Safety, tolerability and pharmacodynamics of apical sodium-dependent bile acid transporter inhibition with volixibat in healthy adults and patients with type 2 diabetes mellitus: a randomised placebo-controlled trial

BMC Gastroenterol. 2018 Jan 5;18(1):3. doi: 10.1186/s12876-017-0736-0.

Abstract

Background: Pathogenesis in non-alcoholic steatohepatitis (NASH) involves abnormal cholesterol metabolism and hepatic accumulation of toxic free cholesterol. Apical sodium-dependent bile acid transporter (ASBT) inhibition in the terminal ileum may facilitate removal of free cholesterol from the liver by reducing recirculation of bile acids (BAs) to the liver, thereby stimulating new BA synthesis from cholesterol. The aim of this phase 1 study in adult healthy volunteers (HVs) and patients with type 2 diabetes mellitus (T2DM) was to assess the safety, tolerability, pharmacokinetics and pharmacodynamics of ASBT inhibition with volixibat (SHP626; formerly LUM002).

Methods: Participants were randomised 3:1 to receive once-daily oral volixibat (0.5 mg, 1 mg, 5 mg or 10 mg) or placebo for 28 days in two cohorts (HV and T2DM). Assessments included safety, faecal BA and serum 7α-hydroxy-4-cholesten-3-one (C4; BA synthesis biomarker).

Results: Sixty-one individuals were randomised (HVs: placebo, n = 12; volixibat, n = 38; T2DM: placebo, n = 3; volixibat, n = 8). No deaths or treatment-related serious adverse events were reported. Mild or moderate gastrointestinal adverse events were those most frequently reported with volixibat. With volixibat, mean total faecal BA excretion on day 28 was ~1.6-3.2 times higher in HVs (643.73-1239.3 μmol/24 h) and ~8 times higher in T2DM (1786.0 μmol/24 h) than with placebo (HVs: 386.93 μmol/24 h; T2DM: 220.00 μmol/24 h). With volixibat, mean C4 concentrations increased by ~1.3-5.3-fold from baseline to day 28 in HVs and by twofold in T2DM.

Conclusions: Volixibat was generally well tolerated. Increased faecal BA excretion and serum C4 levels support the mechanistic rationale for exploring ASBT inhibition in NASH. The study was registered with the Dutch clinical trial authority (Centrale Commissie Mensgebonden Onderzoek; trial registration number NL44732.056.13; registered 24 May 2013).

Keywords: Apical sodium-dependent bile acid transporter; Bile acids; Clinical pharmacology; LUM002; Non-alcoholic fatty liver disease; Non-alcoholic steatohepatitis; Phase 1 clinical trial; SHP626; Type 2 diabetes mellitus; Volixibat.

Publication types

  • Clinical Trial, Phase I
  • Randomized Controlled Trial

MeSH terms

  • Adolescent
  • Adult
  • Aged
  • Benzothiepins / administration & dosage*
  • Benzothiepins / adverse effects*
  • Benzothiepins / pharmacokinetics
  • Bile Acids and Salts / analysis
  • Bile Acids and Salts / metabolism
  • Blood Glucose / metabolism
  • Cholestenones / blood
  • Diabetes Mellitus, Type 2 / drug therapy*
  • Diabetes Mellitus, Type 2 / metabolism
  • Double-Blind Method
  • Feces / chemistry
  • Female
  • Glycosides / administration & dosage*
  • Glycosides / adverse effects*
  • Glycosides / pharmacokinetics
  • Homeostasis
  • Humans
  • Lipid Metabolism
  • Male
  • Membrane Glycoproteins / antagonists & inhibitors*
  • Middle Aged
  • Non-alcoholic Fatty Liver Disease / drug therapy*
  • Organic Anion Transporters, Sodium-Dependent / antagonists & inhibitors*
  • Symporters / antagonists & inhibitors*
  • Young Adult

Substances

  • Benzothiepins
  • Bile Acids and Salts
  • Blood Glucose
  • Cholestenones
  • Glycosides
  • Membrane Glycoproteins
  • Organic Anion Transporters, Sodium-Dependent
  • Symporters
  • sodium-bile acid cotransporter
  • 7 alpha-hydroxy-4-cholesten-3-one
  • volixibat