Use of rilaplat for the preparation of a medicament for the prevention and treatment of pulmonary fibrosis

CN117357523BActive Publication Date: 2026-06-19UNIV OF MACAU
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Patent Information

Authority / Receiving Office
CN · China
Patent Type
Patents(China)
Current Assignee / Owner
UNIV OF MACAU
Filing Date
2023-10-25
Publication Date
2026-06-19

AI Technical Summary

Technical Problem

Currently, there are no effective drugs for the prevention and treatment of pulmonary fibrosis, and existing drugs such as nintedanib and pirfenidone have high levels of toxic side effects.

Method used

By utilizing liranafate as a novel drug, this study aimed to inhibit the TGF-β1 signaling pathway, block the transformation of EMT and fibroblasts into myofibroblasts, and prepare inhibitors of α-SMA, N-cadherin, Collagen I, and Collagen III. It also aimed to promote E-cadherin expression and prepare epithelial-mesenchymal transition inhibitors.

Benefits of technology

It significantly inhibits the progression of pulmonary fibrosis, reduces collagen fiber deposition, improves lung tissue damage, and reduces inflammation, providing a safe and low-side-effect treatment option for pulmonary fibrosis.

✦ Generated by Eureka AI based on patent content.

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Abstract

This invention belongs to the field of pharmaceutical technology and discloses the use of liranafyl ester in the preparation of drugs for the prevention and treatment of pulmonary fibrosis. Specifically, it discloses the use of liranafyl ester or its pharmaceutically acceptable salts in the preparation of drugs for the prevention and / or treatment of pulmonary fibrosis. This invention discloses for the first time that liranafyl ester or its pharmaceutically acceptable salts can significantly inhibit TGF-β1-induced EMT, inhibit the decrease in E-cadherin expression and the increase in N-cadherin expression, significantly inhibit the transformation of fibroblasts into myofibroblasts, inhibit the expression of α-SMA, Collagen I, and Collagen III, and can significantly improve lung damage in pulmonary fibrosis model mice, inhibit collagen deposition in the lungs, and alleviate lung inflammation and damage to lung parenchymal structure.
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