natgillin/translations-raw huggingface dataset:
In this trial, the loading dose and maintenance dose of leflunomide was based on three weight categories: &lt; 20 kg, 20 - 40 kg, and &gt; 40 kg.
V tem preskušanju sta polnilni in vzdrževalni odmerek leflunomida temeljila na treh kategorijah telesne mase: &lt; 20 kg, od 20 do 40 kg in &gt; 40 kg.
In this trial, the loading dose and maintenance dose of leflunomide was based on three weight categories: &lt; 20 kg, 20-40 kg, and &gt; 40 kg.
V tem preskušanju sta polnilni in vzdrževalni odmerek leflunomida temeljila na treh kategorijah telesne mase: &lt; 20 kg, od 20 do 40 kg in &gt; 40 kg.
In those patients that received &gt; 10.6 mg/kg ribavirin (800 mg dose in typical 75 kg patient), regardless of genotype or viral load, response rates were significantly higher than in those patients that received ≤ 10.6 mg/kg ribavirin (Table 6), while response rates in patients that received &gt; 13.2 mg/kg ribavirin were even higher.
Pri bolnikih, ki so prejeli &gt; 10,6 mg/kg ribavirina (800 mg odmerek pri tipičnem bolniku s telesno maso 75 kg, je bil delež odziva bistveno višji kot pri tistih, ki so prejeli ≤ 10,6 mg/kg ribavirina (Preglednica 6), ne glede na genotip ali virusno obremenitev, delež odziva pri tistih, ki so prejeli &gt; 13,2 mg/kg zdravila ribavirina, pa je bil še višji.
In those patients that received &gt; 10.6 mg/kg ribavirin (800 mg dose in typical 75 kg patient), regardless of genotype or viral load, response rates were significantly higher than in those patients that received ≤ 10.6 mg/kg ribavirin (Table 6), while response rates in patients that received &gt; 13.2 mg/kg ribavirin were even higher.
Pri bolnikih, ki so prejeli &gt; 10,6 mg/kg ribavirina (800 mg odmerek pri tipičnem bolniku s telesno maso 75 kg, je bil delež odziva bistveno višji kot pri tistih, ki so prejeli ≤ 10,6 mg/kg ribavirina, ne glede na genotip ali virusno obremenitev (preglednica 6), delež odziva pri tistih, ki so prejeli &gt; 13,2 mg/kg zdravila ribavirina, pa je bil še višji.
In those patients that received &gt; 10.6 mg/kg ribavirin (800 mg dose in typical 75 kg patient), regardless of genotype or viral load, response rates were significantly higher than in those patients that received ≤ 10.6 mg/kg ribavirin (Table 7), while response rates in patients that received &gt; 13.2 mg/kg ribavirin were even higher.
Pri bolnikih, ki so prejeli &gt; 10,6 mg/kg ribavirina (800 mg odmerek pri tipičnem bolniku s telesno maso 75 kg), je bil delež odziva bistveno višji kot pri tistih, ki so prejeli ≤ 10,6 mg/kg ribavirina, ne glede na genotip ali virusno obremenitev (preglednica 7), delež odziva pri tistih, ki so prejeli &gt; 13,2 mg/kg zdravila ribavirina, pa je bil še višji.
In those patients who underwent non-primary PCI &lt; 6 hours after the last dose of fondaparinux, the median dose of UFH was 5000 IU and the incidence of major bleeding was 4.1% (2/49).
Pri bolnikih, pri katerih je bila opravljena neprimarna PCI &lt; 6 ur po zadnjem odmerku fondaparinuksa, je bil povprečni odmerek nefrakcioniranega heparina 5.000 i.e., pojavnost večjih krvavitev pa 4,1 % (2/49).
In three of four patients the change in the sweat chloride test was &lt; 5 mmol/L and this group did not demonstrate a clinically relevant improvement in FEV1 after 8 weeks of treatment.
Pri treh od štirih bolnikov se je test kloridov v znoju spremenil za &lt; 5 mmol/l in ta skupina ni pokazala klinično pomembnega izboljšanja FEV1 po 8 tednih zdravljenja.
In TORCH, older patients, patients with a lower body mass index ( &lt; 25 kg/m2) and patients with very severe disease (FEV1 &lt; 30% predicted) were at greatest risk of developing pneumonia regardless of treatment.
V študiji TORCH so pri starejših bolnikih, bolnikih z nižjim indeksom telesne mase ( &lt; 25 kg/m2) in bolnikih z zelo hudo obliko bolezni (pričakovan FEV1 &lt; 30 %) opazili največje tveganje za pojav pljučnice ne glede na zdravljenje.
In TRA 2°P - TIMI 50, in vorapaxar- treated patients, including those with history of stroke, a higher rate of ICH was observed in patients weighing &lt; 60 kg compared to patients weighing ≥60 kg.
V preskušanju TRA 2ºP-TIMI 50 pri bolnikih, ki so prejemali vorapaksar, vključno s tistimi z možgansko kapjo v anamnezi, so pri tistih, s telesno maso &lt; 60 kg, opazili večji delež ICH kot pri tistih, s telesno maso ≥ 60 kg.
In treatment-naïve MRCC patients receiving IFN-, six (2%) venous thromboembolic events occurred; one patient ( &lt; 1%) experienced a Grade 3 DVT and five patients (1%) had pulmonary embolisms, all with Grade 4.
Med bolniki s še nezdravljenim MRCC, ki so prejemali IFN-, se je pojavilo 6 (2 %) venskih trombemboličnih dogodkov; pri enem bolniku ( &lt; 1 %) je šlo za globoko vensko trombozo 3. stopnje, pet bolnikov (1 %) pa je imelo pljučno embolijo 4. stopnje.
In TRIUMPH, study patients treated with Soliris had significantly reduced (p &lt; 0.001) haemolysis resulting in improvements in anaemia as indicated by increased haemoglobin stabilization and reduced need for RBC transfusions compared to placebo treated patients (see Table 3).
V študiji TRIUMPH so imeli sodelujoči bolniki, zdravljeni z zdravilom Soliris, pomembno zmanjšano (p &lt; 0,001) hemolizo, kar je privedlo do izboljšanja slabokrvnosti, kakor to kaže večja stabilizacija hemoglobina in zmanjšanje potrebe po transfuziji eritrocitov v primerjavi z bolniki, zdravljenimi s placebom (glejte preglednico 3).
In two 12-week, placebo controlled studies (200109 and 200110), the addition of Incruse to fluticasone furoate/vilanterol (FF/VI) (92/22 micrograms) once daily in adult patients with a clinical diagnosis of COPD, resulted in statistically significant and clinically meaningful improvements in the primary endpoint of trough FEV1 at Day 85 compared to placebo plus FF/VI (124 mL (95% CI 93, 154, p &lt; 0.001) and 122 mL (95%CI 91, 152, p &lt; 0.001)).
Zato ni mogoče sklepati o statistični značilnosti te primerjave. in FF/VI pri odraslih bolnikih s klinično diagnozo KOPB po 85 dneh dosegel statistično značilno in klinično pomembno izboljšanje primarnega opazovanega dogodka, najnižje vrednosti FEV1 (124 ml (95-odstotni IZ 93, 154; p &lt; 0,001) in 122 ml (95-odstotni IZ 91, 152; p &lt; 0,001)).
In two controlled double blind clinical trials, the overall rate of thromboembolic events in patients treated with desirudin 15mg s.c. b.i.d. (N=370) was half that in patients treated with a standard dose of unfractionated heparin (N=396) (p &lt; 0.0001); the rate of proximal deep venous thrombosis was only one fifth that observed with the heparin (p &lt; 0.0001).
V dveh kontroliranih dvojno slepih kliničnih preskušanjih je bil celotni delež trombemboličnih dogodkov pri bolnikih, zdravljenih s 15 mg desirudina subkutano dvakrat na dan (n = 370), polovico manjši kot pri bolnikih, zdravljenih s standardnim odmerkom nefrakcioniranega heparina (n = 396) (p &lt; 0,0001); delež proksimalne globoke venske tromboze je bil le petino tistega pri heparinu (p &lt; 0,0001).
In two replicate 12 month studies in a total of 3,255 patients with COPD the incidence of bone fractures overall was low in all treatment groups, with a higher incidence in all Relvar Ellipta groups (2%) compared with the vilanterol 22 micrograms group ( &lt; 1%).
V dveh repliciranih 12-mesečnih študijah pri skupno 3.255 bolnikih s KOPB je bila celotna incidenca zlomov kosti majhna v vseh terapevtskih skupinah, a je bila večja v vseh skupinah z zdravilom Relvar Ellipta (2 %) kot v skupini s 22 mikrogrami vilanterola ( &lt; 1 %).
In two replicate 12 month studies in a total of 3,255 patients with COPD the incidence of bone fractures overall was low in all treatment groups, with a higher incidence in all Revinty Ellipta groups (2%) compared with the vilanterol 22 micrograms group ( &lt; 1%).
V dveh repliciranih 12-mesečnih študijah pri skupno 3.255 bolnikih s KOPB je bila celotna incidenca zlomov kosti majhna v vseh terapevtskih skupinah, a je bila večja v vseh skupinah z zdravilom Revinty Ellipta (2 %) kot v skupini s 22 mikrogrami vilanterola ( &lt; 1 %).
In two separate 12 week pivotal trials (Trials 1 and 2), ospemifene was associated with a statistically significant mean decrease from baseline in the percentage of parabasal cells and vaginal pH and a statistically significant mean increase from baseline in the percentage of superficial cells, compared with placebo (P &lt; 0.001 for each parameter) at weeks 4 and 12.
V dveh ločenih 12-tedenskih ključnih preskušanjih (preskušanji 1 in 2) je bil ospemifen povezan s statistično značilnim povprečnim zmanjšanjem od izhodišča v odstotku parabazalnih celic in nožničnega pH in s statistično značilnim povprečnim povečanjem od izhodišča v odstotku površinskih celic v primerjavi s placebom (P &lt; 0,001 za vsak parameter) v 4. in 12. tednu.
In two years, the risk was 85% in the placebo group and 69% in the Extavia group (Hazard Ratio = 0.57, 95% confidence interval (0.46, 0.71), p &lt; 0.00001).
V dveh letih je bilo tveganje 85-odstotno v skupini s placebom in 69-odstotno v skupini z zdravilom Extavia (razmerje tveganja = 0,57, interval zaupanja = 95 % (0,46, 0,71), p &lt; 0,00001).
In very rare cases ( &lt; 0.01 %) the temporary infertility may last more than 18 months.
V zelo redkih primerih lahko začasna neplodnost traja več kot 18 mesecev.
In very rare cases ( &lt; 0.01%) there has been transitory increased sexual interest, increased testicle size and testicular pain immediately after implantation.
V zelo redkih primerih ( &lt; 0,01%) je prišlo takoj po implantaciji do prehodnega povečanega spolnega zanimanja, povečane velikosti mod in bolečin v modih.
In very rare cases ( &lt; 0.01%), a transient behavioural change has been reported with development of aggression (see section 12 “Special warnings”).
V zelo redkih primerih ( &lt; 0,01%) je prišlo do prehodne spremembe obnašanja z razvojem agresije (glej poglavje 4.4 »Posebna opozorila«)
In very rare cases ( &lt; 0.01%), a transient behavioural change has been reported with the development of aggression (see section 4.4).
V zelo redkih primerih ( &lt; 0,01%) je prišlo do prehodne spremembe obnašanja z razvojem agresije (glej poglavje 4.4 ).
In very rare cases ( &lt; 1/100,000), hypersensitivity can be observed.
V zelo redkih primerih ( &lt; 1/100000) so opazili preobčutljivostne reakcije.
In view of the potential impact of bisphosphonates, including zoledronic acid, on renal function, the lack of clinical safety data in patients with severe renal impairment (in clinical trials defined as serum creatinine ≥ 400 μmol/l or ≥ 4.5 mg/dl for patients with TIH and ≥ 265 μmol/l or ≥ 3.0 mg/dl for patients with cancer and bone metastases, respectively) at baseline and only limited pharmacokinetic data in patients with severe renal impairment at baseline (creatinine clearance &lt; 30 ml/min), the use of Zoledronic Acid Teva is not recommended in patients with severe renal impairment.
Glede na možni vpliv zoledronske kisline na delovanje ledvic ob pomanjkanju kliničnih podatkov o varnosti pri bolnikih s težko izhodiščno okvaro ledvic (v kliničnih preskušanjih opredeljeno s serumskim kreatininom ≥ 400 μmol/l ali ≥ 4,5 mg/dl za bolnike s tumorsko povzročeno hiperkalciemijo - TIH - oziroma s serumskim kreatininom ≥ 265 μmol/l ali ≥ 3,0 mg/dl za bolnike z rakom in zasevki v kosteh) in glede na samo omejene farmakokinetične podatke pri bolnikih s težko izhodiščno ledvično okvaro (očistek kreatinina &lt; 30 ml/min), uporabe zdravila Zoledronska kislina Teva pri bolnikih s težko ledvično okvaro ne priporočamo.
In view of the potential impact of zoledronic acid on renal function, the lack of clinical safety data in patients with severe renal impairment (in clinical trials defined as serum creatinine 400 µmol/l or 4.5 mg/dl for patients with TIH and 265 µmol/l or 3.0 mg/dl for patients with cancer and bone metastases, respectively) at baseline and only limited pharmacokinetic data in patients with severe renal impairment at baseline (creatinine clearance &lt; 30 ml/min), the use of zoledronic acid is not recommended in patients with severe renal impairment.
Glede na možni vpliv zoledronske kisline na delovanje ledvic ob pomanjkanju kliničnih podatkov o varnosti pri bolnikih s težko izhodiščno okvaro ledvic (v kliničnih preskušanjih opredeljeno s serumskim kreatininom ≥ 400 μmol/l ali ≥ 4,5 mg/dl za bolnike s tumorsko povzročeno hiperkalciemijo - TIH - oziroma s serumskim kreatininom ≥ 265 μmol/l ali ≥ 3,0 mg/dl za bolnike z rakom in zasevki v kosteh) in glede na samo omejene farmakokinetične podatke pri bolnikih s težko izhodiščno ledvično okvaro (očistek kreatinina &lt; 30 ml/min), uporabe zoledronske kisline pri bolnikih s težko ledvično okvaro ne priporočamo.
In virologically stable treatment-experienced adults, emtricitabine, in combination with an NRTI (either stavudine or zidovudine) and a protease inhibitor (PI) or an NNRTI was shown to be non-inferior to lamivudine with respect to the proportion of responders ( &lt; 400 copies/ml) through 48 weeks (77% emtricitabine, 82% lamivudine).
Pri virološko stabilnih odraslih, ki se zdravijo že dalj časa, se emtricitabin, v kombinaciji z NRTI (ali stavudinom ali zidovudinom) in zaviralcem proteaz (PI) ali NNRTI, ni obnesel slabše od lamivudina glede na delež odzivov ( &lt; 400 virionov/ml) v obdobju 48 tednov (77 % emtricitabin, 82 % lamivudin).
In vitro apixaban studies showed no inhibitory effect on the activity of CYP1A2, CYP2A6, CYP2B6, CYP2C8, CYP2C9, CYP2D6 or CYP3A4 (IC50 &gt; 45 M) and weak inhibitory effect on the activity of CYP2C19 (IC50 &gt; 20 M) at concentrations that are significantly greater than peak plasma concentrations observed in patients.
Pri in vitro študijah niso ugotovili zaviralnega učinka apiksabana na aktivnost CYP1A2, CYP2A6, CYP2B6, CYP2C8, CYP2C9, CYP2D6 ali CYP3A4 (IC50 &gt; 45 M) in šibek zaviralni učinek na aktivnost CYP2C19 (IC50 &gt; 20 M) pri koncentracijah, ki so bile pomembno večje od največjih plazemskih koncentracij pri človeku.
In vitro binding of axitinib to human plasma proteins is &gt; 99% with preferential binding to albumin and moderate binding to α1-acid glycoprotein.
In vitro delež vezave aksitiniba na plazemske beljakovine pri ljudeh znaša &gt; 99 %, pri čemer gre v glavnem za vezavo na albumin in zmerno vezavo na α1-kisli glikoprotein.
In vitro binding of emtricitabine to human plasma proteins is &lt; 4% and independent of concentrations over the range of 0.02 to 200 µg/ml.
In vitro je bila vezava emtricitabina na človeške plazemske beljakovine &lt; 4 % in neodvisna od koncentracije v razponu med 0,02 in 200 µg/ml.
In vitro binding of emtricitabine to human plasma proteins was &lt; 4% and independent of concentration over the range of 0.02 to 200 µg/mL.
In vitro je bila vezava emtricitabina na humane plazemske proteine manj kot 4 % in je neodvisna od koncentracije v razponu med 0,02 in 200 µg/ml.
In vitro binding of emtricitabine to human plasma proteins was &lt; 4% and independent of concentration over the range of 0.02 to 200 µg/mL.
In vitro je bila vezava emtricitabina na humane plazemske proteine manj kot 4% in je neodvisna od koncentracije v razponu med 0,02 in 200 µg/ml.
In vitro binding of emtricitabine to human plasma proteins was &lt; 4% and independent of concentration over the range of 0.02 to 200 µg/mL.
In vitro je bila vezava emtricitabina na humane plazemske proteine manj kot &lt; 4% in je neodvisna od koncentracije v razponu med 0,02 in 200 µg/ml.
In vitro binding of emtricitabine to human plasma proteins was &lt; 4% and independent of concentration over the range of 0.02 – 200 μg/ml.
In vitro je bila vezava emtricitabina na humane plazemske proteine manj kot 4% in je neodvisna od koncentracije v razponu med 0,02 in 200 μg/ml.
In vitro binding of emtricitabine to human plasma proteins was &lt; 4% and independent of concentration over the range of 0.02-200 µg/mL.
In vitro je bila vezava emtricitabina na humane plazemske proteine &lt; 4 % in je neodvisna od koncentracije v razponu med 0,02–200 µg/ml.
In vitro binding of emtricitabine to human plasma proteins was &lt; 4% and independent of concentration over the range of 0.02-200 µg/ml.
In vitro je bila vezava emtricitabina na humane plazemske proteine manj kot 4 % in je neodvisna od koncentracije v razponu med 0,02 in 200 µg/ml.
In vitro binding of emtricitabine to human plasma proteins was &lt; 4% and independent of concentration over the range of 0.02-200 µg/mL.
In vitro je bila vezava emtricitabina na humane plazemske proteine manj kot 4 % in je neodvisna od koncentracije v razponu med 0,02-200 µg/ml.
In vitro binding of emtricitabine to human plasma proteins was &lt; 4% and independent of concentration over the range of 0.02-200 μg/mL.
In vitro je bila vezava emtricitabina na humane plazemske proteine manj kot 4 % in je neodvisna od koncentracije v razponu med 0,02-200 µg/ml.
In vitro binding of tenofovir to human plasma or serum protein is &lt; 0.7% and 7.2%, respectively over the tenofovir concentration range 0.01 to 25 µg/ml.
V območju koncentracij tenofovirja od 0,01 do 25 μg/ml je vezava tenofovirja na človeške beljakovine v plazmi in vitro &lt; 0,7 %, na serumske beljakovine pa 7,2 %.
In vitro binding of tenofovir to human plasma proteins is &lt; 0.7% and is independent of concentration over the range of 0.01-25 µg/mL.
In vitro je vezava tenofovirja na humane plazemske proteine &lt; 0,7 % in je neodvisna od koncentracije v razponu med 0,01–25 µg/ml.
In vitro binding of tenofovir to human plasma proteins is &lt; 0.7% and is independent of concentration over the range of 0.01-25 μg/mL.
In vitro je bila vezava tenofovirata na humane plazemske proteine &lt; 0,7 % in je neodvisna od koncentracije v razponu med 0,01-25 μg/ml.
In vitro orlistat is &gt; 99 % bound to plasma proteins (lipoproteins and albumin were the major binding proteins).
In vitro se več kot 99 % orlistata veže na beljakovine v plazmi (pretežno na lipoproteine in albumin).
In vitro plasma protein binding in human plasma of fluticasone furoate and vilanterol was high, on average &gt; 99.6% and 93.9%, respectively.
Vezava na plazemske beljakovine v človeški plazmi in vitro je bila visoka: flutikazonfuroata v povprečju &gt; 99,6 % in vilanterola v povprečju 93,9 %.
In vitro selection of darunavir-resistant virus from wild type HIV-1 was lengthy ( &gt; 3 years).
In vitro selekcija virusa, odpornega na darunavir, iz divjega tipa HIV-1 je bila dolgotrajna ( &gt; 3 leta).
In vitro studies demonstrate that varenicline does not inhibit cytochrome P450 enzymes (IC50 &gt; 6,400 ng/ml).
Študije in vitro kažejo, da vareniklin ne zavira encimov citokroma P450 (IK50 &gt; 6.400 ng/ml).
In vitro studies evaluating the percent recovery of total dose delivered with nasogastric or gastrostomy tubes demonstrated the percent of dose recovered was &gt; 99% for doses &gt; 1 ml and 70% for a 0.5 ml dose.
Študije in vitro, ki so ocenjevale odstotek izkoriščenega odmerka pri skupnem odmerku, dostavljenem prek nazogastričnih sond ali gastrostome, so pokazale, da je izkoriščeni odmerek &gt; 99 % za odmerke &gt; 1 ml in 70 % za odmerek 0,5 ml.
In vitro studies evaluating the percent recovery of total dose delivered with nasogastric, nasojejunal or gastrostomy tubes demonstrated the percent of dose recovered was &gt; 99% for doses &gt; 1 ml and 70% for a 0.5 ml dose.
Študije in vitro, ki so ocenjevale odstotek izkoriščenega skupnega odmerka, ki je bil apliciran preko nazogastrične sonde, nazojejunalne sonde ali gastrostome, so pokazale, da je bil odstotek izkoriščenega odmerka &gt; 99 % za odmerke &gt; 1 ml in približno 70 % za odmerek 0,5 ml.
In vitro studies have shown that vardenafil is more potent on PDE5 than on other known phosphodiesterases ( &gt; 15-fold relative to PDE6, &gt; 130-fold relative to PDE1, &gt; 300-fold relative to PDE11, and &gt; 1000-fold relative to PDE2, PDE3, PDE4, PDE7, PDE8, PDE9 and PDE10).
Študije in vitro so pokazale, da vardenafil močneje vpliva na PDE5 kot na druge znane fosfodiesteraze ( &gt; 15-krat v primerjavi s PDE6, &gt; 130-krat v primerjavi s PDE1, &gt; 300-krat v primerjavi s PDE11 in &gt; 1.000-krat v primerjavi s PDE2, PDE3, PDE4, PDE7, PDE8, PDE9 in PDE10).
In vitro studies in human, dog, mouse and rat plasma showed a high plasma protein binding ( &gt; 99.5 %), mainly to albumin and α-1-acid glycoprotein.
Študije in vitro v plazmi ljudi, psov, miši in podgan kažejo na visoko vezavo na beljakovine v plazmi ( &gt; 99,5 %), pretežno na albumin in α-1 kisli glikoprotein.
In vitro studies using human liver microsomes show no or little ( &lt; 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 ( &lt; 25 %) inhibicijo izoencimov 1A2, 2A6, 2B6, 2C8, 2C9, 2C19, 2D6, 2E1 ali 3A4 citokroma P450, pri koncentracijah zonisamida, ki so bile dva ali večkrat višje od klinično pomembnih serumskih koncentracij nevezane učinkovine.
In vitro studies using human liver microsomes show no or little ( &lt; 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 ( &lt; 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, apremilast has little to no inhibitory effect (IC50 &gt; 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 &gt; 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 a substrate, and a weak inhibitor of P-glycoprotein (IC50 &gt; 50µM), however clinically relevant drug interactions mediated via P-gp are not expected to occur.
In vitro je apremilast substrat in šibek zaviralec P-glikoproteina (IC50 &gt; 50µM), vendar ne pričakujemo, da bo prišlo do klinično pomembnih interakcij med zdravili, posredovanih s P-gp.
In vitro, cytochrome P450 3A4 was demonstrated as the predominant ( &gt; 80%) isoform involved in the P450-mediated metabolism of lenvatinib.
In vitro so pokazali, da je citokrom P450 3A4 prevladujoča ( &gt; 80 %) izooblika vpletena v presnovo lenvatiniba, ki poteka preko P450.
In vitro, dolutegravir demonstrated no direct, or weak inhibition (IC50 &gt; 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 &gt; 50 μM) na encime citokrom P450 (CYP)1A2, CYP2A6, CYP2B6, CYP2C8, CYP2C9, CYP2C19, CYP2D6,
In vitro, lurasidone demonstrated no direct, or weak inhibition (direct or time-dependent) (IC50 &gt; 5.9 μM) of the enzymes cytochrome P450 (CYP)1A2, CYP2B6, CYP2C8, CYP2C9,
Lurasidon in vitro ni neposredno ali šibko zaviral (neposredno ali v odvisnosti od časa) (IC50 &gt; 5,9 μM) encimov citokroma P450 (CYP)1A2, CYP2B6, CYP2C8, CYP2C9, CYP2C19,
In vitro, orlistat is &gt; 99% bound to plasma proteins (lipoproteins and albumin were the major binding proteins).
In vitro se več kot 99 % orlistata veže na beljakovine v plazmi (večinoma na lipoproteine in albumin).
In vitro, this metabolite shows minimal inhibition of acetylcholinesterase ( &lt; 10 %).
In vitro kaže ta presnovek zelo majhno stopnjo zaviranja acetilholinesteraze ( &lt; 10 %).
In vitro, this metabolite shows minimal inhibition of acetylcholinesterase ( &lt; 10 %).
In vitro ta presnovek kaže minimalno zaviranje acetilholinesteraze ( &lt; 10 %).
In vitro, this metabolite shows minimal inhibition of acetylcholinesterase ( &lt; 10%).
In vitro kaže ta presnovek zelo majhno stopnjo zaviranja holinesteraze ( &lt; 10 %).