natgillin/translations-raw huggingface dataset:
In vitro data kan ikke udelukke at abacavir hæmmer P-pg og BCRP i tarmsystemet.
In vitro data indicate that inhibition of P-pg and BCRP by abacavir cannot be excluded at intestinal level.
In vitro data og studier på forsøgsdyr viser, at 99mTc-depreotid binder med høj affinitet til somatostatin receptorerne (SSTR) subtyperne 2, 3 og 5.
In vitro data and studies in laboratory animals indicate that 99mTc-depreotide binds with high affinity to somatostatin receptor (SSTR) subtypes 2, 3 and 5.
In vitro data på humane levermikrosomer indikerer dannelsen af små mængder af N-demethyleret topotecan.
In vitro data using human liver microsomes indicate the formation of small amounts of N- demethylated topotecan.
In vitro data tydede på, at lægemiddelinteraktioner med afatinib som følge af hæmning af transportørerne OATB1B1, OATP1B3, OATP2B1, OAT1, OAT3, OCT1, OCT2 og OCT3 kan anses for usandsynlige.
In vitro data indicated that drug-drug interactions with afatinib due to inhibition of OATB1B1, OATP1B3, OATP2B1, OAT1, OAT3, OCT1, OCT2, and OCT3 transporters are considered unlikely.
In vitro data tydede på, at lægemiddelinteraktioner med afatinib som følge af hæmning af UGT1A1 er usandsynlige.
In vitro data indicated that drug-drug interactions with afatinib due to inhibition of UGT1A1 are considered unlikely.
In vitro eksperimenter har vist at den hepatiske metabolisme af saquinavir mættes ved koncentrationer over 2 g/ml.
In vitro experiments have shown that the hepatic metabolism of saquinavir becomes saturable at concentrations above 2 g/ml.
In vitro eksperimenter har vist at den hepatiske metabolisme af saquinavir mættes ved koncentrationer over 2g/ml.
In vitro experiments have shown that the hepatic metabolism of saquinavir becomes saturable at concentrations above 2 g/ml.
In vitro er brivaracetam ikke et substrat af humant P-glycoprotein (P-gp), multimedicinske resistensproteiner (MRP) 1 og 2, og sandsynligvis ikke organisk anion-transporter polypeptid 1B1 (OATP1B1) og 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 er dasatinib aktivt i leukæmiske cellelinjer, der repræsenterer varianter af imatinibfølsom og - resistent sygdom.
In vitro, dasatinib is active in leukaemic cell lines representing variants of imatinib-sensitive and resistant disease.
In vitro er der en omvendt korrelation mellem graden af resistens over for tipranavir og virus’ replikationskapacitet.
In vitro, there is an inverse correlation between the degree of resistance to tipranavir and the capacity of viruses to replicate.
In vitro er der ikke fundet nogen cytokrom P450- metabolisme.
No cytochrome P 450 catalysed metabolism has been detected in vitro.
In vitro er der set hurtig udvikling af hiv-stammer, som er krydsresistente over for NNRTI-hæmmere..
Rapid emergence of HIV-strains which are cross-resistant to NNRTIs has been observed in vitro.
In vitro er lenalidomid et substrat for P-gp, men det er ikke en P-gp-hæmmer.
In vitro, lenalidomide is a substrate of P-gp, but is not a P-gp inhibitor.
In vitro evaluering indikerede, at trifluridin og FTY ikke har induktiv effekt på humane CYP-isozymer (se pkt.
In vitro evaluation indicated that trifluridine and FTY had no inductive effect on human CYP isoforms (see section 5.2).
In vitro evaluering viste, at trifluridin og FTY ikke havde induktiv effekt på human CYP1A2, CYP2B6 eller CYP3A4/5.
In vitro evaluation indicated that trifluridine and FTY had no inductive effect on human CYP1A2, CYP2B6 or CYP3A4/5.
In vitro fandtes der ingen relevant telaprevir-relateret hæmning af den organiske kation-transportør (OCT) OCT2.
No relevant inhibition by telaprevir of the organic cation transporter (OCT) OCT2 was observed in vitro.
In vitro forsøg har vist, at aclidiniumbromid ved den terapeutiske dosis eller dets metabolitter ikke hæmmer eller inducerer cytokrom P450 (CYP450)-enzymer og ikke hæmmer esteraser (carboxylesterase, acetylcholinesterase og butyrylcholinesterase).
In vitro studies have shown that aclidinium bromide at the therapeutic dose or its metabolites do not inhibit or induce any of the cytochrome P450 (CYP450) enzymes and do not inhibit esterases (carboxylesterase, acetylcholinesterase and butyrylcholinesterase).
In vitro forsøg viser, at levetiracetam påvirker de intraneuronale Ca2+ niveauer ved delvis hæmning af Ca2+ strømme af N-type og ved at reducere frigivelsen af Ca2+ fra intraneuronale lagre.
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 granulocyt funktionstest viste imidlertid ingen signifikant forskel når IMMU-MN3-Fab'-SH blev tilsat.
However, in vitro granulocyte function tests did not show significant changes when the sulesomab was added.
In vitro har ketoconazol, klassificeret som en kraftig CYP3A4- og P-glykoprotein (P-gp)-hæmmer, vist sig at være en multipathway CYP- og P-gp/brystcancer-resistensprotein (BCRP)-hæmmer for riociguat-metabolismen og udskillelsen (se pkt.
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 har lurasidon ikke udvist nogen, eller kun svag hæmning (direkte eller tidsafhængig) (IC50>5,9 μM) af enzymerne CYP1A2, CYP2B6, CYP2C8, CYP2C9, CYP2C19, CYP2D6, CYP2E1
In vitro, lurasidone demonstrated no direct, or weak inhibition (direct or time-dependent) (IC50>5.9 μM) of the enzymes cytochrome P450 (CYP)1A2, CYP2B6, CYP2C8, CYP2C9,
In vitro har maraviroc ingen aktivitet mod virus, der bruger CXCR4 som deres indtrædende co- receptor (dual-tropisme eller CXCR4-tropisme, der tilsammen benævnes CXCR4-using virus, se nedenfor).
Maraviroc has no antiviral activity in vitro against viruses which can use CXCR4 as their entry co- receptor (dual-tropic or CXCR4-tropic viruses, collectively termed ‘CXCR4-using’ virus below).
In vitro har verteporfin forårsaget et lavt niveau af komplementaktivering i humant blod ved koncentrationer, der var 5 gange den forventede maksimale plasmakoncentration hos behandlede patienter.
Verteporfin at more than 5 times the expected maximum plasma concentration in treated patients, caused a low level of complement activation in human blood in vitro.
In vitro hæmmede emtricitabin ikke metabolisme medieret af en af de følgende humane CYP450- isoformer: 1A2, 2A6, 2B6, 2C9, 2C19, 2D6 og 3A4.
In vitro, emtricitabine did not inhibit metabolism mediated by any of the following human CYP450 isoforms: 1A2, 2A6, 2B6, 2C9, 2C19, 2D6 and 3A4.
In vitro hæmmede perampanel en AMPA-induceret (men ikke NMDA-induceret) forøgelse i intracellulært calcium.
In vitro, perampanel inhibited AMPA- induced (but not NMDA-induced) increase in intracellular calcium.
In vitro hæmmede siltuximab dosisafhængigt væksten af en IL-6-afhængig plasmacytomacellelinje i mus som reaktion på humant IL-6.
In vitro, siltuximab dose-dependently inhibited the growth of an IL-6-dependent murine plasmacytoma cell line in response to human IL-6.
In vitro hæmmede topotecan hverken de menneskelige P450-enzymer CYP1A2, CYP2A6, CYP2C8/9, CYP2C19, CYP2D6, CYP2E, CYP3A eller CYP4A eller de menneskelige cytosoliske enzymer dihy- dropyrimidin eller xanthinoxidase.
In vitro, topotecan did not inhibit human P450 enzymes CYP1A2, CYP2A6, CYP2C8/9, CYP2C19, CYP2D6, CYP2E, CYP3A, or CYP4A nor did it inhibit the human cytosolic enzymes dihydropyrimidine or xanthine oxidase.
In vitro hæmmede topotecan hverken de menneskelige P450-enzymer CYP1A2, CYP2A6, CYP2C8/9, CYP2C19, CYP2D6, CYP2E, CYP3A eller CYP4A eller de menneskelige cytosoliske enzymer dihydropyrimidin eller xanthinoxidase.
In vitro, topotecan did not inhibit human P450 enzymes CYP1A2, CYP2A6, CYP2C8/9, CYP2C19, CYP2D6, CYP2E, CYP3A, or CYP4A nor did it inhibit the human cytosolic enzymes dihydropyrimidine or xanthine oxidase.
In vitro hæmmede topotecan hverken de menneskelige P450-enzymer CYP1A2, CYP2A6, CYP2C8/9, CYP2C19, CYP2D6, CYP2E, CYP3A og CYP4A eller de menneskelige cytosoliske enzymer dihydropyrimidin eller xanthinoxidase.
In vitro, topotecan did not inhibit human P450 enzymes CYP1A2, CYP2A6, CYP2C8/9, CYP2C19, CYP2D6, CYP2E, CYP3A, of CYP4A nor did it inhibit the human cytosolic enzymes dihydropyrimidine or xanthine oxidase.
In vitro hæmmede topotecan hverken de menneskelige P450-enzymer CYP1A2, CYP2A6, CYP2C8/9, CYP2C19, CYP2D6, CYP2E, CYP3A og CYP4A eller de menneskelige cytosoliske enzymer dihydropyrimidin eller xanthinoxidase.
In vitro, topotecan did not inhibit human P450 enzymes CYP1A2, CYP2A6, CYP2C8/9, CYP2C19, CYP2D6, CYP2E, CYP3A, or CYP4A nor did it inhibit the human cytosolic enzymes dihydropyrimidine or xanthine oxidase.
In vitro hæmmer crizotinib ikke de humane hepatiske transportproteiner organisk anion-transport- polypeptid (OATP) 1B1 og OATP1B3 eller de renale transportproteiner organisk anion-transporter (OAT) 1 eller OAT3 ved klinisk relevante koncentrationer.
In vitro, crizotinib did not inhibit the human hepatic uptake transport proteins organic anion transporting polypeptide (OATP)1B1 or OATP1B3 or the renal uptake transport proteins organic anion transporter (OAT)1 or OAT3 at clinically relevant concentrations.
In vitro hæmmer Imatinib cytochrom P450 isoenzym CYP2D6-aktivitet ved koncentrationer svarende til dem, der påvirker CYP3A4-aktivitet.
In vitroimatinib inhibits the cytochrome P450 isoenzyme CYP2D6 activity at concentrations similar to those that affect CYP3A4 activity.
In vitro hæmmer lamivudin OCT1 og OCT2.
In vitro, lamivudine inhibited OCT1 and OCT2.
In vitro hæmmer olaparib efflukstransportøren P-gp (IC50 = 76 µm), hvorfor det ikke kan udelukkes, at olaparib kan forårsage klinisk relevante lægemiddelinteraktioner med substrater for P-gp (fx simvastatin, pravastatin, dabigatran, digoxin, colchicin).
In vitro, olaparib inhibits the efflux transporter P-gp (IC50 = 76µM), therefore it cannot be excluded that olaparib may cause clinically relevant drug interactions with substrates of P-gp (e.g. simvastatin, pravastatin, dabigatran, digoxin, colchicine).
In vitro hæmmer osimertinib ikke OAT1, OAT3, OATP1B1, OATP1B3 og MATE2K i klinisk relevante koncentrationer.
In vitro, osimertinib does not inhibit OAT1, OAT3, OATP1B1, OATP1B3 and MATE2K at clinically relevant concentrations.
In vitro hæmningsforsøg i humane levermikrosomer tyder på, at cytochrom P450 (CYP) 1A2, 2C19 og 3A4 er involverede i leflunomids metabolisering..
In vitro inhibition studies in human liver microsomes suggest that cytochrome P450 (CYP) 1A2, 2C19 and 3A4 are involved in leflunomide metabolism.
In vitro hæmningsforsøg med humane levermikrosomer tyder på, at cytochrom P450 (CYP) 1A2, 2C19 og 3A4 er involverede i leflunomids metabolisering.
In vitro inhibit ion studies in human liver microsomes suggest that cytochrome P450 (CYP) 1A2, 2C19 and 3A4 are involved in leflunomide metabolism.
In vitro inhiberer visse makrolidantibiotika, f.eks. erythromycin, aktiviteten af bovin Cytochrom P 450-enzymer (CYP3A4-underklasse).
In vitro, some macrolide antibiotics like erythromycin inhibited the activity of bovine Cytochrom P 450-enzymes (CYP3A4-subclass).
In vitro medførte dolutegravir ingen direkte eller kun svag hæmning (IC50 > 50 μM) af enzymerne CYP1A2, CYP2A6, CYP2B6, CYP2C8, CYP2C9, CYP2C19, CYP2D6, CYP3A,
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 metaboliseres N-desmethyl-enzalutamid til carboxylsyremetabolitten af carboxylesterase 1, som også spiller en mindre rolle i metaboliseringen af enzalutamid til carboxylsyremetabolitten.
In vitro, N-desmethyl enzalutamide is metabolized to the carboxylic acid metabolite by carboxylesterase 1, which also plays a minor role in the metabolism of enzalutamide to the carboxylic acid metabolite.
In vitro metabolismestudier har vist, at CYP2D6- og i mindre omfang CYP3A4- og CYP1A2-isoenzymerne er involveret i metabolismen af palonosetron.
In vitro metabolism studies have shown that CYP2D6 and to a lesser extent, CYP3A4 and CYP1A2 isoenzymes are involved in the metabolism of palonosetron.
In vitro metabolismestudier indikerer, at der ikke er induktion eller hæmning i betydelig grad af cytochrom P450, CYP2A6, 2B6, 2C8, 2C9, 2C19, 2D6, 2E1 og 3A3/5 ved relevante koncentrationer (Cmax af frit safinamid 0,4 µM ved 100 mg/dag) hos mennesker.
In vitro metabolism studies have indicated that there is no meaningful induction or inhibition of cytochrome P450, CYP2A6, 2B6, 2C8, 2C9, 2C19, 2D6, 2E1 and 3A3/5 at concentrations which are relevant (Cmax of free safinamide 0.4 µM at 100 mg/day) in man.
In vitro og in vivo bliver clopidogrel metaboliseret via to primære veje: En esterasemedieret, hvorved det hydrolyseres til dets inaktive carboxylsyrederivat (85 % af de cirkulerende metabolitter) og en medieret af flere cytochrom P450- isoenzymer.
In vitro and in vivo, clopidogrel is metabolised according to two main metabolic pathways: one mediated by esterases and leading to hydrolysis into its inactive carboxylic acid derivative (85% of circulating metabolites), and one mediated by multiple cytochromes P450.
In vitro og in vivo bliver clopidogrel metaboliseret via to primære veje: En esterasemedieret, hvorved det hydrolyseres til dets inaktive carboxylsyrederivat (85 % af de cirkulerende metabolitter), og en medieret af flere cytochrom P450- isoenzymer.
In vitro and in vivo, clopidogrel is metabolised according to two main metabolic pathways: one mediated by esterases and leading to hydrolysis into its inactive carboxylic acid derivative (85% of circulating metabolites), and one mediated by multiple cytochromes P450.
In vitro og in vivo bliver clopidogrel metaboliseret via to primære veje: En esterasemedieret, hvorved det hydrolyseres til dets inaktive carboxylsyrederivat (85% af de cirkulerende metabolitter), og en medieret af flere cytochrom P450- isoenzymer.
In vitro and in vivo, clopidogrel is metabolised according to two main metabolic pathways: one mediated by esterases and leading to hydrolysis into its inactive carboxylic acid derivative (85% of circulating metabolites), and one mediated by multiple cytochromes P450.
In vitro og in vivo data fra andre dyrearter end hund antyder at vaccinen kan give nogen grad af krydsbeskyttelse mod L. interrogans serogruppe Icterohaemorrhagiae serovar Icterohaemorrhagiae og
In vitro and in vivo data in non-target species suggests that the vaccine may provide a degree of cross- protection against L. interrogans serogroup Icterohaemorrhagiae serovar Icterohaemorrhagiae and
In vitro og in vivo data fra andre dyrearter end hunde antyder at vaccinen kan give nogen grad af krydsbeskyttelse mod L. interrogans serogruppe Icterohaemorrhagiae serovar Icterohaemorrhagiae og
In vitro and in vivo data in non-target species suggests that the vaccine may provide a degree of cross- protection against L. interrogans serogroup Icterohaemorrhagiae serovar Icterohaemorrhagiae and
In vitro og in vivo data tyder på, at axitinib hovedsageligt metaboliseres i leveren.
In vitro and in vivo data indicate that axitinib is primarily metabolised by the liver.
In vitro og in vivo forsøg tyder på, at den biologiske aktivitet af PegIntron stammer fra dets interferon alfa- 2b-del.
In vitro and in vivo studies suggest that the biological activity of PegIntron is derived from its interferon alfa-2b moiety.
In vitro og in vivo studier har vist, at meloxicam i højere grad hæmmer cyclooxygenase-2 (COX-2) end cyclooxygenase-1 (COX-1).
In vitro and in vivo studies demonstrated that meloxicam inhibits cyclooxygenase-2 (COX-2) to a greater extent than cyclooxygenase-l (COX-I).
In vitro og in vivo studier har vist, atmeloxicam i højere grad hæmmer cyclooxygenase-2 (COX-2) end cyclooxygenase-1 (COX-1).
In vitro and in vivo studies demonstrated that meloxicam inhibits cyclooxygenase-2 (COX-2) to a greater extent than cyclooxygenase-1 (COX-1).
In vitro og in vivo undersøgelser har vist, at ritonavir i betydelig grad hæmmer CYP3A- og CYP2D6- medierede biotransformationer.
In vitro and in vivo studies have demonstrated that ritonavir is a potent inhibitor of CYP3A- and CYP2D6- mediated biotransformations.
In vitro og in vivo-studier har vist, at meloxicam i højere grad hæmmer cyclooxygenase-2 (COX-2) end cyclooxygenase-1 (COX-1).
In vitro and in vivo studies demonstrated that meloxicam inhibits cyclooxygenase-2 (COX-2) to a greater extent than cyclooxygenase-1 (COX-1).
In vitro og kliniske farmakokinetiske interaktionsstudier har vist et lavt potentiale for CYP450- medierede interaktioner, hvor emtricitabin og tenofovirdisoproxil er involveret sammen med andre lægemidler.
In vitro and clinical pharmacokinetic interaction studies have shown the potential for CYP450 mediated interactions involving emtricitabine and tenofovir disoproxil with other medicinal products is low.
In vitro og kliniske farmakokinetiske interaktionsstudier har vist et lavt potentiale for CYP450- medierede interaktioner, hvor emtricitabin og tenofovirdisoproxilfumarat er involveret sammen med andre lægemidler.
In vitro and clinical pharmacokinetic interaction studies have shown the potential for CYP450 mediated interactions involving emtricitabine and tenofovir disoproxil fumarate with other medicinal products is low.
In vitro resultater viste, at CYP3A4 var det primære P450- enzym i katalyseringen af biotransformationen af imatinib.
The in vitro results showed that CYP3A4 was the major human P450 enzyme catalysing the biotransformation of imatinib.
In vitro studier af CYP- og UGT-hæmning og -induktion
In vitro studies of CYP and UGT inhibition and induction
In vitro studier antyder, at axitinib ikke hæmmer CYP2A6, CYP2C9, CYP2C19, CYP2D6, CYP2E1, CYP3A4/5 eller UGT1A1 ved terapeutiske plasmakoncentrationer.
In vitro studies indicated that axitinib does not inhibit CYP2A6, CYP2C9, CYP2C19, CYP2D6, CYP2E1, CYP3A4/5, or UGT1A1 at therapeutic plasma concentrations.
In vitro studier har vist, at aclidinium eller dets metabolitter ikke er substrater eller hæmmere af P-glykoprotein
In vitro studies have shown that aclidinium or its metabolites are not substrates or inhibitors of P-glycoprotein.
In vitro studier har vist, at eltrombopag er substrat for og hæmmer af brystcancer-resistent protein (BCRP).
In vitro studies demonstrated that eltrombopag is a breast cancer resistance protein (BCRP) substrate and inhibitor.
In vitro studier i levermikrosomer viste, at eluxadolin ikke hæmmer CYP3A4 ved klinisk relevante koncentrationer, men i tarmmikrosomer hæmmede eluxadolin CYP3A4 med en Ki på 450 µM (256 µg/ml).
In vitro studies in liver microsomes showed that eluxadoline is not an inhibitor of CYP3A4 at clinically relevant concentrations, but in intestinal microsomes, eluxadoline inhibited CYP3A4 with a Ki of 450 µM (256 µg/mL).
In vitro studier indikerede, at eluxadolin er substrat for og hæmmer af leveroptagelsestransportøren OATP1B1 og substrat for levereffluxtransportøren MRP2, men ikke substrat for eller hæmmer af P- gp- og BCRP-transportørerne.
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.
In vitro studier indikerer, at aktivering af stavudin hæmmes af doxorubicin og ribavirin men ikke af andre lægemidler til behandling af HIV-infektion, som fosforyleres på lignende måde, (f.eks. didanosin, zalcitabin, ganciclovir og foscarnet); der bør derfor udvises forsigtighed ved samtidig administration af stavudin og doxorubicin eller ribavirin.
In vitro studies indicate that the activation of stavudine is inhibited by doxorubicin and ribavirin but not by other medicinal products used in HIV infection which are similarly phosphorylated, (e.g. didanosine, zalcitabine, ganciclovir and foscarnet) therefore, coadministration of stavudine with either doxorubicin or ribavirin should be undertaken with caution.
In vitro studier indikerer, at CYP2D6 (aromatisk hydroxylation), CYP1A2 (kæde- oxidation) og i mindre grad CYP2C19 var involveret i propranolol metabolisme.
In vitro studies indicated that CYP2D6 (aromatic hydroxylation), CYP1A2 (chain oxidation) and to a less extent CYP2C19 were involved in propranolol metabolism.
In vitro studier med humane hepatocytter antyder at crizotinib kan inducere preganan-X-receptor (PXR)- og konstitutiv androstanreceptor (CAR)-regulerede enzymer (fx CYP3A4, CYP2B6, CYP2C8, CYP2C9, UGT1A1).
In vitro studies in human hepatocytes indicated that crizotinib may induce pregnane X receptor (PXR)- and constitutive androstane receptor (CAR)-regulated enzymes (e.g., CYP3A4, CYP2B6, CYP2C8, CYP2C9, UGT1A1).
In vitro studier med tafamidismeglumin indikerer, at tafamidismeglumin ved klinisk relevante koncentrationer sandsynligvis ikke forårsager lægemiddelinteraktioner med substrater for UDP- glukuronosyltransferase (UGT), P-gp-transportører eller organisk anion-transporterende polypeptid- transportører (OATP1B1 og 1B3).
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 studier tyder på, at dasatinib er et CYP3A4-substrat.
In vitro studies indicate that dasatinib is a CYP3A4 substrate.
In vitro studier viser, at eluxadolin hverken inducerer CYP1A2, CYP2B6, CYP2C9, CYP2C19 eller CYP3A4 og heller ikke hæmmer CYP1A2, CYP2A6, CYP2B6, CYP2C9, CYP2C19, CYP2C8 og
In vitro studies indicate that eluxadoline is neither an inducer of CYP1A2, CYP2B6, CYP2C9, CYP2C19, and CYP3A4, nor an inhibitor of CYP1A2, CYP2A6, CYP2B6, CYP2C9, CYP2C19,
In vitro studies hebben aangetoond dat de verhoogde blootstelling aan repaglinide het gevolg is van de remming van CYP2C8 door de glucuronide metaboliet van clopidogrel.
In vitro studies have shown the increase in repaglinide exposure is due to inhibition of CYP2C8 by the glucuronide metabolite of clopidogrel.
In vitro tests viste, at plerixafor ikke metaboliseres af CYP- enzymer, og at det ikke hæmmer eller inducerer CYP-enzymer.
In vitro tests showed that plerixafor was not metabolised by P450 CYP enzymes, did not inhibit or induce P450 CYP enzymes.
In vitro undersøgelser af human megakaryocytopoiese har fastslået, at anagrelids hæmmende virkning på dannelsen af blodplader hos mennesker fremkaldes via forsinkelse af modningen af megakaryocytter, og ved at reducere deres størrelse og ploidi.
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 undersøgelser antyder, at ligesom med andre NSAID’er, er ibuprofen kraftigt bundet til plasma-albumin, selvom denne synes at være signifikant lavere (95 %) sammenlignet med plasma hos voksne (99 %).
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 %).
In vitro undersøgelser har også vist, at bivalirudin forlænger den aktiverede partielle tromboplastintid (aPTT), trombintiden (TT) og pro-trombintiden (PT) i normal human plasma på en koncentrationsafhængig måde og at bivalirudin ikke inducerer blodpladeaggregationsrespons mod sera fra patienter med kendt tidligere Heparin-Induceret-Trombocytopeni/Trombose Syndrom (HIT/HITTS).
In vitro studies have also shown that bivalirudin prolongs the activated partial thromboplastin time (aPTT) thrombin time (TT) and pro-thrombin time (PT) of normal human plasma in a concentration- dependent manner and that bivalirudin does not induce a platelet aggregation response against sera from patients with a history of Heparin-Induced Thrombocytopenia/Thrombosis Syndrome (HIT/HITTS).