ReviewFrontiers in immunology2026
Significant improvement with ivarmacitinib after suboptimal response to tofacitinib in severe alopecia areata: a case report and literature review.
Review in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- Real-World Efficacy and Safety of Tofacitinib for Patients With Alopecia Areata: A Retrospective Multi-Center Cohort Study.Clinical and translational science · 2026Article
- JAK Inhibitors for Alopecia Areata: Approved Therapies, Efficacy, and Unanswered Questions.Drug design, development and therapy · 2026Review
Corrections and comments
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Authors and funding
3 authors.
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Abstract
Alopecia areata (AA) is a chronic, immune-mediated hair loss disorder, in which the JAK-STAT signaling pathway plays an important pathogenic role. Available agents for AA include minoxidil, corticosteroids, immunosuppressants and Janus kinase (JAK) inhibitors, among others. For adults with severe AA, JAK inhibitors have emerged as cornerstone systemic treatments, but the responses to them are variable. Ivarmacitinib is a novel and highly selective JAK1 inhibitor, which has been approved for AA in China recently with little real-world evidence. We present a case of a patient with severe AA who achieved significant improvement with ivarmacitinib after suboptimal response to tofacitinib, and review previous studies on switching therapy between different JAK inhibitors for AA. This case suggests that ivarmacitinib is a viable alternative for tofacitinib-refractory AA, possibly due to its higher JAK1 selectivity. Further studies are required to define ivarmacitinib's optimal position in AA treatment algorithm, and to elucidate underlying mechanisms behind JAK inhibitors, which is essential for more personalized and targeted therapy for severe AA.
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