natgillin/translations-raw huggingface dataset:
Safinamide may be taken with or without food. 
Safinamid se lahko jemlje s hrano ali brez.
Safinamide is a highly selective and reversible MAO-B inhibitor causing an increase in extracellular levels of dopamine in the striatum. 
Safinamid je visoko selektiven in reverzibilen zaviralec MAO-B, ki povzroča zvišanje zunajceličnih ravni dopamina v striatumu.
If an important overdose occurs, safinamide treatment should be discontinued and supportive treatment should be administered as clinically indicated. 
Če pride do pomembnega prevelikega odmerjanja, je treba zdravljenje s safinamidomprekiniti in začeti podporno zdravljenje, kot je klinično indicirano.
Therefore, caution is necessary when safinamide is taken concomitantly with medicinal products that are OCT1 substrates and have a tmax similar to safinamide (2 hours) (e.g. metformin, aciclovir, ganciclovir) as exposure to these substrates might be increased as a consequence. 
Zato je potrebna previdnost ob sočasnem jemanju safinamida z zdravili, ki so substrati za OCT1 in imajo Tmax podoben kot safinamid (2 uri) (npr. metformin, aciklovir, ganciklovir), saj se lahko posledično poveča izpostavljenost tem substratom.
Responder analyses (post-hoc) (e) n(%) ON time increase ≥60 minutes p-value ≥60 minutes increase ON time and decrease in OFF time and ≥ 30% improvement UPDRS III p-value 
Analize odziva (post-hoc) (e) n (%) Zvečanje obdobja brez težav z gibanjem ≥ 60 minut p-vrednost minutnozvečanje obdobja brez težav z gibanjem in zmanjšanje obdobja s težavami z gibanjem in ≥ 30odstotno izboljšanje lestvice UPDRS
Impulse control disorders can occur in patients treated with dopamine agonists and/or dopaminergic treatments. 
Motnje nadzora impulzov se lahko pojavijo pri bolnikih, ki prejemajo dopaminske agoniste in/ali dopaminergična zdravila.
Available pharmacodynamic/toxicological data in animals have shown excretion of safinamide in milk (for details see 5.3). 
Razpoložljivi farmakodinamični/toksikološki podatki pri živalih kažejo na izločanje safinamida v mleko (za podrobnosti glejte poglavje 5.3).
Safinamide absorption is rapid after single and multiple oral dosing, reaching Tmax in the time range 1.82.8 h after dosing under fasting conditions. 
Absorpcija safinamida je po enkratnem in večkratnem peroralnem odmerjanju hitra, saj doseže Tmax v časovnem razponu 1,8-2,8 ure po odmerjanju na tešče.
Xadago is not recommended for use in children and adolescents, below 18 years old due to the lack of data on safety and efficacy in this population. 
Jemanje zdravila Xadago ni priporočeno pri otrocih in mladostnikih, mlajših od 18 let, saj pri tej populaciji ni zadostnih podatkov o varnosti in učinkovitosti zdravila.
If a dose is missed the next dose should be taken at the usual time the next day. 
Če bolnik izpusti odmerek, naj naslednji odmerek zdravila vzame naslednji dan ob običajnem času.
Animal studies indicate that safinamide treatment is associated with adverse reactions on female rat reproductive performance and sperm quality. 
Študije na živalih nakazujejo, da je zdravljenje s safinamidom povezano z neželenimi reakcijami na sposobnost razmnoževanja pri podganjih samicah in na kakovost sperme.
Pharmacotherapeutic group: Anti-Parkinson-Drugs, monoamine oxidase -B inhibitors, ATC code: N04BD03. 
Farmakoterapevtska skupina: Antiparkinsoniká, Inhibítory monoaminooxidázy typu B, oznaka ATC: N04BD03.
Toxic effects on the liver and accompanying symptoms as yellow/orange skin and skull, in pups exposed to safinamide during lactation are mediated mainly via in utero exposure, whereas exposure via the mother's milk had only a minor influence. 
Toksični učinki na jetra in spremljajoči simptomi, kot so rumena/oranžna koža in lobanja pri mladičih, ki so bili med laktacijo izpostavljeni safinamidu, so predvsem posledica izpostavljenosti v maternici, medtem ko je imela izpostavljenost prek materinega mleka le manjši vpliv.
Secondary efficacy parameters included OFF Time, UPDRS II and III (Unified Parkinson's Disease Rating Scale - sections II and III), and CGI-C (Clinical Global Impression of Change) 
Sekundarni parametri učinkovitosti so vključevali obdobje brez težav z gibanjem, UPDRS II in III (Unified Parkinson's Disease Rating Scale; Združena ocenjevalna lestvica Parkinsonove boleznirubriki II in III) ter CGI-C (Clinical Global Impression of Change; Celostni klinični odziv).
It acts to increase the level of a substance called dopamine in the brain, which is involved in the control of movement and is present in reduced amounts in the brain of patients with Parkinson's disease. 
Ta deluje tako, da zviša raven snovi, imenovane dopamin, v možganih, ki sodeluje pri nadziranju gibov, in je v možganih bolnikov s parkinsonovo boleznijo prisotna v nižjih ravneh.
Moderate or severe renal impairment did not alter the exposure to safinamide, compared to healthy subjects (see section 4.2). 
Zmerna ali huda ledvična okvara ni spremenila izpostavljenosti safinamidu v primerjavi z zdravimi preskušanci (glejte poglavje 4.2).
Xadago is supplied in packs containing 14, 28, 30, 90 or 100 film coated tablets. 
Xadago je na voljo v škatlah, ki vsebujejo 14, 28, 30, 90 ali 100 filmsko obloženih tablet.
Potential for retinal degeneration in patients with prior history of retinal disease 
Potencial za degeneracijo mrežnice pri bolnikih z boleznijo mrežnice v anamnezi
Safinamide exposure in patients with mild hepatic disease increased marginally (30% in AUC), while in patients with moderate hepatic impairment exposure increased by approximately 80% (see section 
Izpostavljenost safinamidu pri bolnikih z blago jetrno okvaro se je rahlo povečala (30 % AUC), medtem ko se je pri bolnikih z zmerno jetrno okvaro izpostavljenost povečala za približno 80 % (glejte poglavje 4.2).
The systemic exposure of NW-1153 is low (1/10 of parent safinamide). 
Sistemska izpostavljenost NW1153 je nizka (1/10 parenteralnega safinamida).
What you need to know before you take Xadago 
Kaj morate vedeti, preden boste vzeli zdravilo Xadago
In vitro experiments indicated that inhibition of amidases in human hepatocytes led to complete suppression of the NW-1153 formation. 
In vitro eksperimenti so pokazali, da je inhibicija amidaz v človeških hepatocitih povzročila popolno supresijo tvorjenja NW-1153.
The pharmacokinetics of safinamide are linear after single and repeated doses. 
Farmakokinetika safinamida je linearna po enkratnem in večkratnih odmerkih.
Medicinal products that are inhibitors of OAT3 given concomitantly with safinamide may reduce clearance of NW-1153, i.e., and thus may increase its systemic exposure. 
Zdravila, ki so inhibitorji OAT3 in jih dajemo sočasno s safinamidom, lahko zmanjšajo npr. očistek NW-1153 in lahko na ta način povečajo sistemsko izpostavljenost.
Absolute bioavailability is high (95%), showing that safinamide is almost completely absorbed after oral administration and first pass metabolism is negligible. 
Absolutna biološka uporabnost je visoka (95 %), kar pomeni, da se safinamid po peroralnem dajanju skoraj v celoti absorbira in da je presnova prvega prehoda zanemarljiva.
D- 73614 Schorndorf Germany 
D- 73614 Schorndorf, Nemčija
Somnolence and dizziness may occur during safinamide treatment, therefore patients should be cautioned about using hazardous machines, including motor vehicles, until they are reasonably certain that safinamide does not affect them adversely. 
Med zdravljenjem s safinamidom se lahko pojavita zaspanost in omotica, zato je treba bolnike opozoriti na previdnost pri upravljanju z nevarnimi stroji, vključno z motornimi vozili, dokler ne bodo prepričani, da safinamid nanje nima neželenih učinkov.
The primary efficacy parameter was the change from baseline to endpoint in ‘ON Time without troublesome dyskinesia'. 
Parameter primarne učinkovitosti je bila sprememba od izhodišča do končne točke v trajanju obdobja brez težav z gibanjem (»vklop«), brez moteče diskinezije.
In one patient suspected of consuming more than the daily prescribed dose of 100 mg for one month, symptoms of confusion, sleepiness, forgetfulness and dilated pupils were reported. 
Pri enem bolniku, za katerega so domnevali, da je en mesec užival večji odmerek od predpisanega 100 mg/dan, so poročali o naslednjih simptomih: zmedenost, zaspanost, pozabljivost in razširjene zenice.
Xadago is a medicine that contains the active substance safinamide. 
Xadago je zdravilo, ki vsebuje učinkovino safinamid.
Dose (mg/day) (a) 
Odmerek (mg/dan) (a)
This effect was not seen when safinamide was used as an adjunct to dopamine agonists in early stage PD patients. 
Tega učinka niso opazili pri uporabi safinamida kot dodatka dopaminskim agonistom pri bolnikih s parkinsonovo boleznijo v zgodnjem stadiju.
Hypromellose Macrogol (6000) Titanium dioxide (E171) Iron oxide red (E172) Mica (E555) 
Filmska obloga hipromeloza makrogol (6000) titanov dioksid (E171) rdeč železov oksid (E172) sljuda (E555)
At concentrations of 50µM, safinamide inhibited OATP1A2 and OATP2P1. 
Pri koncentracijah 50µM je safinamid zaviral OATP1A2 in OATP2P1.
Dedicated drug-drug interaction studies performed with ketoconazole, L-dopa and CYP1A2 and CYP3A4 substrates (caffeine and midazolam), did not detect any clinically significant effects on the pharmacokinetics of safinamide, or L-dopa, caffeine and midazolam. 
V namenskih študijah medsebojnega delovanja zdravil, ki so jih opravili s ketokonazolom, L-dopo ter substrati CYP1A2 in CYP3A4 (kofein in midazolam), niso opazili nobenih klinično pomembnih učinkov na farmakokinetiko safinamida ali L-dope, kofeina in midazolama.
When safinamide is co-administered with products that are BCRP substrates, please refer to the SmPC for that particular medicinal product. 
Če je safinamid uporabljen sočasno z zdravili, ki so substrati BCRP, prosimo upoštevajte Povzetek glavnih značilnosti zdravila tistega določenega to zdravila.
Total clearance was determined to be 4.6 L/h classifying safinamide as a low clearance substance. 
Ugotovljeno je bilo, da je celotni očistek 4,6 l/h, zato se safinamid uvršča med snovi z nizkim očistkom.
The tabulation below includes all adverse reactions in clinical trials where adverse reactions were considered related. 
V spodnji preglednici so navedene vse neželene reakcije v kliničnih preskušanjih, v katerih so neželene učinke opredelili kot povezane z zdravilom.
This potential increase is most likely of no clinical relevance as NW-1153, the first product in the metabolic pathway, is further transformed to secondary and tertiary metabolites. 
To potencialno povečanje najverjetneje nima klinične pomembnosti, saj se NW-1153, prvi produkt v presnovni poti, nadalje transformira v sekundarne in terciarne presnovke.
Phospholipidosis was seen mainly in the lungs in rodents (at exposures similar to humans) and monkeys (at exposures greater than 12 fold higher than human). 
Fosfolipidozo so opazili zlasti v pljučih glodavcev (pri izpostavljenostih, podobnim izpostavljenostim človeka), in opic (pri izpostavljenosti, ki več kot 12krat presega izpostavljenost človeka.
Breast Feeding Xadago is likely to be excreted in breast milk. 
Velika verjetnost je, da se zdravilo Xadago izloča v materino mleko.
In drug-drug-interaction studies in human, a weak interaction was observed with rosuvastatin (AUC increase between 1.25 and 2.00 fold) but no significant interaction was found with diclofenac. 
V študijah medsebojnega delovanja zdravili, opravljenih z rosuvastatinom, so pri ljudeh opazili šibko medsebojno delovanje (vrednost AUC je narasla med 1,25- in 2,0-krat), v študijah z diklofenakom pa niso opazili pomembnih medsebojnih delovanj.
Xadago may be taken with or without food. 
Zdravilo Xadago se lahko jemlje s hrano ali brez.
14 film-coated tablets 28 film-coated tablets 30 film-coated tablets 90 film-coated tablets 100 film-coated tablets 
14 filmsko obloženih tablet 28 filmsko obloženih tablet 30 filmsko obloženih tablet 90 filmsko obloženih tablet 100 filmsko obloženih tablet
You must wait at least 7 days after stopping Xadago treatment before starting treatment with MAO inhibitors or pethidine. 
Ko zaključite zdravljenje z zdravilom Xadago, morate počakati vsaj 7 dni, preden začnete zdravljenje z zaviralci MAO ali petidinom.
The amidase FAAH was able to catalyse the formation of NW-1153 at low rates only. 
Amidaza FAAH je katalizirala tvorjenje NW-1153 le v majhni meri.
Population PK models developed from studies in patients with Parkinson's disease indicate that the pharmacokinetic and pharmacodynamics effects of safinamide were not dependent on age, gender, weight, renal function and exposure to levodopa, indicating that dose adjustments will not be required based on these variables. 
Populacijski farmakokinetični (PK) modeli, ki so jih razvili na podlagi študij pri bolnikih s parkinsonovo boleznijo, kažejo, da farmakokinetični in farmakodinamični učinki safinamida niso odvisni od starosti, spola, telesne mase, delovanja ledvic in izpostavljenosti levodopi, kar nakazuje, da prilagajanje odmerkov na podlagi teh spremenljivk ne bo potrebno.
In general, safinamide may be used with selective serotonin re-uptake inhibitors (SSRIs) at the lowest effective dose, with caution for serotoninergic symptoms. 
Safinamid je na splošno mogoče uporabljati s selektivnimi zaviralci ponovnega privzema serotonina (SSRI) v najmanjšem učinkovitem odmerku, pri čemer je treba biti pozoren na simptome serotoninergičnega sindroma.
The effect on ON Time was maintained at the end of the 24-month double-blind treatment period for both safinamide doses as compared to placebo. 
Učinek obdobja brez težav z gibanjem se je v primerjavi s placebom ohranil do konca 24-mesečnega obdobja dvojno slepega zdravljenja za obe skupini s safinamidom.
Safinamide acts through both dopaminergic and non-dopaminergic mechanisms of action. 
Safinamid deluje prek dopaminergičnega in nedopaminergičnega mehanizma delovanja.
Preliminary in vitro studies have shown that safinamide is not a substrate for the transporters P-gp, BCRP, OAT1B1, OAT1B3, OATP1A2 or OAT2P1. 
Preliminarne in vitro študije so pokazale, da safinamid ni substrat za prenašalce OAT3, P-gp, BCRP, OAT1B1, OAT1B3, OATP1A2 ali OAT2P1.
The high absorption classifies safinamide as a highly permeable substance. 
Zaradi svoje visoke absorpcije se safinamid uvršča med visoko permeabilne snovi.
Therefore, other amidases are likely to be involved in the conversion to NW-1153. 
Zato so v konverzijo v NW-1153 najverjetneje vključene druge amidaze.
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 študije presnove so pokazale, da ne prihaja do pomembne indukcije ali inhibicije citokroma P450, CYP2A6, 2B6, 2C8, 2C9, 2C19, 2D6, 2E1 in 3A3/5 v koncentracijah, ki so relevantne (Cmax prostega safinamida 0,4 µM pri 100 mg/dan) za človeka.
In particular, the concomitant use of safinamide and fluoxetine or fluvoxamine should be avoided, or if concomitant treatment is necessary these medicinal products should be used at low doses (see section 4.5). 
Zlasti se je treba izogibati sočasni uporabi safinamida in fluoksetina ali fluvoksamina, če pa je sočasno zdravljenje potrebno, je treba ta zdravila uporabljati v nizkih odmerkih (glejte poglavje 4.5).
There are no or limited amount of data from the use of safinamide in pregnant women. 
Podatkov o uporabi safinamida pri nosečnicah ni oziroma so omejeni.
The efficacy of safinamide as add-on treatment in mid-to late-stage PD (LSPD) patients with motor fluctuations, currently receiving L-dopa alone or in combination with other PD medicinal products, was evaluated in two double-blind, placebo-controlled studies: Study SETTLE (Study 27919; 50-100 mg/day; 24 weeks), and Study 016/018 (50 and 100 mg/day; 2-year, double-blind, placebo-controlled study). 
Učinkovitost safinamida kot dodatnega zdravljenja pri bolnikih s parkinsonovo boleznijo v srednjem do poznem stadiju (LSPD) z motoričnimi fluktuacijami, ki trenutno prejemajo L-dopo v monoterapiji ali v kombinaciji z drugimi zdravili za zdravljenje parkinsonove bolezni, je bila ocenjena v dveh dvojno slepih, s placebom nadzorovanih študijah: študiji SETTLE (študija 27919; 50-100 mg/dan; 24 tednov) in študiji 016/018 (50 in 100 mg/dan; 2-letna dvojno slepa, s placebom nadzorovana študija).
Safinamide must not be administered along with other MAO inhibitors (including moclobemide) as there may be a risk of non-selective MAO inhibition that may lead to a hypertensive crisis (see section 4.3). 
Safinamida se ne sme dajati sočasno z drugimi zaviralci MAO (vključno z moklobemidom) zaradi možnosti tveganja neselektivnega zaviranja monoaminooksidaze, ki lahko povzroči hipertenzivno krizo (glejte poglavje 4.3).
The metabolite NW-1153 is a substrate for OAT3 at clinically relevant concentrations. 
Presnovek NW-1153 je substrat za OAT3 v klinično pomembnih koncentracijah.
Metabolite structure elucidation revealed three metabolic pathways of safinamide. 
Obrazložitev strukture presnovkov je razkrila tri presnovne poti safinamida.
In view of the selective and reversible MAO-B inhibitory activity of safinamide, antidepressants may be administered but used at the lowest doses necessary. 
Z vidika selektivne in reverzibilne zaviralne aktivnosti safinamida na MAO-B se antidepresive sme uporabljati, a v najnižjih potrebnih odmerkih.
Safinamide used as an adjunct to levodopa may potentiate the side effects of levodopa, and preexisting dyskinesia may be exacerbated, requiring a decrease of levodopa. 
Safinamid, ki je uporabljen kot dodatek k levodopi, lahko potencira neželene učinke levodope in poslabša predobstoječo diskinezijo, zaradi česar je potrebno zmanjšanje odmerka levodope.
Do not use this medicine after the expiry date which is stated on the carton and blister after “EXP” The expiry date refers to the last day of that month. 
Tega zdravila ne smete uporabljati po datumu izteka roka uporabnosti, ki je naveden na škatli in pretisnem omotu poleg oznake „EXP“.
Safinamide is almost exclusively eliminated via metabolism, largely by high capacity amidases that have not yet been characterized. 
Safinamid se skoraj v celoti izloča s presnovo, večinoma prek visokozmogljivih amidaz, ki pa še niso bile opredeljene.
Film-coated tablet (tablet) 
Filmsko obložena tableta (tableta)
Skip the missed dose and take the next dose at the time you normally take it. 
Izpustite zamujeni odmerek in naslednji odmerek vzemite ob običajnem času, kot ga sicer jemljete.
This interaction has the potential to reduce the clearance of NW1153 and increase its exposure; however the systemic exposure of NW-1153 is low (1/10 of parent safinamide), and as it is metabolised to secondary and tertiary metabolites, it is unlikely to be of any clinical relevance. 
To medsebojno delovanje ima potencial za zmanjšanje očistka NW-1153 in za povečanje izpostavljenosti le-temu; kljub temu pa je sistemska izpostavljenost NW-1153 nizka (1/10 parenteralnega safinamida) in ker se presnavlja v sekundarne in terciarne presnovke, najverjetneje nima nobene klinične pomembnosti.
The combination of safinamide with levodopa/carbidopa resulted in additive effects in the embryo-foetal development studies with a higher incidence of foetal skeletal abnormalities than seen with either treatment alone. 
Kombinacija safinamida z levodopo/karbidopo je povzročila aditivne učinke v študijah embriofetalnega razvoja z večjo pojavnostjo okvar na okostju plodu, kot so jih opazili pri vsakem od obeh posamičnih zdravljenj.
If you forget to take Xadago 
Če ste pozabili vzeti zdravilo Xadago
What Xadago is and what it is used for What you need to know before you take Xadago How to take Xadago 
Kaj je zdravilo Xadago in za kaj ga uporabljamo Kaj morate vedeti, preden boste vzeli zdravilo Xadago Kako jemati zdravilo Xadago Možni neželeni učinki
Safinamide may transiently inhibit BCRP in vitro. 
Safinamid lahko prehodno inhibira BCRP in vitro.
NW-1153 is not an inhibitor of OCT2, MATE1, or MATE2-K up to concentrations of 5µM. 
NW-1153 ni zaviralec OCT2, MATE1 ali MATE2-K do koncentracij 5µM.
Use in patients with albinism, retinal degeneration, uveitis, inherited retinopathy or severe progressive diabetic retinopathy (see sections 4.4 and 5.3). 
Uporaba pri bolnikih z albinizmom, bolnikih z degeneracijo mrežnice, uveitisom, dedno retinopatijo ali hudo napredovalo diabetično retinopatijo (glejte poglavji 4.4 in 5.3).
No retinal degeneration was noted in monkeys despite higher systemic exposure than in rodents or in patients at the maximum human dose. 
Pri opicah niso opazili degeneracije mrežnice kljub višji sistemski izpostavljenosti kot pri glodavcih ali pri bolnikih, ki so prejemali najvišji odmerek za človeka.
In human liver microsomes (HLM), the N-dealkylation step appears to be catalysed by CYP3A4, as safinamide clearance in HLM was inhibited by ketoconazole by 90%. 
V človeških jetrnih mikrosomih (human liver micromsomes, HLM) se N-dealkilacija najverjetneje katalizira z encimi CYP3A4, saj je ketokonazol očistek safinamida v mikrosomih v človeških jetrnih mikrosomih zavrl za 90 %.
Pooled analyses of adverse event data from placebo controlled studies in Parkinson's disease patients indicate that the concomitant administration of safinamide together with a broad category of commonly used medicinal products in this patient population (antihypertensive, beta-blockers cholesterol lowering, non-steroidal anti-inflammatory medicinal products, proton pump inhibitors, antidepressants, etc.) was not associated with an increased risk for adverse events. 
Združene analize podatkov o neželenih učinkih iz s placebom nadzorovanih študij pri bolnikih s parkinsonovo boleznijo kažejo, da sočasno dajanje safinamida skupaj s široko kategorijo pogosto uporabljenih zdravil v tej populaciji bolnikov (antihipertenzivna zdravila, zdravila za zniževanje holesterola iz skupine antagonistov adrenergičnih receptorjev beta, nesteroidna protivnetna zdravila, antidepresivi itd.) ni bilo povezano s povečanim tveganjem za neželene učinke.
Safinamide inhibits OCT1 in vitro at clinically relevant portal vein concentrations. 
Safinamid zavira OCT1 in vitro v klinično pomembnih koncentracijah v portalni veni.
- If you have been told that you have severe liver problems - If you have an eye condition which might put you at risk of potential damage to your retina (the light sensitive layers at the back of your eyes), e.g. albinism (lack of pigment in your skin and eyes), retinal degeneration (loss of cells from light sensitive layer at the back of the eye), or uveitis (inflammation inside of the eye), inherited retinopathy (inherited disorders of the vision), or severe progressive diabetic retinopathy (a progressive decrease of the vision due to diabetes). 
- če so vam povedali, da imate močno oslabljeno delovanje jeter - če imate očesno bolezen, zaradi katere bi lahko pri vas obstajalo povečano tveganje za morebitne poškodbe mrežnice (na svetlobo občutljiv sloj v ozadju očesa), npr. če imate albinizem (pomanjkanje barvila v koži in očeh), degeneracijo mrežnice (izguba celic v na svetlobo občutljivem sloju v ozadju očesa) ali uveitis (vnetje srednjega sloja očesa), dedno retinopatijo (dedna motnja vida) ali hudo progresivno diabetično retinopatijo (napredujoče slabšanje vida zaradi sladkorne bolezni).