116 results about "Altersbedingte makuladegeneration" patented technology

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.

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.

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.

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 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 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 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 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.

This application provides a screening method and animal model related to intraocular diseases, such as age-related macular degeneration (AMD), for identifying candidate therapeutic agents for treating or preventing eye diseases, such as AMD. [Solution] The present application also provides compounds / compositions that can kill or inhibit the growth of microorganisms such as Bacillus megatherium. The present application further provides methods for treating infections caused by microorganisms such as Bacillus megatherium, and for treating or preventing diseases or disorders associated with such infections, such as AMD, using the compounds / compositions.

The present invention belongs to the field of tumor immunotherapy, and relates to a humanized anti-VEGF antibody Fab fragment. The present invention discloses nucleic acid sequences (including heavy / light chain variable regions) encoding said antibody fragment, and vectors, pharmaceutical compositions and kits containing said nucleic acid sequences. The anti-VEGF antibody Fab fragments disclosed in the present invention can specifically bind to VEGF with high affinity and block the binding of VEGF to the receptor VEGFR2, and also neutralize the proliferative effect of VEGF on HUVEC cells. Compared to the full-length antibody, antibodies in the form of Fab fragments have stronger penetrability and less toxic in terms of gastrointestinal perforation, hypertension and hemorrhage and do not stimulate the complement cascade reaction, thus reducing the risk of endophthalmitis and autoimmune inflammatory reactions. Thus it could be used in clinical treatment of ocular diseases characterized by choroidal neovascularization, including but not limited to age-related macular degeneration (AMD), diabetic macular edema (DME), retinal edema, degenerative myopia, choroidal neovascularization (CNV).

Biomarkers that can support the diagnosis of inflammatory diseases and methods of their use. [Solution] A composition and method for detecting inflammasome components in a sample from a subject as a marker for inflammasome-related diseases or disorders such as multiple sclerosis, stroke, mild cognitive impairment, Alzheimer's disease, age-related macular degeneration, NASH, inflammatory aging, or traumatic brain injury. Methods for using such inflammasome markers to determine prognosis, prescribe treatment, and monitor response to treatment in subjects with inflammasome-related diseases or disorders such as multiple sclerosis, stroke, mild cognitive impairment, Alzheimer's disease, age-related macular degeneration, NASH, inflammatory aging, or traumatic brain injury are also described.

The present disclosure relates to methods of removing lipids (e.g., cholesterol) or preventing lipid accumulation in an eye of an individual (e.g., a human), and methods of preventing or treating an eye disease characterized by lipid accumulation (e.g., age-related macular degeneration) in an individual, such as an eye disease characterized by age-related macular degeneration. The method comprises administering to an eye of an individual an effective amount of a pharmaceutical composition comprising a plurality of nanodisks, wherein the nanodisks comprise a membrane scaffold protein (MSP) and a phospholipid.

The current invention relates to the use of bispecific antibodies that bind to human vascular endothelial growth factor (VEGF) and to human angiopoietin-2 (ANG-2) for the treatment of ophthalmologic diseases, such as age-related macular degeneration and diabetic macular edema, where the bispecific antibodies are administered intravitreally every 8 weeks or less frequently.

The invention belongs to the technical field of biological medicine, and particularly relates to superoxide dismutase HSTM-SOD and application thereof. The amino acid sequence of the superoxide dismutase HSTM-SOD provided by the invention is selected from at least one of sequences as shown in SEQ ID NO: 1 to SEQ ID NO: 8, or a sequence with more than 80% of homology with the amino acid sequence. The HSTM-SOD with different sequences, which is provided by the invention, generally has excellent thermal stability, pH stability, good compatibility and super-strong membrane crossing capability; the HSTM-SOD shows remarkable capabilities in the aspects of promoting cell sunburn repair, promoting cell oxidative damage repair, resisting ferroptosis caused by TalaA, promoting wound healing of diabetic patients, improving age-related macular degeneration and the like, and has a wide application prospect.

The invention discloses an application of a fluorinated modified peptide in preparation of a medicine for treating dry age-related macular degeneration, the fluorinated modified peptide FNBP can effectively pass through a retinal barrier and exert antioxidant and neuroprotective effects in RPE cells, and the dry age-related macular degeneration is treated by activating a Keap1 / Nrf2 pathway. The new application of the fluorinated modified peptide in dry AMD treatment is provided for the first time, and a new strategy is provided for medicine development of posterior ocular diseases.

Microparticulate (MP) formulations formed from one or more poly(hydroxyacid) polymers having a molecular weight ranging from 5kD to 60kD, and one or more active agents are injected into the eye of a subject to address eye disorders. The MP formulations assure high drug loading and extended delivery of the active agent of six to twelve months. The active agents may include peroxisome proliferator-activated receptor alpha (PPARα) signaling agonists such as PPARα agonist A190 (IUPAC name 3-((4-((4-fluorobenzyl)oxy)- 3- methylbenzyl)amino)benzoic acid). The formulations have therapeutic and protective effects against retinal degeneration diseases such as age-related macular degeneration (AMD), but may also be used for treating or relieving the symptoms of retinal inflammation, retinal neovascularization, retinal vascular leakage, retinopathy of prematurity (ROP), diabetic retinopathy (DR), and diabetic macular edema (DME).

Methods of treating ocular diseases such as age-related macular degeneration may include the administration of peptides comprising complement factor H and factor H-like protein domains to reduce an amount of geographic atrophy in a subject in need thereof. These methods may be administered by intraocular, intervascular or subcutaneous injection.

To provide treatment of AMD using an AAV2 variant with aflibercept.SOLUTION: The present disclosure provides pharmaceutical compositions and methods thereof for treatment of age-related macular degeneration (AMD) in a subject by administering intravitreally a pharmaceutical composition adapted for gene therapy, comprising a vector having a nucleic acid sequence that encodes aflibercept. The present disclosure relates to pharmaceutical compositions and methods for prevention or treatment of neovascular (wet) age-related macular degeneration (AMD), macular edema following retinal vein occlusion (RVO), diabetic macular edema (DME), diabetic retinopathy (DR) in patients with DME, retinal vein occlusion, and related eye diseases or conditions, in a primate or human subject by administering intravitreally or subretinally a pharmaceutical composition comprising a pharmaceutically effective amount of a vector or viral particles (e.g., rAAV) comprising a nucleic acid encoding aflibercept or a functional fragment or variant thereof.SELECTED DRAWING: None