39 results about "Geographic atrophy" patented technology

An apparatus for delivering therapeutic agent to an eye comprises a body, a cannula, a hollow needle, and an actuation assembly. The cannula extends distally from the body and is sized and configured to be insertable between a choroid and a sclera of a patient's eye. The actuation assembly is operable to actuate the needle relative to the cannula to thereby drive a distal portion of the needle along an exit axis that is obliquely oriented relative to the longitudinal axis of the cannula. The cannula may be inserted through a sclerotomy incision to position a distal end of the cannula at a posterior region of the eye, between the choroid and sclera. The needle may be advanced through the choroid to deliver the therapeutic agent adjacent to the potential space between the neurosensory retina and the retinal pigment epithelium layer, adjacent to the area of geographic atrophy.

The present invention is directed to the treatment of disorders involving the accumulation of drusen, such as dry age-related macular degeneration and geographic atrophy via administration of therapeutically effective amounts of at least one monomeric or polymeric cyclodextrin.

The present disclosure provides therapeutic agents for the treatment of age-related macular degeneration (AMD) and other eye disorders. One or more therapeutic agents can be used to treat any stages (including the early, intermediate and advance stages) of AMD, and any phenotypes of AMD, including geographic atrophy (including non-central GA and central GA) and neovascularization (including types 1, 2 and 3 NV). In certain embodiments, an anti-dyslipidemic agent (e.g., an apolipoprotein mimetic and/or a statin) is used alone to treat or slow the progression of atrophic AMD (including early AMD and intermediate AMD), and/or to prevent or delay the onset of AMD, advanced AMD and/or neovascular AMD. In further embodiments, two or more therapeutic agents (e.g., any combinations of an anti-dyslipidemic agent, an antioxidant, an anti-inflammatory agent, a complement inhibitor, a neuroprotector and an anti-angiogenic agent) that target multiple underlying factors of AMD (e.g., formation of lipid-rich deposits, oxidative stress, local inflammation, cell death and neovascularization) are used to treat or slow the progression of atrophic AMD (including non-central GA and central GA) or neovascular AMD (including types 1, 2 and 3 NV), and/or to prevent or delay the onset of AMD, advanced AMD and/or neovascular AMD.

The application discloses methods and compositions for the inhibition of the alternative complement pathway. The methods and compositions involve the use of aptamers for inhibiting complement Factor D. The application further provides anti-Factor D aptamers for the treatment of dry age-related macular degeneration, geographic atrophy, wet age-related macular degeneration or Stargardt disease.

The present invention provides biomarkers of oxidative stress in subjects with retinitis pigmentosa, age-related macular degeneration, diabetic retinopathy, Fuchs' dystrophy, diabetic macular edema (DME), geographic atrophy, Stargardt's disease, or retinal vein occlusion (RVO), and their use in identifying subjects in need of treatment and methods for staging the severity of the disease.

Pharmacogenetic analysis revealed an effect of risk alleles in ARMS2 and CFH genes on the response of subjects to anti-C5 antibodies in the treatment of the progression of geographic atrophy.

Described herein are methods and devices for the long term treatment of ophthalmic disorders. Also disclosed are encapsulated cell therapy (ECT) devices that secrete a biologically active molecule and methods for using the same for the treatment of various kinds of ophthalmic disorders, including retinitis pigmentosa, geographic atrophy (dry age-related macular degeneration), glaucoma and/or macular telangiectasia.

The invention provides a solution to the clinical problem of retinal pigment epithelium (RPE) degeneration or geographic atrophy (GA) associated with AMD. PPARΥ selective agonists, e.g., troglitazone and analogs thereof are used to reduce or inhibit RPE degeneration, GA, and/or the progression of dry AMD.

The present invention relates to a method and compositions for the treatment of age-related macular degeneration (AMD), in particular dry-AMD, specifically geographic atrophy (GA) or advanced dry-AMD. Specifically, the invention relates to an inner-blood-retinal-barrier (iBRB) or blood-brain-barrier (BBB) tight junction protein and/or a circadian clock protein for use in the prevention and/or treatment of age-related macular degeneration.

This invention is directed to novel aliphatic prolinamide derivatives of Formula I, and pharmaceutically acceptable salts, solvates, solvates of the salt and prodrugs thereof, useful in the prevention (e.g., delaying the onset of or reducing the risk of developing) and treatment (e.g., controlling, alleviating, or slowing the progression of) of age-related macular degeneration (AMD) and related diseases of the eye. These diseases include dry-AMD, wet-AMD, geographic atrophy, diabetic retinopathy, retinopathy of prematurity, polypoidal choroidal vasculopathy, and degeneration of retinal or photoreceptor cells. The invention disclosed herein is further directed to methods of prevention, slowing the progress of, and treatment of dry-AMD, wet-AMD, and geographic atrophy, diabetic retinopathy, retinopathy of prematurity, polypoidal choroidal vasculopathy, and degeneration of retinal or photoreceptor cells, comprising: administration of a therapeutically effective amount of compound of the invention. The compounds of the invention are inhibitors of HTRA1. Thus, the compounds of the invention are useful in the prevention and treatment of a wide range of diseases mediated (in whole or in part) by HTRA1. The compounds of the invention are also useful for inhibiting HTRA1 protease activity in an eye or locus of an arthritis or related condition.

The invention discloses applications of a small molecule drug (+)-JQ1 in drugs for treating geographic atrophy type age-related macular degeneration, and specifically discloses the small molecule drug(+)-JQ1 having effects of inhibiting cGAS-STING signal pathways and regulatory and anti-inflammatory effects of the small molecule drug on autoimmunity. In a mouse disease model of sodium iodate injection induced geographic atrophy type age-related macular degeneration, the (+)-JQ1 is firstly provided that the (+)-JQ1 can inhibit the expression of cGAS and STING genes and achieve immunoregulationand anti-inflammatory effects by inhibiting the functions of the cGAS-STING signal pathways. The inhibition of the (+)-JQ1 on the cGAS-STING signal pathways and the anti-inflammatory effects of the(+)-JQ1 in the disease model of geographic atrophy type age-related macular degeneration are a promising clinical strategy of new use for old drugs, so that reference can be provided for researches on small molecular compounds for anti-autoimmune response and treatment of age-related macular degeneration diseases.

There are provided inter alia compounds capable of inhibiting retinal pigment epithelium (RPE) degeneration or geography atrophy (GA) associated with age-related macular degeneration (AMD), and methods of using the same.