Researchers Review Available Efficacy, Safety Data on Ozanimod in RMS

Researchers analyzed the available evidence on the treatment’s efficacy and safety profile from the RADIANCE and SUNBEAM trials.

In March, ozanimod became the first FDA-approved sphingosine-1-phosphate receptor (S1PR) modulator for patients with relapsing forms of multiple sclerosis (RMS) that doesn’t require a genetic test or first-dose observation. With this recent addition to the MS treatment landscape, researchers took a look at the available evidence on ozanimod’s efficacy and safety profile using data from the RADIANCE and SUNBEAM trials.


Efficacy data gleaned from the trials demonstrated ozanimod’s favorable cumulative number of gadolinium-enhancing lesions and favorable relapsed rates compared with placebo.

In the phase 2, 24-week randomized, double-blind, placebo-controlled RADIANCE trial of 258 patients, the cumulative mean number of gadolinium-enhancing lesions was drastically lower for patients receiving ozanimod 0.5 mg and 1 mg (1.5 and 1.5, respectively) compared with patents receiving placebo (11.1). At 24 weeks, patients treated with either dose of ozanimod exhibited fewer total gadolinium-enhancing lesions, as well as a smaller cumulative number of new or enlarging T2 lesions.

Similar findings emerged from the phase 3 RADIANCE trial of 1300 patients, which compared the same 2 doses of ozanimod with intramuscular interferon beta-1a 30 μg. At 24 months, the mean number of gadolinium-enhancing lesions was 0.20 and 0.18 in the patients receiving ozanimod 0.5 mg and 1 mg, respectively, compared with 0.37 in patients receiving interferon beta-1a.

The phase 3 trial also looked at the adjusted relapse rate (ARR)—the study’s primary endpoint—across the 3 groups, which were 0.22 and 0.17 for patients receiving ozanimod 0.5 mg and 0.1 mg, respectively, compared with 0.28 for patients receiving interferon beta-1a. Compared with interferon beta-1a, ozanimod also resulted in a reduced loss of whole-brain volume, cortical grey matter, and thalamic volume.

The phase 3 SUNBEAM trial included the same 3 treatment groups as the phase 3 RADIANCE trial but included another 1300 patients. SUNBEAM found an adjusted ARR of 0.24 for the ozanimod 0.5 mg group, 0.18 for the ozanimod 1 mg group, and 0.35 for the interferon beta-1a group.

“As in the RADIANCE phase III trial, this study reported a reduction in the loss of whole-brain volume, cortical grey matter, and thalamic volume with ozanimod when compared to interferon beta-1a,” wrote the researchers. “SUNBEAM also concluded that both low and high-dose ozanimod was as effective as interferon beta-1a in reducing active disease in relapsing MS, with ozanimod 1 mg demonstrating numerically greater efficacy than ozanimod 0.5 mg.”


The same studies established the safety profile of ozanimod. All trials concluded that ozanimod was well tolerated among patients, with the phase 2 RADIANCE trial also finding no evident differences in safety between the 2 ozanimod doses.

In the phase 2 RADIANCE trial, 60% of patients reported at least one treatment-emergent adverse event (TEAE), the most common being nasopharyngitis and headache. There were no reported cases of macular edema, notable infectious, malignancy-related, or pulmonary adverse events.

In the phase 3 RADIANCE trial, fewer patients reported TEAEs in both the ozanimod 0.5 mg group and 1 mg group (74.3% and 74.7%, respectively) compared with 83% who reported TEAEs in the interferon beta-1a group.

The most common TEAEs in the ozanimod cohorts were nasopharyngitis, ALT increase, hypertension, γ-glutamyltransferase increase, pharyngitis, and urinary tract infection, while the most common TEAEs in the interferon beta-1a group were influenza-like illness, headache, nasopharyngitis, upper respiratory tract infection, pyrexia, and orthostatic hypotension.

Reference: Lassiter G, Melancon C, Rooney T, et al. Ozanimod to treat relapsing forms of multiple sclerosis: a comprehensive review of disease, drug efficacy and side effects. Neurol Int. 2020;12(3):89-108. doi: 10.3390/neurolint12030016