Примери за използване на Efflux transporter на Английски и техните преводи на Български
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Eliglustat is a substrate of the efflux transporter P-gp.
Inhibition of efflux transporters(P-gp, BCRP, BSEP, and MATE1/2) Niraparib is not an inhibitor of BSEP.
Trametinib is an in vitro substrate of the efflux transporter P-gp.
Teriflunomide is a substrate of the efflux transporter BCRP, which could be involved in direct secretion.
In vitro data indicate that enzalutamide may be an inhibitor of the efflux transporter P-gp.
Amiodarone is an inhibitor of the efflux transporter P-glycoprotein and dabigatran etexilate a substrate of this transporter. .
Based on in vitro data, ceritinib is a substrate of the efflux transporter P-glycoprotein(P-gp).
The effects of potent inducers of the efflux transporters BCRP and P-glycoprotein(P-gp) on the bioavailability and disposition of cladribine have not been formally studied.
Enzalutamide is not a substrate of the efflux transporters P-gp or BCRP.
In vitro, olaparib inhibits the efflux transporter P-gp(IC50= 76µM), therefore it cannot be excluded that olaparib may cause clinically relevant drug interactions with substrates of P-gp(e.g. simvastatin, pravastatin, dabigatran, digoxin and colchicine).
In vitro studies have demonstrated that vemurafenib is a substrate of the efflux transporters P-gp and BCRP.
In vitro, olaparib is a substrate of the efflux transporter P-gp, however, this is unlikely to be of clinical significance(see section 4.5).
The non-linear exposure increase<120 mg may be related to saturation of efflux transporters.
In vitro, alectinib and M4 are inhibitors of the efflux transporter Breast Cancer Resistance Protein(BCRP).
Migalastat is not a substrate for MDR1 or BCRP, nor is it an inhibitor of BCRP, MDR1, orBSEP human efflux transporters.
In vitro, olaparib is a substrate of the efflux transporter P-gp, however this is unlikely to be of clinical significance(see section 4.5).
Valsartan Inhibitors of the uptake transporter(rifampicin,ciclosporin) or efflux transporter(ritonavir).
Lurasidone is an in vitro inhibitor of the efflux transporter BCRP and the clinical relevance of intestinal BCRP inhibition cannot be excluded.
Based on in vitro data pasireotide appears to be a substrate of efflux transporter P-gp(P-glycoprotein).
In vitro, olaparib inhibits the efflux transporter P-gp(IC50= 76 µM), therefore it cannot be excluded that olaparib may cause clinically relevant drug interactions with substrates of P-gp(e.g. simvastatin, pravastatin, dabigatran, digoxin and colchicine).
In vitro, alectinib andits major active metabolite M4 are inhibitors of the efflux transporter P-glycoprotein(P-gp).
Based on in vitro data pasireotide is not a substrate of the efflux transporter BCRP(breast cancer resistance protein) nor of the influx transporters OCT1(organic cation transporter 1), OATP(organic anion-transporting polypeptide) 1B1, 1B3 or 2B1.
Co-administration with medicinal products that are BCRP inhibitors In vitro,sunitinib is a substrate of the efflux transporter BCRP.
An increase in plasma concentrations of substrates of the P-gp efflux transporter, such as digoxin or dabigatran, should be anticipated(see table 2).
Edoxaban is a substrate for the efflux transporter P-glycoprotein(P-gp), but not a substrate for uptake transporters such as organic anion transporter polypeptide OATP1B1, organic anion transporters OAT1 or OAT3 or organic cation transporter OCT2.
Therefore, a clinically meaningful interaction related to an inhibition of these efflux transporters although unlikely, cannot be excluded.
However, in vitro tafamidis meglumine inhibits the efflux transporter BCRP(breast cancer resistant protein) with IC50=1.16 µM and may cause drug-drug interactions at clinically relevant concentrations with substrates of this transporter(e.g. methotrexate, rosuvastatin, imatinib).
Based on in vivo studies,brexpiprazole is neither a substrate nor an inhibitor of efflux transporters, such as Multi Drug Resistance(MDR) 1(P-gp) and BCRP.
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.
Neither trifluridine nor tipiracil hydrochloride was an inhibitor of orsubstrate for human uptake and efflux transporters based on in vitro studies, except for OCT2 and MATE1.