National Institutes of Health, Public Health Service, HHS.
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.
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.
Photosensitization by Nuclear Receptor-Ligand Complexes and Cell Ablation Uses Thereof
Description of Technology: Androgen receptors (AR) mediate the effects of male steroid hormones and contribute to a wide variety of physiological and pathophysiological conditions. Prostate cancer development and progression are mediated through AR, a ligand-dependent transcription factor, and it is present in all stages of prostate carcinoma. Increased levels of PSA, an AR-induced prostate tumor-specific protein, are indicative of prostate cancer. Benign, non-cancerous conditions are also AR-dependent and can be therapeutic targets as well.
This technology is a method to cause AR-induced cell death (apoptosis) through photoactivation of a non-steroidal androgen receptor antagonist 1,2,3,4-tetrahydro-2,2-dimethyl-6-(trifluoromethyl)-8-pyridono[5,6-g] quinoline (TDPQ). Upon TDPQ binding to AR, a highly potent photocytoxic reaction induced once the TDPQ-AR complex is exposed to visible light irradiation of a specific wavelength. The inventors have cell-culture results demonstrating that cell death is a function of TDPQ, AR and light irradiation. This treatment method can potentially target AR-containing cancerous cells, while sparing nearby cells that lack AR.
The process has been extended to other nuclear receptors by choice of other photoactivatable ligands for these receptors. Certain suitable ligands are marketed drugs.
Applications: Therapeutic compounds to treat AR related conditions such as prostate cancer, baldness, hirsutism, and acne; Potential therapeutics for progesterone and glucorticoid receptor ligand related conditions such as breast and brain cancers, lymphoma, leukemia and arthritis; Method to treat androgen, Start Printed Page 39825progesterone, and glucorticoid receptor related conditions.
Market: Prostate cancer is the second most common type of cancer among men, wherein one in six men will be diagnosed with prostate cancer; An estimated 218,890 new cases of prostate cancer and 27,050 deaths due to prostate cancer in the U.S. in 2007; Hirsutism affects approximately 5% of adult women in the United States; Hair loss and acne industries are worth several billions of dollars.
Development Status: The technology is currently in the pre-clinical stage of development.
Inventors: William T. Schrader et al. (NIEHS).
1. B Risek et al. Androgen Receptor-Mediated Apoptosis is Regulated by Photoactivatable AR Ligands. Abstract submitted to the Endocrine Society; To be presented at the Annual Meeting of the Endocrine Society in Toronto, Canada in June 2007.
2. B Risek et al. Photocytotoxic Properties of the Non-Steroidal Androgen Receptor Antagonist TDPQ. Presented at the Annual Meeting of the Endocrine Society in Boston, MA in June 2006.
Patent Status: U.S. Provisional Application No. 60/926,218 filed 24 Apr 2007 (HHS Reference No. E-108-2007/0-US-01).
Licensing Status: Available for exclusive or non-exclusive licensing.
Licensing Contact: Jennifer Wong; 301/435-4633; email@example.com.
Method of Treating or Preventing Oxidative Stress-Related Diseases (Stroke and Neurodegenerative Diseases, Wound Healing and Cardiovascular Diseases)
Description of Technology: Reactive oxygen species (ROS) and reactive nitrogen species (RNS) produce oxidative stress to DNA, lipids and proteins thus causing cellular and tissue damage. A number of diseases are associated with oxidative stress including Alzheimer's disease, ischemic stroke, heart disease, cancer, hepatitis, and autoimmune disease. Uric acid is a natural antioxidant effective in reducing ROS and research has shown that uric acid contributes approximately two-thirds of all free radical scavenging capacity in plasma. Because uric oxide is too insoluble to be used as a therapeutic agent, scientists at the NIH developed uric acid analogs with improved anti-oxidative and solubility properties for use as free radical scavengers or antioxidants. These analogs increased survival of PC12 and hippocampal neurons after challenge by Fe, MPP and Glutamate. When administered to a mouse model of focal ischemic stroke, these compounds protect neuronal cells from ROS and reduce brain damage and ameliorate neurological deficits. Other studies show a single application of these analogs on skin lacerations in mice decreased the time for wound repair. Available for licensing are methods of treating ischemic stroke and wound healing, and for the prevention or treatment of other oxidative stress-related diseases, such as epilepsy, Parkinson's disease and dementia.
Applications: Novel uric acid analogs for use as antioxidants to help reduce the risk of stroke, neurological diseases and assisting with wound repair.
Market: Stroke is the third-leading cause of death and the leading cause of severe neurological disability worldwide; Americans will pay approximately $62.7 billion dollars in 2007 for stroke-related medical costs and disability.
Development Status: Pre-clinical data.
Inventors: Nigel H. Greig (NIA), Mark P. Mattson (NIA), et al.
Patent Status: U.S. Provisional Application No. 60/839,800 filed 23 Aug 2006 (HHS Reference No. E-059-2006/0-US-01).
Licensing Status: Available for licensing.
Licensing Contact: Norbert Pontzer, PhD, J.D.; 301/435-5502; firstname.lastname@example.org.
Collaborative Research Opportunity: The National Institute on Aging, Laboratory of Neurosciences, is seeking statements of capability or interest from parties interested in collaborative research to further develop, evaluate, or commercialize the described uric acid analogue technology in the treatment of neurodegenerative diseases, wound healing and cardiovascular disease. Please contact John D. Hewes, PhD at 301-435-3121 or email@example.com for more information.
Thiazepine Inhibitors of HIV-1 Integrase
Description of Technology: The human immunodeficiency virus (HIV) is the causative agent of acquired immunodeficiency syndrome (AIDS). Drug resistance is a critical factor contributing to the gradual loss of clinical benefit of treatments for HIV infection. Accordingly, combination therapies have further evolved to address the mutating resistance of HIV. However, there has been great concern regarding the apparent growing resistance of HIV strains to current therapies.
It has been found that a certain class of compounds including thiazepines and analogs and derivatives thereof are effective and selective anti-integrase inhibitors. These compounds have been found to inhibit both viral replication and the activity of purified HIV-1 integrase. The subject invention provides for such compounds and for methods of inhibiting HIV integrase.
Inventors: Yves Pommier et al. (NCI).
Patent Status: U.S. Patent No. 7,015,212 issued 21 Mar 2006 (HHS Reference No. E-036-1999/0-US-03).
Licensing Status: Available for exclusive or non-exclusive licensing.
Licensing Contact: Sally Hu, PhD, MBA; 301/435-5606; firstname.lastname@example.org.
Collaborative Research Opportunity: The Laboratory of Molecular Pharmacology of the National Cancer Institute is seeking statements of capability or interest from parties interested in collaborative research to further develop, evaluate, or commercialize anti-integrase inhibitors. Please contact John D. Hewes, PhD at 301-435-3121 or email@example.com for more information.Start Signature
Dated: July 13, 2007.
Steven M. Ferguson,
Director, Division of Technology Development and Transfer, Office of Technology Transfer, National Institutes of Health.
[FR Doc. E7-14031 Filed 7-19-07; 8:45 am]
BILLING CODE 4140-01-P