ArticleMarine life science & technology2025
MR2938 relieves DSS-induced colitis in mice through inhibiting NF-κB signaling and improving epithelial barrier.
Article in Marine life science & technology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Targeting Inflammation and Immune Regulation in Chronic Inflammation Associated Cancers.Cancer science · 2026Review
- EngineeredFrontiers in immunology · 2026Article
- Quinazolinone derivatives as potential anti‑tumor agents: Structural features and molecular mechanisms in inducing cell death (Review).International journal of molecular medicine · 2025Review
- Newly Isolated Aromatic Compounds from Ailanthus altissima and Their Anti-inflammatory Activity.ACS omega · 2025Article
- Quinazolinone Derivative MR2938 Protects DSS-Induced Barrier Dysfunction in Mice Through Regulating Gut Microbiota.Pharmaceuticals (Basel, Switzerland) · 2025Article
Corrections and comments
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Authors and funding
11 authors.
Funding
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Abstract
Damage to the epithelial barrier is among key processes contributing to initiation and chronic inflammation in inflammatory bowel diseases (IBD). Only management therapy exists for IBD (e.g., anti-inflammatory and immunomodulatory agents, JAK/STAT inhibitors), and while novel therapeutic approaches have shown great potential, issues remain including route of administration, development of resistance to therapy and toxicity. Thus, novel small molecule inhibitors which can alleviate colonic inflammation and restore intestinal barrier functions are needed. Our previous study identified a new quinazolinone derivative MR2938, inspired by marine natural product penipanoid C, displaying impressive anti-inflammatory effects. In vivo efficacy study indicated that MR2938 had a dose-dependent effect on improving colitis symptoms, gut-barrier disruption, and colonic inflammation in an acute dextran sulfate sodium (DSS)-induced murine colitis as a model of epithelial injury relevant to IBD. Evaluation of potential mechanism involved in MR2938 efficacy demonstrated that MR2938 inhibited NF-κB-mediated inflammatory responses, and attenuated intestinal epithelial tight junction damage by restoring the expression of Occludin and ZO-1. Taken together, these data suggest that MR2938 is a promising lead compound for the treatment of IBD. Supplementary Information: The online version contains supplementary material available at 10.1007/s42995-025-00285-x.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.