0%; placebo, 22.0%; P = .002; relative risk, 2.3; 95% CI, 1.3–4.2). Prespecified exploratory subgroup analysis results by concomitant corticosteroid or immunosuppressive use for clinical remission at weeks 6 and 10 and CDAI-100 response at week 6 for the TNF antagonist–failure and overall populations are shown in Supplementary Figures 2 and 3. Among patients

in the TNF antagonist–failure and overall populations with increased baseline CRP levels, median changes in CRP concentration were improved modestly from baseline to weeks 6 and 10; these improvements were more pronounced at week 10 than at week 6 (Supplementary Figure 4). Nominal P values for between-group differences in median change in fecal calprotectin E7080 molecular weight levels from baseline to week 6

were not less than .05 among the TNF antagonist–failure population (vedolizumab, -22.1 μg/g stool; placebo, -5.0 μg/g stool; P = .883) or the overall population (vedolizumab, -26.2 μg/g stool; placebo, -7.8 μg/g stool; P = .744). Sixty percent of placebo-treated patients and 56% of vedolizumab-treated patients experienced 1 or more AEs during the study (Table 2). Selleckchem ERK inhibitor Serious infection and drug-related SAEs were experienced by 1% or less of patients in both groups, and 2% of patients in both groups had SAEs leading to study discontinuation. No deaths were reported in the study. The most common AEs in both groups were similar and included infections (vedolizumab, 19%; placebo, 17%). Gastrointestinal infections occurred in 5 (2%) vedolizumab-treated patients and in 3 (1%) placebo-treated patients. In vedolizumab-treated patients, the most common AEs Obeticholic Acid nmr were nausea, vomiting, headache, upper respiratory tract infection, arthralgia, nasopharyngitis, and abdominal pain (Table 2). Incidences of nausea, upper respiratory tract infection, arthralgia, abdominal pain, aphthous stomatitis, vomiting, fatigue, urinary tract infection, and anemia were higher with vedolizumab, whereas incidences of CD exacerbation, pyrexia, and headache were higher with placebo. Two vedolizumab-treated patients had SAEs of infection, including

1 anal abscess and 1 urinary tract infection, which were treated successfully during the study; neither led to study discontinuation. No placebo-treated patients had SAEs of infection. Infusion-related AEs occurred in 4 (2%) vedolizumab-treated patients and in 2 (<1%) placebo-treated patients. In the 1 patient who reported new neurologic symptoms during the study and was evaluated by an independent adjudication committee, PML formally was excluded. This vedolizumab-treated patient was later withdrawn from the study because of an ependymoma and had the only reported neoplasm in the study. The mean ± SD week 6 trough vedolizumab serum concentration was 26.5 ± 15.8 μg/mL (n = 195), which was similar to that observed in GEMINI 2.24 The week 10 vedolizumab serum concentration was 28.4 ± 17.9 μg/mL (n = 190).