ABSTRACT
Interferon (IFN)-β is a first-line therapy for relapsingremitting multiple sclerosis (MS). Three IFN-β preparations are currently available for the treatment of MS: IFN-β-1b (Betaseron®/Betaferon®) administered subcutaneously every other day; IFNβ-1a (Avonex®) administered intramuscularly once weekly; and IFN-β-1a (Rebif®) administered subcutaneously three times weekly. All three preparations have a moderate effect on the occurrence of relapses, a pronounced effect on disease activity measured on magnetic resonance imaging (MRI) and a small, but significant, effect on short-term disability progression demonstrated in large phase III trials1-3. Of the three commercially available IFN-β preparations, IFN-β-1b (Betaseron/Betaferon) is produced in an Escherichia coli cell line. It differs from the human IFN-β by having cysteine at position 17 substituted by serine, and the N-terminal methionine has been deleted so that the final protein has only 165 amino acids. Further, IFN-β-1b is not glycosylated, because bacteria are unable to attach sugar molecules. IFN-β-1a (Avonex or Rebif) has the full 166 amino-acid sequence of the human IFN-β. Because it is genetically engineered in a Chinese hamster ovary cell line the molecule is glycosylated, but not necessarily with the same pattern
as human IFN-β. The relative potency in vivo of IFN-β-1b is only about 10% that of IFN-β-1a, and IFN-β-1b is administered in approximately ten times higher doses to achieve an equivalent in vivo activity to that of IFN-β-1a.
