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NEUROLOGY 2010;74:S41-S46
© 2010 American Academy of Neurology

Mitoxantrone and cytotoxic drugs' mechanisms of action

Timothy Vollmer, MD, Thomas Stewart, MS, JD, PA-C and Nancy Baxter

From the Department of Neurology (T.V.), University of Colorado Health Sciences Center, Aurora; The Rocky Mountain MS Center (T.V., T.S.), Englewood, CO; and Expert Medical Education (N.B.), Washington, DC.

Address correspondence and reprint requests to Dr. Timothy Vollmer, Department of Neurology, University of Colorado Denver, Rm L15-5511, A01, 12631 E 17th Avenue, Mail Stop B185, Aurora, CO 80045 Timothy.Vollmer{at}UCD.edu

Evidence has suggested that early, aggressive intervention may improve both short- and long-term outcomes in patients with multiple sclerosis (MS). Cytotoxic agents may offer advantages in this setting, particularly when used as an induction or add-on therapy with immunomodulators. Immunosuppression is the mechanism of action common to all cytotoxic drugs; individual subtleties in immunoregulatory actions are likely of minor importance. In the United States, mitoxantrone is currently the only cytotoxic agent approved for the treatment of MS (secondary-progressive, progressive-relapsing, and worsening relapsing-remitting forms). Therapies in phase III development include cyclophosphamide, mycophenolate mofetil, cladribine, and teriflunomide. All these drugs have exhibited efficacy in controlled clinical trials, although the degree of benefit with respect to MRI and clinical endpoints has varied both within and among the various agents. Further investigations are needed to determine whether cytotoxic drugs represent a substantial improvement over treatments that have a more targeted impact on the immune system.

Abbreviations: ACTH = adrenocorticotropic hormone; CIS = clinically isolated syndrome; EDSS = Expanded Disability Status Scale; CI = confidence interval; GA = glatiramer acetate; RRMS = relapsing-remitting MS; MS = multiple sclerosis; MSFC = Multiple Sclerosis Functional Composite; IFN = interferon; IL = interleukin.

This supplement was supported by an educational grant from Teva Neuroscience. Expert Medical Education contributed to the editorial refinement of this article and to the production of this supplement. Authors may have accepted honoraria for their supplement contributions.

Disclosure: Author disclosures are provided at the end of the article.

Neurology® supplements are not peer-reviewed. Information contained in Neurology® supplements represents the opinions of the authors. These opinions are not endorsed by nor do they reflect the views of the American Academy of Neurology, Editor-in-Chief, or Associate Editors of Neurology®.






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