Government-Owned Inventions; Availability for Licensing, 61458-61460 [05-21118]
Download as PDF
<![CDATA[
61458
Federal Register / Vol. 70, No. 204 / Monday, October 24, 2005 / Notices
parents/guardians of children who were
seen in an emergency department for an
injury. This information will be
collected in conjunction with the
Consumer Product Safety Commission’s
(CPSC’s) National Electronic Injury
Surveillance System (NEISS). The
NEISS is part of CPSC’s routine data
collection. Through this system, trained
abstractors code information from all
injury-related emergency department
visits in the participating hospital.
Additional information will be collected
through ‘‘follow-back’’ phone interviews
with parents/guardians of injured
children seen in participating hospitals.
NICHD will collect information on
developmental disabilities among
injured children e.g., cerebral palsy,
blindness, deafness or trouble hearing,
autism, and mental retardation),
medical/psychological conditions e.g.
epilepsy/seizures, ADHD), medication
use, and other potential risk factors for
injury including family structure,
sibling characteristics, and caregiver
supervision practices. Finally, NICHD
would like to determine if typically
developing children who have a sibling
with a developmental disability, who
may compete for supervisory time, are
at a greater risk of injury than other
children. This Interagency Agreement
provides funds from NICHD to CPSC to
complete 8000 telephone interviews
with parents/guardians of injured
children. The sample of interviewees
will be derived from a larger sample of
children who will be systematically
selected from the NEISS system.
Sampling will cover an entire year to
account for seasonal variations in injury
Estimated
numbers of
respondents
Type of respondents
Parents/guardians ............................................................................................
Request for Comments
Written comments and/or suggestions
from the public and affected agencies
should address one or more of the
following points: (1) Evaluate whether
the proposed collection of information
is necessary for the proper performance
of the function of the agency, including
whether the information will have
practical utility; (2) Evaluate the
accuracy of the agency’s estimate of the
burden of the proposed collection of
information, including the validity of
the methodology and assumptions used;
(3) Enhance the quality, utility, and
clarity of the information to be
collected; and (4) Minimize the burden
of the collection of information on those
who are to respond, including the use
of appropriate automated, electronic,
mechanical, or other technological
collection techniques or other forms of
information technology.
To
request more information on the
proposed project or to obtain a copy of
the data collection plans and
instruments, contact: Gitanjali Saluja,
Ph.D., 6100 Executive Blvd. Suite 7B03,
Rockville, MD 20852. Phone: 301–435–
6917. E-mail: salujag@mail.nih.gov
FOR FURTHER INFORMATION CONTACT:
Comments Due Date
Comments regarding this information
collection are best assured of having
their full effect if received within 60days of the date of this publication.
VerDate Aug<31>2005
15:19 Oct 21, 2005
Jkt 208001
BILLING CODE 4140–01–P
DEPARTMENT OF HEALTH AND
HUMAN SERVICES
National Institutes of Health
Government-Owned Inventions;
Availability for Licensing
National Institutes of Health,
Public Health Service, DHHS.
ACTION: Notice.
AGENCY:
SUMMARY: The inventions listed below
are owned by an agency of the U.S.
Government and are available for
licensing in the U.S. in accordance with
35 U.S.C. 207 to achieve expeditious
commercialization of results of
federally-funded research and
development. Foreign patent
applications are filed on selected
inventions to extend market coverage
for companies and may also be available
for licensing.
ADDRESSES: Licensing information and
copies of the U.S. patent applications
listed below may be obtained by writing
to the indicated licensing contact at the
Office of Technology Transfer, National
Institutes of Health, 6011 Executive
Boulevard, Suite 325, Rockville,
Maryland 20852–3804; telephone: 301/
Frm 00036
Fmt 4703
Sfmt 4703
Estimated
number of
responses per
respondent
8000
Dated: October 13, 2005.
Paul L. Johnson,
Project Clearance Liaison, NICHD, National
Institutes of Health.
[FR Doc. 05–21116 Filed 10–21–05; 8:45 am]
PO 00000
rates. Two thousand interviews will be
conducted in 4 different age groups: 0–
4 years, 5–9 years, 10–14 years, and 15–
19 years. Intentional injuries will not be
included in the sampling pool. Further,
deaths and hospitalizations will be
excluded. Interviews will be limited to
those who can complete an interview in
English or Spanish. Frequency of
Response: One interview; Affected
Public: Individuals or households; Type
of Respondents: Parents or Guardians;
The annual reporting burden is as
follows: Estimated Number of
Respondents: 8000. Estimated Number
of Responses per Respondent: 1;
Average Burden Hours Per Response
0.33; and Estimated Total Annual
Burden Hours Requested: 2640. There
are no Capital Costs, Operating Costs
and/or Maintenance Costs to report.
1
Average
burden hours
per response
.33
Estimated total
annual burden
hours
requested
2640
496–7057; fax: 301/402–0220. A signed
Confidential Disclosure Agreement will
be required to receive copies of the
patent applications.
NIH3T3 Cell Lines Carrying c-Met
Mutations Including G3906A, G3522A,
G3810T, T3936C, T3936G, T3997C,
C3528T, C3564G, C3831G, A3529T, and
T3640C
Laura S. Schmidt (NCI).
HHS Reference No. E–327–2005/0—
Research Tool.
Licensing Contact: John Stansberry; 301/
435–5236: stansbej@mail.nih.gov.
MET is over expressed in a variety of
cancers including hereditary papillary
renal cell carcinoma and non-small cell
lung cancer. These cell lines carry
naturally-occurring Met mutations and
were derived from the germline of
patients with hereditary papillary renal
cell carcinoma. These cell lines can be
used as drug discovery research
reagents.
These cell lines were described in
part in Schmidt et al., ‘‘Novel mutations
of the MET proto-oncogene in papillary
renal carcinomas. Oncogene. (1999)
18:2343–2350 and Jeffers et al.,
‘‘Activating mutations for the met
tyrosine kinase receptor in human
cancer.’’ PNAS (1997) 94:11445–11450.
In addition to licensing, the
technology is available for further
development through collaborative
research opportunities with the
inventors.
E:\FR\FM\24OCN1.SGM
24OCN1
Federal Register / Vol. 70, No. 204 / Monday, October 24, 2005 / Notices
Mouse Fibroblasts Stably Expressing CType Lectin Receptors DC–SIGN and L–
SIGN
Vineet N. KewelRamani and Thomas
Martin (NCI).
HHS Reference Nos. E–321–2005/0 and
E–322–2005/0—Research Tools.
Licensing Contact: Susan Ano; 301/435–
5515; anos@mail.nih.gov.
The NIH is pleased to offer for
licensing mouse fibroblasts that stably
express the C-type lectin receptors DC–
SIGN and L–SIGN (CD209 and CD209L,
respectively). L–SIGN and DC–SIGN
both exhibit selectivity for highly
mannosylated glycoproteins. DC–SIGN
is also selective for certain Lewis X
sugar groups. These types of
interactions allow L–SIGN and DC–
SIGN to interact with a wide spectrum
of pathogens including HIV, hepatitis C
virus, and SARS coronavirus, which
appear to use L–SIGN and DC–SIGN to
facilitate their replication. In addition to
HIV, HCV, and SARS, pathogens such as
Ebola virus, some herpes viruses, and
tuberculosis interact with DC–SIGN. In
contrast to primary cells expressing L–
SIGN and DC–SIGN, the subject
fibroblasts are resilient, adhere to coated
tissue culture plates, grow rapidly and
continually express high levels of their
respective receptor. The subject
materials could be used to study the
interaction of pathogens with L–SIGN or
DC–SIGN and to screen for compounds
that block these interactions.
Additionally, the materials could be
used for the development of antibodies
or compounds through rational design
that interacted with L–SIGN or DC–
SIGN. The NIH3T3/DC–SIGN and
NIH3T3/L–SIGN cells are further
described in Journal of Virology, 2002,
vol. 26(12), pages 5905–5914. The
subject technologies are available for
licensing from the NIH through
biological materials license agreements.
Murine Mast Cell Line Useful for
Toxicity and Immunopotency Screens
Michael Potter (NCI).
HHS Reference No. E–274–2005/0—
Research Tool.
Licensing Contact: John Stansberry; 301/
435–5236; stansbej@mail.nih.gov.
The technology is a mouse cell line
(P815) that could be useful for screening
biological and chemical agents for
toxicity and immunopotency.
Specifically, the cell line is useful for
screening for toxic effects of
immunopotentiators including
Mycobacterium bovis, Bacillus
Calmette-Gurerin strain, zymosan,
lipopolysaccharide and dextran sulfate.
The cell line may also have application
in screening other compounds.
VerDate Aug<31>2005
15:19 Oct 21, 2005
Jkt 208001
The cell line may also prove useful for
studies of cancer and tumor
immunology as injection of mice with
P815 leads to progressive tumors. The
P815 tumors express cell surface
antigens that could provide a model for
cancer vaccine development.
Mutated Pseudomonas Exotoxins with
Reduced Antigenicity
Ira H. Pastan et al. (NCI).
U.S. Provisional Patent Application
filed 29 Jul 2005 (HHS Reference No.
E–262–2005/0–US–01).
Licensing Contact: Jesse S. Kindra; 301–
435–5559; kindraj@mail.nih.gov.
The use of Pseudomonas exotoxins
(PE) for treatment of solid tumors, in
particular, has been limited because of
the development of neutralizing
antibodies to the immunotoxin after the
first administration. These antibodies
develop before most protocols would
call for a second administration of the
immunotoxin, and therefore render
further use of the immunotoxins
ineffective against solid tumors in
previously exposed patients.
The studies underlying this novel
invention reveal that the predominant
immune response of patients to PEimmunotoxins is the PE portion of the
immunotoxin. This finding indicates
that reducing the antigenicity of the PE
molecules used for immunotoxins
would reduce the overall antigenicity of
the immunotoxin, and increase their
utility.
Therefore, this invention relates to
mutated Pseudomonas exotoxins (PE)
that have reduced antigenicity
compared to PEs containing the native
sequence. The PEs of this invention
have one or more individual mutations
that reduce antibody binding to one or
more epitopes of PE.
In addition to licensing, the
technology is available for further
development through collaborative
research opportunities with the
inventors.
61459
(5,10-methylenetrahydrofolate
dehydrogenase, 5,10methenyltetrahydrofolate
cyclohydrolase, 10formyltetrahydrofolate synthase) and
methylenetetrahydrofolate
dehydrogenase (NADP+ dependent) 1like (MTHFD1L). These enzymes are
extremely important in the promotion of
DNA synthesis, a process that is critical
for normal placental and fetal
development.
Recently, the inventors have
discovered that a MTHFD1
polymorphism is also a strong maternal
genetic risk factor for placental
abruption, premature separation of a
normally implanted placenta. This
polymorphism may also be a risk factor
for first and second trimester
miscarriages. Diagnostic and therapeutic
methods are provided in this invention
involving the correlation of
polymorphic variants in MTHFD1 and
other genes with relative susceptibility
for various pregnancy-related and other
complications such as cancer,
cardiovascular disease, and
developmental anomalies. Both nutrient
status and genetic background are
independent yet interacting risk factors
for impaired folate metabolism.
However, the mechanisms that lead to
pathology or the mechanisms whereby
folate prevents these disorders are
unknown. Therefore, a diagnostic and
therapeutic invention of this kind
would significantly improve the
detection and treatment of disorders
associated with folate metabolism.
For further information, see Brody
et al., July 28, 2005, ‘‘A polymorphism
in the MTHFD1 gene increases a
mother’s risk of having an unexplained
second trimester pregnancy loss,’’ Mol.
Hum. Reprod. 10.1093/molehr/gah204.
In addition to licensing, the
technology is available for further
development through collaborative
research opportunities with the
inventors.
AAV5 Vector and Uses Thereof
John A. Chiorini, Robert M. Kotin
(NHLBI).
U.S. Provisional Application No. 60/
Lawrence C. Brody (NHGRI) et al.
087,029 filed 28 May 1998 (HHS
PCT Application No. PCT/US05/21288
Reference No. E–127–1998/0–US–01).
filed 16 Jun 2005 (HHS Reference No. U.S. Patent Application No. 09/717,789
E–149–2005/0–PCT–01).
filed 21 Nov 2000 (HHS Reference No.
Licensing Contact: Marlene Shinn-Astor;
E–127–1998/0–US–07).
301/435–4426; shinnm@mail.nih.gov. U.S. Patent Application Serial No. 11/
184,380 filed 19 Jul 2005 (HHS
This invention relates to materials
Reference No. E–127–1998/0–US–08).
and methods associated with
Licensing Contact: Jesse S. Kindra; 301/
polymorphic variants in two enzymes
435–5559; kindraj@mail.nih.gov.
involved in folate-dependent and oneThe invention described and claimed
carbon metabolic pathways important in
in this patent application provides for
pregnancy-related complications and
novel vectors and viral particles which
neural tube birth defects: MTHFD1
Methods and Materials for Identifying
Polymorphic Variants, Diagnosing
Susceptibilities, and Treating Disease
PO 00000
Frm 00037
Fmt 4703
Sfmt 4703
E:\FR\FM\24OCN1.SGM
24OCN1
61460
Federal Register / Vol. 70, No. 204 / Monday, October 24, 2005 / Notices
comprise adeno-associated virus
serotype 5 (AAV5). AAV5 is a singlestranded DNA virus of either plus or
minus polarity which, like other AAV
serotypes (e.g., AAV4, AAV2) requires a
helper virus for replication. AAV type 2
has the interesting and potentially
useful ability to integrate into human
chromosome 19 q 13.3-q ter. This
activity is dependent on the nonstructural, Rep, proteins of AAV2. The
Rep proteins of AAV types 2 and 5 are
dissimilar and are not able to substitute
in DNA replication of the heterologous
serotype.
AAV5 offers several advantages which
make it attractive for use in gene
therapy: 1. Increased production (10–50
fold greater than AAV2); 2. distinct
integration locus when compared to
AAV2; 3. Rep protein and ITR regions
do not complement other AAV
serotypes; and 4. appears to utilize
different cell surface attachment
molecules than those of AAV type 2.
In addition to licensing, the
technology may be available for further
development through collaborative
research opportunities with the
inventors.
The Use of Nitroxides in the
Prophylactic and Therapeutic
Treatment of Cancer Due to Genetic
Defects
James Mitchell, Angelo Russo, Anne
Deluca and Murali Cherukuri (NCI).
U.S. Patent Application No. 09/424,519
filed 03 Mar 2000, claiming priority to
27 May 1997 (HHS Reference No. E–
167–1997/0–US–07).
Licensing Contact: George Pipia; 301/
435–5560; pipiag@mail.nih.gov.
The invention is a method for
preventing or treating cancer, especially
cancers associated with defects in the
p53 gene. This gene is generally
considered to be a tumor-suppressor
gene, and in a large percentage of
malignancies including pancreatic,
colon, lung, and breast, the gene is
found to be inactive in the cancer. It is
believed that many individuals have
genetic defects in p53 predisposing
them to cancer.
The invention involves the use of
certain nitroxides as agents to slow the
appearance or progression of tumors
associated with p53 knockout. Thus,
these compounds could serve as
preventative agents for people
predisposed to cancer, or as therapeutic
agents for certain cancers. As nitroxides
have already been identified as
antioxidants, such agents could become
part of a cancer prevention and antiaging regimen. A new method of use for
these compounds now include their use
in imaging, which correlates functional
VerDate Aug<31>2005
15:19 Oct 21, 2005
Jkt 208001
information about the tumor with
magnetic resonance imaging data.
Dated: October 13, 2005.
Steven M. Ferguson,
Director, Division of Technology Development
and Transfer, Office of Technology Transfer,
National Institutes of Health.
[FR Doc. 05–21118 Filed 10–21–05; 8:45 am]
BILLING CODE 4140–01–P
DEPARTMENT OF HEALTH AND
HUMAN SERVICES
National Institutes of Health
National Cancer Institute; Notice of
Closed Meeting
Pursuant to section 10(d) of the
Federal Advisory Committee Act, as
amended (5 U.S.C. Appendix 2), notice
is hereby given of the following
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 Cancer
Institute Special Emphasis Panel PAR–04–
020: Small Grants for Behavioral Research in
Cancer Control
Date: November 9, 2005.
Time: 8 a.m. to 5 p.m.
Agenda: To review and evaluate grant
applications
Place: Gaithersburg Marriott
Washingtonian Center, 9751 Washington
Boulevard, Gaithersburg, MD 20878
Contact Person: C. Michael Kerwin, PhD,
MPH, Scientific Review Administrator,
Special Review and Logistics Branch,
Division of Extramural Activities, National
Cancer Institute, National Institutes of
Health, 6116 Executive Boulevard, Room
8057, MSC 8329, Bethesda, MD 20892–8329,
301–496–7421, kerwinm@mail.nih.gov.
(Catalogue of Federal Domestic Assistance
Program Nos. 93.392, Cancer Construction;
93.393, Cancer Cause and Prevention
Research; 93.394, Cancer Detection and
Diagnosis Research; 93.395, Cancer
Treatment Research; 93.396, Cancer Biology
Research; 93.397, Cancer Centers Support;
93.398, Cancer Research Manpower; 93.399,
Cancer Control, National Institutes of Health,
HHS)
PO 00000
Frm 00038
Fmt 4703
Sfmt 4703
Dated: October 13, 2005.
Anthony M. Coelho, Jr.,
Acting Director, Office of Federal Advisory
Committee Policy.
[FR Doc. 05–21124 Filed 10–21–05; 8:45 am]
BILLING CODE 4140–01–M
DEPARTMENT OF HEALTH AND
HUMAN SERVICES
National Institutes of Health
National Heart, Lung, and Blood
Institute; Notice of Closed Meeting
Pursuant to section 10(d) of the
Federal Advisory Committee Act, as
amended (5 U.S.C. Appendix 2), notice
is hereby given of the following
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 contract proposals and
the discussions could disclose
confidential trade secrets or commercial
property such as patentable material,
and personal information concerning
individuals associated with the contract
proposals, the disclosure of which
would constitute a clearly unwarranted
invasion of personal privacy.
Name of Committee: National Heart, Lung,
and Blood Institute Special Emphasis Panel
Large-Scale Genotyping of NHLBI Cohorts
Date: October 20, 2005.
Time: 1 p.m. to 4 p.m.
Agenda: To review and evaluate contract
proposals
Place: National Institutes of Health, 6701
Rockledge Drive, Bethesda, MD 20892,
(Telephone Conference Call).
Contact Person: Valerie L Prenger, PhD,
Chief, Review Branch, Division of Extramural
Affairs, National Heart, Lung, and Blood
Institute, 6701 Rockledge Drive, MSC 7924,
Room 7214, Bethesda, MD 20892–7924, 301–
435–0270, prengerv@nhlbi.nih.gov.
This notice is being published less than 15
days prior to the meeting due to the timing
limitations imposed by the review and
funding cycle.
(Catalogue of Federal Domestic Assistance
Program Nos. 93.233, National Center for
Sleep Disorders Research; 93.837, Heart and
Vascular Diseases Research; 93.838, Lung
Diseases Research; 93.839, Blood Diseases
and Resources Research, National Institutes
of Health, HHS)
October 24, 2005.
Anthony M. Coelho, Jr.,
Acting Director, Office of Federal Advisory
Committee Policy.
[FR Doc. 05–21133 Filed 10–21–05; 8:45 am]
BILLING CODE 4140–01–M
E:\FR\FM\24OCN1.SGM
24OCN1
]]>Agencies
[Federal Register Volume 70, Number 204 (Monday, October 24, 2005)]
[Notices]
[Pages 61458-61460]
From the Federal Register Online via the Government Printing Office [www.gpo.gov]
[FR Doc No: 05-21118]
-----------------------------------------------------------------------
DEPARTMENT OF HEALTH AND HUMAN SERVICES
National Institutes of Health
Government-Owned Inventions; Availability for Licensing
AGENCY: National Institutes of Health, Public Health Service, DHHS.
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.
NIH3T3 Cell Lines Carrying c-Met Mutations Including G3906A, G3522A,
G3810T, T3936C, T3936G, T3997C, C3528T, C3564G, C3831G, A3529T, and
T3640C
Laura S. Schmidt (NCI).
HHS Reference No. E-327-2005/0--Research Tool.
Licensing Contact: John Stansberry; 301/435-5236:
stansbej@mail.nih.gov.
MET is over expressed in a variety of cancers including hereditary
papillary renal cell carcinoma and non-small cell lung cancer. These
cell lines carry naturally-occurring Met mutations and were derived
from the germline of patients with hereditary papillary renal cell
carcinoma. These cell lines can be used as drug discovery research
reagents.
These cell lines were described in part in Schmidt et al., ``Novel
mutations of the MET proto-oncogene in papillary renal carcinomas.
Oncogene. (1999) 18:2343-2350 and Jeffers et al., ``Activating
mutations for the met tyrosine kinase receptor in human cancer.'' PNAS
(1997) 94:11445-11450.
In addition to licensing, the technology is available for further
development through collaborative research opportunities with the
inventors.
[[Page 61459]]
Mouse Fibroblasts Stably Expressing C-Type Lectin Receptors DC-SIGN and
L-SIGN
Vineet N. KewelRamani and Thomas Martin (NCI).
HHS Reference Nos. E-321-2005/0 and E-322-2005/0--Research Tools.
Licensing Contact: Susan Ano; 301/435-5515; anos@mail.nih.gov.
The NIH is pleased to offer for licensing mouse fibroblasts that
stably express the C-type lectin receptors DC-SIGN and L-SIGN (CD209
and CD209L, respectively). L-SIGN and DC-SIGN both exhibit selectivity
for highly mannosylated glycoproteins. DC-SIGN is also selective for
certain Lewis X sugar groups. These types of interactions allow L-SIGN
and DC-SIGN to interact with a wide spectrum of pathogens including
HIV, hepatitis C virus, and SARS coronavirus, which appear to use L-
SIGN and DC-SIGN to facilitate their replication. In addition to HIV,
HCV, and SARS, pathogens such as Ebola virus, some herpes viruses, and
tuberculosis interact with DC-SIGN. In contrast to primary cells
expressing L-SIGN and DC-SIGN, the subject fibroblasts are resilient,
adhere to coated tissue culture plates, grow rapidly and continually
express high levels of their respective receptor. The subject materials
could be used to study the interaction of pathogens with L-SIGN or DC-
SIGN and to screen for compounds that block these interactions.
Additionally, the materials could be used for the development of
antibodies or compounds through rational design that interacted with L-
SIGN or DC-SIGN. The NIH3T3/DC-SIGN and NIH3T3/L-SIGN cells are further
described in Journal of Virology, 2002, vol. 26(12), pages 5905-5914.
The subject technologies are available for licensing from the NIH
through biological materials license agreements.
Murine Mast Cell Line Useful for Toxicity and Immunopotency Screens
Michael Potter (NCI).
HHS Reference No. E-274-2005/0--Research Tool.
Licensing Contact: John Stansberry; 301/435-5236;
stansbej@mail.nih.gov.
The technology is a mouse cell line (P815) that could be useful for
screening biological and chemical agents for toxicity and
immunopotency. Specifically, the cell line is useful for screening for
toxic effects of immunopotentiators including Mycobacterium bovis,
Bacillus Calmette-Gurerin strain, zymosan, lipopolysaccharide and
dextran sulfate. The cell line may also have application in screening
other compounds.
The cell line may also prove useful for studies of cancer and tumor
immunology as injection of mice with P815 leads to progressive tumors.
The P815 tumors express cell surface antigens that could provide a
model for cancer vaccine development.
Mutated Pseudomonas Exotoxins with Reduced Antigenicity
Ira H. Pastan et al. (NCI).
U.S. Provisional Patent Application filed 29 Jul 2005 (HHS Reference
No. E-262-2005/0-US-01).
Licensing Contact: Jesse S. Kindra; 301-435-5559; kindraj@mail.nih.gov.
The use of Pseudomonas exotoxins (PE) for treatment of solid
tumors, in particular, has been limited because of the development of
neutralizing antibodies to the immunotoxin after the first
administration. These antibodies develop before most protocols would
call for a second administration of the immunotoxin, and therefore
render further use of the immunotoxins ineffective against solid tumors
in previously exposed patients.
The studies underlying this novel invention reveal that the
predominant immune response of patients to PE-immunotoxins is the PE
portion of the immunotoxin. This finding indicates that reducing the
antigenicity of the PE molecules used for immunotoxins would reduce the
overall antigenicity of the immunotoxin, and increase their utility.
Therefore, this invention relates to mutated Pseudomonas exotoxins
(PE) that have reduced antigenicity compared to PEs containing the
native sequence. The PEs of this invention have one or more individual
mutations that reduce antibody binding to one or more epitopes of PE.
In addition to licensing, the technology is available for further
development through collaborative research opportunities with the
inventors.
Methods and Materials for Identifying Polymorphic Variants, Diagnosing
Susceptibilities, and Treating Disease
Lawrence C. Brody (NHGRI) et al.
PCT Application No. PCT/US05/21288 filed 16 Jun 2005 (HHS Reference No.
E-149-2005/0-PCT-01).
Licensing Contact: Marlene Shinn-Astor; 301/435-4426;
shinnm@mail.nih.gov.
This invention relates to materials and methods associated with
polymorphic variants in two enzymes involved in folate-dependent and
one-carbon metabolic pathways important in pregnancy-related
complications and neural tube birth defects: MTHFD1 (5,10-
methylenetrahydrofolate dehydrogenase, 5,10-methenyltetrahydrofolate
cyclohydrolase, 10-formyltetrahydrofolate synthase) and
methylenetetrahydrofolate dehydrogenase (NADP+ dependent) 1-like
(MTHFD1L). These enzymes are extremely important in the promotion of
DNA synthesis, a process that is critical for normal placental and
fetal development.
Recently, the inventors have discovered that a MTHFD1 polymorphism
is also a strong maternal genetic risk factor for placental abruption,
premature separation of a normally implanted placenta. This
polymorphism may also be a risk factor for first and second trimester
miscarriages. Diagnostic and therapeutic methods are provided in this
invention involving the correlation of polymorphic variants in MTHFD1
and other genes with relative susceptibility for various pregnancy-
related and other complications such as cancer, cardiovascular disease,
and developmental anomalies. Both nutrient status and genetic
background are independent yet interacting risk factors for impaired
folate metabolism. However, the mechanisms that lead to pathology or
the mechanisms whereby folate prevents these disorders are unknown.
Therefore, a diagnostic and therapeutic invention of this kind would
significantly improve the detection and treatment of disorders
associated with folate metabolism.
For further information, see Brody et al., July 28, 2005, ``A
polymorphism in the MTHFD1 gene increases a mother's risk of having an
unexplained second trimester pregnancy loss,'' Mol. Hum. Reprod.
10.1093/molehr/gah204.
In addition to licensing, the technology is available for further
development through collaborative research opportunities with the
inventors.
AAV5 Vector and Uses Thereof
John A. Chiorini, Robert M. Kotin (NHLBI).
U.S. Provisional Application No. 60/087,029 filed 28 May 1998 (HHS
Reference No. E-127-1998/0-US-01).
U.S. Patent Application No. 09/717,789 filed 21 Nov 2000 (HHS Reference
No. E-127-1998/0-US-07).
U.S. Patent Application Serial No. 11/184,380 filed 19 Jul 2005 (HHS
Reference No. E-127-1998/0-US-08).
Licensing Contact: Jesse S. Kindra; 301/435-5559; kindraj@mail.nih.gov.
The invention described and claimed in this patent application
provides for novel vectors and viral particles which
[[Page 61460]]
comprise adeno-associated virus serotype 5 (AAV5). AAV5 is a single-
stranded DNA virus of either plus or minus polarity which, like other
AAV serotypes (e.g., AAV4, AAV2) requires a helper virus for
replication. AAV type 2 has the interesting and potentially useful
ability to integrate into human chromosome 19 q 13.3-q ter. This
activity is dependent on the non-structural, Rep, proteins of AAV2. The
Rep proteins of AAV types 2 and 5 are dissimilar and are not able to
substitute in DNA replication of the heterologous serotype.
AAV5 offers several advantages which make it attractive for use in
gene therapy: 1. Increased production (10-50 fold greater than AAV2);
2. distinct integration locus when compared to AAV2; 3. Rep protein and
ITR regions do not complement other AAV serotypes; and 4. appears to
utilize different cell surface attachment molecules than those of AAV
type 2.
In addition to licensing, the technology may be available for
further development through collaborative research opportunities with
the inventors.
The Use of Nitroxides in the Prophylactic and Therapeutic Treatment of
Cancer Due to Genetic Defects
James Mitchell, Angelo Russo, Anne Deluca and Murali Cherukuri (NCI).
U.S. Patent Application No. 09/424,519 filed 03 Mar 2000, claiming
priority to 27 May 1997 (HHS Reference No. E-167-1997/0-US-07).
Licensing Contact: George Pipia; 301/435-5560; pipiag@mail.nih.gov.
The invention is a method for preventing or treating cancer,
especially cancers associated with defects in the p53 gene. This gene
is generally considered to be a tumor-suppressor gene, and in a large
percentage of malignancies including pancreatic, colon, lung, and
breast, the gene is found to be inactive in the cancer. It is believed
that many individuals have genetic defects in p53 predisposing them to
cancer.
The invention involves the use of certain nitroxides as agents to
slow the appearance or progression of tumors associated with p53
knockout. Thus, these compounds could serve as preventative agents for
people predisposed to cancer, or as therapeutic agents for certain
cancers. As nitroxides have already been identified as antioxidants,
such agents could become part of a cancer prevention and anti-aging
regimen. A new method of use for these compounds now include their use
in imaging, which correlates functional information about the tumor
with magnetic resonance imaging data.
Dated: October 13, 2005.
Steven M. Ferguson,
Director, Division of Technology Development and Transfer, Office of
Technology Transfer, National Institutes of Health.
[FR Doc. 05-21118 Filed 10-21-05; 8:45 am]
BILLING CODE 4140-01-P
