Examples of using Does not inhibit in English and their translations into Hungarian
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Rimonabant does not inhibit or induce other CYP enzymes or P-glycoprotein(P-gp) in vitro.
In vitro studies demonstrated that vildagliptin does not inhibit/induce CYP 450 enzymes.
Empagliflozin does not inhibit other glucose transporters important for glucose transport into peripheral tissues and is 5000 times more selective for SGLT2 versus SGLT1, the major transporter responsible for glucose absorption in the gut.
Based on in vitro studies, empagliflozin does not inhibit, inactivate, or induce CYP450 isoforms.
Linagliptin is a weak competitive and a weak to moderatemechanism-based inhibitor of CYP isozyme CYP3A4, but does not inhibit other CYP isozymes.
In vitro studies indicated that axitinib does not inhibit CYP2A6, CYP2C9, CYP2C19, CYP2D6, CYP2E1, CYP3A4/5, or UGT1A1 at therapeutic plasma concentrations.
At high caffeine concentrations, however, the activation of the pyramidal cell is so strong thateven the increased buffering effect of interneurons does not inhibit it and the cramps become stronger.
In vitro studies inhuman liver microsomes indicate that tigecycline does not inhibit metabolism mediated by any of the following 6 cytochrome P450(CYP) isoforms.
Dapagliflozin does not inhibit other glucose transporters important for glucose transport into peripheral tissues and is> 1,400 times more selective for SGLT2 versus SGLT1, the major transporter in the gut responsible for glucose absorption.
Raltegravir is not a substrate of cytochrome P450(CYP) enzymes, does not inhibit CYP1A2, CYP2B6, CYP2C8, CYP2C9, CYP2C19, CYP2D6 or CYP3A, and does not induce CYP3A4.
The Commission considers that valuation comparability could be enhanced in order to ensure that such variety, which may be linked togenuine needs in domestic housing markets, does not inhibit cross-border activity on the lending or the funding side.
In vitro studies inhuman liver microsomes indicate that tigecycline does not inhibit metabolism mediated by any of the following 6 cytochrome P450(CYP) isoforms: 1A2, 2C8, 2C9, 2C19, 2D6, and 3A4 by competitive inhibition.
Reporting formats should be succinct and user-friendly so thatthe volume of information that could be generated by this Directive does not inhibit meaningful action on schemes that are being reported.
In vitro metabolism studies suggest that methylnaltrexone bromide does not inhibit the activity of CYP1A2, CYP2E1, CYP2B6, CYP2A6, CYP2C9, CYP2C19 or CYP3A4, while it is a weak inhibitor of the metabolism of a model CYP2D6 substrate.
Consequently, respect for norms which prohibit such acts and oblige"semper et pro semper," that is, without any exception,not only does not inhibit a good intention, but actually represents its basic expression.
Since vildagliptin is not a cytochrome P(CYP) 450 enzyme substrate and does not inhibit or induce CYP 450 enzymes, it is not likely to interact with active substances that are substrates, inhibitors or inducers of these enzymes.
It is unlikely that atosiban is involved in cytochrome P450 mediated drug-drug interactions as in vitro investigations have shown that atosiban isnot a substrate for the cytochrome P450 system, and does not inhibit the drug metabolising cytochrome P450 enzymes.
In vitro studies indicate that alogliptin does not induce CYP1A2,CYP2B6 and CYP2C9 and does not inhibit CYP1A2, CYP2B6, CYP2C8, CYP2C9, CYP2C19, CYP2D6 or CYP3A4 at concentrations achieved with the recommended dose of 25 mg alogliptin.
Regadenoson does not inhibit the metabolism of substrates for CYP1A2, CYP2C8, CYP2C9, CYP2C19, CYP2D6, or CYP3A4 in human liver microsomes, indicating that it is unlikely to alter the pharmacokinetics of medicinal products metabolised by these cytochrome P450 enzymes.
In vitro studies indicate that raltegravir is not a substrate of cytochromeP450(CYP) enzymes, does not inhibit CYP1A2, CYP2B6, CYP2C8, CYP2C9, CYP2C19, CYP2D6 or CYP3A, does not induce CYP3A4 and does not inhibit P-glycoprotein-mediated transport.
Dapagliflozin does not inhibit other glucose transporters important for glucose transport into peripheral tissues and is> 1,400 times more selective for SGLT2 versus SGLT1, the major transporter in the gut responsible for glucose absorption.
The secretory pathway of renal elimination does not appear to include known acidic or basic transport systems involved in the excretion ofother active substances In addition, ibandronic acid does not inhibit the major human hepatic P450 isoenzymes and does not induce the hepatic cytochrome P450 system in rats.
Based on in vitro data, ceritinib does not inhibit apical efflux transporter 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.
Pregabalin is excreted in the urine, mostly unchanged, undergoes minimal human metabolism(less than 2% of thedose is excreted as metabolites in the urine), does not inhibit the metabolism of other drugs in vitro and does not bind to plasma proteins, therefore, it is unlikely to enter in pharmacokinetic interaction.
Ambrisentan does not inhibit or induce phase I or II drug metabolizing enzymes at clinically relevant concentrations in in vitro and in vivo non-clinical studies, suggesting a low potential for ambrisentan to alter the profile of medicinal products metabolized by these pathways.
Since pregabalin is predominantly excreted unchanged in the urine, undergoes negligible metabolism in humans(<2% of a dose recovered in urine as metabolites), does not inhibit drug metabolism in vitro, and is not bound to plasma proteins, it is unlikely to produce, or be subject to, pharmacokinetic interactions.
Dasabuvir does not inhibit organic anion transporter(OAT1) in vivo and is not expected to inhibit organic cation transporters(OCT2), organic anion transporters(OAT3), or multidrug and toxin extrusion proteins(MATE1 and MATE2K) at clinically relevant concentrations; therefore, Exviera does not affect medicinal product transport by these proteins.
Fluconazole, being highly selective for the cytochrome P450 fungi,practically does not inhibit cytochrome P-450 in humans(as compared to itraconazole, clotrimazole, econazole and ketoconazole less suppresses dependent cytochrome P450 oxidative processes in human liver microsome).
Fluconazole, being highly selective for fungal cytochrome P450,practically does not inhibit these enzymes in the human body(in comparison with itraconazole, clotrimazole, econazole and ketoconazole less inhibits cytochrome P450 dependent oxidative processes in human liver microsomes).