Pyrolotriazine and imidazotriazine derivatives as regulators of the NLRP3 inflammasome pathway

JP2025524640A5Pending Publication Date: 2026-06-15AC IMMUNE SA
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Patent Information

Authority / Receiving Office
JP · JP
Patent Type
Applications
Current Assignee / Owner
AC IMMUNE SA
Filing Date
2023-07-14
Publication Date
2026-06-15

AI Technical Summary

⚠Technical Problem

Current treatments for NLRP3-related diseases, such as Alzheimer's disease and gout, are limited by the biological availability of existing compounds, particularly in the central nervous system, and existing small molecules have overlapping modes of action and limited efficacy.

⚗Method used

Development of novel pyrrolotriazine and imidazotriazine derivatives that modulate the NLRP3 inflammasome pathway by inhibiting its activation and reducing IL-1 beta and/or IL-18 levels, providing specific and effective treatment options for diseases responsive to NLRP3 inflammasome modulation.

🎯Benefits of technology

The compounds effectively inhibit the NLRP3 inflammasome pathway, reducing IL-1 beta and IL-18 levels, offering potential therapeutic benefits for diseases like Alzheimer's disease, Parkinson's disease, non-alcoholic fatty liver disease, and gout, with improved efficacy and specificity compared to existing treatments.

✦ Generated by Eureka AI based on patent content.

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Abstract

This application relates to pyrrolotriazine and imidazotriazine derivatives of general formula (I) for the treatment, alleviation, or prevention of a group of diseases, disorders, and abnormalities that respond to the modulation or inhibition of the activation of components of the NLRP3 inflammasome pathway. In particular, the components of the inflammasome pathway are the NOD-like receptor (NLR) family, pyrin domain-containing protein 3 (NLRP3) inflammasome. More specifically, the compounds have the ability to modulate the NLRP3 inflammasome pathway and are suitable for the treatment, alleviation, or prevention of a group of diseases, disorders, and abnormalities that respond to the modulation, particularly the reduction, of IL-I beta and / or IL-I8 levels, such as Alzheimer's disease, Parkinson's disease, non-alcoholic fatty liver disease, and gout. JPEG2025524640000115.jpg56170
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