Arthur Kavanaugh1, Iain B McInnes2, Philip J Mease2, Stephen Hall2, Hector Chinoy2, Alan J Kivitz2, Zailong Wang2, Shephard Mpofu2. 1. From the University of California-San Diego, School of Medicine, LaJolla, California, USA; Immunology, Infection and Inflammation, University of Glasgow, Glasgow, UK; Swedish Medical Centre, and University of Washington School of Medicine, Seattle, Washington, USA; Monash University, Melbourne, Australia; UK National Institute for Health Research (NIHR) Manchester Musculoskeletal Biomedical Research Unit, Central Manchester University Hospitals National Health Service NHS Foundation Trust, University of Manchester, UK; Altoona Center for Clinical Research, Duncansville, Pennsylvania; Novartis Pharmaceuticals Corp., East Hanover, New Jersey, USA; Novartis Pharma AG, Basel, Switzerland.A. Kavanaugh, MD, Professor of Clinical Medicine, Director of Center for Innovative Therapy, University of California-San Diego, School of Medicine; I.B. McInnes, MD, PhD, Professor of Experimental Medicine (Immunology), Muirhead Chair of Medicine and Director of Institute (School of Medicine), Immunology, Infection and Inflammation, University of Glasgow; P.J. Mease, MD, Clinical Professor, University of Washington School of Medicine, Director of the Rheumatology Clinical Research Division of Swedish Medical Center; S. Hall, MBBS, Professor, Director-Emeritus Research, Monash University; H. Chinoy, PhD, Senior Lecturer, Rheumatology, NIHR Manchester Musculoskeletal Biomedical Research Unit, Central Manchester University Hospitals NHS Foundation Trust, University of Manchester; A.J. Kivitz, MD, CPI, President, Altoona Center for Clinical Research; Z. Wang, PhD, Associate Director, Biometrician, Novartis; S. Mpofu, MD, Senior Global Program Medical Director, Novartis. akavanaugh@ucsd.edu. 2. From the University of California-San Diego, School of Medicine, LaJolla, California, USA; Immunology, Infection and Inflammation, University of Glasgow, Glasgow, UK; Swedish Medical Centre, and University of Washington School of Medicine, Seattle, Washington, USA; Monash University, Melbourne, Australia; UK National Institute for Health Research (NIHR) Manchester Musculoskeletal Biomedical Research Unit, Central Manchester University Hospitals National Health Service NHS Foundation Trust, University of Manchester, UK; Altoona Center for Clinical Research, Duncansville, Pennsylvania; Novartis Pharmaceuticals Corp., East Hanover, New Jersey, USA; Novartis Pharma AG, Basel, Switzerland.A. Kavanaugh, MD, Professor of Clinical Medicine, Director of Center for Innovative Therapy, University of California-San Diego, School of Medicine; I.B. McInnes, MD, PhD, Professor of Experimental Medicine (Immunology), Muirhead Chair of Medicine and Director of Institute (School of Medicine), Immunology, Infection and Inflammation, University of Glasgow; P.J. Mease, MD, Clinical Professor, University of Washington School of Medicine, Director of the Rheumatology Clinical Research Division of Swedish Medical Center; S. Hall, MBBS, Professor, Director-Emeritus Research, Monash University; H. Chinoy, PhD, Senior Lecturer, Rheumatology, NIHR Manchester Musculoskeletal Biomedical Research Unit, Central Manchester University Hospitals NHS Foundation Trust, University of Manchester; A.J. Kivitz, MD, CPI, President, Altoona Center for Clinical Research; Z. Wang, PhD, Associate Director, Biometrician, Novartis; S. Mpofu, MD, Senior Global Program Medical Director, Novartis.
Abstract
OBJECTIVE: To determine the effect of prior tumor necrosis factor inhibitor (TNFi) therapy on secukinumab efficacy in psoriatic arthritis (PsA). METHODS: Patients were randomized to secukinumab 300 mg, 150 mg, 75 mg, or placebo. RESULTS: American College of Rheumatology 20 responses at Week 24 with secukinumab 300 mg, 150 mg, 75 mg, and placebo were 58.2%, 63.5%, 36.9%, and 15.9% in TNFi-naive (n = 258), and 45.5%, 29.7%, 14.7%, and 14.3% in TNFi-exposed patients (n = 139), respectively. Week 52 responses with secukinumab 300 mg, 150 mg, and 75 mg were 68.7%, 79.4%, and 58.5% in TNFi-naive, and 54.5%, 37.8%, and 35.3% in TNFi-exposed patients, respectively. CONCLUSION:Secukinumab was efficacious in TNFi-naive and TNFi-exposed patients with PsA, with greatest improvements in TNFi-naive patients.
RCT Entities:
OBJECTIVE: To determine the effect of prior tumor necrosis factor inhibitor (TNFi) therapy on secukinumab efficacy in psoriatic arthritis (PsA). METHODS:Patients were randomized to secukinumab 300 mg, 150 mg, 75 mg, or placebo. RESULTS: American College of Rheumatology 20 responses at Week 24 with secukinumab 300 mg, 150 mg, 75 mg, and placebo were 58.2%, 63.5%, 36.9%, and 15.9% in TNFi-naive (n = 258), and 45.5%, 29.7%, 14.7%, and 14.3% in TNFi-exposed patients (n = 139), respectively. Week 52 responses with secukinumab 300 mg, 150 mg, and 75 mg were 68.7%, 79.4%, and 58.5% in TNFi-naive, and 54.5%, 37.8%, and 35.3% in TNFi-exposed patients, respectively. CONCLUSION:Secukinumab was efficacious in TNFi-naive and TNFi-exposed patients with PsA, with greatest improvements in TNFi-naive patients.
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Authors: Iain B McInnes; Philip J Mease; Christopher T Ritchlin; Proton Rahman; Alice B Gottlieb; Bruce Kirkham; Radhika Kajekar; Eumorphia-Maria Delicha; Luminita Pricop; Shephard Mpofu Journal: Rheumatology (Oxford) Date: 2017-11-01 Impact factor: 7.580