Use of a new compound in the preparation of a medicament for preventing and treating ischemic stroke

By promoting microglia phagocytosis through compound I, the problems of narrow treatment time window and aggravated inflammatory response in ischemic stroke were solved, and the effects of improved neurological function, increased cerebral blood flow and neuronal protection were achieved.

CN119970733BActive Publication Date: 2026-06-19NANJING MEDICAL UNIV
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Patent Information

Authority / Receiving Office
CN · China
Patent Type
Patents(China)
Current Assignee / Owner
NANJING MEDICAL UNIV
Filing Date
2025-02-28
Publication Date
2026-06-19

AI Technical Summary

Technical Problem

Existing treatments for ischemic stroke have problems such as a narrow treatment window, limited indications, and postoperative reperfusion injury. Furthermore, impaired microglial phagocytic function after ischemic stroke leads to an inflammatory response that exacerbates brain damage.

Method used

The novel compound shown in Formula I crosses the blood-brain barrier, promotes phagocytosis by microglia, significantly improves neurological function, increases cerebral blood flow, reduces cerebral infarction volume, alleviates neuronal damage, and promotes the clearance of apoptotic neurons by microglia.

Benefits of technology

It significantly improves neurological function after ischemic stroke, increases cerebral blood flow, reduces infarct volume, alleviates neuronal damage, and promotes microglia to phagocytose and clear apoptotic neurons, providing a novel treatment approach.

✦ Generated by Eureka AI based on patent content.

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Abstract

This invention discloses the application of a novel structural compound in the preparation of drugs for the prevention and treatment of ischemic stroke. The novel structural compound, as shown in formula (I), can cross the blood-brain barrier and has been found to significantly improve neurological function and behavioral scores, increase cerebral blood flow, reduce infarct volume, and reduce neuronal damage after cerebral ischemia-reperfusion. This indicates that the novel structural compound has a significant protective effect against cerebral ischemia-related injury. Furthermore, the novel structural compound can induce the phagocytosis and clearance of apoptotic neurons by microglia after cerebral ischemia-reperfusion, suggesting that promoting the phagocytosis and clearance of apoptotic neurons by microglia may be an important mechanism by which the novel structural compound exerts its protective effect against cerebral ischemia-related injury.
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