35 results about "Optic neuropathy" patented technology

The invention provides an application of a human retina organ in preparation of a medicament for treating traumatic optic neuropathy. According to the invention, the induced and differentiated human retina-like organ is applied to the optic nerve injury area, and the eye and brain nerve connection can be functionally reconstructed, so that the damaged visual function is recovered.

The present invention relates to IL-8 inhibitor compounds, preferably dual CXCR1 / CXCR2 receptor inhibitors, useful in the treatment and / or prevention of chemotherapy-induced neuropathy, preferably in the treatment and / or prevention of chemotherapy-induced peripheral neuropathy (CIPN) or chemotherapy-induced optic neuropathy.

The present invention relates generally to compositions and methods useful for treating brain injuries such as stroke, optic neuropathy, traumatic brain injury, and cerebral palsy. The methods comprise administering to a subject HMC obtained by in vitro differentiation of pluripotent stem cells and / or extracellular vesicles (EV) derived from these HMCs (HMC-EV).

Provided is a method for preventing or treating optic neuropathy, comprising administering a pharmaceutical composition including neural progenitor cells as an active ingredient, where the neural progenitor cells not only exhibit remarkably superior neuroprotective and pro-regenerative effects compared to mesenchymal stem cells such as placenta-derived stem cells (e.g., PSCs), but also can be administered by non-invasive and safe subtenon injection, and therefore the method may be advantageously used as a cell therapy for treating optic neuropathy.

The present invention generally relates to compositions and methods useful for treating a brain injury such as stroke, optic neuropathy, traumatic brain injury, and cerebral palsy. The methods include administering HMCs obtained by in vitro differentiation of pluripotent stem cells and / or extracellular vesicles (EVs) derived from such HMCs (HMC-EVs) into a subject.

The invention provides an application of a human retina organ in preparation of a medicament for treating traumatic optic neuropathy. According to the invention, the induced and differentiated human retina-like organ is applied to the optic nerve injury area, and the eye and brain nerve connection can be functionally reconstructed, so that the damaged visual function is recovered.

The present disclosure relates to nanoemulsions of 5-amino-[4-(4-chlorobenzoyl)-3,5-dichlorobenzyl]-1,2,3-triazole-4-carboxamide (carboxy-amido-triazole or CAI), methods of preparing thereof, and their use in the treatment of inflammatory optic neuropathies.

Methods and compositions are provided for the treatment of glaucoma and other optic neuropathies by administering an effective dose of an HDAC4 coding sequence or protein.

Provided are: a kit for inducing differentiation, which is for inducing the differentiation of a Muller glial cell into a retinal ganglion cell in vivo in a mammal; and a pharmaceutical composition for treating glaucoma or optic neuropathy. The kit and the pharmaceutical composition each include: a nucleic acid encoding NEUROG2; a combination of a nucleic acid encoding ASCL1, a nucleic acid encoding BRN3B, and a nucleic acid encoding ATOH7; or a combination of a nucleic acid encoding ASCL1, a nucleic acid encoding BRN3B, and a nucleic acid encoding ISL1.

The invention relates to application of GMFB in preparation of a medicine for treating traumatic optic neuropathy. Research finds that on the third day of a rat ONC model, compared with normal control, GMFB expression is remarkably up-regulated; cholera toxin B subunit (Cholera Toxin Subunit B, CTB) tracing shows that the axons of a rat ONC model with the GMFB knocked out are remarkably lengthened (compared with those of a wild rat ONC model), and LFB (luxoLuxol Fast Blue) myelination staining shows that remyelination of the denatured axons can be effectively improved, axon regeneration is promoted, and the visual function is improved by knockout of the GMFB.

The present invention relates to a base correction system that corrects mitochondrial DNA mutations G3460A, G11778A, or T14484C, which are present in patients with Leber's hereditary optic neuropathy (LHON), to a normal genotype. Specifically, the present invention provides a base editor capable of correcting a mutation site in a mitochondrial gene of an LHON patient to a normal genotype. The present invention also provides a method for correcting a mitochondrial gene mutation using a fusion protein or a polynucleotide encoding such a fusion protein that recognizes a specific site in the mitochondrial gene of an LHON patient and specifically corrects the adenine base at position 3460, the adenine base at position 11778, or the cytosine base at position 14484. The base editor or polynucleotide according to the present invention can be used in cells or in an extracellular test tube environment to correct DNA mutations specifically expressed in LHON, and more preferably, can be used as a gene therapy agent to prevent or treat the disease. Thus, the present invention also provides a use of the substance for preventing or treating Leber's hereditary optic neuropathy.

The invention relates to the technical field of biology, in particular to a polypeptide compound, a medicine for preventing and treating eye diseases and application. According to the present invention, a mitochondrial targeting module (triphenylphosphine) and a superoxide-initiated persulfide donor (SOPD) are integrated into a specific polypeptide to obtain the ROS-responsive mitochondrial targeting polypeptide compound; experiments show that the polypeptide compound has remarkable oxidative stress resistance, can effectively relieve RGC damage caused by intraocular hypertension, has a good prevention and treatment effect on glaucoma optic neuropathy, has the prevention and treatment effect obviously improved compared with that of other polypeptide compounds with similar structures, and has good biocompatibility and biological safety.

The present disclosure relates to nanoemulsions of 5-amino-[4-(4-chlorobenzoyl)-3,5-dichlorobenzyl]-1,2,3-triazole-4-carboxamide (carboxy-amido-triazole or CAI), methods of preparing thereof, and their use in the treatment of inflammatory optic neuropathies.

Methods of treating an optic neuropathy or an optic nerve injury in a subject are provided. Aspects of the methods include administering an effective amount of an agonist of a Piezo mechanosensitive ion channel, a recombinant nucleic acid or an expression vector expressing a Piezo mechanosensitive ion channel, or a Piezo mechanosensitive ion channel to the subject. Also provided are pharmaceutical formulations comprising an agonist of a Piezo mechanosensitive ion channel, a recombinant nucleic acid or an expression vector expressing a Piezo mechanosensitive ion channel, or a Piezo mechanosensitive ion channel. In some embodiments, the agonist of the Piezo mechanosensitive ion channel, the recombinant nucleic acid or expression vector expressing the Piezo mechanosensitive ion channel, or the Piezo mechanosensitive ion channel is administered to treat glaucoma, ischemic optic neuropathy, optic neuritis, or traumatic optic neuropathy.

The present disclosure provides compositions and methods for treating a mammalian subject for an ON neuropathies and / or reducing or ameliorating degeneration of axons and / or soma of RGCs. Aspects of the composition include a neuroprotective agent and a pharmaceutically acceptable excipient, where the neuroprotective agent inhibits HRH1 activity. A variety of ON neuropathies may be treated by practicing the methods, including retinal ganglion cell degeneration, glaucoma, optic neuritis, ON traumatic injury and other ON-related diseases.

The present disclosure provides methods and uses of aminonaphthoquinone compounds in treatment and / or prevention of an optic neuropathy.

The present invention relates to IL-8 inhibitor compounds, preferably dual CXCR1 / CXCR2 receptor inhibitors, useful in the treatment and / or prevention of chemotherapy-induced neuropathy, preferably in the treatment and / or prevention of chemotherapy-induced peripheral neuropathy (CIPN) or chemotherapy-induced optic neuropathy.

The present invention discloses the application of GSK-872 in the preparation of a drug for treating traumatic optic neuropathy, and relates to the field of biomedical technology. The present invention provides the application of GSK-872 in the preparation of a drug for treating traumatic optic neuropathy. The present invention has found that GSK-872 has the effects of inhibiting autophagy, anti-inflammatory and neuroprotection. GSK-872 is used to treat traumatic optic neuropathy. Early intravitreal injection of GSK-872 can significantly inhibit the autophagic death caused by excessive activation of autophagy in retinal microglia, reduce local retinal neuroinflammation, improve the inflammatory microenvironment, thereby delaying the process of retinal ganglion cell death, effectively preventing the loss of neurons, and having a significant effect on the protection of visual function, thereby achieving the purpose of treating traumatic optic nerve injury. The present invention provides a new strategy for treating traumatic optic neuropathy.

Disclosed is a method of producing ganglion progenitor cells from pluripotent stem cells and their use for treating ocular disorders. In particular, disclosed is a method of producing ganglion progenitor cells from pluripotent stem cells by transducing pluripotent stem cells with the neuronal differentiation transcription factor Neuronal Differentiation 1 (NEUROD1) in a chemically-defined and xenogenic-free culture medium and their use for treating ocular disease and / or an optic neuropathy.

The invention discloses an optic nerve image enhancement and lesion recognition method based on multi-modal fusion, and the method comprises the following steps: S1, collecting the image data of an optic nerve lesion patient, and carrying out the denoising processing, spatial position alignment and data normalization; s2, constructing an improved conditional diffusion probability model, and establishing a reverse diffusion process for image detail enhancement; s3, gradually enhancing image data details by using a reverse diffusion process; s4, calculating high-dimensional conditional probability feature joint distribution of different modal image space domains and frequency domains, and establishing a cross-modal feature set; s5, performing image adaptive fusion by adopting a conditional guidance mechanism; s6, optimizing model parameters to obtain a fused image; and S7, identifying the feature vector of the lesion area by using a Transform classification model to realize lesion identification and classification diagnosis. According to the invention, the image fusion quality and the lesion diagnosis precision are obviously improved.

The disclosure provides compositions and methods useful for treating conditions related to Dual Leucine Zipper (DLK), e.g., neurodegenerative disorders including optic neuropathy. The disclosure provides gene constructs and vectors that regulate the activity of Dual Leucine Zipper Kinase (DLK) or Leucine Zipper Kinase (LZK). The disclosure also provides dominant negative DLK (DN-DLK) proteins that inhibit the kinase and / or signaling activity of DLK. The disclosure also provides vectors, pharmaceutical compositions, and methods of inhibiting DLK.

The present application relates to the field of medicine, in particular to the use of a substance specifically binding to NSE protein or its encoding gene in the preparation of a diagnostic product or a prognostic product for ARN. By detecting NSE protein or its encoding gene, the optic neuropathy caused by acute retinal necrosis can be understood, and doctors can identify ARN conditions earlier, so as to promptly implement appropriate medical intervention. Therefore, the present application can not only significantly reduce the risk of retinal detachment and vision loss, but also assist clinicians in accurately assessing the severity of the disease and predicting the possibility of vision recovery, which can promote the individualization and precision of treatment. In addition, by avoiding unnecessary drug use and wasting of medical resources, it also brings economic benefits, which benefits patients and society.

Methods of treating an optic neuropathy or an optic nerve injury in a subject are provided. Aspects of the methods include administering an effective amount of an agonist of a Piezo mechanosensitive ion channel, a recombinant nucleic acid or an expression vector expressing a Piezo mechanosensitive ion channel, or a Piezo mechanosensitive ion channel to the subject. Also provided are pharmaceutical formulations comprising an agonist of a Piezo mechanosensitive ion channel, a recombinant nucleic acid or an expression vector expressing a Piezo mechanosensitive ion channel, or a Piezo mechanosensitive ion channel. In some embodiments, the agonist of the Piezo mechanosensitive ion channel, the recombinant nucleic acid or expression vector expressing the Piezo mechanosensitive ion channel, or the Piezo mechanosensitive ion channel is administered to treat glaucoma, ischemic optic neuropathy, optic neuritis, or traumatic optic neuropathy.

The invention discloses application of GSK-872 in preparation of a medicine for treating traumatic optic neuropathy, and relates to the technical field of biological medicines. The invention provides an application of GSK-872 in preparation of a medicine for treating traumatic optic neuropathy. The research finds that the GSK-872 has the effects of inhibiting autophagy, resisting inflammation and protecting nerves, the GSK-872 is used for treating traumatic optic neuropathy, and early intravitreal injection of the GSK-872 can obviously inhibit autophagy death caused by over-activation of autophagy of retina microglia cells, relieve local neuroinflammation of retina, improve the inflammatory microenvironment and prevent and treat traumatic optic neuropathy. Therefore, the death process of retinal ganglion cells is delayed, the loss of neurons is effectively prevented, the obvious effect of protecting the visual function is achieved, and the purpose of treating traumatic optic nerve injury is achieved. The invention provides a new strategy for treating traumatic optic neuropathy.

The present disclosure provides novel approaches and methods for treating various eye diseases or conditions including optic neuropathies. In particular, the disclosed methods and treatments are directed to those eye diseases or conditions involving mitochondrial dysfunction. More particularly, the methods and treatments provided can restore mitochondrial homeostasis.

The present invention provides aminonaphthoquinone compounds for the treatment and / or prevention of optic neuropathy. [Solution] This disclosure provides methods and uses of aminonaphthaquinone compounds in the treatment and / or prevention of optic neuropathy. The present invention also provides a pharmaceutically acceptable composition for use in a method for preventing and / or treating optic neuropathy associated with apoptosis of RGCs, wherein the pharmaceutically acceptable composition comprises a compound of formula (I) described herein. The use of a pharmaceutically acceptable composition in the manufacture of a pharmaceutically acceptable composition for preventing and / or treating optic neuropathy associated with apoptosis of RGCs is also provided, wherein the pharmaceutically acceptable composition comprises a compound of formula (I) described herein.

A method of treating optic neuropathy that provides surprising efficacy while minimizing toxicity using a specific administration regimen with an effective amount of a compound of Formula (I):

The application discloses a gene medicine for treating deafness-dystonia-optic neuropathy syndrome caused by TIMM8A gene defect and application. The medicine core is a modularly designed adeno-associated virus vector system which carries an expression cassette containing a tissue-specific promoter and a human TIMM8A treatment gene. The application realizes precise treatment through local minimally invasive injection according to different symptoms: AAV-Anc80L65-MYO15-TIMM8A is injected into the cochlea to treat sensorineural hearing loss; AAV2 / 4-Brn3b-TIMM8A is injected into the vitreous body of the eyeball to treat optic neuropathy; AAV9-hSyn-TIMM8A is injected into the central lateral ventricle to treat dystonia. Preclinical studies have confirmed that the strategy can efficiently express TIMM8A protein in the corresponding target cells, significantly repair hearing, visual and motor function defects, and correct mitochondrial dysfunction from the pathological mechanism.

The invention relates to the field of medicine, in particular to application of a substance specifically combined with NSE protein or a coding gene thereof to preparation of an ARN diagnosis product or a prognosis product. By detecting the NSE protein or the encoding gene thereof, optic neuropathy caused by acute retinal necrosis can be informed, and doctors can recognize ARN diseases earlier, so that proper medical intervention can be implemented quickly. Therefore, the risk of retinal abscission and visual loss can be remarkably reduced, clinical doctors can be assisted in accurately evaluating the severity of the illness state and predicting the possibility of visual recovery, and individuation and precision of treatment can be promoted. In addition, by avoiding unnecessary medicine use and medical resource waste, economic benefits are brought, and both the patient and the society are benefited.

The application belongs to the technical field of biological medicine, and discloses application of plerixafor in preparation of a medicine for treating traumatic optic neuropathy. Researches of the application show that the plerixafor has a repairing effect of promoting survival of retinal ganglion cells (RGC) and axon regeneration after optic nerve injury, and can achieve and improve the effect of treating traumatic optic nerve injury.