Restricted brain penetration of the tyrosine kinase inhibitor erlotinib due to the drug transporters P-gp and BCRP

Invest New Drugs. 2012 Apr;30(2):443-9. doi: 10.1007/s10637-010-9569-1. Epub 2010 Oct 21.

Abstract

Purpose: Erlotinib (Tarceva®, OSI-774) is a small molecule inhibitor of the epidermal growth factor receptor (EGFR) tyrosine kinase. As high-grade gliomas frequently show amplification, overexpression and/or mutation of EGFR, this drug has been tested in several clinical trials with glioblastoma patients, but unfortunately, with little success. As erlotinib is a known substrate of P-glycoprotein (P-gp) and breast cancer resistance protein (BCRP) we have investigated the effect of these ABC-transporters on the brain penetration of erlotinib.

Study design: Erlotinib (50 mg/kg) was given by i.p. administration to wild-type (WT), Mdr1ab(-/-) (single P-gp knockout), Bcrp1(-/-) (single Bcrp1 knockout) and Mdr1ab(-/-)Bcrp1(-/-) (compound P-gp and Bcrp1 knockout) mice. Drug levels in plasma and tissues were determined by reversed-phase high-performance liquid chromatography.

Results: Relative to Mdr1ab(-/-)Bcrp1(-/-) mice that are deficient for both drug transporters, the area under the concentration time curve in brain tissue (AUC)(brain) of erlotinib decreased significantly by 1.6-fold in Mdr1ab(-/-) mice where Bcrp1 is present (49.6 ± 3.95 versus 31.1 ± 1.7, μg/g*h; P < 0.01). In Bcrp1(-/-) mice, were P-gp is present, a more pronounced 3.8-fold decrease to 13.0 ± 0.70, μg/g*h (P < 0.01) was observed, which is close to the 4.5-fold decrease in the AUC(brain) of erlotinib found in WT mice where both drug transporters are present (11.0 ± 1.35, P < 0.01). The plasma clearance of erlotinib was similar in mice deficient for P-gp and/or Bcrp1 compared with wild-type mice. In all other tissues the differences between the genotypes were negligible.

Conclusions: Both P-gp and Bcrp1 reduce the brain penetration of erlotinib. Although P-gp appears to be the most effective factor limiting the brain penetration of erlotinib, the highest brain accumulation was observed when Bcrp1 was also absent. Strategies to inhibit P-gp/BCRP in patients to improve delivery of (novel molecular-targeted) substrate agents, such as erlotinib, to the brain may be required for treatment of intracranial malignancies.

MeSH terms

  • ATP Binding Cassette Transporter, Subfamily B / deficiency
  • ATP Binding Cassette Transporter, Subfamily B / genetics
  • ATP Binding Cassette Transporter, Subfamily B / metabolism*
  • ATP Binding Cassette Transporter, Subfamily G, Member 2
  • ATP-Binding Cassette Sub-Family B Member 4
  • ATP-Binding Cassette Transporters / genetics
  • ATP-Binding Cassette Transporters / metabolism*
  • Animals
  • Antineoplastic Agents / administration & dosage
  • Antineoplastic Agents / blood
  • Antineoplastic Agents / pharmacokinetics*
  • Area Under Curve
  • Blood-Brain Barrier / metabolism*
  • Capillary Permeability*
  • Chromatography, High Pressure Liquid
  • Chromatography, Reverse-Phase
  • Erlotinib Hydrochloride
  • Female
  • Injections, Intraperitoneal
  • Metabolic Clearance Rate
  • Mice
  • Mice, Knockout
  • Protein Kinase Inhibitors / administration & dosage
  • Protein Kinase Inhibitors / blood
  • Protein Kinase Inhibitors / pharmacokinetics*
  • Quinazolines / administration & dosage
  • Quinazolines / blood
  • Quinazolines / pharmacokinetics*
  • Tissue Distribution

Substances

  • ATP Binding Cassette Transporter, Subfamily B
  • ATP Binding Cassette Transporter, Subfamily G, Member 2
  • ATP-Binding Cassette Transporters
  • Abcg2 protein, mouse
  • Antineoplastic Agents
  • Protein Kinase Inhibitors
  • Quinazolines
  • multidrug resistance protein 3
  • Erlotinib Hydrochloride