Examples of using P-gp in English and their translations into German
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Medicine
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Colloquial
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Official
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Ecclesiastic
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Financial
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Ecclesiastic
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Political
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Computer
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Programming
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Official/political
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Political
P-gp interactions.
P-gp substrates or weak inhibitors.
Ketoconazole is a potent inhibitor of CYP3A4 and P-gp.
Mechanism: P-gp inhibition by dasabuvir.
Caution required with concomitant use P-gp interactions.
Coadministration of lurasidone with P-gp and BCRP inhibitors may increase exposure to lurasidone.
In vitro studiessuggest that crizotinib is a substrate for P-glycoprotein P-gp.
Empagliflozin does not inhibit P-gp at therapeutic doses.
Inhibitors of P-gp may decrease the efflux of sirolimus from intestinal cells and increase sirolimus levels.
Therefore, apixaban does not inhibit P-gp mediated substrate transport.
Dronedarone can increase exposure of statins that are substrates of CYP 3A4 and/or P-gp substrates.
Therefore, concomitant treatment with other P-gp substrates could lead to enhanced toxicity.
The increased aliskiren exposure in juvenile rats appears tobe attributed mainly to lack of maturation of P-gp in the gastrointestinal tract.
In vitro: Cysteamine bitartrate is a substrate of P-gp and OCT2, but not a substrate of BCRP, OATP1B1, OATP1B3, OAT1, OAT3 and OCT1.
Medicinal products affected by ivacaftor: CYP3A, P-gp or CYP2C9 substrates.
Co-administration of pazopanib with a CYP3A4, P-gp, and BCRP inhibitor, such as lapatinib, will result in an increase in plasma pazopanib concentrations.
Clinically significant PK interactions between vismodegib and P-gp inhibitors are not expected.
Clarithromycin(a potent inhibitor of CYP3A4 and P-gp) did not have a clinically meaningful effect on the pharmacokinetics of laropiprant.
Based on in vitro data,ceritinib is predicted to inhibit intestinal P-gp and BCRP at clinically relevant concentrations.
Ketoconazole HRA is also a potent inhibitor of P-gp: inhibition of P-gp by Ketoconazole HRA can increase patients' exposure to medicinal products which are P-gp substrates see section 4.5.
Active substances strongly inhibiting only one of the rivaroxaban elimination pathways, either CYP3A4 or P-gp, are expected to increase rivaroxaban plasma concentrations to a lesser extent.
Concomitant administration of potent inducers of P-gp, glucuronidation, CYP3A4(e.g. rifampicin, rifabutin, carbamazepine, phenytoin or St John's Wort[hypericin]) should be avoided when possible see section 4.5.
Clarithromycin(500 mg twice a day),for instance, considered as a strong CYP3A4 inhibitor and moderate P-gp inhibitor, led to a 1.5 fold increase in mean rivaroxaban AUC and a 1.4 fold increase in Cmax.
Sonidegib did not inhibit apical efflux transporters, P-gp or MRP2, hepatic uptake transporters OATP1B1 or OATP1B3, renal organic anion uptake transporters OAT1 and OAT3, or the organic cation uptake transporters OCT1 or OCT2 at clinically relevant concentrations.
Coadministration of apixaban with ketoconazole(400 mg once a day),a strong inhibitor of both CYP3A4 and P-gp, led to a 2-fold increase in mean apixaban AUC and a 1.6-fold increase in mean apixaban Cmax.
Co-administration of Sovaldi with medicinal products that inhibit P-gp and/or BCRP may increase sofosbuvir plasma concentration without increasing GS-331007 plasma concentration, thus Sovaldi may be co-administered with P-gp and/or BCRP inhibitors.
The inhibitory effect of ritonavir(with or without other protease inhibitors) on P-gp activity may decrease over time eg digoxin and fexofenadine-see table“Ritonavir effects on non-antiretroviral drugs” below.
Ranolazine is a moderate to potent inhibitor of P-gp and a mild inhibitor of CYP3A4, and may increase plasma concentrations of P-gp or CYP3A4 substrates.
Clinically significant medicinal product interactions with Epclusa mediated by P-gp, BCRP, OATP, or CYP450 inhibitors are not expected; Epclusa may be co-administered with P-gp, BCRP, OATP and CYP inhibitors.