Kristin K Jørgensen1, Inge C Olsen2, Guro L Goll2, Merete Lorentzen3, Nils Bolstad4, Espen A Haavardsholm2,5, Knut EA Lundin5,6,7, Cato Mørk Professor8, Tore K Kvien2,5, Jørgen Jahnsen1,5
on behalf of the Nor-Switch study group
1Section for Gastroenterology, Department of Gastroenterology, Akershus University Hospital, Lørenskog. 2Dept. of Rheumatology, Diakonhjemmet Hospital, Box 23 Vinderen, 0319 Oslo, Norway. 3Dept.of Dermatology, Oslo University Hospital, Rikshospitalet, 0027 Oslo. 4Dept. of Medical Biochemistry, Oslo University Hospital, Radiumhospitalet, Ullernchausseen 70, 0310 Oslo, Norway. 5Faculty of Medicine, University of Oslo, P.O. Box 1171 Blindern, N-0318 Oslo, Norway. 6Dept. of Gastroenterology, Oslo University Hospital, Rikshospitalet, Sognsvannsveien 20, N-0372 Oslo. 7Centre for Immune Regulation, Department of Immunology, P.O. Box 4956 Nydalen, N-0424 Oslo, Norway. 8Institute of Cancer Research and Molecular Medicine, Faculty of Medicine, Norwegian University of Science and Technology, 7491 Trondheim, Norway
TNF-inhibitors (TNFi) have improved treatment of Crohn’s disease (CD), ulcerative colitis (UC), spondyloarthritis (SpA), rheumatoid arthritis (RA), psoriatic arthritis (PsA) and chronic plaque psoriasis (Ps). The NOR-SWITCH study was funded by the Norwegian government. The aim of the study was to examine switching from originator to biosimilar infliximab regarding efficacy, safety and immunogenicity.
The study was designed as a 52-week randomized, double-blind, non-inferiority, phase IV trial. Patients with a diagnosis of CD, UC, SpA, RA, PsA or Ps on stable treatment with the originator infliximab (Remicade®, INX) were randomized 1:1 to either continued INX or switch to CT-P13 treatment (biosimilar infliximab, Remsima®), using unchanged dosing regimen. Data were collected at infusion visits. The primary endpoint was disease worsening during follow-up.
Between October 6, 2014 and July 8, 2016, 481 patients (INX 241, CT-P13 240, Full Analysis Set, FAS) at 40 Norwegian study centres were randomized, received treatment and were followed for 52 weeks. The main demographic and baseline characteristics are shown in the table. Disease worsening occurred in 26.2% and 29.6% of patients in the INX and CT-P13 arms, respectively (PPS). The 95% confidence interval of the adjusted treatment difference (-4.4%) was -12.7 – 3.9 which was within the pre-specified non-inferiority margin. Changes in the generic disease variables and disease specific composite measures were similar in both arms (table). Likewise, the incidence of anti-drug antibodies detected (table), the trough drug levels and the frequencies of reported adverse events were also similar (data not shown).
The NOR-SWITCH trial demonstrated that switch from INX to CT-P13 was not inferior to continued treatment with INX.