Evidence for the Use of Janus Kinase ( <scp>JAK</scp> ) Inhibitors in the Management of Stevens‐Johnson Syndrome and Toxic Epidermal Necrolysis: A Scoping Review

Stevens-Johnson Syndrome (SJS) and Toxic Epidermal Necrolysis (TEN) are severe mucocutaneous adverse drug reactions associated with high morbidity and mortality. Current treatment regimens are largely supportive, and evidence for adjunctive systemic therapies remains limited. Recent research has implicated the Janus Kinase (JAK) signal transducer and activator of transcription (STAT) pathway in SJS/TEN pathogenesis, raising interest in JAK inhibitors as potential targeted therapies. This scoping review aimed to evaluate the existing literature on the use of JAK inhibitors in the management of SJS/TEN, summarise clinical outcomes and identify key research gaps. This scoping review was conducted in accordance with PRISMA-ScR guidelines. A systematic search of Medline, Web of Science, Embase and Scopus was conducted from inception up to 12 June 2025. Nine studies were included, comprising eight case reports and one translational research study, reporting on 15 patients (median age 45 years) treated with ruxolitinib (n = 7), tofacitinib (n = 5) or abrocitinib (n = 3). Most cases involved severe or treatment-refractory disease. Among the eight cases where time to re-epithelialisation was reported, six described 20%-30% re-epithelialisation by day 7 and one described 95% re-epithelialisation by day 16. No JAK inhibitor-related adverse events were reported. Preclinical studies supported a mechanistic role for the JAK/STAT pathway in keratinocyte apoptosis and inflammation. JAK inhibitors show promise as a novel therapeutic approach in SJS/TEN; however, current evidence is limited by small sample sizes, disease severity, concomitant therapies and potential publication bias. Well-designed prospective trials are needed to determine efficacy, safety and optimal use in this life-threatening condition.