Clinical pharmacokinetics of tyrosine kinase inhibitors.

Article Details

Citation

van Erp NP, Gelderblom H, Guchelaar HJ

Clinical pharmacokinetics of tyrosine kinase inhibitors.

Cancer Treat Rev. 2009 Dec;35(8):692-706. doi: 10.1016/j.ctrv.2009.08.004. Epub 2009 Sep 5.

PubMed ID
19733976 [ View in PubMed
]
Abstract

In the recent years, eight tyrosine kinase inhibitors (TKIs) have been approved for cancer treatment and numerous are under investigation. These drugs are rationally designed to target specific tyrosine kinases that are mutated and/or over-expressed in cancer tissues. Post marketing study commitments have been made upon (accelerated) approval such as additional pharmacokinetic studies in patients with renal- or hepatic impairment, in children, additional interactions studies and studies on the relative or absolute bioavailability. Therefore, much information will emerge on the pharmacokinetic behavior of these drugs after their approval. In the present manuscript, the pharmacokinetic characteristics; absorption, distribution, metabolism and excretion (ADME), of the available TKIs are reviewed. Results from additional studies on the effect of drug transporters and drug-drug interactions have been incorporated. Overall, the TKIs reach their maximum plasma levels relatively fast; have an unknown absolute bioavailability, are extensively distributed and highly protein bound. The drugs are primarily metabolized by cytochrome P450 (CYP) 3A4 with other CYP-enzymes playing a secondary role. They are predominantly excreted with the feces and only a minor fraction is eliminated with the urine. All TKIs appear to be transported by the efflux ATP binding-cassette transports B1 and G2. Additionally these drugs can inhibit some of their own metabolizing enzymes and transporters making steady-state metabolism and drug-drug interactions both complex and unpredictable. By understanding the pharmacokinetic profile of these drugs and their similarities, factors that influence drug exposure will be better recognized and this knowledge may be used to limit sub- or supra-therapeutic drug exposure.

DrugBank Data that Cites this Article

Drug Targets
DrugTargetKindOrganismPharmacological ActionActions
ErlotinibNuclear receptor subfamily 1 group I member 2ProteinHumans
Yes
Agonist
Details
Drug Enzymes
DrugEnzymeKindOrganismPharmacological ActionActions
DasatinibCytochrome P450 1A1ProteinHumans
Unknown
Substrate
Details
DasatinibCytochrome P450 1A2ProteinHumans
Unknown
Substrate
Details
DasatinibCytochrome P450 1B1ProteinHumans
Unknown
Substrate
Details
DasatinibCytochrome P450 3A4ProteinHumans
Unknown
Substrate
Inhibitor
Details
DasatinibCytochrome P450 3A5ProteinHumans
Unknown
Substrate
Details
ErlotinibCytochrome P450 1A1ProteinHumans
Unknown
Substrate
Details
ErlotinibCytochrome P450 1A2ProteinHumans
Unknown
Substrate
Details
ErlotinibCytochrome P450 1B1ProteinHumans
Unknown
Substrate
Details
ErlotinibCytochrome P450 2C8ProteinHumans
Unknown
Substrate
Inhibitor
Details
ErlotinibCytochrome P450 2D6ProteinHumans
Unknown
Substrate
Details
ErlotinibCytochrome P450 3A4ProteinHumans
Unknown
Substrate
Inhibitor
Details
ErlotinibCytochrome P450 3A5ProteinHumans
Unknown
Substrate
Details
LapatinibCytochrome P450 2C19ProteinHumans
Unknown
Substrate
Details
LapatinibCytochrome P450 3A4ProteinHumans
Unknown
Substrate
Inhibitor
Details
LapatinibCytochrome P450 3A5ProteinHumans
Unknown
Substrate
Details
SorafenibCytochrome P450 3A4ProteinHumans
Unknown
Substrate
Inhibitor
Details
SorafenibUDP-glucuronosyltransferase 1A9ProteinHumans
Unknown
Substrate
Inhibitor
Details