personnel from radiation injuries resulting from
occupational exposure to ionizing radiation, military exposure, or
terrorist acts.
Development Status: Mouse data available. In vitro data available
in mouse, bovine, porcine, and human cells.
Inventors: Jeffery S. Isenberg, David D. Roberts, Justin B.
Maxhimer (NCI)
Related Publications:
1. JB Maxhimer, DR Soto-Pantoja, LA Ridnour, HB Shih, WG DeGraff, M
Tsokos, DA Wink, JS Isenberg, DD Roberts. Radioprotection in normal
tissue and delayed tumor growth by blockade of CD47 signaling. Sci
Transl Med. 21 October 2009; Vol 1, Issue 3, pg. 3ra7; DOI:10.1126/
scitranslmed.3000139.
2. JS Isenberg, G Martin-Manso, JB Maxhimer, DD Roberts. Regulation
of nitric oxide signaling by thrombospondin-1: implications for anti-
angiogenic therapies. Nat Rev Cancer. 2009 Mar;9(3):182-194. [PubMed:
19194382]
3. JS Isenberg, JB Maxhimer, F Hyodo, ML Pendrak, LA Ridnour, WG
DeGraff, M Tsokos, DA Wink, DD Roberts. Thrombospondin-1 and CD47 limit
cell and tissue survival of radiation injury. Am J Pathol.
2008;173(4):1100-1112. [PubMed: 18787106]
Patent Status: PCT/US2009/052902 filed 05 Aug 2009 (HHS Reference
No. E-153-2008/0-PCT-02).
Licensing Status: Available for licensing.
Licensing Contact: Charlene A. Sydnor, Ph.D.; 301-435-4689;
sydnorc@mail.nih.gov.
Collaborative Research Opportunity: The 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-targeting agents as
radioprotectants and tumor sensitizers. Please contact John D. Hewes,
Ph.D. at 301-435-3121 or hewesj@mail.nih.gov for more information.
Mouse Lacking the Chemokine Receptor CX3CR1
Description of Invention: This mouse has been generated by targeted
gene disruption. The mouse provides a model to investigate the function
of the chemokine receptor CX3CR1, which is a proinflammatory receptor
for the leukocyte chemoattractant CX3CL1 (aka fractalkine). As an
example, the mouse is in use in the study of atherosclerosis. Further,
the mouse may serve as a model study the role of the immune system
during infection with pathogens as well as other immunologically
mediated diseases and responses to tumors.
Inventors: Philip Murphy, Christopher Combadi[egrave]re, Ji-liang
Gao (NIAID).
Related Publication: C Combadi[egrave]re et al. Decreased
atheroscelerotic lesion formation in CX3R1/ApoE double knockout mice.
Circulation 2003 Feb 25;107(7):1009-1016. [PubMed: 12600915].
Patent Status: HHS Reference No. E-216-2003/0--Research Tool.
Patent protection is not being pursued for this technology.
Licensing Status: Available for licensing under a biological
materials license.
Licensing Contact: Susan Ano, Ph.D.; 301-435-5515;
anos@mail.nih.gov.
Oligonucleotides Which Specifically Bind Retroviral Nucleocapsid
Proteins
Description of Invention: The human immunodeficiency virus (HIV) is
the causative agent of acquired immunodeficiency syndrome (AIDS). A
retroviral protein species, the gag polyprotein, is involved in the
assembly of retrovirus particles and capable of specific interactions
with nucleic acids. After the virion is released from the cell, the
polyprotein is cleaved by the virus-encoded protease. One of the
cleaved products, the nucleocapsid (NC) protein, then binds to genomic
RNA, forming the ribonucleoprotein core of the mature particle. The
interaction between gag and genomic RNA is known to involve the NC
domain of the polyprotein. In addition, the NC protein plays crucial
roles in both the reverse transcription and integration steps in the
viral life cycle.
The present invention relates to retroviral nucleocapsid proteins,
such as NC and the gag precursor, and their ability to bind to specific
nucleic acid sequences with high affinity. The high affinity of this
interaction has potential applications in the design of new antiviral
approaches and in sensitive detection of HIV particles. Accordingly,
the invention provides for oligonucleotides which bind to nucleocapsid
proteins with high affinity, molecular decoys for retroviral
nucleocapsid proteins which inhibit viral replication, targeted
molecules
[[Page 10289]]
comprising high affinity oligonucleotides, assays for selecting test
compounds, and related kits.
Inventors: Alan R. Rein et al. (NCI).
Patent Status: U.S. Patent No. 6,316,190 issued 13 Nov 2001 (HHS
Reference No. E-107-1996/0-US-06).
Licensing Status: Available for licensing.
Licensing Contact: Sally Hu, PhD; 301-435-5606; hus@mail.nih.gov.
Dated: March 1, 2010.
Richard U. Rodriguez,
Director, Division of Technology Development and Transfer, Office of
Technology Transfer, National Institutes of Health.
[FR Doc. 2010-4757 Filed 3-4-10; 8:45 am]
BILLING CODE 4140-01-P
