Примери за използване на Did not inhibit на Английски и техните преводи на Български
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DM1 did not inhibit major CYP450 enzymes in vitro.
In-vitro studies showed that delamanid did not inhibit CYP450 isozymes.
Venlafaxine did not inhibit CYP1A2, CYP2C9, or CYP3A4.
In vitro studies indicated that trifluridine, tipiracil hydrochloride and 5-[trifluoromethyl]uracil(FTY) did not inhibit the activity of human cytochrome P450(CYP) isoforms.
Emtricitabine did not inhibit the enzyme responsible for glucuronidation.
In vitro studies indicated that trifluridine, tipiracil hydrochloride andFTY(inactive metabolite of trifluridine) did not inhibit the CYP isoforms tested(CYP1A2, CYP2A6, CYP2B6, CYP2C8, CYP2C9, CYP2C19, CYP2D6, CYP2E1 and CYP3A4/5).
Ribociclib did not inhibit OAT1, OAT3 or MRP2 at clinically relevant concentrations in vitro.
In human liver microsomes,abacavir did not inhibit cytochrome P450 isoforms.
Emtricitabine did not inhibit the glucuronidation reaction of a non-specific UGT substrate in vitro.
In human liver cytosol, lenvatinib did not inhibit aldehyde oxidase activity.
Prasugrel did not inhibit CYP2C9, as it did not affect the pharmacokinetics of S-warfarin.
Ertugliflozin and ertugliflozin glucuronides did not inhibit the activity of UGTs 1A6, 1A9 or 2B7 in vitro.
Alectinib did not inhibit OATP1B1/OATP1B3, OAT1, OAT3 or OCT2 at clinically relevant concentrations in vitro.
Nintedanib, BIBF 1202, andBIBF 1202 glucuronide did not inhibit or induce CYP enzymes in preclinical studies.
Emtricitabine did not inhibit in vitro drug metabolism mediated by the following human CYP450 isoenzymes.
Influence of enfuvirtide on metabolism of concomitant medicinal products: In an in-vivo human metabolism study enfuvirtide,at the recommended dose of 90 mg twice daily, did not inhibit the metabolism of substrates by CYP3A4(dapsone), CYP2D6(debrisoquine), CYP1A2(caffeine), CYP2C19(mephenytoin), and CYP2E1(chlorzoxazone).
In vitro, midostaurin did not inhibit hERG channel activity up to the limit of solubility of 12 µM.
Etoricoxib did not inhibit gastric prostaglandin synthesis and had no effect on platelet function.
In vitro, ospemifene and 4-hydroxyospemifene did not inhibit or induce the activity of CYP450 enzymes at clinically relevant concentrations.
Cabazitaxel did not inhibit in vitro the major biotransformation pathway of warfarin into 7-hydroxywarfarin, which is mediated by CYP2C9.
Medicinal products metabolised by CYP2C9:prasugrel did not inhibit CYP2C9, as it did not affect the pharmacokinetics of S-warfarin.
Memantine did not inhibit CYP 1A2, 2A6, 2C9, 2D6, 2E1, 3A, flavin containing monooxygenase, epoxide hydrolase or sulphation in vitro.
In in vitro studies, ertugliflozin andertugliflozin glucuronides did not inhibit or inactivate CYPs 1A2, 2C9, 2C19, 2C8, 2B6, 2D6, or 3A4, and did not induce CYPs 1A2, 2B6, or 3A4.
Parmodulin 2 did not inhibit the activity of factor V or factor X, proteins that function in blood coagulation.
At relevant clinical concentrations, eribulin did not inhibit BCRP, OCT1, OCT2, OAT1, OAT3, OATP1B1 and OATP1B3 transporter-mediated activity.
Prucalopride did not inhibit specific CYP450 activities in in vitro studies in human liver microsomes at therapeutically relevant concentrations.
In an in-vivo human metabolism study enfuvirtide,at the recommended dose of 90 mg twice daily, did not inhibit the metabolism of substrates by CYP3A4(dapsone), CYP2D6(debrisoquine), CYP1A2(caffeine), CYP2C19(mephenytoin), and CYP2E1(chlorzoxazone).
Also, emtricitabine did not inhibit uridine 5'-diphosphoglucuronyl transferase, the enzyme responsible for glucuronidation.
In vitro studies demonstrated that ceftolozane, tazobactam andthe M1 metabolite of tazobactam did not inhibit CYP1A2, CYP2B6, CYP2C8, CYP2C9, CYP2C19, CYP2D6, or CYP3A4 and did not induce CYP1A2, CYP2B6, or CYP3A4 at therapeutic plasma concentrations.
In vitro cabazitaxel did not inhibit Multidrug-Resistant Proteins(MRP): MRP1 and MRP2 or Organic Cation Transporter(OCT1).