Government-Owned Inventions; Availability for Licensing, 113-114 [E8-31239]

Download as PDF Federal Register / Vol. 74, No. 1 / Friday, January 2, 2009 / Notices 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. mstockstill on PROD1PC66 with NOTICES Novel Inhibitor of NF-kappa B Pathway Description of Technology: Many tumors and blood cell cancers show overactivation of the NF-kappa B signal transduction pathway. This overactivation is associated with cancer forming in the colon, liver and other epithelial sites. In addition, there is evidence that overactivation leads to tumor formation and metastasis. However, this pathway is key for normal immunity, so any inhibition of NFkappa B overactivation must avoid diminishing the body’s ability to fight infection. This invention claims a compound that inhibits NF-kappa B activation without affecting other transcription factors such as AP–1 and SRE binding proteins. It appears to function by blocking IKK beta and is effective at low micromolar concentrations without affecting cell proliferation or cell survival. At this low concentration, NFkappa B is reduced to basal levels so this novel compound has prospects for preventing or treating cancer without being detrimental to immunity. In addition, because NF-kappa B overactivation contributes to a variety of inflammatory disorders including colitis, diabetes, prostatitis, and pancreatitis this compound has therapeutic applications beyond cancer. Applications: • Therapeutic for the chemoprevention or treatment of cancers associated with the overactivation of NF-kappa B signaling pathway. • Therapeutic for the treatment of inflammatory disorders related to NFkappa B overactivation. • Reagent for the diagnosis of conditions related to overexpression of NF-kappa B. Advantages: • Highly specific inhibitor that allows targeting NF-kappa B without inhibiting other transcription factors. • Effective at preventing carcinogenesis without affecting normal cell proliferation and survival. • Therapeutic for treatment of cancer that will not compromise the immune system. Development Status: Early stage. Market: Cancer is the second leading cause of death in the U.S. and it is estimated that 1.4 million Americans develop cancer in a year. VerDate Aug<31>2005 16:23 Dec 31, 2008 Jkt 217001 Inventors: Curtis J. Henrich et al. (NCI). Publications: None related to invention have been published. Patent Status: U.S. Provisional Application No. 61/098,977 filed 22 Sep 2008 (HHS Reference No. E–295–2008/ 0–US–01). Licensing Status: Available for exclusive or non-exclusive licensing. Licensing Contact: Sabarni K. Chatterjee, Ph.D.; 301–435–5587; chatterjeesa@mail.nih.gov. Collaborative Research Opportunity: The National Cancer Institute (SAICFrederick) is seeking statements of capability or interest from parties interested in collaborative research to further develop, evaluate, or commercialize around development of analogs and/or further investigations of mechanism of action of the compound. Please contact John D. Hewes, Ph.D. at 301–435–3121 or hewesj@mail.nih.gov for more information. Method for Predicting and Detecting Tumor Metastasis Description of Technology: Detecting cancer prior to metastasis greatly increases the efficacy of treatment and the chances of patient survival. Although numerous biomarkers have been reported to identify aggressive tumor types and predict prognosis, each biomarker is specific for a particular type of cancer, and no universal marker that can predict metastasis in a number of cancers have been identified. In addition, due to a lack of reliability, several markers are typically required to determine the prognosis and course of therapy. The inventors discovered a novel CPE splice variant designated CPE->N and found its expression levels increase according to the presence of cancer and metastasis wherein this variant is upregulated in tumors and further increased in metastatic cancer. This data has been demonstrated both in vitro and in vivo experiments and in liver, breast, prostate, colon, and head and neck cancers. Metastatic liver cells treated with CPE->N siRNA reversed the cells from being metastatic and arrested cells from further metastasis. Thus, this novel CPE isoform is a biomarker for predicting metastasis and its inhibitors have an enormous potential to increase patient survival. Applications: • Method to prognose multiple types of cancer and determine likelihood of metastasis. • Method to prevent and treat cancer with CPE inhibitors. • Method to determine the stage of cancer development. PO 00000 Frm 00045 Fmt 4703 Sfmt 4703 113 • CPE->N pharmaceutical compositions. Development Status: The technology is currently in the pre-clinical stage of development. Market: • Global cancer market is worth more than eight percent of total global pharmaceutical sales. • Cancer industry is predicted to expand to $85.3 billion by 2010. Inventors: Y. Peng Loh et al. (NICHD). Patent Status: U.S. Provisional Application No. 61/080,508 filed 14 Jul 2008 (HHS Reference No. E–234–2008/ 0–US–01). Licensing Status: Available for exclusive or non-exclusive licensing. Licensing Contact: Jennifer Wong; 301–435–4633; wongje@mail.nih.gov. Collaborative Research Opportunity: The National Institute of Child Health and Human Development, Laboratory of Development Neurobiology, is seeking statements of capability or interest from parties interested in collaborative research to further develop, evaluate, or commercialize Method for Predicting and Detecting Tumor Metastasis. Please contact John D. Hewes, Ph.D. at 301– 435–3121 or hewesj@mail.nih.gov for more information. Dated: December 23, 2008. Richard U. Rodriguez, Director, Division of Technology Development and Transfer, Office of Technology Transfer, National Institutes of Health. [FR Doc. E8–31238 Filed 12–31–08; 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 E:\FR\FM\02JAN1.SGM 02JAN1 114 Federal Register / Vol. 74, No. 1 / Friday, January 2, 2009 / Notices mstockstill on PROD1PC66 with NOTICES 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. Knockout of Aryl Hydrocarbon Receptor (AhR) and Its Binding Partner Aryl Hydrocarbon Receptor Nuclear Translocator (Arnt) Each in Separate Mouse Models Description of Technology: The technology relates to two separate knockout mouse models of related transcription factors that bind each other. The aryl hydrocarbon receptor (AhR) and the aryl hydrocarbon receptor nuclear translocator (Arnt) protein are transcription factors that play an important role in mediating the effects of man-made environmental toxins. They also play a role in mammalian development and physiological homeostasis. Members of the PAS domain/bHLH family of transcription factors, they are obligate dimerization partners with each other and other members of this family, such as hypoxia-inducible factor 1alpha (HIF1alpha). These transcription factors have been shown to be important in a number of specific tissues including ovary, vascular endothelium, keratinocytes, T-cells, and liver. Available for licensing is a knockout mouse line in which the AhR receptor has been knocked-out, and a mouse line containing a floxed allele of the Arnt gene. The Arnt mouse line can be used to disrupt the Arnt gene in different tissues by breeding the Arnt-floxed mice with transgenic mice in which the Cre recombinase is under the control of tissue-specific promoters. These mice may be used as a research tool for drug development where PAS/bHLH transcription factors are targeted. Applications: • Tool for drug studies targeting PAS/ bHLH transcription factors. • Tool to probe the role of the Arnt protein in a tissue-specific manner. Inventors: Frank J. Gonzalez and Pedro M. Fernandez-Salguero (NCI). Related Publications: 1. S Tomita, CJ Sinal, SH Yim, and FJ Gonzalez. Conditional disruption of the aryl hydrocarbon receptor nuclear translocator (Arnt) gene leads to loss of target gene induction by the aryl hydrocarbon receptor and hypoxiainducible factor 1alpha. Mol Endocrinol. 2000 Oct;14(10):1674–1681. 2. SH Yim, Y Shah, S Tomita, HD Morris, O Gavrilova, G Lambert, JM Ward, and FJ Gonzalez. Disruption of VerDate Aug<31>2005 16:23 Dec 31, 2008 Jkt 217001 the Arnt gene in endothelial cells causes hepatic vascular defects and partial embryonic lethality in mice. Hepatology. 2006 Sep;44(3):550–560. 3. P Fernandez-Salguero et al. Immune system impairment and hepatic fibrosis in mice lacking the dioxinbinding Ah receptor. Science 1995 May 5;268(5211):722–726. Patent Status: HHS Reference Nos. E– 046–2009/0 and E–047–2007/0— Research Tools. Patent protection is not being pursued for these technologies. Licensing Status: This technology is available as a research tool under a Biological Materials License. Licensing Contact: Steve Standley, Ph.D.; 301–435–4074; sstand@mail.nih.gov. Collaborative Research Opportunity: The National Cancer Institute, Laboratory of Metabolism, Center for Cancer Research, is seeking statements of capability or interest from parties interested in collaborative research to further develop, evaluate, or commercialize this technology. Please contact John D. Hewes, Ph.D. at 301– 435–3121 or hewesj@mail.nih.gov for more information. Recombineering Vector Description of Technology: Transgenic mouse models have become a common experimental tool for unraveling gene function. Bacterial artificial chromosome (BAC) mediated transgenesis has proven to be a highly reliable way to obtain accurate transgene expression for in vivo studies of gene expression and function. A ratelimiting step in characterizing large numbers of genes by this approach has been the speed and ease by which BACs can be modified. NIH investigators have developed a highly efficient recombineering vector that can be used for modifying BACs in bacteria. This new vector contains tetracycline and chloramphenical resistance as well as the ccdB gene that encodes a protein that interferes with E. coli DNA gyrase. This vector can be propagated in ccdB resistant E. coli strains but not in other strains (DH5a, Top10, DH10B, etc.) unless the ccdB is replaced by DNA inserts flanked by attB1 and attB2 sites. This vector was generated to modify BAC plasmids by RecA-mediated recombination. The vector disclosed here bypasses the rate-limiting step in recombineering protocols; the efficient cloning of a modifying vector. It is well suited for efficient production of engineered BACs for use in a variety of in vivo studies. Applications: PO 00000 Frm 00046 Fmt 4703 Sfmt 4703 • The fusion of fluorescent protein or cre recombinase genes to a gene of interest. • Generation of dominant negative mutations. • Introduction of gene mutations that would mimic disease conditions. • Insertion of lox sites for conditional deletion of transgenes. • Generation of knock-out or knock-in constructs. Inventors: Rafael C. Casellas and Susan E. Lim (NIAMS). Patent Status: HHS Reference No. E– 026–2009/0—Research Material. Patent protection is not being pursued for this technology. Licensing Status: Available for Biological Material Licensing. Licensing Contact: Suryanarayana (Sury) Vepa, Ph.D., J.D.; 301–435–5020; vepas@mail.nih.gov. Collaborative Research Opportunity: The NIAMS/NIH Genomics and Immunity group is seeking statements of capability or interest from parties interested in collaborative research to further develop, evaluate, or commercialize the engineering of mouse transgenic constructs using the new vector and BAC recombineering. Please contact Rafael Casellas, Ph.D. at 301– 402–7858 or e-mail to casellar@mail.nih.gov for more information. Dated: December 22, 2008. Richard U. Rodriguez, Director, Division of Technology Development and Transfer, Office of Technology Transfer, National Institutes of Health. [FR Doc. E8–31239 Filed 12–31–08; 8:45 am] BILLING CODE 4140–01–P DEPARTMENT OF HOMELAND SECURITY Federal Emergency Management Agency [Docket ID FEMA–2008–0017] Voluntary Private Sector Accreditation and Certification Preparedness Program AGENCY: Federal Emergency Management Agency, DHS. ACTION: Public meeting notice. SUMMARY: This notice announces the date, time, location, and discussion topics for a stakeholder meeting open to the public to engage in dialogue with Department of Homeland Security (DHS) leadership and program managers regarding the Voluntary Private Sector Preparedness Accreditation and Certification Program (PS–Prep). E:\FR\FM\02JAN1.SGM 02JAN1

Agencies

[Federal Register Volume 74, Number 1 (Friday, January 2, 2009)]
[Notices]
[Pages 113-114]
From the Federal Register Online via the Government Printing Office [www.gpo.gov]
[FR Doc No: E8-31239]


-----------------------------------------------------------------------

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

[[Page 114]]

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.

Knockout of Aryl Hydrocarbon Receptor (AhR) and Its Binding Partner 
Aryl Hydrocarbon Receptor Nuclear Translocator (Arnt) Each in Separate 
Mouse Models

    Description of Technology: The technology relates to two separate 
knockout mouse models of related transcription factors that bind each 
other. The aryl hydrocarbon receptor (AhR) and the aryl hydrocarbon 
receptor nuclear translocator (Arnt) protein are transcription factors 
that play an important role in mediating the effects of man-made 
environmental toxins. They also play a role in mammalian development 
and physiological homeostasis. Members of the PAS domain/bHLH family of 
transcription factors, they are obligate dimerization partners with 
each other and other members of this family, such as hypoxia-inducible 
factor 1alpha (HIF1alpha). These transcription factors have been shown 
to be important in a number of specific tissues including ovary, 
vascular endothelium, keratinocytes, T-cells, and liver.
    Available for licensing is a knockout mouse line in which the AhR 
receptor has been knocked-out, and a mouse line containing a floxed 
allele of the Arnt gene. The Arnt mouse line can be used to disrupt the 
Arnt gene in different tissues by breeding the Arnt-floxed mice with 
transgenic mice in which the Cre recombinase is under the control of 
tissue-specific promoters. These mice may be used as a research tool 
for drug development where PAS/bHLH transcription factors are targeted.
    Applications:
     Tool for drug studies targeting PAS/bHLH transcription 
factors.
     Tool to probe the role of the Arnt protein in a tissue-
specific manner.
    Inventors: Frank J. Gonzalez and Pedro M. Fernandez-Salguero (NCI).
    Related Publications:
    1. S Tomita, CJ Sinal, SH Yim, and FJ Gonzalez. Conditional 
disruption of the aryl hydrocarbon receptor nuclear translocator (Arnt) 
gene leads to loss of target gene induction by the aryl hydrocarbon 
receptor and hypoxia-inducible factor 1alpha. Mol Endocrinol. 2000 
Oct;14(10):1674-1681.
    2. SH Yim, Y Shah, S Tomita, HD Morris, O Gavrilova, G Lambert, JM 
Ward, and FJ Gonzalez. Disruption of the Arnt gene in endothelial cells 
causes hepatic vascular defects and partial embryonic lethality in 
mice. Hepatology. 2006 Sep;44(3):550-560.
    3. P Fernandez-Salguero et al. Immune system impairment and hepatic 
fibrosis in mice lacking the dioxin-binding Ah receptor. Science 1995 
May 5;268(5211):722-726.
    Patent Status: HHS Reference Nos. E-046-2009/0 and E-047-2007/0--
Research Tools. Patent protection is not being pursued for these 
technologies.
    Licensing Status: This technology is available as a research tool 
under a Biological Materials License.
    Licensing Contact: Steve Standley, Ph.D.; 301-435-4074; 
sstand@mail.nih.gov.
    Collaborative Research Opportunity: The National Cancer Institute, 
Laboratory of Metabolism, Center for Cancer Research, is seeking 
statements of capability or interest from parties interested in 
collaborative research to further develop, evaluate, or commercialize 
this technology. Please contact John D. Hewes, Ph.D. at 301-435-3121 or 
hewesj@mail.nih.gov for more information.

Recombineering Vector

    Description of Technology: Transgenic mouse models have become a 
common experimental tool for unraveling gene function. Bacterial 
artificial chromosome (BAC) mediated transgenesis has proven to be a 
highly reliable way to obtain accurate transgene expression for in vivo 
studies of gene expression and function. A rate-limiting step in 
characterizing large numbers of genes by this approach has been the 
speed and ease by which BACs can be modified. NIH investigators have 
developed a highly efficient recombineering vector that can be used for 
modifying BACs in bacteria. This new vector contains tetracycline and 
chloramphenical resistance as well as the ccdB gene that encodes a 
protein that interferes with E. coli DNA gyrase. This vector can be 
propagated in ccdB resistant E. coli strains but not in other strains 
(DH5a, Top10, DH10B, etc.) unless the ccdB is replaced by DNA inserts 
flanked by attB1 and attB2 sites. This vector was generated to modify 
BAC plasmids by RecA-mediated recombination.
    The vector disclosed here bypasses the rate-limiting step in 
recombineering protocols; the efficient cloning of a modifying vector. 
It is well suited for efficient production of engineered BACs for use 
in a variety of in vivo studies.
    Applications:
     The fusion of fluorescent protein or cre recombinase genes 
to a gene of interest.
     Generation of dominant negative mutations.
     Introduction of gene mutations that would mimic disease 
conditions.
     Insertion of lox sites for conditional deletion of 
transgenes.
     Generation of knock-out or knock-in constructs.
    Inventors: Rafael C. Casellas and Susan E. Lim (NIAMS).
    Patent Status: HHS Reference No. E-026-2009/0--Research Material. 
Patent protection is not being pursued for this technology.
    Licensing Status: Available for Biological Material Licensing.
    Licensing Contact: Suryanarayana (Sury) Vepa, Ph.D., J.D.; 301-435-
5020; vepas@mail.nih.gov.
    Collaborative Research Opportunity: The NIAMS/NIH Genomics and 
Immunity group is seeking statements of capability or interest from 
parties interested in collaborative research to further develop, 
evaluate, or commercialize the engineering of mouse transgenic 
constructs using the new vector and BAC recombineering. Please contact 
Rafael Casellas, Ph.D. at 301-402-7858 or e-mail to 
casellar@mail.nih.gov for more information.

    Dated: December 22, 2008.
Richard U. Rodriguez,
Director, Division of Technology Development and Transfer, Office of 
Technology Transfer, National Institutes of Health.
 [FR Doc. E8-31239 Filed 12-31-08; 8:45 am]
BILLING CODE 4140-01-P

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