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- W2195976321 abstract "The low bioavailability of the anti‐migraine drug sumatriptan is partially caused by first‐pass hepatic metabolism. In this study, we analyzed the impact of the hepatic organic cation transporter OCT1 on sumatriptan cellular uptake, and of OCT1 polymorphisms on sumatriptan pharmacokinetics. OCT1 transported sumatriptan with high capacity and sumatriptan uptake into human hepatocytes was strongly inhibited by the OCT1 inhibitor MPP + . Sumatriptan uptake was not affected by the Met420del polymorphism, but was strongly reduced by Arg61Cys and Gly401Ser, and completely abolished by Gly465Arg and Cys88Arg. Plasma concentrations in humans with two deficient OCT1 alleles were 215% of those with fully active OCT1 ( P = 0.0003). OCT1 also transported naratriptan, rizatriptan, and zolmitriptan, suggesting a possible impact of OCT1 polymorphisms on the pharmacokinetics of other triptans as well. In conclusion, OCT1 is a high‐capacity transporter of sumatriptan and polymorphisms causing OCT1 deficiency have similar effects on sumatriptan pharmacokinetics as those observed in subjects with liver impairment." @default.
- W2195976321 created "2016-06-24" @default.
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- W2195976321 date "2016-01-12" @default.
- W2195976321 modified "2023-10-09" @default.
- W2195976321 title "OCT1 mediates hepatic uptake of sumatriptan and loss-of-function<i>OCT1</i>polymorphisms affect sumatriptan pharmacokinetics" @default.
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- W2195976321 doi "https://doi.org/10.1002/cpt.317" @default.
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