199 results about "Altersbedingte makuladegeneration" patented technology

The present disclosure relates to fusion molecules and chimeric molecules which comprise two components: an Ang-2 antagonist peptide linked to a VEGF-binding moiety. Further disclosed are methods of using said chimeric molecules to treat a patient cancer, proliferative retinopathy, neovascular glaucoma, macular edema, wet age-related macular degeneration (wAMD), macular edema following retinal vein occlusion (RVO), diabetic macular edema (DME), or diabetic retinopathy (DR).

By constructing an age-related macular degeneration animal model, experimental results in multiple aspects of clinical examination (FFA and ERG), pathological detection (RPE-choroidal patch IB4 fluorescent staining) and the like prove that the rucotinib can be used for effectively treating age-related macular degeneration, especially wet age-related macular degeneration.

The present invention relates to superoxide dismutase and a use thereof for preventing or treating dry age-related macular degeneration. More specifically, the present invention relates to a pharmaceutical composition or a therapeutic method for prevention or treatment of dry macular degeneration. The composition and method according to the present invention can be effectively used to prevent or treat dry macular degeneration by reducing or preventing drusen formation and / or drusenoid lesions.

Disclosed herein are methods of treating neovascular age-related macular degeneration ( "nAMD" ) and diabetic macular edema ( "DME" ) in a subject in need thereof using a fusion protein that inhibits both the VEGF and complement pathways (e.g., efdamrofusp alfa). Disclosed herein include, inter alia, treatment regiments comprising a loading phase and a maintenance phase.

The use of Gap Junction-dependent cellular modulators in the treatment or prevention of age-related macular degeneration (AMD) is disclosed, and more particularly to their use for the treatment or prevention of dry AMD (d-AMD) and to prevent progression to wet or neovascular or advanced angiogenic AMD or geographic atrophy (GA).

Methods for treating ocular diseases such as dry age-related macular degeneration include administering non-invasive photobiomodulation light therapy in the context of a prior PBM treatment, on the basis of a subject response to prior PBM treatment, on the basis of a patient pre-treatment characteristic, and combinations thereof. In some embodiments, methods comprise administering PBM therapy to subjects who have received PBM about four to six months prior to the present administering. In some embodiments, methods comprise administering PBM therapy to subjects in early stages of dry age-related macular degeneration.

A method and system delivers customizable microcurrent stimulation to ocular tissue using a three half-bridge driver circuit. The system includes a control circuit that selectively switches high-side and low-side transistors, such as MOSFETs, to generate various electrical waveforms, such as stepped, asymmetric biphasic, pulsed, and triangular waveforms. These waveforms are applied to electrodes in contact with the eye for therapeutic treatment, addressing conditions like age-related macular degeneration (AMD) and other ocular disorders. The system allows for adjustments in amplitude, frequency, and duration of the waveforms, providing personalized treatment protocols tailored to patient-specific needs. High-impedance periods are included between pulses to promote tissue recovery and enhance patient comfort. Additionally, a non-transitory computer-readable storage medium stores a program that controls the system, enabling real-time waveform generation and dynamic adjustment during treatment. This approach offers a flexible and efficient solution for ocular therapy, improving both treatment outcomes and patient experience.

To provide methods for reducing the treatment burden for patients who have an intraocular neovascular disorder.SOLUTION: The present invention provides a method for treating neovascular age-related macular degeneration (nAMD) in a mammal, the method comprising: a) administering to the mammal three individual doses of a VEGF antagonist at 4 week intervals; b) assessing the mammal for best corrected visual acuity (BCVA), visual acuity (VA), central subfield thickness (CSFT), and the presence of intraretinal cysts / fluid at week 12; and c) assessing the mammal for BCVA, VA, CSFT, and the presence of intraretinal cysts / fluid at week 16.SELECTED DRAWING: None

The invention discloses application of cnidium lactone in preparation of a medicine for treating AMD or corneal injury, and belongs to the field of biological medicine. It is found for the first time that the cnidium lactone can inhibit sodium iodate induced retinal pigment epithelial cell injury, and it is also found for the first time that the cnidium lactone can promote injured cornea repair; based on the discovery, the invention respectively provides application of cnidium lactone in preparation of medicines for treating age-related macular degeneration and preparation of medicines for treating corneal injury. Experimental results show that cnidium lactone can remarkably reverse the retinal pigment epithelial cell degradation trend caused by age-related macular degeneration and can also remarkably promote corneal notch healing. The invention provides a new optional medicine for treating age-related macular degeneration and corneal injury, expands the application range of cnidium lactone, and has outstanding clinical practical value and wide application prospect.

Disclosed are direct-binding dual hypoxia-inducible factor (HIF) inhibitors and their use for treating cancer, including, but not limited to, breast, colorectal, lung, melanoma, pancreatic, and prostate cancer as a monotherapy and in combination with anti-CTLA-4 or anti-PD-1 immunotherapies. The dual HIF inhibitors also can be used for treating diseases, disorders, or conditions associated with ocular neovascularization, including, but not limited to, diabetic macular edema, diabetic retinopathy, and other ischemic retinopathies (including, but not limited to retinal vein occlusion, sickle cell retinopathy, retinopathy of prematurity, Norrie's disease, and Coat's disease), corneal neovascularization, and the treatment or prevention of neurovascular (wet-type) age-related macular degeneration.

The present invention relates to antibodies that bind to VEGF and ANG2 for use in the treatment of ocular vascular diseases, such as neovascular AMD (nAMD) (also referred to as choroidal angiogenesis [CNV] secondary to age-related macular degeneration [AMD] or wet AMD), diabetic retinopathy, in particular diabetic macular edema (DME) or macular edema secondary to retinal vein occlusion (RVO).

The present disclosure relates to the pharmaceutical use of antagonists (e.g., antibodies or antigen-binding portions thereof) that specifically bind to FAM19A5 for the treatment of retinopathy (e.g., diabetic retinopathy) and / or maculopathy (e.g., age-related macular degeneration) in an individual in need thereof.

This invention relates to pharmaceutical compositions and methods for treatment of ophthalmic or ocular diseases and conditions. The compositions contain targeting molecules that are made up of a bifunctional hepatoma-derived growth factor-specific antibody covalently attached to a trapper that specifically binds vascular endothelial growth factor and / or transforming growth factor beta. Specific eye conditions that can be beneficially affected by the compositions and methods of the invention include age-related macular degeneration, diabetic retinopathy, peripheral vitreoretinopathy, and retinal vein occlusion.

The invention discloses an application of daidzin to preparation of a medicine and a potency verification method of daidzin, the medicine is applied to improvement of age-related macular degeneration, and the potency verification method comprises in-vitro verification and in-vivo verification; the protection effect of daidzin on oxidative damage caused by SIN-1 is evaluated through an in-vitro experiment, and the protection effect is specifically shown as increase of cell activity and reduction of MDA content; in-vivo verification is completed by means of a rat model, a visual placement reaction experiment is formed, a rat visual function system is evaluated, the MDA content of rat eye peripheral blood is detected, and it is clear that the daidzin can obviously relieve AMD damage, that is, the daidzin has an obvious improvement effect on AMD; and daidzin is good in safety and low in improvement and treatment cost on age-related macular degeneration, and meets the current clinical requirements.

Computer-implemented systems and methods for automated diagnosis of age-related macular degeneration apply machine learning techniques to optical coherence tomography B-scans to diagnose and grade age-related macular degeneration and other eye diseases.

The present invention relates to inhibitors, compositions containing inhibitors, and their use in the treatment or prevention of age-related macular degeneration (AMD).

Compositions and methods are described for the delivery of a fully human post-translationally modified (HuPTM) monoclonal antibody (“mAb”) or the antigen-binding fragment of a mAb against human vascular endothelial growth factor (“hVEGF”)—such as, e.g., a fully human-glycosylated (HuGly) anti-hVEGF antigen-binding fragment—to the retina / vitreal humour in the eye(s) of human subjects diagnosed with ocular diseases caused by increased neovascularization, for example, neovascular age-related macular degeneration (“nAMD”), also known as “wet” age-related macular degeneration (“WAMD”), age-related macular degeneration (“AMD”), and diabetic retinopathy.

The invention discloses a construction method of a dry age-related macular degeneration animal model, which comprises the following steps: sodium iodate is injected into vitreous cavities above macula lutea, the concentration of the sodium iodate is 4 mg / mL-16 mg / mL, and the single injection capacity is 100 [mu] L / eye. The stable and repeatable dry age-related macular degeneration animal model is constructed by adjusting the injection range, the injection dosage and different injection positions, and the severity of the lesion of the model is obviously related to the dosage.

The disclosure provides a method of treating, ameliorating, and / or preventing retinal degenerations, such as but not limited to anterior segment ocular disorders and / or age-related macular degeneration (AMD), in a subject. In certain embodiments, the method comprises administering to the subject a therapeutically effective amount of a compound of the disclosure. In certain embodiments, the compound of the disclosure prevents and / or minimizes cellular assault, such as oxidative stress-related cellular assault, and / or promote cell viability.

The invention discloses application of a DKK1 inhibitor in preparation of a medicine for treating dry age-related macular degeneration. According to the application disclosed by the invention, the expression of DKK1 in dry AMD cells and animal models induced by sodium iodate (NaIO3) is obviously improved. The form of the retinal pigment epithelial cells can be protected and the death rate can be reduced by using the siRNA of the targeted DKK1 in an in-vitro experiment, and the plaque loss of the retinal pigment epithelial cells can be relieved and the retinal pigment epithelial cells can be protected by using the shRNA of the targeted DKK1 in an in-vivo experiment. Therefore, the invention provides a new therapeutic target and therapeutic strategy for dry AMD, and has important clinical application value.

The present disclosure provides pharmaceutical compositions containing nucleic acid molecules encoding PEDF which are codon-optimized, as well as methods for increasing the level of PEDF in the treatment or prophylaxis of retinal degenerative diseases, such as age-related macular degeneration (AMD), or other neurodegenerative diseases.

The present invention provides methods and compositions for treating and / or preventing age related macular degeneration and other conditions involving macular degeneration, ocular neovascularization, or ocular inflammation. In an exemplary embodiment, a method is disclosed that involves administering an expression vector that delivers a secretable and cell penetrating CARD to a subject in need of treatment or prevention of age-related macular degeneration or another condition involving macular degeneration or ocular neovascularization.

The present disclosure describes compositions comprising vitamin C, vitamin E, zinc, copper, lutein, zeaxanthin, and Coenzyme Q10, as well as pharmaceutically acceptable salts of any one of the foregoing. The compositions are useful for treating diseases associated with loss of visual acuity, including, for example, age-related macular degeneration, and supporting cardiac health.

Benzyl derivative compounds having peroxisome proliferator-activated receptor α (PPARα) agonistic activity, kits and compositions containing such compounds, and methods of their use in enhancing PPARα activity for treating diseases and / or conditions involving inflammation and / or angiogenesis, particularly ocular diseases and / or conditions such as but not limited to retinal inflammation, retinal neovascularization, retinal vascular leakage, retinopathy of prematurity, diabetic retinopathy, age-related macular degeneration, and diabetic macular edema.

The described invention provides method for treating a complement disorder such as age-related macular degeneration (AMD) in a subject, comprising administering a pharmaceutical composition into an affected eye of a subject by ocular injection, wherein the composition comprises a nucleic acid encoding a soluble CD59 (sCD59) protein operably linked to a promoter, wherein the nucleic acid encoding sCD59 is packaged into a delivery vector and wherein the administering results in expression and secretion of the sCD59 protein by cells of the affected eye and the expression results in treatment of affected cells in the affected eye.

The invention belongs to the technical field of medical experimental animal models, provides a construction method of a dry age-related macular degeneration animal model, and aims to break through the technical bottlenecks of long construction period, high cost and incomplete pathological feature coverage of an existing model. D-galactose is used for inducing glycosylation end product accumulation and mitochondrial dysfunction, oxidative stress, RPE metabolic disorder and inflammation microenvironment in the dry AMD pathogenesis process can be synchronously simulated, core pathological characteristics such as retina glass membrane wart deposition, RPE atrophy, retina and visual function damage and the like can be accurately reproduced, meanwhile, a multi-dimensional verification system is matched, and the method has the advantages that the method is simple and convenient to operate and high in practicability. The method is suitable for preclinical evaluation of personalized treatment strategies; besides, the method is short in modeling period, the animal model meeting the requirement can be obtained within 8 weeks, the cost advantage is outstanding, and an efficient and reliable experimental animal model can be provided for dry AMD treatment research.

The application discloses application of a GPR146 inhibitor in preparation of a drug for treating wet age-related macular degeneration. The application finds that GPR146 is significantly up-regulated in expression in a mouse model of laser-induced CNV and a mouse model of subretinal fibrosis. In mice, shRNA is used to knock down GPR146, thereby significantly inhibiting CNV, subretinal fibrosis and inflammation. In an in-vitro experiment, siRNA targeting GPR146 can inhibit the in-vitro neovascular function of endothelial cells, such as proliferation, migration and tube formation, and reduce immune cell adhesion and transendothelial cell migration. In addition, targeting GPR146 can also inhibit the expression of TGF-beta, Fibronectin (FN), alpha-SMA, Col1A, MMP9 and other fibrosis-promoting molecules by endothelial cells. Meanwhile, targeting GPR146 can also inhibit the proliferation and migration of smooth muscle cells and reduce the expression of the above fibrosis-promoting molecules. The above results all show that targeting GPR146 can significantly inhibit CNV formation, inflammation and subretinal fibrosis, and has good therapeutic effect.

The present application provides an acesulfame implant which is stable, safe and can achieve at least 6 months of sustained release, can effectively treat various eye diseases including but not limited to glaucoma, cataract, retinal vein obstruction (RVO), uveitis, diabetic macular edema (DME) and age-related macular degeneration (wAMD and nAMD), etc., avoids repeated administration, reduces the formation of side effects, reduces the cost of drug use, and meets the high stability required by drug preparation in production, storage and transportation, has good application prospect, and meets the unmet clinical needs.