34 results about "Macula lutea degeneration" patented technology

The invention belongs to the technical field of nano-drugs, and discloses a multifunctional nano-drug delivery system for treating neovascular eye diseases and a preparation method of the multifunctional nano-drug delivery system. The nano drug delivery system disclosed by the invention is a composite nano preparation which takes dendritic mesoporous silica nanoparticles as a carrier and co-loads cerium zirconium oxide nano enzyme and an anti-VEGF (vascular endothelial growth factor) drug, various active oxygen can be efficiently removed, oxygen is continuously released through catalytic decomposition of hydrogen peroxide, a retina hypoxia microenvironment is improved, and the retina hypoxia effect is improved. According to the present invention, the anti-VEGF drug delivery system can reduce the oxidative stress induced retinal pigment epithelial cell apoptosis rate, reduce the inflammatory reaction, and simultaneously achieve the slow release and the controlled release of the anti-VEGF drug, and the drug effect maintenance time can achieve more than 60 days, such that the multi-target synergistic treatment can be achieved through the synergistic regulation of the multiple pathological links such as oxygen deficit-oxidative stress-inflammation-angiogenesis, and the anti-VEGF drug delivery effect can be achieved. The choroidal neovascularization can be effectively inhibited by single intravitreal injection, and a new strategy of multi-target collaborative treatment is provided for neovascular macular degeneration and other eye diseases.

Disclosed herein are compositions and methods for the modulation of 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR) expression, wherein the compositions include an siRNA duplex or a conjugated siRNA duplex. Also disclosed herein are methods, and compositions for use in methods, of treating age-related macular degeneration (AMD) or hyperlipidemia. The compositions disclosed herein comprise an siRNA duplex that comprises a sense sequence and an antisense sequence, wherein the sense sequence and the antisense sequence are at least partially complementary to each other.

This disclosure relates to RNAi agents capable of inhibiting complement factor B (CFB) gene expression. Pharmaceutical compositions containing CFB RNAi agents and methods of use thereof are also disclosed. The CFB RNAi agents disclosed herein may be conjugated to a targeted ligand containing an N-acetyl-galactosamine ligand to facilitate in vivo delivery to hepatocytes. RNAi agents can be used in methods of treating diseases, disorders, or conditions partially mediated by CFB gene expression, including IgA nephropathy (IgAN), C3 glomerulopathy (C3G), immune complex-mediated membrane proliferative glomerulonephritis (IC-MPGN), lupus nephritis (LN), anti-glomerular basement membrane antibody disease (anti-GBM), ischemia-reperfusion injury and T-cell-mediated rejection in kidney transplantation (TCMR), anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis, age-related macular degeneration (AMD) including early and / or intermediate-stage AMD, geographic atrophy (GA), glaucoma, Doyne honeycomb retinal dystrophy, paroxysmal nocturnal hemoglobinuria (PNH), atypical hemolytic uremic syndrome (aHUS), pre-eclampsia, rheumatoid arthritis (RA), and / or other complement-mediated disorders.

The present invention relates to a nanoparticle comprising a nanomaterial and at least a first ligand and a second ligand tethered to the nanoparticle. The present invention also relates to a nanoparticle for use as a medicament or diagnostic agent. The present invention also relates to a nanoparticle for use in a method for preventing or treating a disease selected from the group consisting of diabetic nephropathy, glomerulonephritis, glomerular VEGF A dysregulation, endothelial VEGF A dysregulation, diabetic retinopathy, rheumatoid arthritis, age-related macular degeneration and cancer, such as breast cancer. Furthermore, the present invention relates to a method of preparing a nanoparticle.

The present invention relates to peptides that have preventive, ameliorative, or therapeutic effects against amyloidosis and / or macular degeneration, are safe for living organisms, and have few side effects including abnormal reactions, as well as pharmaceutical compositions and health functional foods containing the same.

This invention relates to a kit and method for detecting pathogenic genes of hereditary macular degeneration (AMD). The kit includes a hybridization mixture containing a probe set for detecting AMD pathogenic genes. The probe set includes capture probes capable of simultaneously and specifically capturing pathogenic genes ABCA4, BEST1, PRPH2, ELOVL4, PROM1, IMPG1, IMPG2, EFEMP1, RP1L1, and TIMP3, as well as the pathogenic regions of MCDR3 and MCDR1. The capture probes capturing the pathogenic regions of MCDR3 and MCDR1 include probes with sequences shown in SEQ ID NO. 1-174 and SEQ ID NO. 175-235, respectively. This invention proposes a targeted amplification strategy for the non-coding pathogenic region of NCMD, successfully detecting two novel point mutations and one genomic structural variation, achieving the detection of point mutations and structural variations in non-coding regions.

The present invention relates to a vascular endothelial growth factor (VEGF) inhibitor for use in the treatment of wet macular degeneration, wherein the VEGF inhibitor is adapted to be administered intravitreally to a patient, wherein the patient has previously been treated intravitreally with the VEGF inhibitor for approximately one year, and has one or more genetic variants that are single nucleotide polymorphisms selected from rs2106124, rs1879796, rs12148845, rs12148100, rs17482885, and rs17629019.

The present invention pertains to new compounds, possessing unique structural features, effective in blue light absorption. The compounds, named as Cordylutenes, show significant biological activity in the prevention and / or treatment of blue light-induced ocular damage. Also provided includes a method and a pharmaceutical, cosmetical or edible composition for preventing or treating an ocular disease, such as dry eye disease, cataracts, glaucoma, or macular degeneration, comprising the Cordylutenes or a pharmaceutically, cosmetically, or edibly acceptable salt thereof.

Disclosed herein are compositions and methods for the modulation of 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR) expression, wherein the compositions include an siRNA duplex or a conjugated siRNA duplex. Also disclosed herein are methods, and compositions for use in methods, of treating age-related macular degeneration (AMD) or hyperlipidemia. The compositions disclosed herein comprise an siRNA duplex that comprises a sense sequence and an antisense sequence, wherein the sense sequence and the antisense sequence are at least partially complementary to each other.

The present disclosure relates to chimeric molecules which are fusion proteins comprising two components: an Ang-2 binding peptide linked to either a VEGF antibody or a VEGF receptor-Fc fusion protein. The Ang2 peptide, VEGF antibody, and VEGF receptor-Fc fusion proteins are each defined below with reference to percent identity to a reference sequence. The chimeric molecule is a fusion protein, dual antagonist of Ang2 and VEGF for treatment of cancers, proliferative retinopathies, neovascular glaucoma, macular edema, AMD, and rheumatoid arthritis.

The present invention relates to: a novel peptide which has a prophylactic, ameliorative or therapeutic effect on amyloidosis and / or macular degeneration, is safe to a living body, and has few side effects including abnormal reactions; a pharmaceutical composition comprising the same; and a health functional food.

Methods for treatment of damaged corneal endothelium are provided, applicable for treatment or protection of corneal endothelium in various circumstances such as oxidative stress, age-related decline in endothelial cell density, inherited or non-inherited degenerative disease such as Fuchs endothelial corneal dystrophy, surgical trauma, increased intraocular pressure (IOP) or contact lens overuse. Further provided are methods for treatment of retinal degeneration such as in diabetic retinopathy, age-related macular degeneration and glaucoma. The methods comprise the transplantation of viable isolated, exogenous, mitochondria systemically and / or directly to the cornea or the retina.

The invention provides a method for inducing a dry macular degeneration model by injecting sodium iodate into a vitreous cavity of a C57BL / 6J mouse, and belongs to the field of disease model construction. The dry macular degeneration mouse vitreous cavity model is established by regulating and controlling the administration dosage of sodium iodate injected into the vitreous cavity, and stable induction of dry macular degeneration is achieved. The method is simple to operate and high in repeatability, and the established model can successfully simulate pathological characteristics of human dry macular degeneration. The model can be used for screening and evaluating potential therapeutic drugs aiming at the dry macular degeneration, provides an experimental platform for researching pathogenesis of the dry macular degeneration, and provides a theoretical basis for developing a new therapeutic method.

The present disclosure relates to RNAi agents able to inhibit Complement Factor B (CFB) gene expression. Also disclosed are pharmaceutical compositions that include CFB RNAi agents and methods of use thereof. The CFB RNAi agents disclosed herein may be conjugated to targeting ligands, including ligands that comprise N-acetyl-galactosamine, to facilitate the in vivo delivery to hepatocyte cells. The RNAi agents can be used in methods of treatment of diseases, disorders, or symptoms mediated in part by CFB gene expression, including IgA nephropathy (IgAN), C3 glomerulopathy (C3G), immune complex-mediated membranoproliferative glomerulonephritis (IC-MPGN), lupus nephritis (LN), Anti-Glomerular Basement Membrane disease (anti-GBM), ischemia reperfusion injury and T-cell mediated rejection (TCMR) in kidney transplantation, anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis, age-related macular degeneration (AMD), including early and / or intermediate AMD, geographic atrophy (GA), glaucoma, Doyne honeycomb retinal dystrophy, paroxysmal nocturnal hemoglobinuria (PNH), atypical hemolytic uremic syndrome (aHUS), pre-eclampsia, rheumatoid arthritis (RA), and / or other complement-mediated diseases.

The present invention pertains to new compounds, possessing unique structural features, effective in blue light absorption. The compounds, named as Cordylutenes, show significant biological activity in the prevention and / or treatment of blue light-induced ocular damage. Also provided includes a method and a pharmaceutical, cosmetical or edible composition for preventing or treating an ocular disease, such as dry eye disease, cataracts, glaucoma, or macular degeneration, comprising the Cordylutenes or a pharmaceutically, cosmetically, or edibly acceptable salt thereof.

The invention relates to the technical field of biological medicine, in particular to sophocarpine and application of sophocarpine in inhibiting formation of subretinal fibrosis, and the sophocarpine comprises the following steps: selecting 7-week-old male C57BL / 6J mice, adaptively feeding the mice for 1 week, and performing 12-hour illumination / 12-hour dark circulation at the environment temperature of 22-25 DEG C; the method comprises the following steps of: performing intraperitoneal injection of thiobarbital sodium on a C57 mouse fed for 1 week for anesthesia, realizing muscle relaxation by using hypnotic, and anesthetizing ocular surface by using 0.4% tetracaine and 0.5% tropicamide mydriasis; a mouse is randomly divided into a control eye and an experiment eye, and 1 microliter of PBS containing 1.5% of DMSO is injected into the control eye to serve as a carrier for control. The invention finds that injection of sophocarpine in vitreous cavity can inhibit RPE cell epithelial-mesenchymal transition, can be used for preventing or treating age-related macular degeneration subretinal fibrosis, may become a new medicine for treating subretinal fibrosis, has important value for inhibiting EMT of RPE cells, can also inhibit EMT of other cells, and can be used for preventing or treating age-related macular degeneration subretinal fibrosis and treating age-related macular degeneration subretinal fibrosis. Therefore, the method has potential application value on diseases caused by cell EMT.

The present application provides a kind of composition and preparation method and application for preventing cataract, macular lesion and diabetic retinopathy, belong to biological medicine technical field.The composition of the present application includes: nano active ingredient, plant extract, glycyrrhizic acid dipotassium, nicotinamide, taurine, ikdoin, caffeine and lutein;Plant extract is composed of wild chrysanthemum flower extract and gentian extract;Nano active ingredient is composed of nano-encapsulated astaxanthin and nanometer retinol.The composition of the present application effectively inhibits key pathological links such as lens protein oxidative denaturation, retinal pigment epithelial cell function decline and pathological angiogenesis by multi-dimensional synergistic mechanism of antioxidant-anti-inflammatory-vascular protection-metabolic regulation, thereby realizing the prevention and adjuvant therapy effect on three major blinding eye diseases of cataract, age-related macular degeneration and diabetic retinopathy.

Described herein are retinoid compositions comprising (a) a retinoid preferably a C20-deuterated vitamin A that inhibits dimerisation to N-retinylidene-N-retinylethanolamine (A2E), (b) a lipid excipient preferably an omega-3 fatty acid comprising eicosapentaenoic acid (EPA) or docosahexaenoic acid (DHA), and (c) a surfactant, wherein the compositions increase the bioavailability of the retinoid in a subject, and methods of using such retinoid compositions for treating eye conditions including macular degeneration.

Described herein are retinoid compositions comprising (a) a retinoid preferably a C20-deuterated vitamin A that inhibits dimerisation to N-retinylidene-N-retinylethanolamine (A2E), (b) a lipid excipient preferably an omega-3 fatty acid comprising eicosapentaenoic acid (EPA) or docosahexaenoic acid (DHA), and (c) a surfactant, wherein the compositions increase the bioavailability of the retinoid in a subject, and methods of using such retinoid compositions for treating eye conditions including macular degeneration.

This application provides antibody-drug synergistic compounds, compositions, and methods for treating ocular diseases such as dry AMD, GA secondary to AMD, and exudative AMD. The antibody-drug synergistic compounds may include antibodies such as anti-angiogenic antibodies or anti-VEGF antibodies conjugated to small molecule complement inhibitors by a linker, or anti-complement antibodies conjugated to small molecule inhibitors of VEGF, VEGFR, PDGF, PDGFR, FGF, or FGFR by a linker. The linker conjugating the antibody and drug is hydrolyzable over time within the target eye, thereby allowing both the antibody and drug to exert their functions within the target eye. The compounds and compositions can confer superior efficacy compared to either the antibody or the drug alone due to the synergistic effect of the ADS compounds. Methods for treating age-related macular degeneration using ADS compounds and compositions are also provided.

NOD-like receptor protein 3 (NLRP3) inhibitors (NSIs) as anti-inflammatory agents are provided, as are methods of using the NSIs to inhibit inflammation and prevent or treat NRLP3 inflammasome dysregulation associated diseases and conditions, such as multiple sclerosis (MS), Alzheimer's disease (AD), traumatic brain injury (TBI), Parkinson's disease (PD), acute myocardial infarction (AMI), heart failure, gout, rheumatoid arthritis, COVID-19, diabetes, macular degeneration, and autoimmune / autoinflammatory diseases.

The present application provides antibody-drug synergistic compounds, compositions, and methods for treating ocular diseases, such as dry AMD, GA secondary to AMD, and exudative AMD. The antibody-drug synergistic compound may comprise an antibody such as an anti-angiogenic antibody or an anti-VEGF antibody linked to a small molecule complement inhibitor through a linking group; or an anti-complement antibody linked to a small molecule inhibitor of VEGF, VEGFR, PDGF, PDGFR, FGF or FGFR via a linking group. A linking group linking the antibody and the drug may hydrolyze in the eye of the subject over time such that both the antibody and the drug function in the eye of the subject. Due to the synergy of the ADS compounds, the compounds and compositions can confer better efficacy than the antibody or drug alone. Methods of treating age-related macular degeneration using the ADS compounds and compositions are also provided.

NSIs with anti-inflammatory activity are provided, as are methods of using the NSIs to inhibit inflammation and prevent or treat diseases and conditions associated with inflammation, such as multiple sclerosis (MS), Alzheimer's disease (AD), traumatic brain injury (TBI), Parkinson's disease (PD), acute myocardial infarction (AMI), heart failure, gout, rheumatoid arthritis, COVID- 19, diabetes, macular degeneration, or an autoimmune or autoinflammatory disease.

This disclosure features chemical entities (e.g., a compound or a pharmaceutically acceptable salt thereof) that degrade and / or otherwise modulate (e.g., inhibit) NIMA Related Kinase 7 (NEK7). Said chemical entities are useful, e.g., for treating a subject (e.g., a human subject) having one or more disorders or diseases associated with NLRP3 inflammasome activation. Said disorders or diseases include but are not limited to, autoinflammatory and autoimmune disorders (e.g., gout, inflammatory bowel disease, rheumatoid arthritis, multiple sclerosis), neurodegenerative diseases (e.g., Alzheimer's disease, Parkinson's disease), cardiovascular and metabolic disorders (eg. pericarditis, atherosclerosis, Type 2 diabetes, obesity, and metabolic syndrome), fibrotic disorders (e.g. interstitial lung disease, chronic kidney disease), hematology (eg. anemia of inflammation) and eye disorders (eg. macular degeneration). In embodiments, and while not wishing to be bound by theory, it is believed that the chemical entities described herein directly target (e.g., directly bind to) NEK7, thereby altering (e.g., attenuating) the inflammatory response modulated by the NLRP3 inflammasome. This disclosure also features compositions containing the same as well as methods of using and making the same.

In one aspect, the invention provides methods and compositions for inhibiting MASP-3-dependent complement activation in a subject suffering from or at risk for developing, a disease or disorder selected from the group consisting of paroxysmal nocturnal hemoglobinuria, age-related macular degeneration, arthritis, disseminated intravascular coagulation, thrombotic microangiopathy, asthma, dense deposit disease, pauci-immune necrotizing crescentic glomerulonephritis, traumatic brain injury, aspiration pneumonia, endophthalmitis, neuromyelitis optica and Behcet's disease by administering to the subject a composition comprising an amount of a MASP-3 inhibitory agent in an amount effective to inhibit MASP-3-dependent complement activation. In some embodiments, the subject is administered a MASP-2 inhibitory agent and a MASP-1 inhibitory agent, a MASP-2 inhibitory agent and a MASP-3 inhibitory agent administered, a MASP-3 inhibitory agent and a MASP-1 inhibitory agent, or a MASP-1 inhibitory agent, a MASP-2 inhibitory agent and a MASP-3 inhibitory agent.

The present invention is directed to compositions for oral administration comprising two or more active ingredients selected from the group consisting of quercetin, metabolites, derivatives and salts and hydrates thereof, a kaempferol rutinoside and salts and hydrates thereof, indole-3-carbinol and derivatives and metabolites and salts and hydrates thereof and gallic acid and salts and hydrates thereof. The present invention is further directed to methods for treating dry eye disease, treating age-related macular degeneration, increasing Bruch's membrane stiffness, modulating expression of a gene selected from the group consisting of YAP, TAZ, integrin α5, integrin β5, interferon β1, interleukin-6, C-X-C motif chemokine ligand 1, C-X-C motif chemokine ligand 10, and combinations thereof, increasing adhesion of retinal pigment epithelium cells to a Bruch's membrane, and methods of modulating a secretory profile of senescent cells exhibiting the senescence-associated secretory phenotype comprising administering an effective amount of one or more active ingredients selected from the group consisting of kaempferol derivatives and salts thereof and hydrates thereof, quercetin metabolites, derivatives and salts and hydrates thereof, indole-3-carbinol and derivatives and metabolites and salts and hydrates thereof and gallic acid and salts and hydrates thereof to a subject in need thereof.

The present invention relates to in vitro sialylated human factor H protein or biologically active sialylated fragments or biologically active sialylated variants thereof, wherein the protein does not comprise trisia lylated N-glycans of the structure A3G3S3 (NaNaNa), for use in a method of treatment, wherein the method of treatment involves administering subcutaneously said in vitro sialylated human factor H protein or biologically active sialylated fragments or biologically active sialylated variants thereof subcutaneously. The methods of treatment comprise treating complement-mediated diseases such as C3 glomerulopathy (C3G), atypical hemolytic uremic syndrome (aHUS), age-related macular degeneration (AMD) or paroxysmal nocturnal hemoglobinuria.

The present application relates to a gene for regulating cholesterol metabolism and a micropeptide MP19 encoded thereby, and a use thereof, and also relates to a use of the micropeptide in the preparation of a drug or pharmaceutical composition for detecting, preventing, alleviating or treating diseases associated with abnormal cholesterol metabolism, said diseases comprising atherosclerosis, age-related macular degeneration, hyperlipidemia, non-alcoholic hepatitis, hepatocellular carcinoma, coronary heart disease, ischemic stroke, and obesity. By means of endogenous overexpression or exogenous synthesis of the micropeptide, diseases associated with abnormal cholesterol metabolism can be effectively prevented, alleviated, or treated.

In one aspect, the invention provides methods and compositions for inhibiting MASP-3-dependent complement activation in a subject suffering from or at risk for developing, a disease or disorder selected from the group consisting of paroxysmal nocturnal hemoglobinuria, age-related macular degeneration, arthritis, disseminated intravascular coagulation, thrombotic microangiopathy, asthma, dense deposit disease, pauci-immune necrotizing crescentic glomerulonephritis, traumatic brain injury, aspiration pneumonia, endophthalmitis, neuromyelitis optica and Behcet's disease by administering to the subject a composition comprising an amount of a MASP-3 inhibitory agent in an amount effective to inhibit MASP-3-dependent complement activation. In some embodiments, the subject is administered a MASP-2 inhibitory agent and a MASP-1 inhibitory agent, a MASP-2 inhibitory agent and a MASP-3 inhibitory agent administered, a MASP-3 inhibitory agent and a MASP-1 inhibitory agent, or a MASP-1 inhibitory agent, a MASP-2 inhibitory agent and a MASP-3 inhibitory agent.