Brief Communication

Rituximab in relapsing-remitting multiple sclerosis: A 72-week, open-label, phase I trial†

  1. Amit Bar-Or MD1,*,
  2. Peter A. J. Calabresi MD2,
  3. Douglas Arnold MD1,3,
  4. Clyde Markowitz MD4,
  5. Stuart Shafer MD5,
  6. Lloyd H. Kasper MD6,
  7. Emmanuelle Waubant MD7,
  8. Suzanne Gazda MD8,
  9. Robert J. Fox MD9,
  10. Michael Panzara MD10,
  11. Neena Sarkar PhD11,
  12. Sunil Agarwal MD11,
  13. Craig H. Smith MD11

Article first published online: 26 MAR 2008

DOI: 10.1002/ana.21363

Issue

Annals of Neurology

Annals of Neurology

Volume 63, Issue 3, pages 395–400, March 2008

Additional Information

How to Cite

Bar-Or, A., Calabresi, P. A. J., Arnold, D., Markowitz, C., Shafer, S., Kasper, L. H., Waubant, E., Gazda, S., Fox, R. J., Panzara, M., Sarkar, N., Agarwal, S. and Smith, C. H. (2008), Rituximab in relapsing-remitting multiple sclerosis: A 72-week, open-label, phase I trial. Ann Neurol., 63: 395–400. doi: 10.1002/ana.21363

Author Information

  1. 1

    Montreal Neurological Institute, McGill University, Montreal, Quebec, Canada

  2. 2

    Department of Neurology, Johns Hopkins Hospital, Baltimore, MD

  3. 3

    NeuroRx Research, Montreal, Quebec, Canada

  4. 4

    Hospital of the University of Pennsylvania, Philadelphia, PA

  5. 5

    Vero Neurology, Vero Beach, FL

  6. 6

    Dartmouth Medical School, Lebanon, NH

  7. 7

    Department of Neurology, University of California at San Francisco, CA

  8. 8

    Integra Clinical Research, San Antonio, TX

  9. 9

    Mellen Center for Multiple Sclerosis, Cleveland Clinic, Cleveland, OH

  10. 10

    Biogen Idec, Cambridge, MA

  11. 11

    Genentech, Incorporated, South San Francisco, CA

*Neuroimmunology Unit and Experimental Therapeutics Program, Montreal Neurological Institute, McGill University, 3801 University, Room 111, Montreal, QC H3A 2B4, Canada

  1. †

    This article has been corrected since its original publication. Please see Annals of Neurology 2008;63;803 for further details.

Publication History

  1. Issue published online: 26 MAR 2008
  2. Article first published online: 26 MAR 2008
  3. Manuscript Accepted: 18 JAN 2008
  4. Manuscript Revised: 17 JAN 2008
  5. Manuscript Received: 9 OCT 2007

Funded by

  • Biogen Idec
  • Genentech, Incorporated

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This article includes supplementary materials available via the Internet at http://www.interscience.wiley.com/jpages/0364-5134/suppmat

FilenameFormatSizeDescription
ana21363-supplementaryfigure.eps2114KSupplementary Figure. Median Counts per mm 3for total CD19+ B Cells (A), CD19+CD27+ Memory B Cells (B), and CD19+CD27- Naive B Cells (C). As expected from its mechanism of action, treatment with rituximab led to rapid depletion of peripheral B cells (measured by CD19 expression), which was near-complete (99.8%) by Week 2, and sustained through Week 48, with reconstitution to mean 34.5% of baseline by Week 72. The majority of reconstituting cells were CD19+CD27- naive B cells (mean 51% of baseline) rather than CD19+CD27+ memory B cells (mean 14% of baseline).
ana21363-SupplementaryTable1.pdf99KSupplementary Table 1: Patient Baseline Characteristics at Entry (ITT Population).
ana21363-SupplementaryTable2.pdf49KSupplementary Table 2. Adverse Events, N (%).

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