natgillin/translations-raw huggingface dataset:
In vitro studies indicate that lenalidomide is not a substrate of human breast cancer resistance protein (BCRP), multidrug resistance protein (MRP) transporters MRP1, MRP2, or MRP3, organic anion transporters (OAT) OAT1 and OAT3, organic anion transporting polypeptide 1B1 (OATP1B1), organic cation transporters (OCT) OCT1 and OCT2, multidrug and toxin extrusion protein (MATE) MATE1, and organic cation transporters novel (OCTN) OCTN1 and OCTN2.
In vitro ispitivanja pokazuju da lenalidomid nije supstrat humanog proteina otpornosti na rak dojke (BCRP, od engl. breast cancer resistance protein), transportera proteina otpornosti na više lijekova (MRP, od engl. multidrug resistance protein) MRP1, MRP2 ili MRP3, transportera organskog aniona (OAT, od engl. organic anion transporter) OAT1 i OAT3, polipeptidnog transportera organskog aniona 1B1 (OATP1B1, od engl. organic anion transporting polypeptide 1B1), transportera organskog kationa (OCT, od engl. organic cation transporter) OCT1 i OCT2, proteina za ekstruziju više lijekova i toksina (MATE, od engl. multidrug and toxin extrusion) MATE1 i novih transportera organskog kationa (OCTN, od engl. organic cation transporters novel) OCTN1 i OCTN2.
In vitro studies indicate that osimertinib is metabolized predominantly by CYP3A4, and CYP3A5.
In vitro ispitivanja ukazuju da se osimertinib pretežno metabolizira putem CYP3A4 i CYP3A5.
In vitro studies indicate that pitolisant is neither a substrate nor an inhibitor of human P-glycoprotein and breast cancer resistance protein (BCRP).
In vitro ispitivanja ukazuju da pitolizant nije ni supstrat ni inhibitor ljudskog P-glikoproteina i proteina rezistencije na karcinom dojke (engl. breast cancer resistance protein, BCRP).
In vitro studies indicate that raltegravir is not a substrate of cytochrome P450 (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.
Istraživanja in vitro pokazuju da raltegravir nije supstrat enzima citokroma P450 (CYP), ne inhibira CYP1A2, CYP2B6, CYP2C8, CYP2C9, CYP2C19, CYP2D6 ili CYP3A, ne inducira CYP3A4 niti inhibira transport posredovan P-glikoproteinom.
In vitro studies indicate that the active metabolites M-2 and M-5 are substrates for P-glycoprotein and BCRP.
In vitro ispitivanja pokazuju da su djelatni metaboliti M-2 i M-5 supstrati P-glikoproteina i BCRP-a.
In vitro studies indicate that the enzymes CYP1A2, 2B6, and 2C9 are not induced and that CYP1A1, 1A2, 2A6, 2B6, 2C8, 2C9, 2D6, and 2E1 are not inhibited by lacosamide at plasma concentrations observed in clinical trials.
Ispitivanja in vitro ukazuju da enzimi CYP1A2, 2B6 i 2C9 nisu inducirani te da CYP1A1, 1A2, 2A6, 2B6, 2C8, 2C9, 2D6 i 2E1 nisu inhibirani lakozamidom pri koncentracijama u plazmi dosegnutim tijekom kliničkih istraživanja.
In vitro studies indicate that tolvaptan is a substrate and competitive inhibitor of P-glycoprotein (P-gp)
In vitro ispitivanja pokazuju da je tolvaptan supstrat i kompetitivni inhibitor P-glikoproteina (P-gp).
In vitro studies indicate that tolvaptan or its oxobutyric metabolite may have the potential to inhibit OATP1B1, OATP1B3, OAT3, BCRP and OCT1 transporters.
In vitro ispitivanja pokazuju da tolvaptan ili njegov oksobutiratni metabolit imaju potencijal za inhibiciju prijenosnika OATP1B1, OATP1B3, OAT3, BCRP i OCT1.
In vitro studies indicate that zidovudine-resistant virus isolates can become zidovudine sensitive when they simultaneously acquire resistance to lamivudine.
Ispitivanja in vitro pokazuju da zidovudin–rezistentni izolati virusa mogu postati osjetljivi na zidovudin istodobno kad postanu rezistentni na lamivudin.
In vitro studies indicated that axitinib does not inhibit CYP2A6, CYP2C9, CYP2C19, CYP2D6, CYP2E1, CYP3A4/5, or UGT1A1 at therapeutic plasma concentrations.
Ispitivanja in vitro pokazala su da u terapijskim koncentracijama u plazmi aksitinib ne inhibira CYP2A6, CYP2C9, CYP2C19, CYP2D6, CYP2E1, CYP3A4/5 ni UGT1A1.
In vitro studies indicated that CYP2D6 (aromatic hydroxylation), CYP1A2 (chain oxidation) and to a less extent CYP2C19 were involved in propranolol metabolism.
In vitro studije pokazuju da su CYP2D6 (aromatična hidroksilacija), CYP1A2 (lančana oksidacija) i u manjoj mjeri CYP2C19 uključeni u metabolizam propranolola.
In vitro studies indicated that ibrutinib is not a substrate of P-gp, nor other major transporters, except OCT2.
In vitro ispitivanja su pokazala da ibrutinib nije supstrat P-gp-a, niti drugih glavnih prijenosnika, osim OCT2.
In vitro studies indicated that ivacaftor has the potential to inhibit CYP2C9.
In vitro ispitivanja pokazala su da ivakaftor može inhibirati CYP2C9.
In vitro studies indicated that the primary enzyme responsible for the limited metabolism of sitagliptin is CYP3A4, with contribution from CYP2C8.
Istraživanja in vitro ukazuju na to da je za ograničeni metabolizam sitagliptina primarno odgovoran CYP3A4, a pridonosi mu i CYP2C8.
In vitro studies indicated that the primary enzyme responsible for the limited metabolism of sitagliptin is CYP3A4, with contribution from CYP2C8.
Istraživanja in vitro ukazuju na to da je za ograničeni metabolizam sitagliptina primarno odgovoran enzim CYP3A4, a pridonosi mu i CYP2C8.
In vitro studies indicated that the primary enzyme responsible for the limited metabolism of sitagliptin was CYP3A4, with contribution from CYP2C8.
Istraživanja in vitro ukazuju na to da je za ograničeni metabolizam sitagliptina primarno odgovoran CYP3A4, uz doprinos CYP2C8.
In vitro studies indicated that the primary enzyme responsible for the limited metabolism of sitagliptin was CYP3A4, with contribution from CYP2C8.
Istraživanja in vitro ukazuju na to da je za ograničeni metabolizam sitagliptina primarno odgovoran enzim CYP3A4, uz doprinos CYP2C8.
In vitro studies of CYP and UGT inhibition and induction
In vitro ispitivanja inhibicije i indukcije CYP i UGT
In vitro studies of human megakaryocytopoiesis established that anagrelide’s inhibitory actions on platelet formation in man are mediated via retardation of maturation of megakaryocytes, and reducing their size and ploidy.
Ispitivanjem ljudske megakariocitopoeze in vitro ustanovljeno je da su inhibicijska djelovanja anagrelida na stvaranje trombocita u čovjeka posredovana usporavanjem sazrijevanja megakariocita i smanjenjem njihove veličine i ploidnosti.
In vitro studies show that cobimetinib is not a substrate of the liver uptake transporters OATP1B1, OATP1B3 and OCT1, however, it weakly inhibits these transporters.
Ispitivanja in vitro pokazala su da kobimetinib nije supstrat jetrenih prijenosnika za unos tvari OATP1B1, OATP1B3 i OCT1, ali blago inhibira te prijenosnike.
In vitro studies show that levetiracetam affects intraneuronal Ca2+ levels by partial inhibition of N- type Ca2+ currents and by reducing the release of Ca2+ from intraneuronal stores.
Studije in vitro pokazuju da levetiracetam utječe na razinu Ca2+ u neuronima na način da djelomično inhibira N-tip protoka Ca2+ i smanjuje otpuštanje Ca2+ iz skladišta u neuronima.
In vitro studies show that levetiracetam affects intraneuronal Ca2+ levels by partial inhibition of N-type Ca2+ currents and by reducing the release of Ca2+ from intraneuronal stores.
Studije in vitro pokazuju da levetiracetam utječe na razinu Ca2+ u neuronima na način da djelomično inhibira N tip protoka Ca2+ i smanjuje otpuštanje Ca2+ iz skladišta u neuronima.
In vitro studies show that levetiracetam affects intraneuronal Ca2+ levels by partial inhibition of N-type Ca2+ currents and by reducing the release of Ca2+ from intraneuronal stores.
Studije in vitro pokazuju da levetiracetam utječe na razinu Ca2+ u neuronima na način da djelomično inhibira N-tip protoka Ca2+ i smanjuje otpuštanje Ca2+ iz skladišta u neuronima.
In vitro studies show that nateglinide is extensively bound (97–99%) to serum proteins, mainly serum albumin and to a lesser extent alpha1-acid glycoprotein.
In vitro ispitivanja pokazuju da se nateglinid veže u visokom postotku (97-99%) za serumske proteine, uglavnom serumski albumin i u manjoj mjeri alfa1-kiseli glikoprotein.
In vitro studies show that ombitasvir, paritaprevir, and ritonavir are not inhibitors of organic cation transporters (OCT2), organic anion transporters (OAT3), or multidrug and toxin extrusion proteins (MATE1 and MATE2K) at clinically relevant concentrations.
In vitro ispitivanjima dokazano je da ombitasvir, paritaprevir i ritonavir nisu inhibitori prijenosnika organskih kationa (OCT2), prijenosnika organskih aniona (OAT3) niti proteina za izlučivanje više lijekova i toksina (MATE1 i MATE2K) pri klinički značajnim koncentracijama.
In vitro studies showed that rasagiline at a concentration of 1 µg/ml (equivalent to a level that is 160 times the average Cmax ~ 5.9-8.5 ng/ml in Parkinson’s disease patients after 1 mg rasagiline multiple dosing), did not inhibit cytochrome P450 isoenzymes, CYP1A2, CYP2A6, CYP2C9, CYP2C19, CYP2D6, CYP2E1, CYP3A4 and CYP4A.
Ispitivanja in vitro su pokazala da razagilin u koncentraciji od 1 µg/ml (istovjetno razini koja je 160 puta veća od prosječne Cmax ~ 5,9-8,5 ng/ml u bolesnika s Parkinsonovom bolešću nakon višekratnog doziranja 1 mg razagilina) nije inhibirao izoenzime citokroma P450, CYP1A2, CYP2A6, CYP2C9, CYP2C19, CYP2D6, CYP2El, CYP3A4 i CYP4A.
In vitro studies showed that telavancin retained full activity in the presence of pulmonary surfactant.
In vitro ispitivanja su pokazala da je telavancin zadržao punu aktivnost u prisutnosti plućnog surfaktanta.
In vitro studies showed that vinflunine had neither inducing effects on CYP1A2, CYP2B6 or CYP3A4 activity nor inhibition effects on CYP1A2, CYP2B6, CYP2C8, CYP2C9, CYP2C19, CYP2D6 and CYP3A4.
Ispitivanja in vitro pokazala su da vinflunin nema indukcijski učinak na aktivnost CYP1A2, CYP2B6 ili CYP3A4 ni inhibicijski učinak na CYP1A2, CYP2B6, CYP2C8, CYP2C9, CYP2C19, CYP2D6 i CYP3A4.
In vitro studies suggest that, similarly to other NSAIDs, ibuprofen is highly bound to plasma albumin, although this seems to be significantly lower (95 %) compared with adult plasma (99 %).
ln vitro ispitivanja nagoviještaju da je, slično kao i ostali NSAIL, ibuprofen u visokoj mjeri vezan za albumin u plazmi, iako se čini da je to znatno manje (95 %) u usporedbi s vezanjem u plazmi odraslih (99 %).
In vitro studies suggested that stiripentol phase 1 metabolism is catalyzed by CYP1A2, CYP2C19 and CYP3A4 and possibly other enzymes.
Ispitivanja in vitro nagovještavaju da je faza 1 metabolizma stiripentola katalizirana pomoću enzima CYP1A2, CYP2C19 i CYP3A4, a moguće i drugim enzimima.
In vitro studies suggested that the primary route of metabolism of empagliflozin in humans is glucuronidation by the uridine
In vitro ispitivanja ukazuju da je primarni put metabolizma empagliflozina u ljudi glukuronidacija pomoću uridin
In vitro studies suggested that the primary route of metabolism of empagliflozin in humans is glucuronidation by the uridine 5'-diphospho-glucuronosyltransferases UGT2B7, UGT1A3, UGT1A8, and UGT1A9.
In vitro ispitivanja ukazuju da je primarni put metabolizma empagliflozina u ljudi glukuronidacija pomoću uridin 5’-difosfoglukuronoziltransferaza UGT2B7, UGT1A3, UGT1A8 i UGT1A9.
In vitro studies using human liver microsomes indicate that CYP1A1 is the major enzyme responsible for the 7-hydroxylation of granisetron, whereas CYP3A4 contributes to 9’desmethylation.
In vitro ispitivanja na mikrosomima ljudske jetre pokazala su da je CYP1A1 glavni enzim odgovoran za 7- hidroksilaciju granisetrona, dok CYP3A4 pridonosi 9’desmetilaciji.
In vitro studies using human liver microsomes indicate that ranolazine is metabolised primarily by CYP3A4, but also by CYP2D6.
In vitro istraživanja uz korištenje humanih jetrenih mikrosoma upućuju na to da se ranolazin metabolizira prvenstveno putem CYP3A4, ali i putem CYP2D6.
In vitro studies using human liver microsomes show no or little (<25%) inhibition of cytochrome P450 isozymes 1A2, 2A6, 2B6, 2C8, 2C9, 2C19, 2D6, 2E1 or 3A4 at zonisamide levels approximately two- fold or greater than clinically relevant unbound serum concentrations.
Ispitivanja in vitro na mikrosomima ljudske jetre ne pokazuju ili pokazuju malu inhibiciju (< 25%) izoenzima 1A2, 2A6, 2B6, 2C8, 2C9, 2C19, 2D6, 2E1 ili 3A4 citokroma P450 pri koncentracijama zonisamida koje su bile približno dva ili više puta veće od klinički značajnih koncentracija slobodnog zonisamida u serumu.
In vitro studies using human liver microsomes showed little or no potential for retigabine to inhibit the major cytochrome P450 isoenzymes (including CYP1A2, CYP2A6, CYP2C8, CYP2C9, CYP2C19, CYP2D6, CYP2E1 and CYP3A4/5).
Ispitivanja in vitro u kojima su se koristili ljudski mikrosomi jetre pokazala su mali ili nikakav potencijal retigabina za inhibiranje glavnih citokrom P450 izoenzima (uključujući CYP1A2, CYP2A6, CYP2C8, CYP2C9, CYP2C19, CYP2D6, CYP2E1 i CYP3A4/5).
In vitro studies using human microsomes indicate that granisetron neither stimulates nor inhibits the cytochrome P450 enzyme system.
In vitro ispitivanja na ljudskim mikrosomima pokazuju da granisetron ne stimulira niti inhibira enzimski sustav citokroma P450.
In vitro studies with cultured human hepatocytes demonstrated that IL-6 caused a reduction in CYP1A2, CYP2C9, CYP2C19, and CYP3A4 enzyme expression.
U in vitro ispitivanjima na kulturi humanih hepatocita IL-6 je prouzročio smanjenje ekspresije enzima CYP1A2, CYP2C9, CYP2C19, i CYP3A4.
In vitro studies with human platelets indicate that vardenafil has no antiaggregatory effect on its own, but at high (super-therapeutic) concentrations, vardenafil potentiates the antiaggregatory effect of the nitric oxide donor sodium nitroprusside.
In vitro ispitivanja na ljudskim trombocitima pokazuju da vardenafil sam po sebi nema antiagregacijski učinak, ali u visokim (višim od terapijskih) koncentracijama pojačava antiagregacijski učinak natrijevog nitroprusida, koji je donor dušikovog oksida.
In vitro studies with tafamidis meglumine suggest that it is unlikely tafamidis meglumine will cause drug interactions at clinically relevant concentrations with substrates of UDP glucuronosyltransferase (UGT), P-gp transporters, or organic anion-transporting polypeptide transporters (OATP1B1 and 1B3).
In vitro ispitivanja s tafamidismegluminom ukazuju da nije vjerojatno da će tafamidismeglumin uzrokovati interakcije lijekova pri klinički značajnim koncentracijama sa supstratima UDP- glukuronoziltransferaze (UGT), transportera P-glikoproteina ili polipeptidnih transportera organskih aniona (OATP1B1 i 1B3).
In vitro studies, examining more than 60 cell lines, demonstrated that the median cytarabine concentration resulting in 50% growth inhibition (IC50) was approximately 10 M (2.4 g/ml) for two days of exposure and 0.1 M (0.024 g/ml) for 6 days of exposure.
Ispitivanja in vitro na više od 60 staničnih linija, pokazala su da medijan koncentracije citarabina koji izaziva inhibiciju rasta od 50% (IC50) iznosi oko 10 M (2,4 g/ml) za dva dana ekspozicije i 0,1 M (0,024 g/ml) za 6 dana ekspozicije.
In vitro transport studies showed that sitagliptin is a substrate for p-glycoprotein and organic anion transporter-3 (OAT3).
Istraživanja transporta in vitro pokazala su da je sitagliptin supstrat p-glikoproteina i organskog anionskog transportera 3 (OAT3).
In vitro transport studies showed that sitagliptin is a substrate for p-glycoprotein and organic anion transporter-3 (OAT3).
Istraživanja transporta in vitro pokazala su da je sitagliptin supstrat p-glikoproteina i organskog anionskog transportera3 (OAT3).
In vitro, ambrisentan has no inhibitory effect on human transporters at clinically relevant concentrations, including the P-glycoprotein (Pgp), breast cancer resistance protein (BCRP), multi- drug resistance related protein 2 (MRP2), bile salt export pump (BSEP), organic anion transporting polypeptides (OATP1B1 and OATP1B3) and the sodium-dependent taurocholate co-transporting polypeptide (NTCP).
In vitro, ambrisentan u klinički značajnim koncentracijama nema inhibitorni učinak na humane prijenosnike, uključujući P-glikoprotein (Pgp), protein koji uzrokuje rezistenciju raka dojke na lijekove (BCRP, engl. breast cancer resistance protein), protein povezan s rezistencijom na više lijekova 2 (MRP2, engl. multi-drug resistance related protein 2), pumpu za izlučivanje žučnih soli (BSEP, engl. bile salt export pump), polipeptide koji transportiraju organske anione (OATP1B1 i OATP1B3, engl. organic anion transporting polypeptide) i o natriju ovisni kotransportni polipeptid za taurokolat (NTCP, engl. sodium-dependent taurocholate co-transporting polypeptide).
In vitro, apremilast is a substrate, and a weak inhibitor of P-glycoprotein (IC50>50µM), however clinically relevant drug interactions mediated via P-gp are not expected to occur.
In vitro, apremilast je supstrat i slabi inhibitor P-glikoproteina (IC50 > 50µM), međutim, ne očekuje se da će doći do klinički važnih interakcija lijekova posredovanih putem P-gp-a.
In vitro, brivaracetam did ot induce CYP1A2.
In vitro, brivaracetam nije induciro CYP1A2.
In vitro, brivaracetam is not a substrate of human P- glycoprotein (P-gp), multidrug resistance proteins (MRP) 1 and 2, and likely not organic anion transporter polypeptide 1B1 (OATP1B1) and OATP1B3.
In vitro, brivaracetam nije supstrat ljudskog P-glikoproteina (P-gp) ni proteina rezistencije na više lijekova (engl. multidrug resistance proteins, MRP) 1 i 2, te vjerojatno ni prijenosnog polipeptida organskih aniona 1B1 (OATP1B1) i OATP1B3.
In vitro, brivaracetam is not a substrate of human P- glycoprotein (P-gp), multidrug resistance proteins (MRP) 1 and 2, and likely not organic anion transporter polypeptide 1B1 (OATP1B1) and OATP1B3.
In vitro, brivaracetam nije supstrat ljudskog P-glikoproteina (P-gp) ni proteina rezistencije na više lijekova (engl. multidrug resistance proteins, MRP) 1 i 2, te vjerovatno ni prijenosnog polipeptida organskih aniona 1B1 (OATP1B1) i OATP1B3.
In vitro, cobimetinib is a moderate inhibitor of BCRP (Breast Cancer Resistance Protein).
In vitro, kobimetinib je umjereni inhibitor proteina koji uzrokuje rezistenciju raka dojke na lijekove (engl. breast cancer resistance protein, BCRP).
In vitro, cobimetinib produced moderate hERG ion channel inhibition (IC50= 0.5 µM [266 ng/mL]), which is approximately 18 fold higher than peak plasma concentrations (Cmax) at the 60 mg to be marketed dose (unbound Cmax=14 ng/mL [0.03 µM]).
In vitro je kobimetinib uzrokovao umjerenu inhibiciju hERG ionskih kanala (IC50 = 0,5 µM [266 ng/ml]), pri koncentraciji koja je približno 18 puta veća od vršnih plazmatskih koncentracija (Cmax) postignutih nakon primjene doze od 60 mg, koja će se nalaziti na tržištu (Cmax nevezanog lijeka = 14 ng/ml
In vitro, CYP3A4 was shown to be the enzyme primarily responsible for the metabolism of olaparib (see section 4.5).
Pokazalo se da je in vitro CYP3A4 glavni enzim odgovoran za metabolizam olapariba (vidjeti dio 4.5).
In vitro, defibrotide has been shown to bind to various sites on vascular endothelium that are involved in cell regulation, providing a stimulus that promotes protection of activated endothelial cells.
Defibrotid se in vitro veže na različita mjesta na vaskularnom endotelu koja sudjeluju u procesima stanične regulacije, stvarajući podražaje koji potiču zaštitu aktiviranih endotelnih stanica.
In vitro, DM1 was a substrate of P-glycoprotein (P-gp).
In vitro je DM1 bio supstrat P-glikoproteina (P-gp).
In vitro, dolutegravir was not a substrate of human OATP 1B1, OATP 1B3 or OCT 1.
In vitro, dolutegravir nije bio supstrat ljudskih prijenosnika OATP 1B1, OATP 1B3 ili OCT 1.
In vitro, dolutegravir was not a substrate of human OATP 1B1, OATP 1B3 or OCT 1.
In vitro, dolutegravir nije bio supstrat za ljudski OATP 1B1, OATP 1B3 ili OCT 1.
In vitro, fondaparinux is highly and specifically bound to antithrombin protein with a dose-dependant plasma concentration binding (98.6% to 97.0% in the concentration range from 0.5 to 2 mg/l).
Fondaparinuks se in vitro, ovisno o koncentraciji odgovarajuće doze u plazmi, u velikoj mjeri i specifično veže za antitrombinski protein (98,6 % do 97,0 % u rasponu koncentracije od 0,5 do 2 mg/l).
In vitro, glucosylceramide synthase is inhibited by miglustat with an IC50 of 20-37 µM. In addition, inhibitory action on a non-lysosomal glycosylceramidase has been demonstrated experimentally in vitro.
In vitro, glukozilceramid sintazu inhibira miglustat sa IC50 koji iznosi 20-37 µM. Osim toga, inhibitorsko djelovanje nelizosomalne glikozilceramidaze eksperimentalno se pokazalo in vitro.
In vitro, idelalisib was an inducer of several enzymes, and a risk for decreased exposure and thereby decreased efficacy of substrates of inducible enzymes such as CYP2C9, CYP2C19, CYP2B6 and UGT cannot be excluded.
In vitro, idelalisib je inducirao nekoliko enzima pa se ne može isključiti rizik od smanjene izloženosti supstratima inducibilnih enzima kao što su CYP2C9, CYP2C19, CYP2B6 i UGT te posljedično tome njihove smanjene djelotvornosti.
In vitro, imatinib inhibits paracetamol O-glucuronidation with Ki value of 58.5 micromol/l.
In vitro, Imatinib inhibira paracetamol O-glukuronidaciju s Ki vrijednostiod
In vitro, imatinib inhibits paracetamol O-glucuronidation with Ki value of 58.5 micromol/l.
In vitro, Imatinib inhibira paracetamol O-glukuronidaciju s Ki vrijednostiod 58,5 mikromol/l.
In vitro, interaction studies to determine the potential inhibitory effects on transporters concluded that there were no clinically relevant effects, except for OAT3.
Ispitivanja interakcija provedena radi utvrđivanja potencijalnih inhibitornih učinaka na prijenosnike zaključila su da nema klinički značajnih učinaka, osim za OAT3.
In vitro, ketoconazole, classified as a strong CYP3A4 and P-glycoprotein (P-gp) inhibitor, has been shown to be a multi-pathway CYP and P-gp/breast cancer resistance protein (BCRP) inhibitor for riociguat metabolism and excretion (see section 5.2).
In vitro se pokazalo da ketokonazol, koji se klasificira kao jaki inhibitor CYP3A4 i P-glikoproteina (P-gp), inhibira metabolizam i izlučivanje riocigvata preko višestrukih puteva CYP i P-gp/proteina za rezistenciju na karcinom dojke (BCRP) (vidjeti dio 5.2).
In vitro, lamivudine inhibited OCT1 and OCT2.
In vitro je lamivudin inhibirao OCT1 i OCT2.
In vitro, levetiracetam and its primary metabolite have been shown not to inhibit the major human liver cytochrome P450 isoforms (CYP3A4, 2A6, 2C9, 2C19, 2D6, 2E1 and 1A2), glucuronyl transferase (UGT1A1 AND UGT1A6) and epoxide hydroxylase activities.
In vitro je pokazano da levetiracetam i njegov glavni metabolit ne inhibiraju aktivnost glavnih izoformi humanog citokroma P450 (CYP3A4, 2A6, 2C9, 2C19, 2D6, 2E1 i 1A2), glukuronil transferaze (UGT1A1 i UGT1A6) ni epoksid hidroksilaze.
In vitro, levetiracetam and its primary metabolite have been shown not to inhibit the major human liver cytochrome P450 isoforms (CYP3A4, 2A6, 2C9, 2C19, 2D6, 2E1 and 1A2), glucuronyl transferase (UGT1A1 AND UGT1A6) and epoxide hydroxylase activities.
In vitro je pokazano da levetiracetam i njegov glavni metabolit ne inhibiraju aktivnost izoformi glavnog humanog citokroma P450 (CYP3A4, 2A6, 2C9, 2C19, 2D6, 2E1 i 1A2), glukuronil transferaze (UGT1A1 i UGT1A6) i epoksid hidroksilaze.
In vitro, levetiracetam and its primary metabolite have been shown not to inhibit the major human liver cytochrome P450 isoforms (CYP3A4, 2A6, 2C9, 2C19, 2D6, 2E1 and 1A2), glucuronyl transferase (UGT1A1 AND UGT1A6]) and epoxide hydroxylase activities.
In vitro je pokazano da levetiracetam i njegov glavni metabolit ne inhibiraju aktivnost izoformi glavnog humanog citokroma P450 (CYP3A4, 2A6, 2C9, 2C19, 2D6, 2E1 i 1A2), glukuronil transferaze (UGT1A1 i UGT1A6) i epoksid hidroksilaze.
In vitro, liraglutide has shown very low potential to be involved in pharmacokinetic interactions with other active substances related to cytochrome P450 and plasma protein binding.
In vitro je liraglutid pokazao vrlo nizak potencijal za farmakokinetičke interakcije s drugim djelatnim tvarima koje se vežu na citokrom P450 i na proteine plazme.