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Their primary mechanism of action is mediated by binding to sulphonylurea receptors (SUR), which are atypical adenosine triphosphate binding cassette transporters in pancreatic beta cells. This interaction inhibits ATP\u2010sensitive potassium channels to promote insulin release. Off\u2010target actions of sulphonylureas identified in recent studies have demonstrated a range of anti\u2010inflammatory properties mediated by modulation of the nucleotide\u2010binding oligomerization domain\u2010like receptor pyrin domain\u2010containing protein 3 inflammasomes. Inflammasomes are cytosolic protein complexes that assemble in response to infection or stress\u2010associated stimuli, activating inflammatory responses, and are the primary source of pro\u2010inflammatory cytokines. Sulphonylureas and their derivatives have been shown to inhibit various stages of inflammasome activation, leading to the reduction of pro\u2010inflammatory mediators, including IL\u20101\u03b2 and IL\u201018. Recent evidence demonstrates that these agents reduced inflammatory responses, disease severity, and progression in various preclinical autoimmune and inflammatory models. In this narrative review, we consider the complexity of autoimmune conditions and the limited treatment options, and highlight the potential value of repurposing sulphonylureas and their derivatives as adjunct therapeutics for autoimmune conditions.<\/jats:p>","DOI":"10.1002\/prp2.70155","type":"journal-article","created":{"date-parts":[[2025,7,21]],"date-time":"2025-07-21T09:24:13Z","timestamp":1753089853000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":3,"title":["Sulphonylureas as Adjunct Therapeutic Agents in the Treatment of Autoimmune Conditions: A Narrative Review"],"prefix":"10.1002","volume":"13","author":[{"given":"Jasen","family":"Elford","sequence":"first","affiliation":[{"name":"School of Science &amp; Technology University of New England  Armidale New South Wales Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Robert 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