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The multivariate model included terms for treatment and biomarker change by treatment interaction. Missing data were handled using the nonresponder imputation rule, LOCF approach (ACR20 response), or LOCF approach only (biomarker data). 3. Results A total of 150 patients (29.8% of the 504 patients comprising the full study population) provided blood samples for biomarker analysis (placebo: n = 51; apremilast 20?mg BID: n = 51; and apremilast Liothyronine Sodium 30?mg BID: n = 48). Among substudy patients, baseline demographic and disease characteristics, as well as prior and concurrent therapy, were comparable across treatment groups (Table 1). Baseline demographics were similar to those of the full study population, except that prior exposure to methotrexate was higher in the biomarker subset (80.0%), as was prior exposure to a biologic DMARD, such as a TNF blocker (48.8%), than in the overall intent-to-treat population (54.2% and 23.6%, resp.) (Table 1). Prior biologic failure was also higher in the biomarker subset (20.7%) than in the overall intent-to-treat population (9.3%) (Table 1). The biomarker substudy patients, therefore, may have had a more treatment-resistant PsA phenotype than the overall study population. Table 1 Baseline demographic Crenolanib clinical trial and clinical characteristics of biomarker substudy patients (N = 150) and the overall intent-to-treat population (N = 504) [10]. 3.1. Biomarker Changes during the Placebo-Controlled Period (Weeks 0 to 24) Patients who received apremilast 20?mg BID or 30?mg BID exhibited significantly different mean percent changes from baseline in various biomarkers at Weeks 4, 16, and/or 24 compared with placebo (Figure 2). At Week 16 (LOCF), with apremilast 20?mg BID and/or apremilast 30?mg BID buy Lapatinib treatment, significant differences in mean percent change from baseline (versus placebo) were observed for TNF-��, IL-8, IL-6, and ferritin. At Week 24 (LOCF), apremilast 20?mg BID or 30?mg BID treatment was associated with significantly different percent changes from baseline (versus placebo) in TNF-��, IL-8, IL-6, ferritin, MIP-1��, and MCP-1 (Figure 2). Significant mean percent increases (versus placebo) in vWF were also observed with apremilast treatment at Weeks 16 and 24 (Figure 2); however, all vWF values were within normal range (