Send to

Choose Destination
See comment in PubMed Commons below
Drug Healthc Patient Saf. 2013;5:37-47. doi: 10.2147/DHPS.S28822. Epub 2013 Feb 26.

Oral available agents in the treatment of relapsing remitting multiple sclerosis: an overview of merits and culprits.

Author information

Department of Neurology, St JosefHospital Bochum, Ruhr-University Bochum, Bochum, Germany.


Multiple sclerosis (MS) is a chronic immunological disease of the central nervous system characterized by early inflammatory demyelination and subsequent neurodegeneration. Major therapeutic progress has occurred during the past decade, in particular since the introduction of immunomodulatory agents, however, MS is still an incurable disease. In addition, parenteral application of the currently licensed drugs is associated with injection-related adverse events (AEs) and low patient compliance. Thus, there remains an unmet need for the development of more effective and well tolerated oral therapies for the treatment of MS. A number of new orally administered agents including fingolimod, laquinimod, teriflunomide, cladribine, and BG-12 have been licensed recently or are currently under investigation in relapsing remitting MS patients. In multi-center, randomized, placebo-controlled phase III clinical studies, all of these agents have already shown their efficacy on both clinical disease parameters and magnetic resonance imaging-based measures of disease activity in patients with relapsing remitting MS. However, there are essential differences concerning their clinical efficacy and side-effect profiles. Additionally, the mechanisms by which these substances exert clinical efficacy have not been fully elucidated. In this article, we review the pharmaceutical properties of fingolimod, laquinimod, teriflunomide, cladribine, and BG-12; and their suggested mechanisms of action, clinical efficacy, and side-effect profiles.


cladribine; fingolimod (FTY); fumaric acid esters (BG-12); laquinimod; teriflunomide

PubMed Commons home

PubMed Commons

How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Dove Medical Press Icon for PubMed Central
    Loading ...
    Support Center