Quantitative assessment of the contribution of sodium-dependent taurocholate co-transporting polypeptide (NTCP) to the hepatic uptake of rosuvastatin, pitavastatin and fluvastatin

Biopharm Drug Dispos. 2013 Nov;34(8):452-61. doi: 10.1002/bdd.1861. Epub 2013 Oct 3.

Abstract

Hepatic uptake transport is often the rate-determining step in the systemic clearance of drugs. The ability to predict uptake clearance and to determine the contribution of individual transporters to overall hepatic uptake is therefore critical in assessing the potential pharmacokinetic and pharmacodynamic variability associated with drug-drug interactions and pharmacogenetics. The present study revisited the interaction of statin drugs, including pitavastatin, fluvastatin and rosuvastatin, with the sodium-dependent taurocholate co-transporting polypeptide (NTCP) using gene transfected cell models. In addition, the uptake clearance and the contribution of NTCP to the overall hepatic uptake were assessed using in vitro hepatocyte models. Then NTCP protein expression was measured by a targeted proteomics transporter quantification method to confirm the presence and stability of NTCP expression in suspended and cultured hepatocyte models. It was concluded that NTCP-mediated uptake contributed significantly to active hepatic uptake in hepatocyte models for all three statins. However, the contribution of NTCP-mediated uptake to the overall active hepatic uptake was compound-dependent and varied from about 24% to 45%. Understanding the contribution of individual transporter proteins to the overall hepatic uptake and its functional variability when other active hepatic uptake pathways are interrupted could improve the current prediction practice used to assess the pharmacokinetic variability due to drug-drug interactions, pharmacogenetics and physiopathological conditions in humans.

Keywords: NTCP; hepatic transport; hepatocytes; statins.

MeSH terms

  • ATP Binding Cassette Transporter, Subfamily B, Member 11
  • ATP-Binding Cassette Transporters / genetics
  • Cell Line
  • Cells, Cultured
  • Fatty Acids, Monounsaturated / pharmacology*
  • Female
  • Fluorobenzenes / pharmacology*
  • Fluvastatin
  • Hepatocytes / metabolism*
  • Humans
  • Hydroxymethylglutaryl-CoA Reductase Inhibitors / pharmacology*
  • Indoles / pharmacology*
  • Liver / metabolism
  • Middle Aged
  • Organic Anion Transporters, Sodium-Dependent / genetics
  • Organic Anion Transporters, Sodium-Dependent / metabolism*
  • Pyrimidines / pharmacology*
  • Quinolines / pharmacology*
  • Rosuvastatin Calcium
  • Sulfonamides / pharmacology*
  • Symporters / genetics
  • Symporters / metabolism*

Substances

  • ABCB11 protein, human
  • ATP Binding Cassette Transporter, Subfamily B, Member 11
  • ATP-Binding Cassette Transporters
  • Fatty Acids, Monounsaturated
  • Fluorobenzenes
  • Hydroxymethylglutaryl-CoA Reductase Inhibitors
  • Indoles
  • Organic Anion Transporters, Sodium-Dependent
  • Pyrimidines
  • Quinolines
  • Sulfonamides
  • Symporters
  • sodium-bile acid cotransporter
  • Fluvastatin
  • Rosuvastatin Calcium
  • pitavastatin