N Engl J Med 2021 03;384(12):1101-1112
From the University Hospital of Bonn, Bonn (T.B.), and University of Lübeck, Lübeck (D.T.) - both in Germany; Oregon Health and Science University, Portland (E.L.S.); George Washington University School of Medicine and Health Sciences, Washington, DC (J.I.S.); Toulouse University and Centre Hospitalier Universitaire, Toulouse, France (C.P.); St. John's Institute of Dermatology, Guy's and St. Thomas' NHS Foundation Trust, London (A.E.P.); Osaka Habikino Medical Center, Osaka, Japan (Y.K.); the Department of Dermatology, National Taiwan University Hospital and National Taiwan University College of Medicine, Taipei (C.-Y.C.); Pfizer, New York (M.D., P.B., B.M., H.V.); Pfizer, Groton, CT (R.R., J.A., I.I., F.Z.); Sinclair Dermatology, East Melbourne, VIC, Australia (R.S.); ForCare Clinical Research, Tampa, FL (S.F.); and Dermedic Jacek Zdybski, Ostrowiec Świętokrzyski, Poland (J.Z.).
Background: The oral Janus kinase 1 (JAK1) inhibitor abrocitinib, which reduces interleukin-4 and interleukin-13 signaling, is being investigated for the treatment of atopic dermatitis. Data from trials comparing JAK1 inhibitors with monoclonal antibodies, such as dupilumab, that block interleukin-4 receptors are limited.
Methods: In a phase 3, double-blind trial, we randomly assigned patients with atopic dermatitis that was unresponsive to topical agents or that warranted systemic therapy (in a 2:2:2:1 ratio) to receive 200 mg or 100 mg of abrocitinib orally once daily, 300 mg of dupilumab subcutaneously every other week (after a loading dose of 600 mg), or placebo; all the patients received topical therapy. Read More