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David P. Bingaman, Weatherford US

David P. Bingaman, Weatherford, TX US

Patent application numberDescriptionPublished
20080234245Angiostatic Agents for Controlling Choroidal Neovascularisation After Ocular Surgery or Trauma - Compositions of angiostatic agents for treating choroidal neovascularization resulting from ocular surgery or from trauma to ocular tissue and methods for their use are disclosed.09-25-2008
20090012030RNAi-MEDIATED INHIBITIN OF HTRA1 FOR TREATMENT OF MACULAR DEGENERATION - RNA interference is provided for inhibition of HTRA1 mRNA expression for treating patients with an HTRA1-mediated ocular disorder. In particular, methods are provided for treating age-related macular degeneration (AMD) and using interfering RNA molecules that attenuate expression of HTRA1 in patients having AMD or at risk of developing AMD.01-08-2009
20090035225RNAi-RELATED INHIBITION OF TNFa SIGNALING PATHWAY FOR TREATMENT OF GLAUCOMA - RNA interference is provided for inhibition of tumor necrosis factor α (TNFα) by silencing TNFα cell surface receptor TNF receptor-1 (TNFR1) mRNA expression, or by silencing TNFα converting enzyme (TACE/ADAM17) mRNA expression. Silencing such TNFα targets, in particular, is useful for treating patients having a TNFα-related condition or at risk of developing a TNFα-related condition such as the ocular conditions associated with elevated intraocular pressure (IOP), including glaucoma and ocular hypertension.02-05-2009
20090036396RNAi-RELATED INHIBITION OF TNFalpha SIGNALING PATHWAY FOR TREATMENT OF OCULAR ANGIOGENESIS - RNA interference is provided for inhibition of tumor necrosis factor α (TNFα) by silencing TNFα cell surface receptor TNF receptor-1 (TNFR1) mRNA expression, or by silencing TNFα converting enzyme (TACE/ADAM17) mRNA expression. Silencing such TNFα targets, in particular, is useful for treating patients having a TNFα-related condition or at risk of developing a TNFα-related condition, such as ocular angiogenesis, retinal ischemia, and diabetic retinopathy.02-05-2009
20090036397RNAi-RELATED INHIBITION OF TNFa SIGNALING PATHWAY FOR TREATMENT OF MACULAR EDEMA - RNA interference is provided for inhibition of tumor necrosis factor α (TNFα) by silencing TNFα cell surface receptor TNF receptor-1 (TNFR1) mRNA expression, or by silencing TNFα converting enzyme (TACE/ADAM17) mRNA expression. Silencing such TNFα targets, in particular, is useful for treating patients having or at risk of developing macular edema.02-05-2009
20090105182RNAi-MEDIATED INHIBITION OF STROMAL CELL-DERIVED FACTOR 1-RELATED TARGETS FOR TREATMENT OF NEOVASCULARIZATION-RELATED CONDITIONS - RNA interference is provided for inhibition of stromal cell-derived factor 1 (SDF1)-related targets in pathologic neovascularization-related conditions, including those cellular changes resulting from the signal transduction activity of the SDF1 targets that lead directly or indirectly to ocular neovascularization, abnormal angiogenesis, retinal vascular permeability, retinal edema, diabetic retinopathy particularly proliferative diabetic retinopathy, diabetic macular edema, exudative age-related macular degeneration, sequela associated with retinal ischemia, and posterior segment neovascularization, for example.04-23-2009
20090105245METHODS FOR TREATING MACULAR EDEMA AND OCULAR ANGIOGENESIS USING AN ANTI-INFLAMMATORY AGENT AND A RECEPTOR TYROSINE KINASE INHIBITOR - The present invention provides methods for inhibiting increased vascular permeability and/or pathologic ocular angiogenesis via administration of a combination of one or more molecules that potently inhibit select receptor tyrosine kinases (RTKs) or vascular endothelial growth factor (VEGF) and one or more anti-inflammatory agents.04-23-2009
20100048608Histone Deacetylase Inhibitors for the Treatment of Ocular Neovascular or Edematous Disorders and Diseases - Ophthalmic compositions containing HDAC inhibitors and their use for treating ocular neovascular or edematous diseases and disorders are disclosed.02-25-2010
20100204244AGENTS FOR TREATMENT OF DIABETIC RETINOPATHY AND DRUSEN FORMATION IN MACULAR DEGENERATION - Agents that stimulate nuclear translocation of Nrf2 protein and the subsequent increases in gene products that detoxify and eliminate cytotoxic metabolites are provided in a method for treating diabetic retinopathy or drusen formation in age-related macular degeneration. The structurally diverse agents that act on the Nrf2/ARE pathway induce the expression of enzymes and proteins that possess chemically versatile cytoprotective properties and are a defense against toxic metabolites and xenobiotics. Agents include certain electrophiles and oxidants such as a Michael Addition acceptor, diphenol, thiocarbamate, quinone, 1,2-dithiole-3-thione, butylated hydroxyanisole, flavonoid other than genistein, an isothiocyanate, 3,5-di-tert-butyl-4-hydroxytoluene, ethoxyquin, a coumarin, combinations thereof, or a pharmacologically active derivative or analog thereof.08-12-2010
20100267811RNAi-RELATED INHIBITION OF TNFa SIGNALING PATHWAY FOR TREATMENT OF OCULAR ANGIOGENESIS - RNA interference is provided for inhibition of tumor necrosis factor α (TNFα) by silencing TNFα cell surface receptor TNF receptor-1 (TNFR1) mRNA expression, or by silencing TNFα converting enzyme (TACE/ADAM17) mRNA expression. Silencing such TNFα targets, in particular, is useful for treating patients having a TNFα-related condition or at risk of developing a TNFα-related condition, such as ocular angiogenesis, retinal ischemia, and diabetic retinopathy.10-21-2010
201100822005,6,7-TRIHYDROXYHEPTANOIC ACID AND ANALOGS FOR THE TREATMENT OF OCULAR DISEASES AND DISEASES ASSOCIATED WITH HYPERPROLIFERATIVE AND ANGIOGENIC RESPONSES - Compositions containing 5,6,7-trihydroxyheptanoic acid and analogs and their use for treating posterior segment ocular diseases and diseases characterized by cellular hyperproliferation or angiogenesis, are disclosed.04-07-2011
20110135579RNAi-RELATED INHIBITION OF TNFa SIGNALING PATHWAY FOR TREATMENT OF GLAUCOMA - RNA interference is provided for inhibition of tumor necrosis factor α (TNFα) by silencing TNFα cell surface receptor TNF receptor-1 (TNFR1) mRNA expression, or by silencing TNFα converting enzyme (TACE/ADAM17) mRNA expression. Silencing such TNFα targets, in particular, is useful for treating patients having a TNFα-related condition or at risk of developing a TNFα-related condition such as the ocular conditions associated with elevated intraocular pressure (IOP), including glaucoma and ocular hypertension.06-09-2011

Patent applications by David P. Bingaman, Weatherford, TX US