Review of the clinical evidence for interferon β 1a (Rebif®) in the treatment of multiple sclerosis

Abstract

Interferon (INF) β 1a 22 or 44 µg (Rebif ® ) administered s.c. 3 times a week (t.i.w) is a well established immunomodulating treatment for relapsing remitting multiple sclerosis (RRMS). This review focuses on its mechanisms of action, evidence of effi cacy, safety, and tolerability. Several pharmacodynamic properties explain the immunomodulatory actions of INF β 1a 22 or 44 µg s.c. t.i.w. Pivotal trials and post-marketing studies proved that the drug is effective in reducing disease activity and likely in slowing disease progression. Head-to-head comparative studies with other marketed INFs β in RRMS suggested a better therapeutic response associated with higher doses and frequency of administration of Rebif ® . Additional evidence indicated a benefi cial effect of INF β 1a in patients with clinically isolated syndromes (CIS) suggestive of MS, as treatment reduced time to conversion to clinically defi nite (CD) disease. Further, although the drug did not prove to slow time to progression there were benefi ts on relapse-and MRI-related secondary outcome measures in secondary progressive (SP) MS. Pivotal trials, their cross-over extensions, and post-marketing studies consistently showed that INF β 1a 22 or 44 µg s.c. t.i.w. is safe and well tolerated, as adverse drug reactions are usually mild and manageable.

A pilot study on the use of interferon beta-1a in early Alzheimer’s disease subjects

“…Interferon beta (IFNβ) was first tested for its antiviral property for the possible involvement of viral infections in the pathogenesis of MS and is now widely used for its immunomodulatory and antiproliferative properties in the treatment of this demyelinating disease [ 12 ]. Some of the mechanism of action of IFNβ include a shift from pro- to anti-inflammatory cytokines production [ 13 , 14 ]; inhibition of T-cell activation, blockage of production of oxygen free radicals by mononuclear phagocytes, and reduced expression of MHC II [ 15 ]; a protective role against BBB disruption by reducing the activity of metalloproteases and thereby preventing T-cells infiltration in the CNS [ 16 ]; a neuroprotective effect on retinal ganglion cells survival and stimulation of the secretion of nerve growth factors by endothelial cells [ 17 , 18 ].…”

Melanoma Cell Adhesion Molecule Expressing Helper T Cells in CNS Inflammatory Demyelinating Diseases

“… 36 , 37 IFN-β does not change the frequency and the absolute number of Th17 cells; however, IFN-β inhibits the Th17 axis and enhances the production of anti-inflammatory cytokines such as IL-10 and IL-4. 36 , 39 Therefore, it is understandable that IFN-β suppresses the disease activity without decreasing the number of MCAM + lymphocytes. Similar to FTY, DMF reduces the PB lymphocytes, including the Th17 cells.…”

The Effectiveness of Interferon Beta-1a in Management of Multiple Sclerosis: A Case Report

“…High immunogenicity increases the risk of neutralizer antibodies that reduce the effectiveness of treatment. 13 Interferon beta 1a can be given by injection of intramuscular (Avonex) or subcutaneous (Rebif) three times a week with a dose of 22 mcg or 44 mcg. IFN beta 1b is given intramuscularly every interval of one day.…”