[Federal Register Volume 76, Number 227 (Friday, November 25, 2011)]
[Notices]
[Pages 72713-72715]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 2011-30357]


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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.

Genetically Engineered Mouse Model for Use as an Alternative Screening 
Method for Evaluating P-glycoprotein (P-gp) Substrate Toxicity in 
Avermectin-sensitive Dogs

    Description of Technology: A pitfall to avermectins is central 
nervous system (CNS) toxicities in herding dogs. As a result, all new 
avermectins must be tested in a ``Collie Safety Study'' to determine 
the degree of CNS toxicity. The toxicity is due to a 4 base pair 
mutation in the ATP-binding cassette, sub-family B member 1 (ABCB1) 
gene. This gene encodes for the P-glycoprotein (P-gp) that affects 
absorption, distribution and elimination of certain drugs. Researchers 
at FDA have developed an alternate animal model that includes two 
transgenic mouse models, one containing the mutant form of the canine 
ABCB1 gene (Yancy 1 line) and the other containing the canine wild-type 
gene (Yancy 2 line). The paired mouse system can be utilized to assess 
the safety of avermectins and other canine drugs by determining the 
toxicity to canines with the mutated form of the ABCB1 gene. 
Ivermectin, a derivative of the avermectin family of heartworm drugs 
used to treat and control parasitic infections, was used to verify this 
mouse model. This technology will enhance the population predictions 
derived from clinical safety data and serve to reduce the use of dogs 
in avermectin derivative safety studies that are part of the 
Investigational New Animal Drug (INAD) approval process.
    Potential Commercial Applications: Drug screening technology to 
assess the toxicity of canine drugs to canines with the mutated form of 
the ABCB1 gene.
    Competitive Advantages: Use as an alternative in vivo model to 
canines for assessment of drug safety in the presence of the ABCB1 
mutation.
    Development Stage: In vivo data available (animal).
    Inventor: Haile F. Yancy (FDA).
    Publication: Orzechowski K, et al., in press Am J Vet Res.
    Intellectual Property: HHS Reference No. E-292-2011/0--Research 
Tool. Patent protection is not being pursued for this technology.
    Licensing Contact: Jaime Greene; (301) 435-5559; 
[email protected].
    Collaborative Research Opportunity: The FDA Center for Veterinary 
Medicine is seeking statements of capability or interest from parties 
interested in collaborative research to further develop, evaluate or

[[Page 72714]]

commercialize this alternative mouse model. For collaboration 
opportunities, please contact Haile F. Yancy at [email protected] 
or (301) 210-4096.

Treatment of Tuberculosis--Adjuvant Therapies To Increase the 
Efficiency of Antibiotic Treatments

    Description of Technology: There is growing evidence that 
resistance to Mycobacterium tuberculosis infection is governed in large 
part by the regulation of host cell death. Lipid mediators called 
eicosanoids are thought to play a central role in this process. The 
subject invention is a novel method of enhancing the efficacy of 
antibiotic treatments for Mycobacterium tuberculosis infection by co-
administering an inhibitor of 5-lipoxygenase and a COX-2 dependent 
prostaglandin. Inhibition of 5-lipoxygenase and treatment with 
prostaglandin E2 results in alteration of the eicosanoid balance. The 
synergistic effects of altering the eicosanoid balance and treatment 
with antibiotics is believed to result in more efficient reduction of 
the bacterial burden and thus, the period of antibiotic administration 
and antibiotic dosage could potentially be reduced. In vivo data from 
mouse models can be provided upon request.
    Potential Commercial Applications: The subject invention can be 
used as an adjuvant therapy for existing antibiotic treatment regimens 
against tuberculosis.
    Competitive Advantages: The disclosed method can be applied to 
increase the efficacy of existing antibiotic treatments for 
tuberculosis, potentially reducing both the duration and dosage of the 
antibiotic treatment.
    Development Stage:
     Early-stage.
     Pre-clinical.
     In vitro data available.
     In vivo data available (animal).
    Inventors: Katrin D. Mayer, Bruno Bezerril D. Andrade, F. Alan 
Sher, and Daniel L. Barber (NIAID).
    Intellectual Property:
     HHS Reference No. E-189-2011/0 --U.S. Provisional Patent 
Application No. 61/515,229 filed 04 Aug 2011.
     HHS Reference No. E-189-2011/1 --U.S. Provisional Patent 
Application No. 61/515,237 filed 04 Aug 2011.
    Licensing Contact: Kevin W. Chang, Ph.D.; (301) 435-5018; 
[email protected].
    Collaborative Research Opportunity: The National Institute of 
Allergy and Infectious Diseases is seeking statements of capability or 
interest from parties interested in collaborative research to further 
develop, evaluate or commercialize adjuvant therapy for antibiotic 
treatment regimens against tuberculosis. For collaboration 
opportunities, please contact Katrin Mayer, Ph.D. at 
[email protected] or (301) 594-8061.

DPEP1 and TPX2 as Prognostic Biomarkers for Pancreatic Ductal 
Adenocarcinoma

    Description of Technology: Scientists at NIH have developed 
prognostic biomarkers and a candidate therapeutic target for pancreatic 
ductal adenocarcinoma (PDAC). PDAC is a devastating cancer, and 
patients have an average survival of six months. The 5-year survival 
for PDAC patients is only 6%. This high lethality in pancreatic cancer 
is due to the late diagnosis and lack of any effective treatment. 
Greater than 80% of patients are diagnosed in an advanced stage of the 
disease. The instant invention is a discovery of biomarkers to make 
prognostic conclusions about the progression of PDAC by measuring the 
expression of DPEP1 and TPX2. Patients with decreased DPEP1 and 
increased TPX2 expression have poorer outcome. Furthermore, DPEP1 and 
TPX2 are controlled by the MAPK pathway. A MAPK inhibitor can be used 
as a treatment because it can lead to increased DPEP1 and decreased 
TPX2 expression, which is associated with better survival.

Potential Commercial Applications

     Prognostic biomarker to identify high-risk patients.
     Identification of MAPK inhibitor(s) altering DPEP1 and 
TPX2 expression.

Competitive Advantages

     Combination of measuring DPEP1 and TPX2 expression levels 
results in improved prognosis prediction.
     Development of expression level patterns during 
tumorigenesis that are representative of PDAC.
    Development Stage: In vivo data available (human).
    Inventors: Syed P. Hussain and Geng Zhang (NCI).
    Publication: DPEP1 and TPX2 as Independent Predictors of Cancer-
Specific Mortality in Pancreatic Ductal Adenocarcinoma, submitted April 
2011.
    Intellectual Property: HHS Reference No. E-171-2011/0--U.S. Patent 
Application No. 61/512,302 filed 27 July 2011.
    Licensing Contact: Uri Reichman, Ph.D., MBA; (301) 435-4616; 
[email protected].

AAV Mediated CTLA-4 Gene Transfer To Treat Sj[ouml]gren's Syndrome

    Description of Technology: Sj[ouml]gren's syndrome is an autoimmune 
disease that affects over 2 million Americans, primarily over the age 
of 40. One of the major outcomes of Sj[ouml]gren's syndrome is 
xerostomia (dry mouth) that is caused by immune system attack on 
moisture producing salivary glands. Researchers at the National 
Institute of Dental and Craniofacial Research have developed a therapy 
that alleviates xerostomia in a murine model of Sj[ouml]gren's 
syndrome. This technology consists of a local delivery of adeno-
associated virus (AAV) mediated cytotoxic T-lymphocyte antigen 4 
Immunoglobulin-G (CTLA4IgG) fusion protein to salivary glands. The 
system effectively blocks CTLA4 ligand interactions with T cell surface 
receptors, resulting in immune suppression and reversal of autoimmune-
related xerostomia. Targeted delivery of the AAV-CTLA4-IgG system makes 
this invention a novel therapeutic for the prevention of xerostomia-
associated pain and discomfort caused by Sj[ouml]gren's syndrome.
    Potential Commercial Applications: Prevention of salivary gland 
destruction and xerostomia development in patients with Sj[ouml]gren's 
syndrome.

Competitive Advantages

     Current treatments temporarily reduce the discomfort of 
xerostomia but do not prevent the deleterious effects of this disorder.
     AAV gene transfer to salivary glands is highly efficient.
     AAV therapy is safe and noninflammatory.

Development Stage

     In vitro data available.
     In vivo data available (animal).
    Inventors: Hongen Yin and John Chiorini (NIDCR).

Publications

1. Zheng C, et al. Assessment of the safety and biodistribution of a 
regulated AAV2 gene transfer vector after delivery to murine 
submandibular glands. Toxicol Sci. 2011 Sep;123(1):247-255. [PMID: 
21625005]
2. Kanaya K, et al. Combined gene therapy with adenovirus vectors 
containing CTLA4Ig and CD40Ig prolongs survival of composite tissue 
allografts in rat model. Transplantation. 2003 Feb 15;75(3):275-281. 
[PMID: 12589145]
3. Genovese MC, et al. Abatacept for rheumatoid arthritis refractory 
to tumor necrosis factor alpha inhibition. N Engl J Med. 2005 Sep 
15;353(11):1114-1123. [PMID: 16162882]


[[Page 72715]]


    Intellectual Property: HHS Reference No. E-087-2011/0--U.S. 
Provisional Application No. 61/476,168 filed 15 April 2011.
    Licensing Contact: Jaime Greene; (301) 435-5559; 
[email protected].
    Collaborative Research Opportunity: The NIDCR is seeking statements 
of capability or interest from parties interested in collaborative 
research to further develop, evaluate or commercialize this technology. 
For collaboration opportunities, please contact David Bradley at 
[email protected].

    Dated: November 18, 2011.
Richard U. Rodriguez,
Director, Division of Technology Development and Transfer, Office of 
Technology Transfer, National Institutes of Health.
[FR Doc. 2011-30357 Filed 11-23-11; 8:45 am]
BILLING CODE 4140-01-P