Evaluation of the usefulness of breast cancer resistance protein (BCRP) knockout mice and BCRP inhibitor-treated monkeys to estimate the clinical impact of BCRP modulation on the pharmacokinetics of BCRP substrates

Pharm Res. 2015 May;32(5):1634-47. doi: 10.1007/s11095-014-1563-4. Epub 2014 Nov 8.

Abstract

Purpose: To evaluate whether the impact of functional modulation of the breast cancer resistance protein (BCRP, ABCG2 421C>A) on human pharmacokinetics after oral administration is predictable using Bcrp knockout mice and cynomolgus monkeys pretreated with a BCRP inhibitor, elacridar.

Methods: The correlation of the changes of the area under the plasma concentration-time curve (AUC) caused by ABCG2 421C>A with those caused by the Bcrp knockout in mice, or BCRP inhibition in monkeys, was investigated using well-known BCRP substrates (rosuvastatin, pitavastatin, fluvastatin, and sulfasalazine).

Results: In mice, the bioavailability changes, which corrected the effect of systemic clearance by Bcrp knockout, correlated well with the AUC changes in humans, whereas the correlation was weak when AUC changes were directly compared. In monkeys, the AUC changes pretreated with elacridar resulted in a good estimation of those in humans within approximately 2-fold ranges.

Conclusions: This study suggests that pharmacokinetics studies that use the correction of the bioavailability changes in Bcrp knockout mice are effective for estimating clinical AUC changes in ABCG2 421C>A variants for BCRP substrate drugs and those studies in monkeys that use a BCRP inhibitor serve for the assessment of BCRP impact on the gastrointestinal absorption in a non-rodent model.

MeSH terms

  • ATP Binding Cassette Transporter, Subfamily G, Member 2
  • ATP-Binding Cassette Transporters / antagonists & inhibitors
  • ATP-Binding Cassette Transporters / genetics*
  • ATP-Binding Cassette Transporters / metabolism
  • Acridines / pharmacology
  • Animals
  • Anti-Inflammatory Agents, Non-Steroidal / administration & dosage
  • Anti-Inflammatory Agents, Non-Steroidal / blood
  • Anti-Inflammatory Agents, Non-Steroidal / pharmacokinetics*
  • Area Under Curve
  • Caco-2 Cells
  • Fatty Acids, Monounsaturated / administration & dosage
  • Fatty Acids, Monounsaturated / blood
  • Fatty Acids, Monounsaturated / pharmacokinetics*
  • Female
  • Fluvastatin
  • Humans
  • Hydroxymethylglutaryl-CoA Reductase Inhibitors / administration & dosage
  • Hydroxymethylglutaryl-CoA Reductase Inhibitors / blood
  • Hydroxymethylglutaryl-CoA Reductase Inhibitors / pharmacokinetics*
  • Indoles / administration & dosage
  • Indoles / blood
  • Indoles / pharmacokinetics*
  • Intestinal Absorption / drug effects
  • Macaca fascicularis
  • Male
  • Mice, Knockout
  • Quinolines / administration & dosage
  • Quinolines / blood
  • Quinolines / pharmacokinetics*
  • Rosuvastatin Calcium / administration & dosage
  • Rosuvastatin Calcium / blood
  • Rosuvastatin Calcium / pharmacokinetics*
  • Sulfasalazine / administration & dosage
  • Sulfasalazine / blood
  • Sulfasalazine / pharmacokinetics*
  • Tetrahydroisoquinolines / pharmacology

Substances

  • ATP Binding Cassette Transporter, Subfamily G, Member 2
  • ATP-Binding Cassette Transporters
  • Abcg2 protein, mouse
  • Acridines
  • Anti-Inflammatory Agents, Non-Steroidal
  • Fatty Acids, Monounsaturated
  • Hydroxymethylglutaryl-CoA Reductase Inhibitors
  • Indoles
  • Quinolines
  • Tetrahydroisoquinolines
  • Sulfasalazine
  • Fluvastatin
  • Rosuvastatin Calcium
  • pitavastatin
  • Elacridar