These rapid, sustained reductions in annualized relapse rate and risk of relapse with natalizumab treatment occurred regardless of baseline disease activity in the overall population and in the subset of patients with highly active disease

These rapid, sustained reductions in annualized relapse rate and risk of relapse with natalizumab treatment occurred regardless of baseline disease activity in the overall population and in the subset of patients with highly active disease. Observations from a clinical practice setting (TOP) were similar to the clinical trial results but should be interpreted with caution owing to the lack of a reference group. and in the multinational Tysabri? Observational Program (TOP). In AFFIRM, natalizumab reduced the annualized relapse rate within 3?months of treatment initiation compared with placebo in the overall populace (0.30 vs. 0.71; highly active, defined as having 2 relapses in the year before study entry and 1 gadolinium-enhancing lesion at study entry VCH-759 aBaseline relapse rates were not available for 13 patients in TOP The median (range) disease duration prior to starting natalizumab VCH-759 was comparable for the two studies: 5 (0C34) years for AFFIRM and 7 (0C44) years for TOP [15, 23]. The majority (90?%) of TOP patients had used another DMT prior to starting natalizumab [23]. The mean relapse rate at baseline among TOP patients was approximately 2.0, similar to the rate in AFFIRM patients with highly active disease (Table?1). Annualized relapse rate In AFFIRM natalizumab monotherapy reduced annualized relapse rate already within the first 3?months of treatment compared with placebo overall [0.30 (95?% CI 0.23C0.40) vs. 0.71 (95?% CI 0.55C0.91); value0.88930.5578Cumulative risk of relapse at 8?weeks from baseline?Percentage5.712.26.816.6?HR (95?% CI)0.45 (0.29C0.72)0.35 (0.14C0.87) value0.00070.0243Cumulative risk of relapse at 12?weeks from baseline?Percentage7.216.77.420.0?HR (95?% CI)0.41 (0.28C0.61)0.33 (0.14C0.76) value 0.00010.0090Cumulative risk of relapse at 24?weeks from baseline?Percentage11.925.414.233.3?HR (95?% CI)0.43 (0.31C0.59)0.37 (0.20C0.68) value 0.00010.0015Cumulative risk of relapse at 48?weeks from baseline?Percentage20.039.221.758.9?HR (95?% CI)0.45 (0.35C0.57)0.28 (0.17C0.45) value 0.0001 0.0001Cumulative risk of relapse at 104?weeks from baseline?Percentage28.755.729.376.0?HR (95?% CI)0.42 (0.34C0.52)0.25 (0.17C0.39) value 0.0001 0.0001 Open in a individual window highly active, defined as having 2 relapses in the year before study entry and 1 gadolinium-enhancing lesion at study entry At 4, 8, and 12?weeks in TOP, patients treated with natalizumab had an estimated 2.4, 4.0, and 5.7?% cumulative risk of relapse from baseline, respectively. At 2?years, the estimated risk was 32?%, similar to the risk in natalizumab-treated AFFIRM patients at 2?years. At 3?years in TOP, the cumulative risk of relapse was 42?% (Fig.?4). Open in a separate windows Fig.?4 Cumulative probability of relapse in TOP patients is shown as a em sound line /em ; 95?% confidence band is usually indicated by em dashed lines /em . Five patients did not receive natalizumab and were excluded from post-baseline analyses Discussion In AFFIRM, natalizumab had a significant effect on annualized relapse rate within 3?months of initiating therapy, and reductions were sustained over the 2-12 months controlled study period. Combined with the MRI findings of the phase II study in which reductions in the mean number of new gadolinium-enhancing lesions in natalizumab-treated patients versus placebo were apparent after 1?month and remained reduced as long as treatment was continued [14], these data suggest that natalizumab reduces disease activity shortly after initiating treatment. Natalizumab also had a significant effect on the cumulative probability of relapse over 2?years, with significant reductions being observed by 8?weeks after starting treatment. These rapid, sustained reductions in annualized relapse rate and risk of relapse with natalizumab treatment occurred regardless of baseline disease activity in the overall population and in the subset of patients with highly active disease. Observations from a clinical practice setting (TOP) were similar to the clinical trial results but should be interpreted with caution owing to the lack of a reference group. Nevertheless, given the differences in patient demographics and disease characteristics between the clinical studies and TOP, these results suggest that the results from the pivotal studies are applicable to those patients included in the current label of natalizumab. This is particularly remarkable regarding the potential utility of natalizumab for patients experiencing MS disease activity despite treatment with other DMTs to rapidly gain control of disease and help prevent further cumulative damage. Our findings are consistent with those of numerous post-marketing studies that VCH-759 have observed significant improvements in CXCR4 annualized relapse rate, radiologic disease, ambulation, or disability progression in patients, including those with highly active disease, switching to natalizumab from other DMTs, although most assessments were performed at 1?year after initiating natalizumab [18, 19, 21, 22, 26C32]. The results of this analysis are also consistent with a separate AFFIRM analysis that showed an increased probability of sustained improvement in Extended Disability Status Scale (EDSS) scores with natalizumab compared with placebo emerging during the first 24?weeks of treatment [33]. Natalizumabs rapid effects and ability to control disease in patients with highly active MS may be best explained by the inhibition of leukocyte migration into brain tissue that prevents lesion formation and reduces inflammatory cell recruitment into existing lesions [34, 35]. In addition to preventing leukocyte entry into the CNS, there is evidence that natalizumab may dampen ongoing inflammation in the CNS by disrupting interactions between inflammatory leukocytes and extracellular matrix proteins such as fibronectin and osteopontin or by inducing apoptosis of activated T cells [36C38]. In summary, rapid onset of natalizumab clinical efficacy shortly after treatment.