7 results about "Ocular neovascularization" patented technology

This invention involves co-transfecting cells with an AAV vector plasmid carrying the target gene, a packaging plasmid providing Rep / Cap proteins, and a helper plasmid providing adenovirus assistance. The transfected cells are cultured under suitable conditions to produce viral particles containing recombinant AAV. Cells and culture supernatant are collected, cells are lysed to release the virus, and the viral particles are purified by centrifugation. A membrane-penetrating peptides or their derivatives are then modified onto the AAV capsid protein. Results show that the gene editing system combined with membrane-penetrating peptides or their derivatives enhances editing efficiency, effectively penetrates ocular surface tissues, and inhibits ocular neovascularization.

The present disclosure provides pharmaceutical compositions and methods thereof for the prevention or treatment of ocular neovascularization, such as AMD, in a subject, by administering to the subject a pharmaceutical composition comprising a rAAV vector having a nucleic acid sequence that encodes an anti-VEGF agent.

Provided herein are compositions and methods for the treatment of ocular neovascular diseases such as wet age-related macular degeneration.

The application discloses application of NSUN2 in treatment of wet age-related macular degeneration. The application research finds that inhibition or silencing of the NSUN2 gene can significantly inhibit ocular neovascularization, reduce ocular inflammatory response, and effectively inhibit the development of subretinal fibrosis, and the result shows that the NSUN2 can be used as a potential target for treating wet age-related macular degeneration. Therefore, the application provides a new strategy for treating wet age-related macular degeneration.

The present disclosure provides compositions and methods for the prevention or treatment of ocular neovascularization, such as AMD, in a human subject, by administering subretinally a pharmaceutical composition comprising a pharmaceutically effective amount of a vector comprising a nucleic acid encoding soluble Fms-related tyrosine kinase-1 (sFlt-1) protein to the human subject.

The invention discloses application of antisense nucleotide for inhibiting NEAT1 in a targeted parasite assembly domain to treatment, improvement or prevention of fundus neovascularization, and belongs to the technical field of biological medicine. The invention finds that NEAT1 and downstream pro-angiogenesis factors CYR61 and FGF2 are obviously up-regulated in wet age-related macular degeneration patients and CNV model mice. According to the invention, the NEAT1 in the retina and the choroid is efficiently inhibited by designing ASO of a specific targeting lncRNA NEAT1 functional key domain, namely, a para-plaque assembly domain. Furthermore, ASO of a targeted mouse Neat1 homologous domain is subjected to intraocular injection, and laser-induced CNV focus formation can be remarkably inhibited in vivo. The invention provides a candidate drug for treating fundus neovascularization, which is independent of the traditional VEGF pathway and novel in action mechanism, and provides a new solution for patients who are insensitive to anti-VEGF therapy or need long-acting treatment.

This invention provides the use of a reagent for increasing pyruvate kinase expression levels in the preparation of a drug for treating ocular neovascularization in subjects. The drug provides long-acting treatment with a high safety profile.