natgillin/translations-raw huggingface dataset:
In patients with normal renal function (creatinine clearance ≥ 80 ml/min), high doses of non-steroidal anti-inflammatory drugs (NSAIDs, such as ibuprofen &gt; 1600 mg/day) and aspirin at higher doses (≥ 1.3 g daily) may decrease pemetrexed elimination and, consequently, increase the occurrence of pemetrexed adverse events.
U bolesnika s normalnom funkcijom bubrega (klirens kreatinina ≥ 80 ml/min), visoke doze nesteroidnih protuupalnih lijekova (NSAIL, npr. ibuprofen &gt; 1600 mg na dan) i više doze acetilsalicilatne kiseline (≥ 1,3 g na dan) mogu smanjiti eliminaciju pemetrekseda i, posljedično, povećati pojavu nuspojava izazvanih pemetreksedom.
In patients with normal renal function, defined as CLcr &gt; 60 ml/min, zoledronic acid 4 mg/100 ml solution for infusion must not be further diluted.
U bolesnika s normalnom funkcijom bubrega, definiranom klirensom kreatinina većim od 60 ml/min, zoledronatna kiselina 4 mg/100 ml otopina za infuziju ne smije se dodatno razrjeđivati.
In patients with normal renal function, defined as CLcr &gt; 60 ml/min, zoledronic acid 4 mg/100 ml solution for infusion must not be further diluted.
U bolesnika s normalnom funkcijom bubrega, koja se definira kao CLcr &gt; 60 ml/min, zoledronatna kiselina 4 mg/100 ml otopina za infuziju ne smije se dodatno razrijediti.
In patients with polyarticular JIA who were 2 to &lt; 4 years old or aged 4 and above weighing &lt; 15 kg dosed with adalimumab 24 mg/m2 , the mean trough steady-state serum adalimumab concentrations was 6.0 ± 6.1 µg/ml (101% CV) for adalimumab without concomitant methotrexate and 7.9 ± 5.6 µg/ml (71.2% CV) with concomitant methotrexate.
U bolesnika s poliartikularnim JIA u dobi od 2 do manje od 4 godine ili u dobi od 4 godine i starijih i tjelesne težine manje od 15 kg, nakon primjene 24 mg/m2 adalimumaba srednja vrijednost najniže koncentracije adalimumaba u serumu u stanju dinamičke ravnoteže bila je 6,0 ± 6,1 µg/ml (101% CV) za adalimumab bez istodobne primjene metotreksata i 7,9 ± 5,6 µg/ml (71,2% CV) uz istodobnu primjenu metotreksata.
In patients with polyarticular JIA who were 2 to &lt; 4 years old or aged 4 and above weighing &lt; 15 kg dosed with adalimumab 24 mg/m2, the mean trough steady-state serum adalimumab concentrations was 6.0 ± 6.1 µg/ml (101% CV) for adalimumab without concomitant methotrexate and 7.9 ± 5.6 µg/ml (71.2% CV) with concomitant methotrexate.
U bolesnika s poliartikularnim JIA u dobi od 2 do manje od 4 godine ili u dobi od 4 godine i starijih i tjelesne težine manje od 15 kg, nakon primjene 24 mg/m2 adalimumaba srednja vrijednost najniže koncentracije adalimumaba u serumu u stanju dinamičke ravnoteže bila je 6,0 ± 6,1 µg/ml (101% CV) za adalimumab bez istodobne primjene metotreksata i 7,9 ± 5,6 µg/ml (71,2% CV) uz istodobnu primjenu metotreksata.
In patients with previously untreated CLL, the median decreases in B cell counts after the first cycle and prior to the sixth monthly cycle were 94% and &gt; 99% respectively for ofatumumab in combination with chlorambucil and 73% and 97% respectively for chlorambucil alone.
U bolesnika s prethodno neliječenim KLL-om, medijan smanjenja broja B-stanica nakon prvog ciklusa odnosno prije šestog mjesečnog ciklusa iznosio je 94% odnosno &gt; 99% za ofatumumab u kombinaciji s klorambucilom te 73% odnosno 97% za klorambucil u monoterapiji.
In patients with severe hepatic impairment (Child-Pugh C) or severe renal impairment (Creatinine Clearance &lt; 30 mL/min/1.73m2), the potential risks associated with the use of this medicine should be assessed against the medical need (see section 5.2).
U bolesnika s teškim oštećenjem funkcije jetre (Child-Pugh C) ili teškim oštećenjem funkcije bubrega (klirens kreatinina &lt; 30 ml/min/1,73m2), potencijalne rizike povezane s primjenom ovog lijeka treba procijeniti u odnosu na medicinsku potrebu (vidjeti dio 5.2).
In patients with severe renal impairment (CrCL &lt; 30 mL/min, calculated by the Cockroft-Gault formula), the recommended dose of bosutinib is 300 mg daily (see sections 4.4 and 5.2).
U bolesnika s teškim oštećenjem funkcije bubrega (CrCL &lt; 30 ml/min, izračunato Cockroft-Gaultovom formulom), preporučena doza je 300 mg bosutiniba dnevno (vidjeti dijelove 4.4 i 5.2).
In patients with severe renal impairment (creatinine clearance &lt; 30 ml/min) administered 1microgram/kg/min , 80 % inhibition was achieved in more than 80 % of patients at 24 hours.
U bolesnika s teškim oštećenjem bubrežne funkcije (klirens kreatinina &lt; 30 ml/min) u kojih je primijenjen lijek u dozi od 1 mikrogram/kg/min, nakon 24 sata postignuta je 80 % -tna inhibicija u više od 80 % bolesnika.
In patients with severe renal impairment (creatinine clearance &lt; 30 ml/min) administered 1microgram/kg/min , 80 % inhibition was achieved in more than 80 % of patients at 24 hours.
U bolesnika s teškim oštećenjem bubrežne funkcije (klirens kreatinina &lt; 30 ml/min) u kojih je primijenjen lijek u dozi od mikrogram/kg/min, nakon 24 sata postignuta je 80 % -tna inhibicija u više od 80 % bolesnika.
In patients with severe renal impairment (creatinine clearance &lt; 30 ml/min) and in patients who require haemodialysis use of tenofovir disoproxil fumarate is not recommended.
U pacijenta s teškim oštećenjem funkcije bubrega (klirens kreatinina &lt; 30 ml/min) i pacijenta kojima je potrebna hemodijaliza ne preporučuje se primjena tenofovirdizoproksilfumarata.
In patients with severe renal impairment (creatinine clearance &lt; 30 ml/min) or end-stage renal disease requiring haemodialysis or peritoneal dialysis, SIRTURO should be used with caution (see section 5.2).
U bolesnika s teškim oštećenjem bubrega (klirens kreatinina &lt; 30 ml/min) ili sa završnim stadijem bubrežne bolesti koja zahtjeva hemodijalizu ili peritonealnu dijalizu, SIRTURO se mora uzimati s oprezom (vidjeti dio 5.2).
In patients with severe renal impairment (creatinine clearance &lt; 30 ml/min) rivaroxaban plasma levels may be significantly increased (1.6 fold on average) which may lead to an increased bleeding risk.
U bolesnika s teško oštećenom funkcijom bubrega (klirens kreatinina &lt; 30 ml/min) mogu se značajno povisiti razine rivaroksabana u plazmi (prosječno 1,6 puta), što može dovesti do povećanog rizika od krvarenja.
In patients with severe renal impairment (creatinine clearance &lt; 30 ml/min) rivaroxaban plasma levels may be significantly increased (1.6-fold on average) which may lead to an increased bleeding risk.
U bolesnika s teško oštećenom funkcijom bubrega (klirens kreatinina manji 30 ml/min) mogu se značajno povisiti razine rivaroksabana u plazmi (prosječno 1,6 puta), što može dovesti do povećanog rizika od krvarenja.
In patients with severe renal impairment (creatinine clearance &lt; 30 ml/min), clearance was decreased by 22% (n = 5).
U bolesnika s teškim oštećenjem funkcije bubrega (klirens kreatinina &lt; 30 ml/min) klirens je bio smanjen za 22% (n = 5).
In patients with severe renal impairment (creatinine clearance &lt; 30 ml/min.) or patients who may be predisposed to fluid retention parecoxib should be initiated at the lowest recommended dose (20 mg) and the patient's kidney function should be closely monitored (see sections 4.4 and 5.2).
U bolesnika s teškim oštećenjem funkcije bubrega (klirens kreatinina &lt; 30 ml/min.) ili u bolesnika koji mogu biti skloni zadržavanju tekućine, primjena parekoksiba mora se započeti u najnižoj preporučenoj dozi (20 mg), a funkcija bubrega bolesnika mora se pažljivo nadzirati (vidjeti dijelove 4.4 i 5.2).
In patients with severe renal impairment (creatinine clearance &lt; 30 ml/min.) or patients who may be predisposed to fluid retention parecoxib should be initiated at the lowest recommended dose (20 mg) and the patient's kidney function should be closely monitored (see sections 4.4 and 5.2).
U bolesnika s teškim oštećenjem funkcije bubrega (klirens kreatinina &lt; 30 ml/min.) ili u bolesnika koji mogu biti skloni zadržavanju tekućine, primjena parekoksiba mora se započeti u najnižoj preporučenoj dozi (20 mg), a funkcija bubrega bolesnika pažljivo nadzirati (vidjeti dijelove 4.4 i 5.2).
In patients with severe renal impairment (creatinine clearance &lt; 30 ml/min) a starting dose of Levitra 5 mg film-coated tablets should be considered.
U bolesnika s teškim oštećenjem funkcije bubrega (klirens kreatinina &lt; 30 ml/min), trebalo bi započeti liječenje dozom od Levitra 5 mg filmom obloženih tableta.
In patients with severe renal impairment (creatinine clearance &lt; 30 ml/min) a starting dose of Vivanza 5 mg film-coated tablets should be considered.
U bolesnika s teškim oštećenjem funkcije bubrega (klirens kreatinina &lt; 30 ml/min), trebalo bi započeti liječenje dozom od Vivanza 5 mg filmom obloženih tableta.
In patients with severe renal impairment (creatinine clearance &lt; 30 ml/min), a starting dose of 5 mg should be considered.
U bolesnika s teškim oštećenjem funkcije bubrega (klirens kreatinina &lt; 30 ml/min), trebalo bi započeti liječenje dozom od 5 mg.
In patients with severe renal impairment (creatinine clearance &lt; 30mL/min) administered 1microgram/kg/min , 80% inhibition was achieved in more than 80% of patients at 24 hours.
U bolesnika s teškim oštećenjem bubrežne funkcije (klirens kreatinina &lt; 30 ml/min) u kojih je primijenjen lijek u dozi od 1 mikrogram/kg/min, nakon 24 sata postignuta je 80 % -tna inhibicija u više od 80 % bolesnika.
In patients with severe renal impairment (eGFR &lt; 30 mL/min/1.73 m2), caution should be exercised during dose titration.
U bolesnika s teškim oštećenjem funkcije bubrega (eGFR &lt; 30 ml/min/1,73 m2), titraciju treba provoditi uz oprez.
In patients with severe renal impairment (eGFR &lt; 30 ml/min/1.73 m2), including those with end-stage renal disease requiring dialysis, Enurev Breezhaler should only be used in the expected benefit outweighs the potential risk (see section 4.4).
U bolesnika s teškim oštećenjem bubrega (eGFR &lt; 30 ml/min/1,73 m2), uključujući one s bolešću bubrega u završnoj fazi koja zahtijeva dijalizu, Enurev Breezhaler treba koristiti samo ako očekivana korist premašuje potencijalni rizik (vidjeti dio 4.4).
In patients with severe renal impairment (eGFR &lt; 30 ml/min/1.73 m2), including those with end-stage renal disease requiring dialysis, Seebri Breezhaler should only be used in the expected benefit outweighs the potential risk (see section 4.4).
U bolesnika s teškim oštećenjem bubrega (eGFR &lt; 30 ml/min/1,73 m2), uključujući one s bolešću bubrega u završnoj fazi koja zahtijeva dijalizu, Seebri Breezhaler treba koristiti samo ako očekivana korist premašuje potencijalni rizik (vidjeti dio 4.4).
In patients with severe renal impairment (eGFR &lt; 30 ml/min/1.73 m2), including those with end-stage renal disease requiring dialysis, Tovanor Breezhaler should only be used in the expected benefit outweighs the potential risk (see section 4.4).
U bolesnika s teškim oštećenjem bubrega (eGFR &lt; 30 ml/min/1,73 m2), uključujući one s bolešću bubrega u završnoj fazi koja zahtijeva dijalizu, Tovanor Breezhaler treba koristiti samo ako očekivana korist premašuje potencijalni rizik (vidjeti dio 4.4).
In patients without decompensated cirrhosis requiring the addition of ribavirin to their treatment regimen (see Table 1), the daily dose of ribavirin is weight based ( &lt; 75 kg = 1,000 mg and
U pacijenata bez dekompenzirane ciroze čijem je terapijskom režimu potrebno dodati ribavirin (vidjeti tablicu 1) dnevna doza ribavirina temelji se na tjelesnoj težini ( &lt; 75 kg = 1000 mg i
In patients ≥60 kg and age &lt; 75 years, non-CABG-related TIMI major or minor bleeding rates were 3.6% for prasugrel and 2.8% for clopidogrel; rates for fatal bleeding were 0.2% for prasugrel and 0.1% for clopidogrel.
U bolesnika tjelesne težine ≥ 60 kg i mlađih od 75 godina, stopa značajnih ili manjih krvarenja (prema TIMI kriterijima) nevezanih uz CABG iznosila je 3,6% uz prasugrel te 2,8% uz klopidogrel, dok je stopa smrtonosnih krvarenja bila 0,2% uz prasugrel i 0,1% uz klopidogrel.
In Phase 2 and 3 clinical trials of telaprevir, treatment-naïve and prior treatment-failure patients with predominant telaprevir-resistant variants at baseline (pre-treatment) were rare (V36M, T54A and R155K &lt; 1% and T54S 2.7%).
U fazi II i III kliničkih ispitivanja s telaprevirom rijetki su bili bolesnici koji prethodno nisu bili liječeni ili je liječenje u njih bilo neuspješno, a koji su na početku (prije liječenja) imali pretežno varijante rezistentne na telaprevir (V36M, T54A i R155K &lt; 1% i T54S 2,7%).
In phase II-III randomised double-blind monotherapy studies respective increases in QTc interval prolongation that exceeded change from baseline greater than &gt; 60 ms Fridericia-correction and Bazett-correction were 0 (0.0%) and 2 (0.3%) among placebo and 1 (0.1%) and 1 (0.1%) among Intuniv patients.
U randomiziranim, dvostruko slijepim ispitivanjima monoterapijskog liječenja faze II-III, odgovarajuća povećanja produljenja QTc intervala koja su premašila promjenu od početne vrijednosti više od 60 ms nakon korekcije prema Fridericiji i korekcije prema Bazettu iznosila su 0 (0,0%) odnosno 2 (0,3%) u bolesnika koji su primali placebo te 1 (0,1%) odnosno 1 (0,1%) u bolesnika liječenih Intunivom.
In Phase III, 6-month studies umeclidinium/vilanterol provided clinically meaningful improvements over placebo in lung function (as measured by forced expiratory volume in 1 second [FEV1]) over 24 hours following once daily administration, which were evident at 15 minutes following administration of the first dose (improvement over placebo by 112 ml (p &lt; 0.001*).
U 6-mjesečnim ispitivanjima faze III, primjena umeklidinija/vilanterola dovela je do klinički značajnih poboljšanja plućne funkcije (mjereno forsiranim izdisajnim volumenom u 1 sekundi [FEV1]) u odnosu na placebo tijekom 24 sata nakon primjene jedanput na dan, koja su bila primjetna 15 minuta nakon primjene prve doze (poboljšanje za 112 ml u odnosu na placebo (p &lt; 0,001)).
In pigs, after a single oral dose of radiolabelled material &gt; 90% absorption was demonstrated.
U svinja, nakon pojedinačne oralne doze radiooznačenog materijala dokazana je apsorpcija za više od 90 %.
In placebo-controlled studies (studies 1 and 2), the incidence of transaminase elevations ( &gt; 3 x upper limit of normal [ULN]) were similar between subjects in the ivacaftor and placebo treatment groups (see section 4.8).
U placebom kontroliranim ispitivanjima (ispitivanja 1 i 2), incidencija povišenih transaminaza ( &gt; 3 puta iznad gornje granice normale [GGN]) bila je slična u ispitanika liječenih ivakaftorom i onih koji su primali placebo (vidjeti dio 4.8).
In placebo-controlled studies palpitations were reported &gt; 1% more often in the teriflunomide 7 mg group (but not in the teriflunomide 14 mg group) when compared to placebo.
U placebom kontroliranim ispitivanjima palpitacije su bile prijavljene &gt; 1% češće u skupini koja je primala 7 mg teriflunomida (ali ne i u skupini koja je primala 14 mg teriflunomida) u usporedbi sa skupinom koja je primala placebo.
In placebo-controlled studies the following was established: systolic blood pressure was &gt; 140 mm Hg in 19.9% of patients receiving 14 mg/day teriflunomide as compared to 15.5% receiving placebo; systolic blood pressure was &gt; 160 mm Hg in 3.8% of patients receiving 14 mg/day teriflunomide as compared to 2.0% receiving placebo; diastolic blood pressure was &gt; 90 mm Hg in 21.4% of patients receiving 14 mg/day teriflunomide as compared to 13.6% receiving placebo.
Tijekom placebom kontroliranih ispitivanja utvrđeno je sljedeće: sistolički krvni tlak bio je &gt; 140 mm Hg u 19,9% bolesnika koji su primali teriflunomid u dozi od 14 mg/dan u usporedbi sa 15,5% bolesnika koji su primali placebo; sistolički krvni tlak bio je &gt; 160 mm Hg u 3,8% bolesnika koji su primali teriflunomid u dozi od 14 mg/dan u usporedbi s 2,0% bolesnika koji su primali placebo; dijastolički krvni tlak bio je &gt; 90 mm Hg u 21,4% bolesnika koji su primali teriflunomid u dozi od 14 mg/dan u usporedbi sa 13,6% bolesnika koji su primali placebo;
In plasma, both brinzolamide and N- desethylbrinzolamide concentrations are low and generally below assay quantitation limits ( &lt; 7.5 ng/ml).
U plazmi su koncentracije i brinzolamida i N-desetil- brinzolamida niske i općenito su ispod limita testa za određivanje ( &lt; 7,5 ng/ml ).
In plasma, tacrolimus is highly bound ( &gt; 98.8%) to plasma proteins, mainly to serum albumin and α-1-acid glycoprotein.
U plazmi je takrolimus u visokom postotku vezan ( &gt; 98,8%) za proteine plazme, uglavnom za serumski albumin i α-1-kiseli glikoprotein.
In plasma, tacrolimus is highly bound ( &gt; 98.8%) to plasma proteins, mainly to serum albumin and α-1-acid glycoprotein.
U plazmi je takrolimus uglavnom vezan ( &gt; 98,8%) za proteine plazme, uglavnom za serumski albumin i α-1-kiseli glikoprotein.
In plasma, tacrolimus is highly bound ( &gt; 98.8%) to plasma proteins, mainly to serum albumin and α-1-acid glycoprotein.
U plazmi se takrolimus u velikoj mjeri veže ( &gt; 98,8%) na proteine plazme, uglavnom na serumski albumin i α-l-kiseli glikoprotein.
In pooled controlled studies using an every 2 week dosing interval, 796 of 3340 patients (23.8%) treated with Praluent had two consecutive values of LDL-C &lt; 25 mg/dL ( &lt; 0.65 mmol/L), including 288 patients (8.6%) with two consecutive values &lt; 15 mg/dL ( &lt; 0.39 mmol/L).
Prema objedinjenim podacima iz kontroliranih ispitivanja u kojima se koristio interval doziranja od svaka 2 tjedna, 796 od 3340 bolesnika (23,8%) liječenih lijekom Praluent imalo je dvije uzastopno izmjerene vrijednosti LDL-C od &lt; 25 mg/dl ( &lt; 0,65 mmol/l), uključujući 288 bolesnika (8,6%) s dvije uzastopne vrijednosti od &lt; 15 mg/dl ( &lt; 0,39 mmol/l).
In population pharmacokinetic analysis, no clinically significant relationship was observed between erlotinib clearance and creatinine clearance, but there are no data available for patients with creatinine clearance &lt; 15 ml/min.
U farmakokinetičkoj populacijskoj analizi nije uočena klinički značajna povezanost između klirensa erlotiniba i klirensa kreatinina, ali nisu dostupni podaci za bolesnike s klirensom kreatinina &lt; 15 ml/min.
In post marketing very rare cases ( &lt; 1/10,000) of hypersensitivity reactions occurred with palonosetron solution for injection for intravenous use.
Nakon stavljanja lijeka u promet, reakcije preosjetljivosti pojavile su se u vrlo rijetkim slučajevima ( &lt; 1/10 000) primjene otopine palonosetrona za intravensku uporabu.
In post-marketing experience, there have also been reports of eosinophilia (eosinophil count &gt; 1,500/mm3) without clinical symptoms.
Nakon stavljanja lijeka u promet, također su zabilježene pojave eozinofilije (broj eozinofila &gt; 1500/mm3) bez kliničkih simptoma.
In preclinical mutagenesis studies, 40 nM was determined as the concentration of ponatinib sufficient to inhibit viability of cells expressing all tested BCR-ABL mutants by &gt; 50% (including T315I) and suppress the emergence of mutant clones.
U pretkliničkim ispitivanjima mutagenosti, 40 nM je određeno kao koncentracija ponatiniba koja je dovoljna za inhibiciju više od 50% vijabilnosti stanica koje eksprimiraju sve testirane mutacije BCR-ABL (uključujući T315I) i potiskivanje nadiranja mutantskih klonova.
In preclinical studies, olanzapine exhibited a range of receptor affinities (Ki &lt; 100 nM) for serotonin 5 HT2A/2C, 5 HT3, 5 HT6; dopamine D1, D2, D3, D4, D5; cholinergic muscarinic receptors M1-M5; α1 adrenergic; and histamine H1 receptors.
U ispitivanju pomoću pozitronske emisijske tomografije (PET), jednostruka oralna doza (10 mg) olanzapina u zdravih dobrovoljaca dovela je do većeg zauzimanja 5 HT2A nego dopaminskih D2 receptora.
In preclinical studies, olanzapine exhibited a range of receptor affinities (Ki &lt; 100 nM) for serotonin 5 HT2A/2C, 5 HT3, 5 HT6; dopamine D1, D2, D3, D4, D5; cholinergic muscarinic receptors M1-M5; α1 adrenergic; and histamine H1 receptors.
U pretkliničkim ispitivanjima olanzapin je pokazao raspon afiniteta za receptore (Ki &lt; 100 nM) serotonina 5 HT2A/2C, 5 HT3, 5 HT6; dopamina D1, D2, D3, D4, D5; kolinergičke muskarinske receptore M1-M5; α1 adrenergičke; i histaminske H1 receptore.
In preclinical studies, olanzapine exhibited a range of receptor affinities (Ki &lt; 100 nM) for serotonin 5 HT2A/2C, 5 HT3, 5 HT6; dopamine D1, D2, D3, D4, D5; cholinergic muscarinic receptors M1-M5; α1 adrenergic; and histamine H1 receptors.
U pretkliničkim ispitivanjima, olanzapin je pokazao raspon afiniteta za receptore (Ki &lt; 100 nM) serotonina 5 HT2A/2C, 5 HT3, 5 HT6; dopamina D1, D2, D3, D4, D5; kolinergičke muskarinske receptore M1–M5; α1 adrenergičke; i histaminske H1 receptore.
In preclinical studies, olanzapine exhibited a range of receptor affinities (Ki &lt; 100 nM) for serotonin 5 HT2A/2C, 5 HT3, 5 HT6; dopamine D1, D2, D3, D4, D5; cholinergic muscarinic receptors M1-M5; α1 adrenergic; and histamine H1 receptors.
U pretkliničkim ispitivanjima, olanzapin je pokazao raspon afiniteta za receptore (Ki &lt; 100 nM) serotonina 5HT2A/2C, 5HT3, 5HT6; dopamina D1, D2, D3, D4, D5; kolinergičke muskarinske receptore M1-M5; α1 adrenergičke; i histaminske H1 receptore.
In preclinical studies, olanzapine exhibited a range of receptor affinities (Ki &lt; 100 nM) for serotonin 5 HT2A/2C, 5 HT3, 5 HT6; dopamine D1, D2, D3, D4, D5; cholinergic muscarinic receptors M1-M5; 1 adrenergic; and histamine H1 receptors.
U pretkliničkim ispitivanjima olanzapin je pokazao raspon afiniteta za receptore (Ki &lt; 100 nM) serotonina 5HT2A/2C, 5HT3, 5HT6; dopamina D1, D2, D3, D4, D5; kolinergičke muskarinske receptore M1-M5; α1 adrenergičke; i histaminske H1 receptore.
In preclinical studies, olanzapine exhibited a range of receptor affinities (Ki &lt; 100 nM) for serotonin 5 HT2A/2C, 5 HT3, 5 HT6; dopamine D1, D2, D3, D4, D5; cholinergic muscarinic receptors M1-M5; 1 adrenergic; and histamine H1 receptors.
U pretkliničkim ispitivanjima, olanzapin je pokazao raspon afiniteta za receptore (Ki &lt; 100 nM) serotonina 5HT2A/2C, 5HT3, 5HT6; dopamina D1, D2, D3, D4, D5; kolinergičke muskarinske receptore M1-M5; α1 adrenergičke; i histaminske H1 receptore.
In preclinical studies, olanzapine exhibited a range of receptor affinities (Ki &lt; 100 nM) for serotonin 5HT2A/2C, 5HT3, 5HT6; dopamine D1, D2, D3, D4, D5; cholinergic muscarinic receptors M1-M5; α 1 adrenergic; and histamine H1 receptors.
U pretkliničkim ispitivanjima olanzapin je pokazao raspon afiniteta za receptore (Ki &lt; 100 nM) serotonina 5HT2A/2C, 5HT3, 5HT6; dopamina D1, D2, D3, D4, D5; kolinergičke muskarinske receptore M1-M5; α1 adrenergičke; i histaminske H1 receptore.
In preclinical studies, olanzapine exhibited a range of receptor affinities (Ki &lt; 100 nM) for serotonin 5HT2A/2C, 5HT3, 5HT6; dopamine D1, D2, D3, D4, D5; cholinergic muscarinic receptors M1-M5; α 1 adrenergic; and histamine H1 receptors.
U pretkliničkim ispitivanjima, olanzapin je pokazao raspon afiniteta za receptore (Ki &lt; 100 nM) serotonina 5HT2A/2C, 5HT3, 5HT6; dopamina D1, D2, D3, D4, D5; kolinergičke muskarinske receptore M1-M5; α1 adrenergičke; i histaminske H1 receptore.
In preclinical studies, olanzapine exhibited a range of receptor affinities (Ki &lt; 100 nM) for serotonin 5HT2A/2C, 5HT3, 5HT6; dopamine D1, D2, D3, D4, D5; cholinergic muscarinic receptors M1-M5; α1 adrenergic; and histamine H1 receptors.
U pretkliničkim ispitivanjima olanzapin je pokazao raspon afiniteta za receptore (Ki &lt; 100 nM) serotonina 5HT2A/2C, 5HT3, 5HT6; dopamina D1, D2, D3, D4, D5; kolinergičke muskarinske receptore M1-M5; α1 adrenergičke; i histaminske H1 receptore.
In preclinical studies, olanzapine exhibited a range of receptor affinities (Ki &lt; 100 nM) for serotonin 5HT2A/2C, 5HT3, 5HT6; dopamine D1, D2, D3, D4, D5; cholinergic muscarinic receptors M1-M5; α1 adrenergic; and histamine H1 receptors.
U pretkliničkim ispitivanjima, olanzapin je pokazao raspon afiniteta za receptore (Ki &lt; 100 nM) serotonina 5HT2A/2C, 5HT3, 5HT6; dopamina D1, D2, D3, D4, D5; kolinergičke muskarinske receptore M1-M5; α1 adrenergičke; i histaminske H1 receptore.