natgillin/translations-raw huggingface dataset:
In vitro studies in rat hepatocytes also showed that ambrisentan did not induce Pgp, BSEP or MRP2 protein expression.
Tudi študije na podganjih jetrnih celicah in vitro so pokazale, da ambrisentan ne inducira ekspresije beljakovin Pgp, BSEP ali MRP2.
In vitro studies indicate that clinical drug-drug interactions are unlikely to occur at therapeutic doses as a result of inhibition by bosutinib on the metabolism of medicinal products that are substrates for CYP1A2, CYP2A6, CYP2C8, CYP2C9, CYP2C19, CYP2D6, or CYP3A4/5.
Študije in vitro so pokazale, da je pri terapevtskih odmerkih majhna verjetnost za medsebojno delovanje z drugimi zdravili, ki bi se pojavilo zaradi zaviranja (ki ga povzroča bosutinib) metabolizma zdravil, ki so substrati CYP1A2, CYP2A6, CYP2C8, CYP2C9, CYP2C19, CYP2D6 ali CYP3A4/5.
In vitro studies indicate that CYP2D6 and CYP3A4 may be minimally involved in paliperidone metabolism, but there are no indications in vitro nor in vivo that these isozymes play a significant role in the metabolism of paliperidone.
In vitro študije kažejo, da izoencima CYP2D6 in CYP3A4 lahko minimalno sodelujeta v presnovi paliperidona, vendar ni nikakršnih znakov in vitro ali in vivo, da bi imela ta dva izoencima pomembno vlogo pri presnovi paliperidona.
In vitro studies indicate that dasatinib is a CYP3A4 substrate.
In vitro študije kažejo, da je dasatinib substrat za CYP3A4.
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.
Študije in vitro kažejo, da lenalidomid ni substrat humanega proteina odpornosti proti raku dojke (BCRP - breast cancer resistant protein), prenašalcev (MRP - multidrug resistance protein) MRP1, MRP2 ali MRP3, prenašalcev organskih anionov (OAT - organic anion transporter) OAT1 in OAT3, polipeptidnega prenašalca organskih anionov 1B1 (OATP1B1 - organic anion transporting polypeptide 1B1), prenašalcev organskih kationov (OCT - organic cation transporters) OCT1 in OCT2, proteina MATE1 (MATE - multidrug and toxin extrusion protein) in prenašalcev organskih kationov (OCTN - organic cation transporters novel) OCTN1 in OCTN2.
In vitro studies indicate that osimertinib is metabolized predominantly by CYP3A4, and CYP3A5.
Študije in vitro kažejo, da se osimertinib presnavlja predvsem s CYP3A4 in CYP3A5.
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.
Študije in vitro kažejo, da raltegravir ni substrat za encime citokroma P450 (CYP), ne zavira CYP1A2, CYP2B6, CYP2C8, CYP2C9, CYP2C19, CYP2D6 ali CYP3A, ne inducira CYP3A4 in ne zavira s
In vitro studies indicate that the active metabolites M-2 and M-5 are substrates for P-glycoprotein and BCRP.
Študije in vitro kažejo, da sta aktivna presnovka M-2 in M-5 substrata glikoproteina P in BCRP.
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.
Študije in vitro kažejo, da lakozamid v plazemskih koncentracijah, izmerjenih v kliničnih preskušanjih, ne inducira encimov CYP1A2, 2B6 in 2C9 ter ne zavira encimov CYP1A1, 1A2, 2A6, 2B6, 2C8, 2C9, 2D6 in 2E1.
In vitro studies indicate that tolvaptan is a substrate and competitive inhibitor of P-glycoprotein (P-gp)
Študije in vitro kažejo, da je tolvaptan substrat in kompetitivni zaviralec 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.
Študije in vitro kažejo, da lahko tolvaptan ali njegov oksobutirni presnovek zavirata OATP1B1, OATP1B3, OAT3, BCRP in OCT1 prenašalce.
In vitro studies indicate that vismodegib has the potential to act as an inhibitor of breast cancer resistance protein (BCRP).
Študije in vitro kažejo, da ima vismodegib zmožnost, da deluje kot zaviralec beljakovine BCRP (breast cancer resistance protein).
In vitro studies indicated that axitinib does not inhibit CYP2A6, CYP2C9, CYP2C19, CYP2D6, CYP2E1, CYP3A4/5, or UGT1A1 at therapeutic plasma concentrations.
In vitro študije so pokazale, da aksitinib v terapevtskih plazemskih koncentracijah ne zavira CYP2A6, CYP2C9, CYP2C19, CYP2D6, CYP2E1, CYP3A4/5 ali UGT1A1.
In vitro studies indicated that axitinib has a potential to inhibit CYP1A2.
In vitro študije so pokazale, da aksitinib lahko zavira CYP1A2.
In vitro studies indicated that axitinib inhibits P-glycoprotein.
In vitro študije so pokazale, da aksitinib zavira P-glikoprotein.
In vitro studies indicated that eluxadoline is a substrate and an inhibitor of the hepatic uptake transporter OATP1B1; a substrate for the hepatic efflux transporter MRP2 and is not a substrate or inhibitor of the P-gp and BCRP transporters.
Študije in vitro so pokazale, da je eluksadolin substrat in zaviralec jetrnega privzemnega prenašalca OATP1B1, substrat jetrnega izločevalnega prenašalca MRP2 in ni substrat ali zaviralec prenašalcev P-gp in BCRP.
In vitro studies indicated that ibrutinib is not a substrate of P-gp, nor other major transporters, except OCT2.
In vitro študije kažejo, da ibrutinib ni substrat P-glikoproteina, niti drugih pomembnih prenašalcev, razen OCT2.
In vitro studies indicated that ivacaftor has the potential to inhibit CYP2C9.
Študije in vitro so pokazale, da ivakaftor lahko zavira CYP2C9.
In vitro studies indicated that lumacaftor has the potential to both inhibit and induce P-gp.
Študije in vitro so pokazale, da ima lumakaftor potencial tako za zaviranje kot za spodbujanje P-gp.
In vitro studies indicated that the primary enzyme responsible for the limited metabolism of sitagliptin was CYP3A4, with contribution from CYP2C8.
Študije in vitro so pokazale, da je primarni encim, odgovoren za omejeno presnovo sitagliptina, CYP3A4, pri presnovi pa sodeluje tudi CYP2C8.
In vitro studies of CYP and UGT inhibition and induction
In vitro študije zaviranja in induciranja CYP in 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.
In vitro študije človeške megakariocitopoeze so pokazale, da se zaviralno delovanje anagrelida na tvorbo krvnih ploščic pri ljudeh odvija prek upočasnitve razvoja megakariocitov ter zmanjšanja njihove velikosti in ploidnosti.
In vitro studies over the opicapone concentration range 0.3 to 30 mcg/mL showed that binding of
Študije in vitro za razpon koncentracij opikapona od 0,3 do 30 µg/ml kažejo, da je vezavnost
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.
In vitro študije so pokazale, da levetiracetam vpliva na nivo Ca2+ znotraj nevrona preko delne inhibicije Ca2+ kanalčkov tipa N in zmanjšanjem sproščanja Ca2+ iz zalog znotraj nevrona.
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.
In vitro študije so pokazale, da levetiracetam vpliva na nivo Ca2+ znotraj nevrona preko delne inhibicije N-tipa Ca2+ kanalov in znižanjem sproščanja Ca2+ iz zalog znotraj nevrona.
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.
Raziskave in vitro kažejo, da se nateglinid v zelo veliki meri (97–99 %) veže na serumske beljakovine, predvsem na serumske albumine in v manjši meri na α1-kisli glikoprotein.
In vitro studies show that perampanel is not a substrate or significant inhibitor of organic anion transporting polypeptides (OATP) 1B1 and 1B3, organic anion transporters (OAT) 1, 2, 3, and 4, organic cation transporters (OCT) 1, 2, and 3, and the efflux transporters P-glycoprotein and Breast Cancer Resistance Protein (BCRP).
Študije in vitro kažejo, da perampanel ni substrat ali pomemben zaviralec organskih anionskih transportnih polipeptidov (OATP) 1B1 in 1B3, organskih anionskih transporterjev (OAT) 1, 2, 3 in 4, organskih kationskih transporterjev (OCT) 1, 2 in 3 in efluksnih transporterjev P-glikoproteina in proteina dovzetnosti za raka dojke (BCRP – Breast Cancer Resistance Protein).
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.
In vitro študije so pokazale, da razagilin v koncentraciji 1 μg/ml (ekvivalent ravni, ki je 160-kratna povprečna Cmax ~ 5,9 – 8,5 ng/ml pri bolnikih s Parkinsonovo boleznijo po zaužitju večkratnih odmerkov 1 mg razagilina) ne inhibira izoencimov citokroma P450: CYP1A2, CYP2A6, CYP2C9, CYP2C19, CYP2D6, CYP2E1, CYP3A4 in CYP4A9.
In vitro studies showed that telavancin retained full activity in the presence of pulmonary surfactant.
In vitro študije so pokazale, da je telavancin zadržal polno aktivnost v prisotnosti pljučnega surfaktanta.
In vitro studies showed that vinflunine is a Pgp-substrate like other vinca alkaloids, but with a lower affinity.
V študijah in vitro so ugotovili, da je vinflunin substrat Pgp, kot drugi alkaloidi rožnatega zimzelena, vendar z manjšo afiniteto.
In vitro studies suggest that CYP3A4 metabolism and glucuronidation are responsible for the metabolism of vemurafenib.
Študije in vitro kažejo, da sta presnova s CYP3A4 in glukuronidacija odgovorni za presnovo vemurafeniba.
In vitro studies suggest that lumacaftor has the potential to induce CYP2B6, CYP2C8, CYP2C9, and CYP2C19; however, inhibition of CYP2C8 and CYP2C9 has also been observed in vitro.
Študije in vitro kažejo, da ima lumakaftor potencial za spodbujanje CYP2B6, CYP2C8, CYP2C9 in CYP2C19; vendar so in vitro opazili tudi inhibicijo CYP2C8 in CYP2C9.
In vitro studies suggest that pazopanib is a substrate for P-gp and BCRP.
In vitro študije kažejo, da je pazopanib substrat za P- glikoprotein (P-gp) in protein, odporen za raka dojke (BCRP - breast cancer resistant protein).
In vitro studies suggested that stiripentol phase 1 metabolism is catalyzed by CYP1A2, CYP2C19 and CYP3A4 and possibly other enzymes.
In vitro študije so nakazale, da so pri 1 fazi stiripentol metabolizma katalizatorji CYP1A2, CYP2C19, CYP3A4 in verjetno drugi encimi.
In vitro studies suggested that the primary route of metabolism of empagliflozin in humans is glucuronidation by the uridine
Študije in vitro so pokazale, da je glavna presnovna pot empagliflozina pri človeku glukuronidacija z uridinom
In vitro studies using human liver microsomes indicate that aprepitant is metabolised primarily by CYP3A4 and potentially with minor contribution by CYP1A2 and CYP2C19.
Študije in vitro s humanimi jetrnimi mikrosomi kažejo, da se aprepitant presnavlja primarno s CYP3A4 in morda z manjšim prispevkom CYP1A2 in CYP2C19.
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.
Raziskave in vitro, v katerih so uporabljali mikrosome človeških jeter, kažejo, da je glavni encim, odgovoren za 7- hidroksilacijo granisetrona, CYP1A1, medtem ko CYP3A4 prispeva k 9’desmetilaciji.
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.
In vitro študije, v katerih so uporabili humane jetrne mikrosome, niso pokazale ali pa so pokazale nizko (<25 %) inhibicijo izoencimov 1A2, 2A6, 2B6, 2C8, 2C9, 2C19, 2D6, 2E1 ali 3A4 citokroma P450 pri koncentracijah zonisamida, ki so bile dvakrat ali večkrat višje od klinično pomembnih serumskih koncentracij nevezane učinkovine.
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).
Študije in vitro z uporabo človeških jetrnih mikrosomov so pokazale, da ima retigabin majhen potencial ali sploh nima potenciala za zavrtje glavnih izoencimov citokroma P450 (vključno s CYP1A2, CYP2A6, CYP2C8, CYP2C9, CYP2C19, CYP2D6, CYP2E1 in CYP3A4/5).
In vitro studies using human microsomes indicate that granisetron neither stimulates nor inhibits the cytochrome P450 enzyme system.
Študije in vitro na človeških mikrosomih kažejo, da granisetron niti ne spodbuja niti ne zavira encimskega sistema citokroma P450.
In vitro studies with amlodipine have shown that approximately 97.5 % of circulating drug is bound to plasma proteins.
Študije amlodipina in vitro so pokazale, da je na beljakovine v plazmi vezanega približno 97,5% zdravila v obtoku.
In vitro studies with cultured human hepatocytes demonstrated that IL-6 caused a reduction in CYP1A2, CYP2C9, CYP2C19, and CYP3A4 enzyme expression.
Študije in vitro na kulturah človeških jetrnih celic so pokazale, da IL-6 zmanjša ekspresijo encimov CYP1A2, CYP2C9, CYP2C19 in CYP3A4.
In vitro studies with human liver microsomes and human cDNA-expressed cytochrome P450 isozymes indicate that bortezomib is primarily oxidatively metabolised via cytochrome P450 enzymes, 3A4, 2C19, and 1A2.
In vitro študije na humanih jetrnih mikrosomih in izocimih citokroma P450 z izraženo človeško cDNA kažejo, da se bortezomib v prvi vrsti oksidativno presnovi z encimi citokroma P450, 3A4, 2C19 in 1A2.
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).
Študije in vitro s tafamidis megluminom kažejo, da je malo verjetno, da bi tafamidis meglumin v klinično pomembnih koncentracijah povzročil medsebojna delovanja s substrati UDP-glukuronil- transferaze (UGT), prenašalcev P-gp ali polipeptidnih prenašalcev organskih anionov (OATP1B1 in 1B3).
In vitro studies with the following active substances did not show any relevant interaction: acetylsalicylic acid, cephalexin, cinacalcet, ciprofloxacin, clopidogrel, enalapril, hydrochlorothiazide, metformin, metoprolol, nifedipine, pioglitazone and quinidine.
Študije in vitro z naslednjimi zdravilnimi učinkovinami niso pokazale pomembnega medsebojnega delovanja: acetilsalicilna kislina, cefaleksin, cinakalcet, ciprofloksacin, klopidogrel, enalapril, hidroklorotiazid, metformin, metoprolol, nifedipin, pioglitazon in kinidin.
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.
In vitro študije, pri katerih so pregledali več kot 60 celičnih linij, so pokazale, da je bila srednja vrednost koncentracije citarabina, ki je povzročila 50-odstotno zaviranje rasti (IC50), po 2 dneh izpostavljanja približno 10 μM (2,4 μg/ml) in po 6 dneh izpostavljanja približno 0,1μ M (0,024 μg/ml).
In vitro study results demonstrate that ingenol mebutate does not inhibit or induce human cytochrome P450 isoforms.
Rezultati študije in vitro so pokazali, da ingenol mebutat ne zavira in ne inducira izoform humanega citokroma P450.
In vitro susceptibility testing has not been standardised and results may vary according to methodological factors.
Testiranje občutljivosti in vitro ni standardizirano in rezultati se lahko razlikujejo glede na metodološke dejavnike.
In vitro the affinity binding of recombinant hLH to the LH/CG receptor on Leydig tumour cells (MA-10) is between that for hCG and that of pituitary hLH, but within the same order of magnitude.
In vitro je afiniteta vezave rekombinantnega hLH na LH/CG receptor na Leydigovih tumorskih celicah (MA-10) med afiniteto hCG-ja in hipofiznega hLH, vendar v istem redu velikosti.
In vitro transporter interaction studies
Študije medsebojnega delovanja s prenašalci in vitro
In vitro, ambrisentan has no inhibitory effect on human transporters at clinically relevant concentrations, including Pgp, BCRP, MRP2, BSEP, OATP1B1, OATP1B3 and NTCP.
In vitro ambrisentan v klinično pomembnih koncentracijah ne zavira človeških prenašalcev, vključno s Pgp, BRCP, MRP2, BSEP, OATP1B1, OATP1B3 in NTCP.
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 v klinično pomembnih koncentracijah ne zavira humanih prenašalcev, vključno s P-glikoproteinom (Pgp), proteinom odpornosti na rak dojke (BRCP), proteinom 2 za odpornost na več zdravil (MRP2), iztočno črpalko žolčnih soli (BSEP), transportnim polipeptidom organskih anionov (OATP1B1 in OATP1B3) in od natrija odvisnim sotransportnim polipeptidom za tavroholat (NTCP).
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 v klinično pomembnih koncentracijah ne zavira človeških prenašalcev, vključno s P-glikoproteinom (Pgp), odpornostnim proteinom raka dojke (BRCP), proteinom 2, povezanim z odpornostjo proti več zdravilom (MRP2), iztočno črpalko žolčnih soli (BSEP), transportnim polipeptidom organskih anionov (OATP1B1 in OATP1B3) in od natrija odvisnim tavroholat sotransportnim polipeptidom (NTCP)..
In vitro, apremilast has little to no inhibitory effect (IC50>10µM) on Organic Anion Transporter (OAT)1 and OAT3, Organic Cation Transporter (OCT)2, Organic Anion Transporting Polypeptide (OATP)1B1 and OATP1B3, or breast cancer resistance protein (BCRP) and is not a substrate for these transporters.
In vitro ima apremilast malo ali nič zaviralnega učinka (IC50>10µM) na prenašalca organskih anionov (OAT)1 in OAT3, prenašalca organskih kationov (OCT)2, polipeptidnega prenašalca organskih anionov (OATP)1B1 in OATP1B3 ali na protein odpornosti proti raku dojke in ni substrat teh prenašalcev.
In vitro, apremilast is not an inhibitor or inducer of cytochrome P450 enzymes.
In vitro apremilast ni zaviralec ali spodbujevalec encimov s citokromom P450.
In vitro, bedaquiline does not significantly inhibit the activity of any of the CYP450 enzymes tested (CYP1A2, CYP2A6, CYP2C8/9/10, CYP2C19, CYP2D6, CYP2E1, CYP3A4, CYP3A4/5 and
In vitro bedakilin niti ne zavira pomembno delovanja nobenega od testiranih encimov CYP450 (CYP1A2, CYP2A6, CYP2C8/9/10, CYP2C19, CYP2D6, CYP2E1, CYP3A4, CYP3A4/5 in CYP4A)
in vitro, binds rapidly and irreversibly to platelet receptors, thus inhibiting platelet aggregation.
In vitro izolirani aktivni tiolski presnovek se hitro in ireverzibilno veže na trombocitne receptorje in tako zavre agregacijo trombocitov.
In vitro, brivaracetam inhibits OAT3 with a half maximal inhibitory concentration 42-fold higher than the Cmax at the highest clinical dose.
Brivaracetam zavira OAT3 s polovico največje zaviralne koncentracije, ki je 42-krat večja kot Cmax pri največjem kliničnem odmerku.
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.
Brivaracetam in vitro ni substrat za človeški P-glikoprotein (P-gp), proteine odporne proti večim učinkovinam 1 in 2 in verjetno ne za organski anionski prenašalni polipeptid 1B1 (OATP1B1) in OATP1B3.
In vitro, brivaracetam was not an inhibitor of the CYP1A2, 2A6, 2B6, 2C8, 2C9, 2D6, 3A4, or the transporters P-gp, BCRP, BSEP MRP2, MATE-K, MATE-1, OATP1B1, OATP1B3, OAT1 and
In vitro, pri klinično pomembnih koncentracijah, brivaracetam ni bil zaviralec CYP1A2, 2A6, 2B6, 2C8, 2C9, 2D6, 3A4 ali prenašalcev P-gp, BCRP, BSEP MRP2, MATE-K, MATE-1, OATP1B1,
In vitro, cobimetinib is a moderate inhibitor of BCRP (Breast Cancer Resistance Protein).
In vitro kobimetinib zmerno zavira BCRP (Breast Cancer Resistance Protein).
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 povzročil zmerno zavrtje ionskih kanalčkov hERG (IC50 0,5 µM [266 ng/ml]); to je približno 18-krat več od največje koncentracije v plazmi (Cmax) med uporabo odmerka 60 mg, ki bo na trgu (nevezani Cmax 14 ng/ml [0,03 µM]).
In vitro, CYP3A4 was shown to be the enzyme primarily responsible for the metabolism of olaparib (see section 4.5).
In vitro je dokazano, da je CYP3A4 encim, ki je predvsem odgovoren za presnovo olapariba (glejte poglavje 4.5).
In vitro, cytochrome P450 3A4 was demonstrated as the predominant (>80%) isoform involved in the P450-mediated metabolism of lenvatinib.
In vitro so pokazali, da je citokrom P450 3A4 prevladujoča (>80 %) izooblika vpletena v presnovo lenvatiniba, ki poteka preko P450.
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.
Pokazali so, da se defibrotid in vitro veže na različna mesta na žilnem endoteliju, ki so vključena v celično regulacijo, kar omogoča dražljaj, ki spodbuja zaščito aktiviranih endotelijskih celic.
In vitro, dolutegravir demonstrated no direct, or weak inhibition (IC50>50 μM) of the enzymes cytochrome P450 (CYP)1A2, CYP2A6, CYP2B6, CYP2C8, CYP2C9, CYP2C19, CYP2D6 CYP3A,
In vitro dolutegravir ni pokazal neposrednega ali šibkega zaviralnega učinka (IC50>50 μM) na encime citokrom P450 (CYP)1A2, CYP2A6, CYP2B6, CYP2C8, CYP2C9, CYP2C19, CYP2D6,
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.
Glukozilceramid-sintazo in vitro zavira miglustat z IC50, ki je 20-37 µM. Poleg tega je bilo zaviralno delovanje na ne-lizosomalni glikozilceramidazi dokazana eksperimentalno 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 je bil idelalizib induktor številnih encimov, tveganja za zmanjšanje izpostavljenosti in s tem manjše učinkovitosti substratov inducibilnih encimov, kot so CYP2C9, CYP2C19, CYP2B6 in UGT, pa ni mogoče izključiti.
In vitro, imatinib inhibits paracetamol O-glucuronidation with Ki value of 58.5 micromol/L. This inhibition has not been observed in vivo after the administration of imatinib 400 mg and paracetamol 1000 mg.
In vitro imatinib zavira paracetamol O-glukuronidacijo z vrednostjo Ki 58,5 mikromolov/L. Tega zaviranja po uporabi imatiniba 400 mg in paracetamola 1000 mg in vivo niso opažali.