natgillin/translations-raw huggingface dataset:
In vitro data suggests that cysteamine bitartrate is likely to be metabolized by multiple CYP enzymes, including CYP1A2, CYP2B6, CYP2C8, CYP2C9, CYP2C19, CYP2D6, and CYP2E1.
Podaci in vitro ukazuju da se cisteamin bitartrat vjerojatno metabolizira putem više CYP enzima, uključujući CYP1A2, CYP2B6, CYP2C8, CYP2C9, CYP2C19, CYP2D6 i CYP2E1.
In vitro data tend to suggest that the continuation of lamivudine in anti-retroviral regimen despite the development of M184V might provide residual anti-retroviral activity (likely through impaired viral fitness).
Rezultati testova in vitro sugeriraju da nastavak primjene lamivudina u antivirusnom liječenju unatoč razvoju M184V može osigurati ostatnu antiretrovirusnu aktivnost (najvjerojatnije putem smanjenog infektivnog virusnog potencijala).
In vitro data using human liver microsomes indicate the formation of small amounts of N- demethylated topotecan.
In vitro podaci, dobiveni primjenom mikrosomalnih enzima ljudske jetre, upućuju na stvaranje male količine N-demetiliranog topotekana.
In vitro dermal absorption into human skin was studied using Ameluz containing radiolabelled 5- aminolaevulinic acid.
In vitro dermalna apsorpcija u ljudsku kožu ispitivana je s lijekom Ameluz koji je sadržavao radiooznačenu 5-aminolevulinsku kiselinu.
In vitro enzymatic studies with human liver microsomes revealed that arsenic trioxide has no inhibitory activity on substrates of the major cytochrome P450 enzymes such as 1A2, 2A6, 2B6, 2C8, 2C9, 2C19, 2D6, 2E1, 3A4/5, 4A9/11.
Enzimatska in vitro ispitivanja na humanim jetrenim mikrosomima otkrila su da arsenov trioksid ne posjeduje inhibitornu aktivnost spram supstrata najvažnijih enzima citokroma P450 poput 1A2, 2A6, 2B6, 2C8, 2C9, 2C19, 2D6, 2E1, 3A4/5, 4A9/11.
In vitro erythrocyte concentrations of 14C-mirabegron were about 2-fold higher than in plasma.
In vitro koncentracija 14C- mirabegrona u eritrocitima bila je oko 2 puta viša nego u plazmi.
In vitro evaluation indicated that trifluridine and FTY had no inductive effect on human CYP isoforms (see section 5.2).
In vitro ispitivanja ukazuju da trifluridin i FTY nemaju indukcijski učinak na ljudske CYP izoforme (vidjeti dio 5.2).
In vitro evaluation indicated that trifluridine and FTY had no inductive effect on human CYP1A2, CYP2B6 or CYP3A4/5.
In vitro ispitivanja upućuju da ni trifluridin, niti FTY nemaju induktivno djelovanja na ljudske CYP1A2, CYP2B6 i CYP3A4/5.
In vitro evaluation using primary cultures of human hepatocytes indicated that tegafur (0.7-70 µM), gimeracil (0.2-25 µM) and oteracil (0.04-4 µM) had little or no inductive effect on CYP1A2, CYP2B6 or CYP3A4/5 metabolic activities.
In vitro evaluacija korištenjem primarnih kultura humanih hepatocita upućuje da tegafur (0,7 – 70 µM), gimeracil (0,2-25 µM) i oteracil (0,04-4 µM) imaju mali ili nikakav indukcijski učinak na metaboličku aktivnost CYP1A2, CYP2B ili CYP3A4/5.
In vitro experiments have shown that the hepatic metabolism of saquinavir becomes saturable at concentrations above 2 g/ml.
Pokusi in vitro pokazali su da je metabolizam sakvinavira u jetri moguće zasititi pri koncentracijama višima od 2 g/ml.
in vitro human microsomal and hepatocyte studies, hydrolysis of the amide group of the C-terminus amino acid, phenylalanine results in a deamidated metabolite and the formation of this metabolite is not NADPH dependent.
U in vitro istraživanjima ljudskih mikrosoma i hepatocita hidrolizom amidne skupine C-terminalnog kraja aminokiseline fenilalanina nastaje deaminirani metabolit, a stvaranje tog metabolita ne ovisi o NADPH-u.
In vitro imatinib inhibits the cytochrome P450 isoenzyme CYP2D6 activity at concentrations similar to those that affect CYP3A4 activity.
Imatinib in vitro inhibira aktivnost CYP2D6 izoenzima citokroma P450 u koncentracijama koje su slične onima što utječu na aktivnost CYP3A4.
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 ispitivanja inhibicije u ljudskim jetrenim mikrosomima ukazuju da su citokromi P450 (CYP) 1A2, 2C19 i 3A4 uključeni u metabolizam leflunomida.
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 in vitro provedena radi utvrđivanja potencijalnih inhibitornih učinaka na prijenosnike zaključila su da nema klinički značajnih učinaka, osim za OAT3.
In vitro interaction studies with topical antifungal (clotrimazole, econazole, imidazole, nystatin, miconazole, ketoconazole), antibacterial (clindamycin, metronidazole) and antiviral medicinal products (acyclovir), showed no effect on antimicrobial activity.
In vitro interakcijske studije s topikalnim antifungalnim (klotrimazol, ekonazol, imidazol, nistatin, mikonazol, ketokonazol), antibakterijskim (klindamicin, metronidazol) i antivirusnim lijekovima (aciklovir) nisu pokazale učinak na antimikrobnu aktivnost.
in vitro labelling
označavanje in vitro
In vitro lamivudine inhibits the intracellular
In vitro lamivudin inhibira unutarstaničnu
In vitro metabolism data and the human mass balance study results indicated that the cytochrome P450 system is not involved in the metabolism of decitabine.
Podaci za metabolizam in vitro i rezultati ispitivanja ravnoteže između količine primijenjenog i izlučenog lijeka u ljudi (engl. mass balance) pokazali su da sustav citokroma P450 nije uključen u metabolizam decitabina.
In vitro metabolism studies have confirmed that the parent compound is rapidly metabolised to 3-O- acetyltylosin.
Ispitivanja metabolizma in vitro potvrdila su da se osnovni spoj brzo metabolizira u 3-O-acetiltilozin.
In vitro metabolism studies indicate that potential for CYP 450-based drug interactions is low since there is limited metabolism of Neparvis via CYP450 enzymes.
In vitro ispitivanja metabolizma upućuju na to da je potencijal za interakcije s lijekovima na temelju CYP 450 nizak budući da je metabolizam Neparvisa putem CYP450 enzima ograničen.
In vitro olaparib is a substrate for the efflux transporter P-gp and therefore P-gp inhibitors may increase exposure to olaparib (see section 4.4).
In vitro olaparib je supstrat za efluksni prijenosnik P-gp, stoga inhibitori P-gp-a mogu povećati izloženost olaparibu (vidjeti dio 4.4).
In vitro potential for sofosbuvir/velpatasvir drug-drug interations
In vitro potencijal interakcija lijek-lijek sofosbuvira/velpatasvira
In vitro protein binding of tenofovir to plasma or serum protein was less than 0.7 and 7.2%, respectively, over the tenofovir concentration range 0.01 – 25 μg/ml.
Vezivanje tenofovira za proteine u plazmi odnosno serumu in vitro bilo je manje od 0,7% odnosno 7,2%, u rasponu koncentracija tenofovira od 0,01 do 25 µg/ml.
In vitro purified enoxaparin has a high anti factor Xa blood clotting (anti-Xa) (approximately 100 IU/mg) and a low anti factor IIa (anti-IIa) or antithrombin (approximately
In vitro purificirani heparin ima snažno protudjelovanje na faktor zgrušavanja Xa (anti- Xa) (približno 100 IU/mg) i slabo protudjelovanje na faktor IIa (anti-IIa) ili antitrombin (približno
In vitro purified enoxaparin has a high anti factor Xa blood clotting (anti-Xa) (approximately 100 IU/mg) and a low anti factor IIa (anti-IIa) or antithrombin (approximately
In vitro purificirani heparin ima snažno protudjelovanje na faktor zgrušavanja Xa (anti-Xa) (približno 100 IU/mg) i slabo protudjelovanje na faktor IIa (anti-IIa) ili antitrombin (približno
In vitro purified enoxaparin has a high anti factor Xa blood clotting (anti-Xa) (approximately 100 IU/mg) and a low anti factor IIa (anti-IIa) or antithrombin (approximately
In vitro purificirani heparin ima snažno protudjelovanje na faktor zgrušavanja Xa (nti-Xa) (približno 100 IU/mg) i slabo protudjelovanje na faktor IIa (anti-IIa) ili antitrombin (približno
In vitro responses seen in single channel patch clamp experiments using membrane patches from rodent cells expressing mutant CFTR forms do not necessarily correspond to in vivo pharmacodynamic response (e.g., sweat chloride) or clinical benefit.
Odgovori opaženi u pokusima in vitro, u kojima se na djelićima membrane stanica glodavaca s oblicima mutacije CFTR-a metodom priklještenja (engl. patch clamp) ispitivao pojedinačni kanal, ne podudaraju se nužno s farmakodinamičkim odgovorom in vivo (npr. koncentracija klorida u znoju) ili s kliničkom koristi.
In vitro results indicate that different CYP isoforms are able to catalyse the N-dealkylation of rotigotine.
In vitro rezultati ukazuju da različite CYP izoforme mogu katalizirati N- dealkilaciju rotigotina.
In vitro studies
In vitro ispitivanja:
In vitro studies also demonstrated that eltrombopag is a breast cancer resistance protein (BCRP) substrate and inhibitor.
In vitro ispitivanja su također pokazala da je eltrombopag supstrat i inhibitor proteina rezistencije raka dojke (BCRP).
In vitro studies demonstrated that eltrombopag is a breast cancer resistance protein (BCRP) substrate and inhibitor.
In vitro ispitivanja pokazala su da je eltrombopag supstrat i inhibitor proteina rezistencije raka dojke (BCRP).
In vitro studies demonstrated that eltrombopag is not a substrate for the organic anion transporter polypeptide, OATP1B1, but is an inhibitor of this transporter.
In vitro ispitivanja pokazala su da eltrombopag nije supstrat za polipeptidni transporter organskih aniona OATP1B1, nego je njegov inhibitor.
In vitro studies demonstrated that telaprevir is an inhibitor of OATP1B1 and OATP2B1.
In vitro ispitivanja su pokazala da je telaprevir inhibitor OATP1B1 i OATP2B1.
In vitro studies demonstrated that trametinib is metabolised predominantly via deacetylation alone or with mono-oxygenation or in combination with glucuronidation biotransformation pathways.
Ispitivanja in vitro pokazala su da se trametinib prvenstveno metabolizira deacetilacijom, samom ili uz monooksigenaciju, ili u kombinaciji s glukuronidacijskim biotransformacijskim putovima.
In vitro studies did not show any significant involvement of oxidative metabolism by cytochrome P450 enzymes.
In vitro ispitivanja nisu pokazala znatniji udio oksidacijskog metabolizma posredovanog enzimima citokroma P450 .
In vitro studies evaluating the percent recovery of total dose delivered with nasogastric, nasojejunal or gastrostomy tubes demonstrated the percent of dose recovered was > 99% for doses > 1 ml and 70% for a 0.5 ml dose.
In vitro ispitivanja za procjenu postotka povrata ukupne doze primijenjene putem nazogastrične, nazojejunalne sonde ili gastrostome pokazala su postotak povrata doze > 99% za doze > 1 ml, odnosno 70% za dozu od 0,5 ml.
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).
In vitro ispitivanja također su pokazala da bivalirudin, ovisno o koncentraciji, produljuje aktivirano parcijalno tromboplastinsko vrijeme (APTV), trombinsko vrijeme (TV) i protrombinsko vrijeme (PV) normalne ljudske plazme te da bivalirudin ne inducira agregaciju krvnih pločica kao odgovor na serum bolesnika koji imaju povijest sindroma heparinom prouzročene trombocitopenije/tromboze.
In vitro studies have concluded that exposure to oseltamivir is not expected to be increased significantly nor is exposure to the active metabolite expected to be significantly decreased in patients with hepatic impairment (see section 4.2).
Ispitivanja in vitro pokazala su da se u bolesnika s oštećenom funkcijom jetre ne očekuje značajno povećanje izloženosti oseltamiviru ni značajno smanjenje izloženosti aktivnom metabolitu (vidjeti dio 4.2).
In vitro studies have demonstrated that afatinib is a substrate of P-gp and BCRP.
In vitro ispitivanja su pokazala da je afatinib supstrat P-gp-a i BCRP-a.
In vitro studies have demonstrated that nalmefene is a selective opioid receptor ligand with antagonist activity at the μ and δ receptors and partial agonist activity at the κ receptor.
In vitro ispitivanja pokazala su da je nalmefen selektivni ligand opiodnog receptora s antagonističkim djelovanjem na receptore μ i δ i djelomičnim agonističkim djelovanjem na receptor κ.
In vitro studies have demonstrated that the Phase I metabolism of osimertinib is predominantly via CYP3A4 and CYP3A5.
In vitro ispitivanja su pokazala da se I. faza metabolizma osimertiniba pretežno odvija preko CYP3A4 i CYP3A5.
In vitro studies have demonstrated that vemurafenib is a substrate of the efflux transporters P-gp and BCRP.
Ispitivanja in vitro pokazala su da je vemurafenib supstrat efluksnih prijenosnika P-gp i BCRP.
In vitro studies have demonstrated that vemurafenib is an inhibitor of the efflux transporters P-glycoprotein (P-gp) and breast cancer resistance protein (BCRP).
Ispitivanja in vitro pokazala su da je vemurafenib inhibitor efluksnih prijenosnika P-glikoproteina (P-gp) i proteina koji uzrokuje rezistenciju raka dojke na liječenje (BCRP).
In vitro studies have determined that neither tenofovir disoproxil fumarate nor tenofovir are substrates for the CYP enzymes.
In vitro ispitivanja pokazala su da ni tenofovirdizoproksil fumarat niti tenofovir nisu supstrati za CYP enzime.
In vitro studies have determined that neither tenofovir disoproxil fumarate nor tenofovir are substrates for the CYP450 enzymes.
In vitro ispitivanja dokazala su da ni tenofovirdizoproksilfumarat ni tenofovir nisu supstrati za CYP450 enzime.
In vitro studies have determined that neither tenofovir disoproxil fumarate nor tenofovir are substrates for the CYP450 enzymes.
In vitro ispitivanja pokazala su da ni tenofovirdizoproksilfumarat ni tenofovir nisu supstrati za CYP450 enzime.
In vitro studies have determined that neither tenofovir disoproxil fumarate nor tenofovir are substrates for the CYP450 enzymes.
In vitro ispitivanja pokazala su da ni tenofovirdizoproksilfumarat ni tenofovir nisu supstrati za enzime CYP450.
In vitro studies have shown that aclidinium bromide or the metabolites of aclidinium bromide at the therapeutic dose are not expected to cause interactions with P-glycoprotein (P-gp) substrate drugs or drugs metabolised by cytochrome P450 (CYP450) enzymes and esterases (see section 5.2).
Ispitivanja in vitro su pokazala da se ne očekuju interakcije terapijske doze aklidinijeva bromida ili metabolita aklidinijeva bromida s lijekovima koji su supstrati P-glikoproteina (P-gp) ili lijekovima koji se metaboliziraju putem citokroma P450 (CYP 450) i esterazama (vidjeti dio 5.2).
In vitro studies have shown that cabazitaxel is mainly metabolised through CYP3A (80% to 90%) (see section 5.2).
Ispitivanja in vitro pokazala su da se kabazitaksel većinom metabolizira pomoću CYP3A (80% do 90%) (vidjeti dio 5.2).
In vitro studies have shown that ceftaroline is bactericidal and able to inhibit bacterial cell wall synthesis in methicillin-resistant Staphylococcus aureus (MRSA) and penicillin non-susceptible Streptococcus pneumoniae (PNSP) due to its affinity for the altered penicillin-binding proteins (PBPs) found in these organisms.
Ispitivanja in vitro su pokazala da ceftarolin djeluje baktericidno i može spriječiti sintezu bakterijske stanične stijenke u meticilin-rezistentnih sojeva bakterije Staphylococcus aureus (MRSA) te u penicilin neosjetljivih sojeva bakterije Streptococcus pneumoniae (PNSP) zbog svog afiniteta za izmijenjene penicilin-vežuće proteine (engl. penicillin-binding proteins, PBP) u tim organizmima.
In vitro studies have shown that corticotroph tumour cells from Cushing’s disease patients display a high expression of hsst5, whereas the other receptor subtypes either are not expressed or are expressed at lower levels.
In vitro ispitivanja pokazala su da kortikotropne tumorske stanice bolesnika s Cushingovom bolešću imaju visoku ekspresiju hsst5, dok druge podvrste receptora ili nisu izražene ili su izražene u manjoj mjeri.
In vitro studies have shown that degarelix is not a substrate for the human CYP450 system.
In vitro ispitivanja pokazala su da degareliks nije supstrat sustava CYP450 u ljudi
In vitro studies have shown that gefitinib has limited potential to inhibit CYP2D6.
In vitro studije su pokazale da gefitinib ima ograničen potencijal za inhibiciju CYP2D6.
In vitro studies have shown that gefitinib is a substrate of p-glycoprotein (Pgp).
In vitro ispitivanja su pokazala da je gefitinib supstrat P-glikoproteina (Pgp).
In vitro studies have shown that indacaterol, a long-acting beta2-adrenergic agonist, has more than 24-fold greater agonist activity at beta2-receptors compared to beta1-receptors and 20-fold greater agonist activity compared to beta3- receptors.
In vitro ispitivanja pokazala su da indakaterol, dugodjelujući beta2-adrenergički agonist, ima više od 24 puta veće agonističko djelovanje na beta2-receptore u usporedbi s beta1-receptorima te 20 puta veće agonističko djelovanje u usporedbi s beta3-receptorima.
In vitro studies have shown that opicapone is not transported by OATP1B1, but is transported by OATP1B3, and efflux transported by P-gp and BCRP.
In vitro ispitivanja pokazala su da se opikapon ne transportira pomoću OATP1B1, ali se transportira pomoću OATP1B3, a efluks transporteri su P-gp i BCRP.
In vitro studies have shown that tenofovir alafenamide is metabolised to tenofovir (major metabolite) by cathepsin A in PBMCs (including lymphocytes and other HIV target cells) and macrophages; and by carboxylesterase-1 in hepatocytes.
In vitro ispitivanja su pokazala da se tenofoviralafenamid metabolizira u tenofovir (glavni metabolit) pomoću katepsina A u PBMC-ovima (uključujuću limfocite i druge ciljne stanice HIV-a) i makrofazima te pomoću karboksilesteraze-1 u hepatocitima.
In vitro studies have shown that the metabolism of docetaxel may be modified by the concomitant administration of compounds which induce, inhibit or are metabolised by (and thus may inhibit the enzyme competitively) cytochrome P450-3A such as ciclosporine, ketoconazole and erythromycin .
In vitro ispitivanja pokazala su da metabolizam docetaksela može promijeniti istodobna primjena tvari koji induciraju, inhibiraju ili se metaboliziraju (i tako kompetitivno mogu inhibirati enzim) pomoću citokroma P450-3A, kao što su ciklosporin, ketokonazo i eritromicin.
In vitro studies have shown that the metabolism of docetaxel may be modified by the concomitant administration of compounds which induce, inhibit or are metabolised by (and thus may inhibit the enzyme competitively) cytochrome P450-3A such as ciclosporine, ketoconazole and erythromycin .
In vitro ispitivanja pokazala su da metabolizam docetaksela može promijeniti istodobna primjena tvari koji induciraju, inhibiraju ili se metaboliziraju (i tako kompetitivno mogu inhibirati enzim) s pomoću citokroma P450-3A, kao što su ciklosporin, ketokonazol i eritromicin.
In vitro studies have shown that the metabolism of docetaxel may be modified by the concomitant administration of compounds which induce, inhibit or are metabolised by (and thus may inhibit the enzyme competitively) cytochrome P450-3A such as ciclosporine, ketoconazole and erythromycin.
In vitro ispitivanja pokazala su da metabolizam docetaksela može promijeniti istodobna primjena tvari koji induciraju, inhibiraju ili se metaboliziraju (i tako kompetitivno mogu inhibirati enzim) s pomoću citokroma P450-3A, kao što su ciklosporin, ketokonazol i eritromicin.
In vitro studies have shown that the metabolism of docetaxel may be modified by the concomitant administration of compounds which induce, inhibit or are metabolised by (and thus may inhibit the enzyme competitively) cytochrome P450-3A such as ciclosporine, ketoconazole, erythromycin.
In vitro ispitivanja pokazala su da metabolizam docetaksela može promijeniti istodobna primjena tvari koji induciraju, inhibiraju ili se metaboliziraju (i tako kompetitivno mogu inhibirati enzim) s pomoću citokroma P450-3A, kao što su ciklosporin, ketokonazol i eritromicin.
In vitro studies have shown that the metabolism of docetaxel may be modified by the concomitant administration of compounds which induce, inhibit or are metabolised by (and thus may inhibit the enzyme competitively) cytochrome P450-3A such as cyclosporine, ketoconazole and erythromycin.
In vitro ispitivanja pokazala su da metabolizam docetaksela može promijeniti istodobna primjena tvari koji induciraju, inhibiraju ili se metaboliziraju (i tako kompetitivno mogu inhibirati enzim) pomoću citokroma P450-3A, kao što su ciklosporin, ketokonazol i eritromicin.
In vitro studies in human liver microsomes indicate that tedizolid phosphate and tedizolid do not significantly inhibit metabolism mediated by any of the following cytochrome P450 isoenzymes (CYP1A2, CYP2C19, CYP2A6, CYP2C8, CYP2C9, CYP2D6, and CYP3A4).
In vitro ispitivanja na ljudskim jetrenim mikrosomima pokazala su da tedizolidfosfat i tedizolid ne inhibiraju značajno metabolizam posredovan bilo kojim od sljedećih izoenzima citokroma P450: CYP1A2, CYP2C19, CYP2A6, CYP2C8, CYP2C9, CYP2D6 i CYP3A4.
In vitro studies in human, dog, mouse and rat plasma showed a high plasma protein binding (> 99.5 %), mainly to albumin and α-1-acid glycoprotein.
In vitro ispitivanja u plazmi čovjeka, psa, miša i štakora pokazala su visoko vezanje na proteine u plazmi (> 99,5%) uglavnom na albumin i α-1 kiseli glikoprotein.
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 ispitivanja na jetrenim mikrosomima pokazala su da eluksadolin nije inhibitor CYP3A4 pri klinički značajnim koncentracijama, dok je u crijevnim mikrosomima eluksadolin inhibirao CYP3A4 s vrijednošću Ki od 450 µM (256 µg/ml).
In vitro studies indicate that asenapine weakly inhibits CYP2D6.
Istraživanja in vitro ukazuju da je asenapin slab inhibitor CYP2D6.
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.
In vitro ispitivanja pokazuju da pri terapijskim dozama nije izgledna pojava kliničkih interakcija između lijekova kao posljedica inhibicije bosutiniba na metabolizam lijekova koji su supstrati za CYP1A2, CYP2A6, CYP2C8, CYP2C9, CYP2C19, CYP2D6, ili 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 ispitivanja ukazuju na to da CYP2D6 i CYP3A4 mogu biti minimalno uključeni u metabolizam paliperidona, no nema dokaza ni in vitro niti in vivo da ti izoenzimi imaju značajnu ulogu u metabolizmu paliperidona.
In vitro studies indicate that dasatinib is a CYP3A4 substrate.
In vitro ispitivanja pokazuju da je dasatinib supstrat enzima CYP3A4.
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 ispitivanja ukazuju da eluksadolin ne djeluje kao induktor CYP1A2, CYP2B6, CYP2C9, CYP2C19 i CYP3A4, niti kao inhibitor CYP1A2, CYP2A6, CYP2B6, CYP2C9, CYP2C19, CYP2C8
In vitro studies indicate that lenalidomide has no inhibitory effect on human bile salt export pump (BSEP), BCRP, MRP2, OAT1, OAT3, OATP1B1, OATP1B3, and OCT2.
In vitro ispitivanja pokazuju da lenalidomid nema inhibitorni učinak na humanu pumpu za izbacivanje žučne soli (BSEP), BCRP, MRP2, OAT1, OAT3, OATP1B1, OATP1B3 i OCT2.