In REGENERATE, results of the 18-month interim analysis based on surrogate endpoints showed that obeticholic acid (OCA) improved liver fibrosis in F2/F3 patients.1 This secondary analysis assessed the effect of OCA in patients with fibrosis due to NASH including those with early fibrosis but at risk of disease progression. The full efficacy (FE) population included patients with NASH and fibrosis stages F2/F3, and F1 with at least one risk factor (BMI≥30 kg/m2, type 2 diabetes, ALT > 1.5x ULN), who were randomized 1:1:1 to placebo (PBO), OCA 10 mg, or OCA 25mg QD. Primary endpoints were fibrosis improvement (≥1 stage) with no worsening of NASH, or NASH resolution with no worsening of fibrosis. The safety population included all randomized patients who received at least one dose of study treatment (F1-3, N= 1968). The FE population included 1218 patients (PBO [n = 407], OCA 10mg [n = 407] or OCA 25mg [n = 404]), comprised of approximately 24 % F1 and 76 % F2/F3 patients. Overall, in the FE population nearly twice as many patients treated with OCA 25mg met the primary fibrosis and NASH endpoints compared to placebo (PBO) (table). In addition, dose-dependent reductions in ALT, AST andGGT were observed. Overall, pruritus was the most common adverse event (AE) (19 % PBO, 28 % OCA 10 mg, 51 % OCA 25 mg). Serious AEs occurred in 11 % PBO, 11 % OCA 10mg and 14 % OCA 25mg patients. OCA improved liver fibrosis, steatohepatitis and liver biochemistry in F1-F3 patients, demonstrating consistent efficacy with an overall similar safety profile to that previously reported in the REGENERATE primary efficacy analysis population (F2/F3 intention-to-treat).
Obeticholic acid treatment in patients with non-alcoholic steatohepatitis: a secondary analysis in the regenerate study across fibrosis stages
Bugianesi E;
2020-01-01
Abstract
In REGENERATE, results of the 18-month interim analysis based on surrogate endpoints showed that obeticholic acid (OCA) improved liver fibrosis in F2/F3 patients.1 This secondary analysis assessed the effect of OCA in patients with fibrosis due to NASH including those with early fibrosis but at risk of disease progression. The full efficacy (FE) population included patients with NASH and fibrosis stages F2/F3, and F1 with at least one risk factor (BMI≥30 kg/m2, type 2 diabetes, ALT > 1.5x ULN), who were randomized 1:1:1 to placebo (PBO), OCA 10 mg, or OCA 25mg QD. Primary endpoints were fibrosis improvement (≥1 stage) with no worsening of NASH, or NASH resolution with no worsening of fibrosis. The safety population included all randomized patients who received at least one dose of study treatment (F1-3, N= 1968). The FE population included 1218 patients (PBO [n = 407], OCA 10mg [n = 407] or OCA 25mg [n = 404]), comprised of approximately 24 % F1 and 76 % F2/F3 patients. Overall, in the FE population nearly twice as many patients treated with OCA 25mg met the primary fibrosis and NASH endpoints compared to placebo (PBO) (table). In addition, dose-dependent reductions in ALT, AST andGGT were observed. Overall, pruritus was the most common adverse event (AE) (19 % PBO, 28 % OCA 10 mg, 51 % OCA 25 mg). Serious AEs occurred in 11 % PBO, 11 % OCA 10mg and 14 % OCA 25mg patients. OCA improved liver fibrosis, steatohepatitis and liver biochemistry in F1-F3 patients, demonstrating consistent efficacy with an overall similar safety profile to that previously reported in the REGENERATE primary efficacy analysis population (F2/F3 intention-to-treat).
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