Several reports at the 2008 WCTRIMS meeting offered new data from clinical trials of both investigational and established therapies for MS.

Kathleen S. Hawker, Ohio State University, Columbus, Ohio, and colleagues reported on the efficacy and safety of rituximab in PPMS. The study involved 439 patients who were randomized to receive 2 intravenous infusions of rituximab or placebo (each dose separated by 2 weeks) every 24 weeks over a period of 96 weeks (4 treatment courses). The difference in time to confirmed disease progression between the treatment groups was not statistically significant, but the median change in T2 lesion volume from baseline to week 96 was significantly lower with rituximab than with placebo (P=0.0008). No significant differences in brain volume were apparent between treatment groups.

Alemtuzumab showed a significant difference from SC IFN with respect to achieving a clinically disease-free state in a trial of patients with RRMS. Krzysztof Selmaj, Klinika j Katedra Neurologii Akademii, Lodz, Poland, on behalf of the CAMMS223 Study Group, explained that these findings came from a randomized trial of 334 patients who received SC IFN 44 3 times weekly or alemtuzumab infusions of 24 or 12 mg/day for 5 days at Month 0, 3 days at Month 12, and, in some patients, for 3 days at Month 24. Followup data showed that the proportion of patients free from relapse, free from 3- month accumulation of disability, and free from 6-month accumulation of disability was significantly greater with alemtuzumab than with SC IFN at years 1 through 3 (P<0.0001). In addition, the proportion of patients free from clinical disease was significantly higher with alemtuzumab than with IFN at years 1 (86% vs 63%, respectively), 2 (81% vs 48%, respectively), and 3 (71% vs 38%, respectively); P<0.0001 for all comparisons.

A pilot study presented by Omar Khan and colleagues, Wayne State University School of Medicine, Detroit, Michigan, suggested that glatiramer acetate 20 mg SC may be equally effective whether administered once daily or every other day in patients with RRMS. Among 30 patients randomized to the 2 dosage schedules, no differences in relapse rates, disease progression, change in T2-weighted lesion volume, or Gd-enhanced lesions were found at 2 years. Moreover, in vitro proliferation of glatiramer acetate-responsive T cells and Th1/Th2 cytokine expression did not differ between groups at any point. After 2 years, all patients in the once-daily treatment group switched to every-other-day treatment. At 4 years, no differences in the endpoints were found between the crossover group and the patients who had continuously received glatiramer acetate on an every-other-day basis. The researchers suggest that larger, multicenter trials are warranted to confirm these findings and to identify an optimal dosage for glatiramer acetate in RRMS.

Short-term induction therapy with mitoxantrone prior to treatment with glatiramer acetate resulted in substantial suppression of clinical disease activity in patients with active RRMS, according to a study by Jason Ramtahal and Mike Boggild, Walton Centre for Neurology and Neuro surgery, NHS Trust, Liverpool, United Kingdom. The study enrolled 77 patients, all of whom received mito xantrone induction therapy: 58 received 48 mg/m² over 8 months and the others (earlier-treated patients) received somewhat higher total dosages. This mitoxantrone induction overlapped with glatiramer acetate therapy for the final 3 months, after which all patients received glatiramer acetate alone. The annualized relapse rate was reduced from 1.85 pre-induction to 0.16 or less at a mean follow-up of 44 months and was sustained up to 6 years.

Heather B. Streeter and colleagues, University of Bristol, United Kingdom, described data showing that ATXMS1467, a peptide vaccine for MS, was safe and well tolerated in a study of 6 patients with SPMS. After receiving escalating doses of ATX-MS1467 (25 to 800 mg), these patients exhibited no treatment-related or serious adverse events. In 4 patients who had a significant T-cell response to myelin basic protein before the trial, this response was significantly suppressed at 1 month after the administration of ATX-MS1467 (P=0.0313).