Cladribine versus fingolimod, natalizumab and interferon β for multiple sclerosis

Jokubaitis, Vilija G./0000-0002-3942-4340; Lugaresi, Alessandra/0000-0003-2902-5589; McCombe, Pamela/0000-0003-2704-8517; Kermode, Allan/0000-0002-4476-4016; Slee, Mark/0000-0003-4323-2453; Kalincik, Tomas/0000-0003-3778-1376; Pedrini, Marzena/0000-0002-2614-8607; Butzkueven, Helmut/0000-0003-3940-8727; Trojano, Maria/0000-0002-6329-8946 WOS: 000447789100014 PubMed: 28857680 Objective: This propensity score-matched analysis from MSBase compared the effectiveness of cladribine with interferon , fingolimod or natalizumab. Methods: We identified all patients with relapse-onset multiple sclerosis, exposure to the study therapies and 1-year on-treatment follow-up from MSBase. Three pairwise propensity score-matched analyses compared treatment outcomes over 1year. The outcomes were hazards of first relapse, disability accumulation and disability improvement events. Sensitivity analyses were completed. Results: The cohorts consisted of 37 (cladribine), 1940 (interferon), 1892 (fingolimod) and 1410 patients (natalizumab). The probability of experiencing a relapse on cladribine was lower than on interferon (p=0.05), similar to fingolimod (p=0.31) and higher than on natalizumab (p=0.042). The probability of disability accumulation on cladribine was similar to interferon (p=0.37) and fingolimod (p=0.089) but greater than natalizumab (p=0.021). The probability of disability improvement was higher on cladribine than interferon (p=0.00017), fingolimod (p=0.0025) or natalizumab (p=0.00099). Sensitivity analyses largely confirmed the above results. Conclusion: Cladribine is an effective therapy for relapse-onset multiple sclerosis. Its effect on relapses is comparable to fingolimod and its effect on disability accrual is comparable to interferon and fingolimod. Cladribine may potentially associate with superior recovery from disability relative to interferon, fingolimod and natalizumab. National Health and Medical Research Council of AustraliaNational Health and Medical Research Council of Australia [1129189, 1083539, 1080518]; MerckMerck & Company; BiogenBiogen; NovartisNovartis; RocheRoche Holding; Bayer ScheringBayer AG; Sanofi Genzyme; Teva The author(s) disclosed receipt of the following financial support for the research, authorship and/or publication of this article: This study was financially supported by National Health and Medical Research Council of Australia (project grants 1129189 and 1083539 and practitioner fellowship 1080518). The MSBase Foundation is a not-for-profit organisation that receives support from Merck, Biogen, Novartis, Roche, Bayer Schering, Sanofi Genzyme and Teva.