期刊
JOURNAL OF VETERINARY PHARMACOLOGY AND THERAPEUTICS
卷 46, 期 1, 页码 1-16出版社
WILEY
DOI: 10.1111/jvp.13102
关键词
ABCB1; cat; dog; MDR1; P-glycoprotein
This paper reviews important discoveries about P-glycoprotein and discusses how they impact drug selection and dosing in dogs and cats with genetically mediated P-glycoprotein deficiency or P-glycoprotein dysfunction resulting from drug-drug interactions.
In 2001 the molecular genetic basis of so-called ivermectin sensitivity in herding breed dogs was determined to be a P-glycoprotein deficiency caused by a genetic variant of the MDR1 (ABCB1) gene often called the MDR1 mutation. We have learned a great deal about P-glycoprotein's role in drug disposition since that discovery, namely that P-glycoprotein transports many more drugs than just macrocyclic lactones that P-glycoprotein mediated drug transport is present in more places than just the blood brain barrier, that some cats have a genetic variant of MDR1 that results in P-glycoprotein deficiency, that P-glycoprotein dysfunction can occur as a result of drug-drug interactions in any dog or cat, and that the concept of P-glycoprotein inhibitors versus P-glycoprotein substrates is somewhat arbitrary and artificial. This paper will review these discoveries and discuss how they impact drug selection and dosing in dogs and cats with genetically mediated P-glycoprotein deficiency or P-glycoprotein dysfunction resulting from drug-drug interactions.
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