Interferon-beta-1b: in newly emerging multiple sclerosis

Abstract

The mechanism of action of interferon-[beta]-1b in multiple sclerosis (MS) is not clearly understood, but is thought to involve immunoregulatory activities, including enhancing the suppressor activity of peripheral blood mononuclear cells. In the planned 3-year analysis of the BENEFIT study in patients with a single clinical event suggestive of MS, the relative risk of clinically definite (CD) MS was reduced by 41% in those receiving interferon-[beta]-1b 250 [micro]g every other day for 3 years (early-treatment group) compared with patients who were initially randomized to placebo then switched to interferon-[beta]-1b 250 [micro]g every other day at the end of 2 years or at the onset of CDMS (delayed-treatment group) [p < 0.01]. The relative risk of confirmed progression of the expanded disability status scale (EDSS) was reduced by 40% in the early-treatment group compared with the delayed-treatment group over 3 years (p < 0.05). At the end of the 2-year, randomized, placebo-controlled period of the BENEFIT study, the risk of developing CDMS (p < 0.0001) and McDonald-defined MS (p < 0.00001) was significantly lower in the interferon-[beta]-1b group than in the placebo group, and in the magnetic resonance imaging analysis, fewer newly active lesions developed in the interferon-[beta]-1b group (p < 0.001). Interferon-[beta]-1b was generally well tolerated. In the 3-year BENEFIT study, neutralizing activity, which was reported in about one-third of the early-treatment group, had no effect on outcome.