Examples of using In vitro data indicate in English and their translations into Slovak
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Medicine
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In vitro data indicate that ruxolitinib may inhibit P-gp and BCRP.
In vitro data indicate that the following species are not susceptible to ceftaroline.
In vitro data indicate cobimetinib is not an inhibitor of OAT1, OAT3 or OCT2.
In vitro data indicate that sacubitril inhibits OATP1B1 and OATP1B3 transporters.
In vitro data indicate that enzalutamide may be an inhibitor of the efflux transporter P-gp.
In vitro data indicate that the following species are not susceptible to ceftolozane/tazobactam.
In vitro data indicate that gefitinib is a substrate for the membrane transport protein Pgp.
In vitro data indicate that repaglinide is metabolised predominantly by CYP2C8, but also by CYP3A4.
In vitro data indicate a potential risk for interaction with CYP2C8 substrates, such as glitazones.
In vitro data indicate that selexipag could be an inducer of both CYP3A4 and CYP2C9 in the intestine.
In vitro data indicate that CYP2D6 and CYP3A4 contribute to the limited metabolism of alogliptin.
In vitro data indicate that the MMAE metabolism that occurs is primarily via oxidation by CYP3A4/5.
In vitro data indicate that repaglinide is metabolised predominantly by CYP2C8, but also by CYP3A4.
In vitro data indicate that ulipristal acetate and its active metabolite are not P-gp(ABCB1) substrates.
In vitro data indicate that this is predominantly mediated by the cytochrome P450 3A4 isoform(CYP3A4).
In vitro data indicate that eribulin is a mild inhibitor of the important drug metabolising enzyme CYP3A4.
In vitro data indicate that this is predominantly mediated by CYP3A4, and to a small extent by CYP1A2 and CYP2A6.
In vitro data indicate that IL-5 and reslizumab are unlikely to affect CYP1A2, 3A4 or 2B6 activity.
In vitro data indicate that ulipristal acetate may be an inhibitor of P-gp at clinically relevant concentrations.
In vitro data indicate that silodosin does not have the potential to inhibit or induce cytochrome P450 enzyme systems.
In vitro data indicate that ketoconazole is an inhibitor of CYP1A2 and does not significantly inhibit CYP 2A6 and 2E1.
In vitro data indicate that ledipasvir may be a weak inducer of metabolising enzymes such as CYP3A4, CYP2C and UGT1A1.
In vitro data indicate that CYP3A4 and CYP2D6 are the major P450 isozyme involvedin the oxidative metabolism of gefitinib.
In vitro data indicate that regorafenib is metabolized by cytochrome CYP3A4 and uridine diphosphate glucuronosyl transferase UGT1A9.
In vitro data indicate that ulipristal acetate may be an inhibitor of BCRP(Breast Cancer Resistance Protein) transporters at the intestinal level.
In vitro data indicate that enzalutamide is not a substrate for OATP1B1, OATP1B3, or OCT1; and N-desmethyl enzalutamide is not a substrate for P-gp or BCRP.
In vitro data indicate that ulipristal acetate may be an inhibitor of P-gp at clinically relevant concentrations in the gastrointestinal wall during absorption.
In vitro data indicate that enzalutamide and its major metabolites do not inhibit the following transporters at clinically relevant concentrations: OATP1B1, OATP1B3, OCT2, or OAT1.
In vitro data indicate that neither tazobactam nor the tazobactam metabolite M1 inhibit P-gp, BCRP, OATP1B1, OATP1B3, OCT1, OCT2, or BSEP transporters at therapeutic plasma concentrations.
In vitro data indicate that ceftolozane did not inhibit P-gp, BCRP, OATP1B1, OATP1B3, OCT1, OCT2, MRP, BSEP, OAT1, OAT3, MATE1, or MATE2-K in vitro at therapeutic plasma concentrations.