An antisense oligonucleotide jag-i9 aso and applications thereof
By designing an antisense oligonucleotide Jag-i9 ASO that specifically targets the binding site of heterogeneous ribonucleoprotein K and the Jag2 gene, the problem of broad target sites in the treatment of myocardial ischemia-reperfusion injury by existing drugs has been solved, achieving efficient and precise treatment results and reducing side effects.
CN121538217BActive Publication Date: 2026-03-31广东医科大学附属第二医院
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Patent Information
- Application Number
- CN202610071442.8
- Authority / Receiving Office
- CN · China
- Patent Type
- Patents(China)
- Current Assignee / Owner
- Filing Date
- 2026-01-20
- Publication Date
- 2026-03-31
- Estimated Expiration
- 2046-01-20
AI Technical Summary
Technical Problem
Existing drugs have broad targets when treating myocardial ischemia-reperfusion injury, which makes it difficult to guarantee efficacy and easily causes systemic side effects.
Method used
An antisense oligonucleotide Jag-i9 ASO is provided, which specifically targets the binding site of heterologous ribonucleoprotein K and the Jag2 gene. Through the modification of the main chain thiophosphate and 2'-O-methoxyethyl structure, it precisely regulates the alternative splicing of the Jag2 gene and inhibits the generation of pro-inflammatory Jag2 isoforms.
Benefits of technology
It achieves precise targeted intervention for myocardial ischemia-reperfusion injury, reduces cardiomyocyte apoptosis and inflammatory response, improves treatment efficacy and reduces side effects.
✦ Generated by Eureka AI based on patent content.
Abstract
The application provides an antisense oligonucleotide Jag-i9 ASO and application thereof, relates to the technical field of biological medicine, and the antisense oligonucleotide Jag-i9 ASO has the sequence of 5'-ACTGGGCCCTGCACCTGA-3'. By providing the antisense oligonucleotide of a specific sequence, the binding site of target heterogeneous ribonucleoprotein K and the Jag2 gene is targeted, the expression of the pro-inflammatory Jag2 subtype is inhibited, the Jag2 gene splicing site can be accurately targeted, the heterogeneous ribonucleoprotein K binding function is specifically blocked, a targeted intervention means is provided for the treatment of myocardial ischemia-reperfusion injury, the generation of the pro-inflammatory subtype is inhibited by efficiently and accurately regulating the alternative splicing of a specific gene, myocardial cell apoptosis and inflammatory response are reduced, myocardial function is improved, and a new approach is provided for the prevention and treatment of myocardial ischemia-reperfusion injury, the treatment effect is improved, and the advantages of reducing side effects are achieved.
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