Celgene announced new Phase 3 data evaluating the safety and efficacy of ozanimod vs. Avonex (interferon beta-1a [IFN]; Biogen), a first-line treatment, for patients with relapsing multiple sclerosis (RMS). Findings were presented at the 7th Joint ECTRIMS – ACTRIMS Meeting in Paris, France.
The multicenter, randomized, double-blind, double-dummy, active-controlled SUNBEAM study (n=1,346) evaluated oral ozanimod 0.5mg and 1mg in patients with RMS for 1 year. The data showed a significant reduction in annualized relapse rate (ARR) for ozanimod 0.5mg (ARR 0.24; P=0.0013) and 1mg (ARR 0.18; P<0.0001) vs. IFN (ARR 0.35) over an average treatment duration of 13.6 months.
Treatment with ozanimod also significantly reduced new or enlarging T2 lesions over 1 year for ozanimod 0.5mg (25% P=0.0032) and 1mg (48%; P<0.0001) vs. IFN. In addition, ozanimod demonstrated a significant reduction in gadolinium-enhanced MRI lesions at 1 year for both doses vs. IFN: 0.5mg (34%; P=0.0182) and 1mg (63%; P<0.0001).
Brain volume loss, an indicator of MS disease progression, was reduced with ozanimod treatment arms vs. the IFN arm. Ozanimod 0.5mg reduced brain volume loss by 12% (median change from baseline to 1 year: –0.50%; P=0.06) and ozanimod 1mg reduced loss by 33% (median change from baseline to 1 year: –0.39; P<0.0001), compared with IFN (median change from baseline to 1 year: –0.57).
Pooled analysis data from SUNBEAM and the Phase 3 study RADIANCE Part B (n=1,320) showed ozanimod did not reach statistical significance vs. IFN in the time to 3-month confirmed disability progression. There was a very low rate of disability progression observed across all treatment groups by the end of the study.
Regarding safety, treatment-emergent adverse events (TEAEs) were seen in 57.2% of patients on ozanimod 0.5mg, 59.8% of patients on ozanimod 1mg vs. 75.5% of patients on IFN.
Ozanimod is a novel, oral, selective sphingosine 1-phosphate 1 (S1PR1) and 5 (S1PR5) receptor modulator under investigation for immune-inflammatory conditions. Selective binding with S1PR1 is thought to inhibit a specific subset of activated lymphocytes from migrating to sites of inflammation. Selective binding with S1PR5 is thought to activate specific cells within the CNS that can potentially enhance remyelination and prevent synaptic defects.
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