Notices. Notice
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BILLING CODE 4140-01-M DEPARTMENT OF HEALTH AND HUMAN SERVICES National Institutes of Health, Clinical Center Proposed Collection; Comment Request; Customer and Other Partners Satisfaction Surveys *Summary:* In compliance with the requirement of Section 3506(c)(2)(A) of the Paperwork Reduction Act of 1995 for the opportunity for pubic comment on the proposed data collection projects, the Warren Grant Magnuson Clinical Center (CC), the National Institutes of Health,
(NIH)will publish periodic summaries of proposed projects to be submitted to the Office of Management and Budget
(OMB)for review and approval. *Proposed Collection:* *Title:* Customer and Other Partners Satisfaction Surveys. *Type of Information Collection Request:* New request/waiver. *Need and Use of Information Collection:* The information collected in these surveys will be used by Clinical Center personnel:
(1)To evaluate the satisfaction of various Clinical Center customers and other partners with Clinical Center services;
(2)to assist with the design of modifications of these services, based on customer input;
(3)to develop new services, based on customer need; and
(4)to evaluate the satisfaction of various Clinical Center customers and other partners with implemented service modifications. These surveys will almost certainly lead to quality improvement activities that will enhance and/or streamline the Clinical Center's operations. The major mechanisms by which the Clinical Center will request customer input is through surveys and focus groups. The surveys will be tailored specifically to each class of customer and to that class of customer's needs. Surveys will either be collected as written documents, as faxed documents, mailed electronically or collected by telephone from customers. Information gathered from these surveys of Clinical Center customers and other partners will be presented to, and used directly by, Clinical Center management to enhance the services and operations of our organization. *Frequency of Response:* The participants will respond yearly. *Affected public:* Individuals and households; businesses and other for profit, small businesses and organizations. *Types of respondents:* These surveys are designed to assess the satisfaction of the Clinical Center's major internal and external customers with the services provided. These customers include, but are not limited to, the following groups of individuals: Clinical Center patients, family members of Clinical Center patients, visitors to the Clinical Center, National Institutes of Health investigators, NIH intramural collaborators, private physicians or organizations who refer patients to the Clinical Center, volunteers, vendors and collaborating commercial enterprises, small businesses, regulators, and other organizations. The annual reporting burden is as follows: Customer Number of respondents Frequency of response Average time per response Annual hour burden FY 2007: Clinical Center Patients 5000 1 .5 2500 Family Members of Patients 2000 1 .5 1000 Visitors to the Clinical Center 1000 1 .17 170 Clinical Center Employees 2500 1 .25 625 NIH Investigators 2000 1 .25 625 NIH Intramural Collaborators 2000 1 .17 340 Vendors and Collaborating Commercial Enterprises 2500 1 .33 833 Professionals and Organizations Referring Patients 2000 1 .33 833 Regulators 30 1 .33 10 Volunteers 275 1 .5 138 Total 19,305 7074 FY 2008: Clinical Center Patients 5000 1 .5 2500 Family Members of Patients 3000 1 .5 1500 Visitors to the Clinical Center 1500 1 .17 255 Clinical Center Employees 2500 1 .33 833 NIH Investigators 2400 1 .5 1200 NIH Intramural Collaborators 1500 1 .25 375 Vendors and Collaborating Commercial Enterprises 2000 1 .25 500 Professionals and Organizations Referring Patients 1000 1 .33 333 Regulators 30 1 .33 10 Volunteers 275 1 .33 92 Total 19,205 7598 FY 2009: Clinical Center Patients 5000 1 .5 2500 Family Members of Patients 2000 1 .5 1000 Visitors to the Clinical Center 1000 1 .17 170 Clinical Center Employees 2500 1 .33 833 NIH Investigators 2500 1 .33 833 NIH Intramural Collaborators 1000 1 .17 170 Vendors and Collaborating Commercial Enterprises 2500 1 .25 625 Professionals and Organizations Referring Patients 3000 1 .33 1000 Regulators 25 1 .25 6 Volunteers 300 1 .25 75 Total 19,825 7212 Estimated costs to the respondents consists of their time; time is estimated using a rate of $10.00 per hour for patients and the public; $30.00 for vendors, regulators, organizations and $55.00 for health care professionals. The estimated annual costs to respondents for each year for which the generic clearance is requested is $159,250 for 2007, $194,540 for 2008, and $194,540 for 2009. Estimated Capital Costs are $7,000. Estimated Operating and Maintenance costs are $73,000. *Requests for Comments:* Written comments and/or suggestions from the public and affected agencies are invited on one or more of the following points:
(1)Whether the proposed collection of information is necessary for the proper performance of the functions of the Clinical Center and the agency, including whether the information shall have practical utility;
(2)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)Ways to enhance the quality, utility, and clarity of the information to be collected; and
(4)Ways to minimize the burden of the collection of information on those who are to respond, including the use of automated, electronic, mechanical, or other technological collection techniques or other forms of information technology *For Further Information:* To request more information on the proposed project, or to obtain a copy of the data collection plans and instruments, contact: Dr. David K. Henderson, Deputy Director for Clinical Care, National Institutes of Health Clinical Center, Building 10, Room 6-1480, 10 Center Drive, Bethesda, Maryland 20892, or call non-toll free: 301-496-3515, or e-mail your request or comments, including your address to: *dkh@nih.gov* . *Comments Due Date:* Comments regarding this information collection are best assured of having their full effect if received within 60 days of the date of this publication. Dated: May 2, 2007. David K. Henderson, Deputy Director for Clinical Care, CC, National Institutes of Health. [FR Doc. E7-8885 Filed 5-8-07; 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. Selenocysteine Mediated Hybrid Antibody Molecules *Description of Technology:* Available for licensing is a new class of hybrid molecules composed of an antibody, or antibody fragment, and a small synthetic molecule (such as a small molecule inhibitor, or cytotoxic compound). These biological and chemical components are covalently linked at an engineered selenocysteine near the C-terminus of the antibody, or antibody fragment. Through this covalent linkage, the chemical and the biological component can acquire properties of one another. For example, the synthetic molecule acquires antibody properties such as circulatory half-life, effector functions, and ability to interfere with protein interactions whereas the antibody, or antibody fragment, acquires properties of the small synthetic molecule such as specificity, affinity, and stability to bind to targets that are sterically inaccessible to immunoglobulins. The technology can also be used to equip an antibody, or antibody fragment, with a small synthetic molecule that enhances target destruction or imaging capabilities through site-selective biotinylation, PEGylation, addition of an imaging agent, or addition of a cytotoxic agent such as a chemotherapeutic drug or a chelate for radioisotope labeling. The hybrid antibody molecules can be engineered with a variety of small synthetic molecules, and the combination of immunogenic properties and those of the small synthetic molecules results in compounds with powerful target destruction or imaging capabilities. This technology could be applied towards the targeted delivery of small synthetic molecules to various cell surface receptors, and may have applicability as a prevention, diagnosis, or therapy for numerous disease states. *Applications:* Potent novel compositions that retains immunogenic properties and those of small synthetic molecules that can be produced at a large scale; Method to prevent, diagnose, and treat cancer, infectious diseases and autoimmune diseases. *Market:* Monoclonal antibody market is projected to exceed $30 billion by 2010; Revenue from antibodies for therapeutics and diagnostic uses are expected to grow at an average annual growth rate of 11.5%. *Development Status:* The technology is currently in the pre-clinical stage of development. *Inventors:* Christoph Rader *et al.* (NCI). *Patent Status:* U.S. Provisional Application No. 60/909,665 filed 02 Apr 2007 (HHS Reference No. E-146-2007/0-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 Cancer Institute, Center for Cancer Research, Experimental Transplantation and Immunology Branch, is seeking statements of capability or interest from parties interested in collaborative research to further develop, evaluate, or commercialize Selenocysteine Mediated Hybrid Antibody Molecules. Please contact Dr. Christoph Rader at
(301)451-2235 or *raderc@mail.nih.gov* for more information. Mutant Alleles of Hsp90 that Modulates the Lifespan of Yeast *Description of Technology:* Heat shock protein 90 (Hsp90) are a class of chaperone proteins that are up-regulated in response to elevated temperature and other environmental stresses. They act as chaperones to other cellular proteins and facilitate their proper folding and repair, and aid in the refolding of misfolded client proteins. This invention identifies Hsp90 mutant residues that affect the chronological lifespan of yeast. These mutations in addition to a deletion in the sch9 allele, the yeast homolog to human kinase AKT, can increase yeast lifespan from 45 to 57 days, approximately 20% longer than the wildtype strain. These genetically engineered yeast strains may have the longest chronological lifespan reported to date. *Applications:* Model to study aging and longevity factors; Model to screen compounds that affect lifespan; A long-lived yeast strain could be used to ferment alcohol in a more efficient and cost effective as an alternative fuel source; Method to extend lifespan of transgenic farm animals. *Market:* Anti-aging and alternative fuel industries are worth billions of dollars. *Development Status:* The technology is currently in the pre-clinical stage of development. *Inventors:* Bradley T. Scroggins
(NCI)*et al.* *Related Publication:* BT Scroggins et al. An acetylation site in the middle domain of Hsp90 regulates chaperone function. Mol Cell. 2007 Jan 12;25(1):151-159. *Patent Status:* U.S. Provisional Application No. 60/848,346 filed 09 Sep 2006 (HHS Reference No. E-319-2006/0-US-01). *Licensing Status:* Available for non-exclusive licensing. *Licensing Contact:* Jennifer Wong; 301/435-4633; *wongje@mail.nih.gov* . *Collaborative Research Opportunity:* The National Cancer Institute's Urologic Oncology Branch is seeking statements of capability or interest from parties interested in collaborative research to further develop, evaluate, or commercialize models to study aging and longevity factors. Please contact John D. Hewes, Ph.D. at 301-435-3121 or *hewesj@mail.nih.gov* for more information. Inhibitors of Ubiquitin E1 *Description of Technology:* The present invention discloses novel pyrazolidinyl compounds that inhibit undesired cell proliferation. The compounds inhibit ubiquitin E1 and can be useful for regulating protein ubiquitination. Specifically, the novel pyrazolidinyl compounds can stabilize p53 and induce apoptosis in mammalian cells through selective inhibition of ubiquitin E1. Ubiquitin-mediated proteolysis is an important pathway of non-lysosomal protein degradation that controls the timed destruction of a number of cellular regulatory proteins including p53. The ubiquitin pathway leads to the covalent attachment of poly-ubiquitin chains to target substrates which are then degraded by a multi-catalytic proteosome complex. The compounds can be useful in the treatment of solid and disseminated cancers or other undesired cell proliferation disease or retroviral infections such as HIV. *Applications and Modality:* Treatment of disorders related to ubiquitin E1, such as HIV and viral infections; Compounds are the first general inhibitors of Ubiquitin E1 with broader biological effects than existing proteosome inhibitors; The compounds can serve as a probe to understand the ubiquitin system. *Market:* Bortezomib (marketed as Velcade TM by Millennium Pharmaceuticals) is the first therapeutic proteasome inhibitor approved by the FDA. Severe side effects such as peripheral neuropathy occur in 30% of patients treated with Bortezomib. New drugs targeting proteins in ubiquitination pathway are needed that will have broader efficacy and reduced side effects. *Development Status:* The technology is in the pre-clinical stage of development. *Inventors:* Allan M. Weissman *et al.* (NCI). *Related Publications:* 1. A manuscript related to this technology will be available as soon as it is accepted for publication. 2. Y Yang et al. Small molecule inhibitors of HDM2 ubiquitin ligase activity stabilize and activate p53 in cells. Cancer Cell. 2005 Jun;7(6):547-559. *Patent Status:* U.S. Provisional Application No. 60/738,242 filed 19 Nov 2005, entitled “Inhibitors of Ubiquitin E1” (HHS Reference No. E-070-2005/0-US-01); International Patent Application No. PCT/US2006/0045032 filed 20 Nov 2006, entitled “Inhibitors of Ubiquitin E1” (HHS Reference No. E-070-2005/0-PCT-02) *Licensing Status:* Available for exclusive and non-exclusive licensing. *Licensing Contact:* Thomas P. Clouse; 301/435-4076; *clousetp@mail.nih.gov* . *Collaborative Research Opportunity:* The National Cancer Institute's Laboratory of Protein Dynamics and Signaling is seeking statements of capability or interest from parties interested in collaborative research to further develop, evaluate, or commercialize inhibitors of ubiquitin E1. Please contact John D. Hewes, Ph.D. at 301-435-3121 or *hewesj@mail.nih.gov* for more information. Biomarkers for Tissue Status *Description of Technology:* Tissue regeneration and tumorigenesis are complex, adaptive processes controlled by cues from the tissue microenvironment. There are complex processes both characterized by cell proliferation, migration, and angiogenesis suggesting that wounds and cancer share a number of phenotypic similarities including cellular behavior, signaling molecules, and gene expression. Utilizing the kidneys as a model to compare renal regeneration and repair
(RRR)from ischemically-injured tissues and renal cellular carcinoma (RCC), the inventors have identified biomarkers which are differentially expressed. The invention relates to methods of quickly and accurately diagnosing RCC and monitoring renal tissue health as well as RCC treatment. *Applications:* Method to accurately diagnose RCC; RCC biomarker inhibitors such siRNA; Method to treat RCC; Method to determine and monitor renal tissue health status; Method for improving renal ischemia recovery without promoting RCC; Biomarkers for immunotherapy, drug targeting and drug screening, for targeting tumors and not normal regenerating tissue; Biomarkers for immunotherapy, drug targeting and drug screening, for targeting ischemic tissue and not tumors. *Market:* Kidney cancer is one of the top ten most prevalent cancers in the U.S. and it accounts for 12,200 deaths annually; Approximately 35,000 new cases of kidney cancer are diagnosed annually; 50% survival rate after five years of diagnosis; Renal cancer accounts for 3% of all adult male malignancies. *Development Status:* The technology is currently in the pre-clinical stage of development. *Inventors:* Joseph Riss
(NCI)*et al.* *Publications:* 1. Journal of Urology, May 2007, Vol. 177 No. 5, in press. 2. J Riss et al. Cancers as wounds that do not heal: differences and similarities between renal regeneration/repair and renal cell carcinoma. Cancer Res. 2006 July 15;66(14):7216-7224. *Patent Status:* U.S. Provisional Application No. 60/649,208 filed 01 Feb 2005 (HHS Reference No. E-064-2005/0-US-01); PCT Application No. PCT/US2006/003611 filed 01 Feb 2006 (HHS Reference No. E-064-2005/0-PCT-02). *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 Cancer Institute, Center for Cancer Research, Laboratory of Cancer Biology and Genetics, Wound Healing and Oncogenesis (NCI/CCR/LCBG), is seeking statements of capability or interest from parties interested in collaborative research to further develop, evaluate, or commercialize topics of invention or related to cancer biology, metastasis, wound healing, bioinformatics, pharmacogenomics and therapeutic. Please contact John D. Hewes, Ph.D. at 301-435-3121 or *hewesj@mail.nih.gov* for more information. New Maleiimide Anti-Phosphatase Inhibitors *Description of Technology:* The present invention describes novel phenyl maleiimide phosphatase inhibitors that appear to target the Cdc25 family of phosphatases. The new compounds are inhibitors of several human tumor cell lines. The compounds have potent activity against human liver cancer cells in vitro and in vivo against an orthotopic liver cancer in rats. In tumor cells, these new inhibitors appear to target the phosphorylation status of several cell cycle proteins that are important for cell survival and thus could represent a novel class of chemotherapeutic agents targeting cancer cells. *Applications and Modality:* Compound targets Cdc25 family of phosphatases and inhibit growth of several human tumor cell lines; Potent activity in vitro against human liver cancer cells and in vivo against orthotopic liver cancer in rats; Targets phosphorylation of cell cycle proteins important for cell survival. *Market:* 600,000 deaths from cancer related diseases were estimated in 2006; In 2006, cancer drug sales were estimated to be $25 billion. *Development Status:* The technology is currently in the pre-clinical stage of development. *Inventors:* Christopher Michejda
(NCI)*et al.* *Relevant Publication:* S Kar, M Wang, W Yao, CJ Michejda, BI Carr. PM-20, A novel inhibitor of Cdc25A, induces extracellular signal-regulated kinase 1/2 phosphorylation and inhibits hepatocellular carcinoma growth in vitro and in vivo. Mol Cancer Ther. 2006 Jun;5(6):1511-1519. *Patent Status:* PCT Patent Application No. PCT/US2005/05742 filed 22 Feb 2005, which published as WO 2005/081972 on 09 Sep 2005 (HHS Reference No. E-110-2004/0-PCT-02); U.S. Patent Application No. 11/508,605 filed 22 Aug 2006 (HHS Ref. No. E-110-2004/0-US-06). *Licensing Status:* Available for exclusive and non-exclusive licensing. *Licensing Contact:* Adaku Nwachukwu, J.D.; 301/435-5560; *madua@mail.nih.gov* . Leu574 of HIF-1alpha as a Molecular Basis for Therapeutic Application *Description of Technology:* The hypoxia-inducible factor 1 (HIF-1) is a transcription factor that plays a pivotal role in cellular adaptation to oxygen availability. HIF-1alpha protein is a subunit of HIF-1. Although the gene for HIF-1alpha is constitutively expressed, it is an extremely short-lived protein under normoxic conditions and is targeted for destruction via the proteosome pathway by an E3 ubiquitin ligase involving the VHL protein. The invention relates to the discovery that mutations or deletions of Leu574 result in a more stable and more active form of HIF-1alpha. Therefore, the invention relates to methods and compositions for modulating oxygen homeostasis for therapeutic application. In one aspect, the inventors contemplate the use of a more stable form of HIF-1alpha protein for therapeutic angiogenesis purposes such as may be useful in ischemic vascular disease. In another aspect, the inventors contemplate the use of this particular site in a screen for targeted drugs that modulates HIF-1alpha activity. The inventors also suggest that Leu574 could be used for developing drugs targeted to HIF hydroxylase binding, thereby altering HIF-1alpha stability. *Inventor:* L. Eric Huang (NCI). *Patent Status:* U.S. Patent No. 7,193,053 issued 20 Mar 2007 (HHS Reference No. E-281-2002/0-US-02). *Licensing Status:* This technology is available for licensing on an exclusive or a non-exclusive basis. *Licensing Contact:* Jesse S. Kindra, J.D.; 301/435-5559; *kindraj@mail.nih.gov* . Dated: April 30, 3007. Steven M. Ferguson, Director, Division of Technology Development and Transfer,Office of Technology Transfer, National Institutes of Health. [FR Doc. E7-8893 Filed 5-8-07; 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. New Compounds and Methods for the Treatment of Spinal Muscular Atrophy and Other Diseases *Description of Technology:* Spinal muscular atrophy
(SMA)is caused by mutations in the *SMN1* gene that result in reduced expression of the survival motor neuron
(SMN)protein and a loss of spinal motor neurons. An *SMN2* gene paralog that differs from SMN by a single base pair has inadequate expression of SMN to support motor neuron survival. Alternative splicing caused by the single base substitution in the *SMN2* gene results in a slightly truncated and highly unstable SMN protein. Drugs that allow translational read through of the stop codons introduced by the alternative splice event have been shown to stabilize the mutant protein, resulting in increased levels of SMN. A chemical library screen identified indoprofen, a nonsteroidal anti-inflammatory drug, as an inducer of SMN expression in cultured cells. However, indoprofen cannot enter the brain in satisfactory amounts, has a relatively low level of activity and can cause substantial side-effects in part due to its cyclooxygenase inhibitory activity. NIH inventors designed indoprofen derivatives without cyclooxygenase activity that can enter the CNS and increase expression of a SMN protein from the *SMN2* gene with increased potency and efficacy. The mechanism of action of these indoprofen analogs appears to be translational readthrough of stop codons introduced by the alternative *SMN2* splicing event. In addition to treating SMA, novel drugs that allow read through of stop codons could potentially treat many other diseases caused by such mutations such as cystic fibrosis and muscular dystrophy. Available for licensing are compounds and methods useful for the treatment of spinal muscular atrophy by increasing SMN expression and increasing the expression from any nucleic acid that encodes a translational stop codon. *Applications:* Efficacious treatment for SMA, utilizing indoprofen analogs that increase SMN protein expression; Treatment of any genetic disease caused by premature termination of protein translation. *Market:* SMA is a rare genetic disease that affects approximately 1 in 6,000 live births, and is the leading genetic cause of death in infants and toddlers. The projected market size for SMA is between $250 million and $750 million. *Development Status:* Clinical candidate selection scheduled for June 2007. *Inventors:* Jill Heemskerk (NINDS), et al. *Publication:* MR Lunn, DE Root, AM Martino, SP Flaherty, BP Kelley, DD Coovert, AH Burghes, NT Man, GE Morris, J Zhou, EJ Androphy, CJ Sumner, BR Stockwell. Indoprofen upregulates the survival motor neuron protein through a cyclooxygenase-independent mechanism. Chem. Biol. 2004 Nov;11(11):1489-1493. *Patent Status:* U.S. Provisional Application No. 60/783,292 filed 17 Mar 2006 (HHS Reference No. E-133-2006/0-US-01); PCT Application No. PCT/2007/006772 filed 16 Mar 2007 (HHS Reference No. E-133-2006/1-PCT-01) *Licensing Availability:* Available for exclusive and non-exclusive licensing. *Licensing Contact:* Norbert Pontzer, J.D., Ph.D.; 301/435-5502; *pontzern@mail.nih.gov.* STAMP, a Novel Cofactor and Possible Steroid Sparing Agent, Modulates Steroid-Induced Induction or Repression of Steroid Receptors *Description of Technology:* Steroid hormones such as androgens, glucocorticoids, and estrogens are used in the treatments of many diseases. They act to regulate many physiological responses by binding to steroid receptors. However, because steroid receptors are expressed in many tissues, efforts to therapeutically modify the effects of steroid hormones on a specific tissue or on a specific receptor of the steroid receptor family often cause undesirable effects in other tissues or on other receptors. STAMP (SRC-1 and TIF-2 Associated Modulatory Protein), a novel protein that acts to lower the concentration of steroid hormone needed to induce (or repress) selected target genes by regulating steroid receptor synthesis, offers an novel approach for reducing the severity of unwanted side-effects, thereby increasing the ability to use steroid hormone therapies. Applications 1. Diseases requiring chronic steroid treatment such as rheumatoid arthritis, psoriatic arthritis, asthma, inflammatory and auto-immune diseases; 2. Diseases characterized by excess or deficiency of glucocorticoids such as obesity, diabetes, hypertension, Cushing's Syndrome, Parkinson's Disease, Addison's Disease; 3. Diseases in which glucocorticoid-responsive gene expression is deranged, so deranging carbohydrate, protein or lipid metabolism; 4. Cancers responsive to androgen or estrogen, such as breast cancer or prostate cancer; 5. Therapeutic applications related to male or female hormone replacement, symptoms related to menopause, birth control, menstrual cycle/amenorrhea, fertility or endometriosis. Advantages 1. STAMP reduces the severity of unwanted side-effects of steroid hormone therapies; 2. STAMP modulates the gene induction properties of androgen and progesterone receptors; 3. STAMP modulates both induction and repression properties of glucocorticoid receptors; 4. STAMP is inactive toward alpha and beta estrogen receptors, thyroid receptor beta, PPAR gamma 2, retinoid receptor alpha or RXR alpha; 5. The siRNAs could be useful as therapeutics. *Market:* The protein, STAMP, offers a novel approach for reducing the severity of unwanted side-effects of steroid hormone therapies. Therefore, STAMP would be helpful in the treatment of diseases requiring chronic steroid treatments, those characterized by excess or deficiency of glucocorticoid response, therapies related to male or female hormone replacement or cancers responsive to androgen or estrogen. Development Status 1. STAMP, a protein which is a novel nuclear receptor cofactor, has been identified; 2. STAMP siRNAs have been shown to change the dose response curve of endogenous glucocorticoid receptor induced genes; 3. A STAMP antibody has been prepared. Further Research & Development Required 1. Further in-vivo studies into the role of STAMP in glucocorticoid receptor-mediated repression; 2. Further study into the activity of STAMP in androgen receptor-mediated responses; 3. Investigation into the mechanism of action of STAMP; 4. Development of STAMP knockout mouse. *Inventors:* Drs. S. Stoney Simons Jr (NIDDK) and Yuanzheng He (NIDDK) *Publication:* Y He and SS Simons Jr. STAMP: A Novel Predicted Factor Assisting TIF2 Actions in Glucocorticoid Receptor-mediated Induction and Repression. Mol Cell Biol. 2007 Feb;27(4);1467-1485. *Patent Status:* PCT International No. PCT/US2005/006393 filed 25 Feb 2005 (priority date 26 Feb 2004), which published as WO 2005/082935 on 09 Sep 2005, entitled “A Novel Cofactor that Modulates Steroid Receptor Activities”; National Stage U.S., Europe, Canada, Australia (HHS Reference No. E-056-2004/0). *Related Technologies:* HHS Reference No. E-015-2000/0, “Antiprogestins with Partial Agonist Activity.” Global IP pending: US, Europe, Australia, Canada, Japan. *Licensing Status:* Available for exclusive and non-exclusive licensing. *Licensing Contact:* Dr. Susan Carson; 301/435-5020; *carsonsu@mail.nih.gov.* *Collaborative Research Opportunity:* The National Institute of Diabetes, Digestive and Kidney Diseases, Laboratory of Molecular and Cellular Biology is seeking statements of capability or interest from parties interested in collaborative research to further develop, evaluate or commercialize this technology. Please contact Dr. Stoney Simons, Chief, Steroid Hormones Section (NIDDK) at *steroids@helix.nih.gov;* Tel: 301-4960-6796 for more information. TMC1, a Deafness-Related Gene *Description of Technology:* Hearing loss is a common communication disorder affecting nearly 1 in 1,000 children in the United States alone, and nearly 50% of adults by the age of eighty. Hearing loss can be caused by environmental and disease-related factors; however, hearing loss due to genetic factors accounts for approximately 50% of cases. The NIH announces the isolation of two novel genes involved in hearing; TMC1, short for transmembrane channel-like gene 1. The inventors have discovered that dominant and recessive mutations in TMC1 underlie two forms of hereditary deafness, known as DFNA36 and DFNB7/11. TMC1 encodes a protein required for normal function of the mammalian hair cell, which plays a critical role within the hearing pathway that detects sound in the inner ear. The invention discloses TMC1 nucleic acids, vectors, and cells. Also disclosed are methods of detecting hearing loss, or a predisposition to hearing loss, due to a mutation in TMC1, as well as methods for identifying agents that interact with the TMC1 gene in a cell. Nucleic acids and methods of use for TMC2, a gene closely related to TMC1, are also disclosed. *Applications:* Development of a genetic diagnostic test for hearing loss; Development of pharmaceuticals to treat hearing loss. *Market:* Hearing loss with a genetic component accounts for 50% of all cases of hearing loss. *Development Status:* Early stage. *Inventors:* Andrew J. Griffith et al. (NIDCD). *Publication:* K Kurima et al. Dominant and recessive deafness caused by mutations of a novel gene, TMC1, required for cochlear hair-cell function. Nat Genet. 2002 Mar;30(3):277-284. Patent Status 1. HHS Reference No. E-168-2001/0: a. U.S. Provisional Application No. 60/323,275 filed 19 Sep 2001. b. PCT Application No. PCT/US02/29614 filed 19 Sep 2002, which published as WO 03/025140 on 27 Mar 2003. c. U.S. Patent No. 7,192,705 issued 20 Mar 2007. d. U.S. Patent Application No. 11/615,250 filed 22 Dec 2006. e. Foreign counterparts in Australia, Canada, Europe, and Japan. 2. HHS Reference No. E-168-2001/1: a. U.S. Patent No. 7,116,433 issued 23 Jan 2007. b. Foreign counterparts in Australia and Canada. *Licensing Status:* Available for non-exclusive licensing. *Licensing Contact:* Tara L. Kirby, Ph.D.; 301/435-4426; *tarak@mail.nih.gov.* *Collaborative Research Opportunity:* The NIDCD Otolaryngology Branch is seeking statements of capability or interest from parties interested in collaborative research to further develop, evaluate, or commercialize this technology as well as collaborate on further pre-clinical and clinical studies with the TMC2 gene mutations. Please contact Ms. Marianne Lynch at 301-402-5579 or via e-mail at *lynchm@nhlbi.nih.gov* for more information. Dated: April 30, 2007. Steven M. Ferguson, Director, Division of Technology Development and Transfer, Office of Technology Transfer, National Institutes of Health. [FR Doc. E7-8894 Filed 5-8-07; 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. Influenza Vaccines and Antiviral Agents *Description of Technology:* The subject invention offers candidate DNA vaccines to target H5N1, H1N1, H3N2 and other subtypes of influenza. These candidates are designed primarily to elicit neutralizing antibodies. The candidate vaccines express hemagglutinin (H/HA) or neuramidase (N/NA) protein that has been codon optimized and/or modified at the protease cleavage site. The modified genes could be used in DNA vaccines, in viral vectors, recombinant proteins/particles or combination. The studies use proprietary expression systems that increase protein expression relative to commonly used alternatives. This invention potentially provides a vaccine strategy for controlling influenza epidemics, including avian flu, should it cross over to humans; the 1918 strain of flu; and seasonal flu strains. In addition, this invention is designed to lead to a combination vaccine to provide a broadly protective vaccine. The incorporation of specific cleavage site types to facilitate preparation of pseudotypes from a variety of strains is an important aspect of this invention. In addition, HA pseudotyped lentiviral vectors are being tested to screen for neutralizing abs in patients and to screen for diagnostic and therapeutic monoclonal abs. *Applications and Advantages:* Influenza vaccine for pandemic or epidemic application; Potential for combination vaccine for broad protection, removing need for seasonal strain monitoring; DNA vaccines are easy to produce and store; No risk of reversion to pathogenic strain as with live-attenuated virus vaccines. *Development Status Highlights:* Phase I clinical trials planned for select candidates; DNA vaccine encoding 1918 influenza virus HA protein protects mice against lethal viral challenge; Codon optimized for expression in human cells. *Inventors:* Gary J. Nabel (VRC/NIAID), Wing-pui Kong (VRC/NIAID), Zhi-yong Yang (VRC, NIAID), *et al.* *Publication:* Certain aspects of this technology were published in WP Kong et al. Protective immunity to lethal challenge of the 1918 pandemic influenza virus by vaccination. Proc Natl Acad Sci USA. 2006 Oct 24;103(43):15987-15991. Epub 2006 Oct 16, doi: 10.1073/pnas.0607564103. *Patent Status:* U.S. Provisional Application No. 60/774,923 filed 16 Feb 2006 (HHS Reference No. E-116-2006/0-US-01) and PCT Application No. PCT/US2007/004506 filed 16 Feb 2007 (influenza) (HHS Reference No. E-116-2006/1-PCT-01); U.S. Patent No. 7,094,598 issued 22 Aug 2006 (CMV/R) (HHS Reference No. E-241-2001/1-US-01) and associated foreign rights. *Licensing Status:* Available for exclusive or non-exclusive licensing. *Licensing Contact:* Susan Ano, Ph.D.; 301/435-5515; *anos@mail.nih.gov* . Enhanced, Targeted Delivery for DNA Vaccines *Description of Technology:* Available for licensing from the NIH is a fusion protein for enhanced gene delivery. Exemplary proteins for achieving this improvement comprise an adenovirus serotype 5 fiber, penton base and core protein V fused to the DNA binding domain of HMG. In vitro studies have shown the effectiveness of the chimeric protein-DNA vaccine co-administration by an increase in uptake of ten to twenty fold. In particular, the plasmid with the chimeric core protein V was delivered efficiently to dendritic cells
(DC)as well as 293T cells. The utilization of this chimeric protein could further enhance the immune response elicited by DNA vaccines. *Potential Applications:* Improved DNA vaccine delivery and uptake. *Inventors:* Gary J. Nabel and Wataru Akahata (VRC/NIAID). *Patent Status:* U.S. Provisional Application No. 60/737,896 filed 18 Nov 2005 (HHS Reference No. E-043-2006/0-US-01); U.S. Provisional Application No. 60/795,529 filed 26 Apr 2006 (HHS Reference No. E-043-2006/1-US-01); PCT Application No. PCT/US2006/044525 filed 20 Nov 2006 (HHS Reference No. E-043-2006/3-PCT-01) *Licensing Status:* Available for non-exclusive or exclusive licensing. *Licensing Contact:* Susan Ano, Ph.D.; 301/435-5515; *anos@mail.nih.gov* . Dated: April 30, 2007. Steven M. Ferguson, Director, Division of Technology Development and Transfer, Office of Technology Transfer, National Institutes of Health. [FR Doc. E7-8895 Filed 5-8-07; 8:45 am] BILLING CODE 4140-01-P DEPARTMENT OF HEALTH AND HUMAN SERVICES National Institutes of Health National Cancer Institute; Notice of Meeting Pursuant to section 10(a) of the Federal Advisory Committee Act, as amended (5 U.S.C. Appendix 2), notice is hereby given of a meeting of the National Cancer Institute Director's Consumer Liaison Group. The meeting will be open to the public, with attendance limited to space available. Individuals who plan to attend and need special assistance, such as sign language interpretation or other reasonable accommodations, should notify the Contact Person listed below in advance of the meeting. *Name of Committee:* National Cancer Institute Director's Consumer Liaison Group. *Date:* June 13, 2007. *Time:* 1 p.m. to 2:30 p.m. *Agenda:* 1. Approval of Minutes; 2. Report from Dr. John E. Niederhuber, NCI Director; 3. Reports on NCI Budget; DCLG member activity; 4. Report on the National Community Cancer Center Program, Advisory Committee and Pilot Project; 5. Public Comment; 6. Action Items and Conclusion. *Place:* National Institutes of Health, 6116 Executive Boulevard, Rockville, MD 20852 (Telephone Conference Call). *Contact Person:* Barbara Guest, Executive Secretary, Office of Liaison Activities, National Cancer Institute, National Institutes of Health, 6116 Executive Blvd, Room 2202, Bethesda, MD 20892-8324, 301-496-0307, *guestb@mail.nih.gov* . Information is also available on the Institute's/Center's home page: *deainfo.nci.nih.gov/advisory/dclg/dclg.htm* , where an agenda and any additional information for the meeting will be posted when available. (Catalogue of Federal Domestic Assistance Program Nos. 93.392, Cancer Construction; 93.393, Cancer Cause and Preventive 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) Dated: April 30, 2007. Jennifer Spaeth, Director, Office of Federal Advisory Committee Policy. [FR Doc. 07-2294 Filed 5-8-07; 8:45 am]
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