natgillin/translations-raw huggingface dataset:
As with other nicotinic acid medicinal products, elevations in fasting glucose (a median increase of approximately 4 mg/ dL), and uric acid (mean change from baseline of +14.7%), and reductions in platelet counts (a mean change from baseline of -14.0%) were reported in
Tako kot pri drugih zdravilih z nikotinsko kislino so v kontroliranih kliničnih študijah z zdravilom Pelzont (2000 mg/ 40 mg) poročali o povišanju glukoze na tešče (mediano povišanje za približno 4 mg/ dl) in sečne kisline (povprečna sprememba glede na izhodišče +14, 7%) ter zmanjšanju števila trombocitov (povprečna sprememba glede na izhodišče - 14, 0%) (glejte poglavje 4. 4).
In diabetic patients a median increase in HbA1c of 0.2% was observed (where modification of hypoglycaemic therapy was allowed).
Pri sladkornih bolnikih so opazili srednje povečanje HbA1c za 0, 2% (pri čemer je bila dovoljenja prilagoditev antidiabetičnega zdravljenja).
Nicotinic acid-related adverse reactions The following nicotinic acid-related adverse reactions have been seen in clinical trials or post-marketing experience with other nicotinic acid medicinal products at unknown frequency or in clinical trials with Pelzont (or the nicotinic acid component of Pelzont) in < 1% of the patients treated:
Neželeni učinki, povezani z nikotinsko kislino Naslednje z nikotinsko kislino povezane neželene učinke so z neznano pogostnostjo opazili v kliničnih preskušanjih in med pomarketinško uporabo drugih zdravil z nikotinsko kislino ali pri < 1% zdravljenih bolnikov v kliničnih preskušanjih z zdravilom Pelzont (ali nikotinskokislinsko sestavino zdravila Pelzont):
Atrial fibrillation and other cardiac arrhythmias, palpitations, tachycardia.
Srčne bolezni: atrijska fibrilacija in druge motnje srčnega ritma, palpitacije, tahikardija.
Migraine, syncope.
Bolezni živčevja: migrena, sinkopa.
Cystoid macular oedema, toxic amblyopia.
Očesne bolezni: cistoiden edem makule, toksična ambliopija.
Respiratory, thoracic, and mediastinal disorders:
Bolezni dihal, prsnega koša in mediastinalnega prostora: dispneja.
Abdominal pain, mouth oedema, eructation, peptic ulcer.
Bolezni prebavil: bolečine v trebuhu, edem v ustih, spahovanje, peptična razjeda.
Acanthosis nigricans, dry skin, hyperpigmentation, macular rash, sweating (night or cold sweat), vesicular rash.
Bolezni kože in podkožja: acanthosis nigricans, suha koža, hiperpigmentacija, makularen izpuščaj, znojenje (ponoči ali hladno znojenje), vezikularen izpuščaj.
Musculoskeletal and connective tissue disorders:
Bolezni mišično- skeletnega sistema in vezivnega tkiva: šibkost mišic, mialgija.
Metabolism and nutrition disorders:
Presnovne in prehranske motnje: motena toleranca za glukozo, protin.
Infections and infestations:
Infekcijske in parazitske bolezni: rinitis.
Vascular disorders:
Žilne bolezni: hipotenzija, ortostatska hipotenzija.
General disorders and administration site conditions:
Splošne težave in spremembe na mestu aplikacije: astenija, mrzlica, edem obraza, generaliziran edem, bolečine, periferni edemi.
Immune system disorders:
Bolezni imunskega sistema: angioedem, preobčutljivost tipa I.
Hepatobiliary disorders:
Bolezni jeter, žolčnika in žolčevodov: zlatenica.
Anxiety, insomnia.
Psihiatrične motnje: anksioznost, nespečnost.
Pelzont In the event of an overdose, it is reasonable to employ the usual symptomatic and supportive measures.
Pelzont 8 V primeru prevelikega odmerjanja je smiselno uporabiti običajne simptomatske in podporne ukrepe.
Cases of overdose have been reported; the maximum dose of Pelzont taken was 5000 mg/ 100 mg.
Opisani so primeri prevelikega odmerjanja; največji zaužiti odmerek zdravila Pelzont je bil 5000 mg/ 100 mg.
The most commonly reported adverse reactions from the subjects who received this higher dose were consistent with a high dose of nicotinic acid and included: flushing, headache, pruritus, nausea, dizziness, vomiting, diarrhoea, epigastric and abdominal pain/ discomfort, and back pain.
Osebe, ki so dobivale ta višji odmerek, so najpogosteje navajale neželene učinke, ki so se skladali z velikim odmerkom nikotinske kisline, med drugim: zardevanje, glavobol, srbenje, navzejo, omotico, bruhanje, drisko, bolečine ali nelagodje v epigastriju in trebuhu, bolečine v hrbtu.
Laboratory abnormalities included increased amylase and lipase, decreased haematocrit and occult blood in the stool.
Med laboratorijskimi nepravilnostmi so bile zvišanje amilaze in lipaze, znižanje hematokrita in okultna kri v blatu.
Laropiprant During controlled clinical trials in healthy subjects, single doses of up to 900 mg laropiprant and multiple doses up to 450 mg once daily for 10 days were generally well tolerated.
Laropiprant V kontroliranih kliničnih preskušanjih so zdravi preiskovanci praviloma dobro prenašali posamične odmerke do 900 mg laropipranta in večkratne odmerke do 450 mg enkrat na dan 10 dni.
There is no experience with doses of laropiprant above 900 mg in humans.
Izkušenj z odmerki več kot 900 mg laropipranta pri človeku ni.
Prolongation of collagen-induced platelet aggregation was observed in subjects taking multiple doses of 300 mg or greater (see section 5.1).
Pri preiskovancih, ki so jemali večkratne odmerke 300 mg ali več, so opazili podaljšanje s kolagenom izzvane agregacije trombocitov (glejte poglavje 5. 1).
Pharmacotherapeutic group: nicotinic acid and derivatives, ATC code:
Oznaka ATC:
Pelzont contains nicotinic acid, which at therapeutic doses is a lipid-modifying agent, and laropiprant, a potent, selective antagonist of the prostaglandin D2 (PGD2) receptor subtype 1 (DP1).
Pelzont vsebuje nikotinsko kislino, ki v terapevtskih odmerkih vpliva na lipide, in laropiprant, močan, selektiven antagonist receptorja prostaglandina D2 (PGD2) podvrste 1 (DP1).
Nicotinic acid lowers the levels of low-density lipoprotein cholesterol (LDL-C), total cholesterol (TC), very low density lipoprotein cholesterol (VLDL-C), apolipoprotein B (apo B, the major LDL protein), triglycerides (TG), and lipoprotein(a) (Lp(a), a modified LDL particle) and elevates the levels of high-density lipoprotein cholesterol (HDL-C) and apolipoprotein A-I (apo A-I, the major protein component of HDL).
Nikotinska kislina znižuje koncentracijo LDL holesterola (hLDL), celotnega holesterola (Ch), VLDL holesterola (hVLDL), apolipoproteina B (apo B, glavne beljakovine LDL), trigliceridov (TG) in lipoproteina( a) (Lp( a), spremenjenega delca LDL) ter zvišuje koncentracijo HDL holesterola (hHDL) in apolipoproteina A- I (apo A- I, glavne beljakovinske sestavine HDL).
Nicotinic acid Mechanism of action The mechanisms by which nicotinic acid modifies the plasma lipid profile are not fully understood.
Nikotinska kislina Mehanizem delovanja Mehanizmi delovanja nikotinske kisline na sestavo lipidov v plazmi niso povsem pojasnjeni.
Nicotinic acid inhibits release of free fatty acids (FFA) from adipose tissue, which may contribute to the reduced plasma LDL-C, TC, VLDL-C, apo B, TG, and Lp(a), as well as elevated HDL-C, and apo A-I, all of which are associated with lower cardiovascular risk.
To morda pripomore k znižanju hLDL, Ch, hVLDL, apo B, TG, in Lp( a) v plazmi ter k zvišanju HDL in apo A- I; vse to zmanjšuje srčno- žilno tveganje.
Additional explanations that do not invoke plasma FFA reduction as the central driver of lipid profile modification include nicotinic acid-mediated inhibition of de novo lipogenesis or esterification of fatty acids into TG in the liver.
Med drugimi razlagami, po katerih osrednje gibalo spremenjene sestave lipidov ni znižanje PMK v plazmi, sta zavrtje de novo lipogeneze z nikotinsko kislino in esterifikacija maščobnih kislin v trigliceride v jetrih.
Pharmacodynamic effects Nicotinic acid causes a relative shift in the distribution of LDL subclasses from small, dense (most atherogenic) LDL particles to larger LDL particles.
Farmakodinamični učinki Nikotinska kislina povzroči relativen premik porazdelitve podskupin LDL od majhnih, gostih (najbolj aterogenih) delcev LDL proti večjim delcem LDL.
Nicotinic acid also elevates the HDL2 subfraction to a greater extent than the HDL3 subfraction, thereby increasing the HDL2: HDL3 ratio, which is associated with decreased cardiovascular disease risk.
Nikotinska kislina tudi bolj zviša podfrakcijo HDL2 kot podfrakcijo HDL3.
Treatment with nicotinic acid reduces the risk of death and cardiovascular events, and slows progression or promotes regression of atherosclerotic lesions.
9 Zdravljenje z nikotinsko kislino zmanjšuje tveganje za smrt in srčno- žilne dogodke ter upočasni napredovanje ali pripomore k nazadovanju aterosklerotičnih sprememb.
The Coronary Drug Project, a five year study completed in 1975, showed that nicotinic acid had a statistically significant benefit in decreasing nonfatal, recurrent myocardial infarctions (MI) in men 30 to 64 years old with a history of MI.
Raziskava Coronary Drug Project, petletna, leta 1975 končana študija je pokazala, da nikotinska kislina statistično značilno pripomore k zmanjšanju števila neusodnih ponovnih miokardnih infarktov (MI) pri moških od 30. do 64. leta starosti z anamnezo MI.
Though total mortality was similar in the two groups at five years, in a fifteen-year cumulative follow-up there were 11% fewer deaths in the nicotinic acid group compared to the placebo cohort.
Po petih letih je bila sicer celotna umrljivost v obeh skupinah podobna, a med petnajstletnim kumulativnim spremljanjem so v skupini, ki je dobivala nikotinsko kislino, ugotovili 11% manj smrti kot v kohorti s placebom.
10 Laropiprant Mechanism of action Nicotinic acid-induced flushing is mediated primarily by release of prostaglandin D2 (PGD2) in the skin.
Laropiprant Mehanizem delovanja Zardevanje zaradi nikotinske kisline je predvsem posledica sproščanja prostaglandina D2 (PGD2) v koži.
Genetic and pharmacologic studies in animal models have provided evidence that PGD2, acting through DP1, one of the two receptors for PGD2, plays a key role in nicotinic acid-induced flushing.
Z genetskimi in farmakološkimi študijami na živalskih modelih so dokazali, da je za zardevanje zaradi nikotinske kisline ključno delovanje PGD2 na DP1, ki je eden od dveh receptorjev za PGD2.
Pharmacodynamic effects Laropiprant has been shown to be effective in reducing flushing symptoms induced by nicotinic acid.
Farmakodinamični učinki Dokazano je, da laropiprant učinkovito zmanjša simptome zardevanja, ki jih povzroča nikotinska kislina.
The reduction in flushing symptoms (assessed by patient questionnaires) was correlated with a reduction in nicotinic acid-induced vasodilatation (assessed by measurements of skin blood flow).
Zmanjšanje simptomov zardevanja (ocenjeno z vprašalniki za bolnike) je koreliralo z zmanjšanjem vazodilatacije zaradi nikotinske kisline (vazodilatacijo so ugotavljali z merjenjem pretoka krvi skozi kožo).
In healthy subjects receiving Pelzont, pretreatment with acetylsalicylic acid 325 mg had no additional beneficial effects in reducing nicotinic acid-induced flushing symptoms compared to Pelzont alone (see section 4.8).
Pri zdravih preiskovancih, ki so dobivali zdravilo Pelzont, predhodna uporaba 325 mg acetilsalicilne kisline ni dodatno ublažila simptomov zardevanja zaradi nikotinske kisline v primerjavi s samim zdravilom Pelzont (glejte poglavje 4. 8).
TP plays a role in platelet function; however, therapeutic doses of laropiprant had no clinically relevant effect on bleeding time and collagen-induced platelet aggregation (see section 4.5).
TP igra vlogo pri delovanju trombocitov; vendar terapevtski odmerki laropipranta niso klinično pomembno vplivali na čas krvavitve ali agregacijo trombocitov, izzvano s kolagenom (glejte poglavje 4. 5).
Clinical studies Effect on lipids Pelzont was consistently efficacious across all prespecified patient subpopulations defined by race, gender, baseline LDL-C, HDL-C and TG levels, age and diabetes status.
Klinične študije Učinek na lipide Pelzont je učinkovit v zelo različnih populacijah odraslih bolnikov s primarno hiperholesterolemijo ali mešano dislipidemijo, ne glede na raso, spol, izhodiščno koncentracijo hLDL, hHDL in trigliceridov, ali glede na starost, pa tudi v posebnih populacijah, npr. pri sladkornih bolnikih.
4.3%) as measured by percent change from baseline.
Bolnikom, ki so jemali zdravilo Pelzont 2000 mg/ 40 mg s statinom ali brez njega, so se v primerjavi s prejemniki placeba bistveno znižali hLDL (- 18, 9% v prim. z - 0, 5%), trigliceridi (- 21, 7% v prim. s 3, 6%), razmerje hLDL: hHDL (- 28, 9% v prim. z 2, 3%), ne- HDL- holesterol (- 19, 0% v prim. z 0, 8%), apo B (- 16, 4% v prim. z 2, 5%), Ch (- 9, 2% v prim. z - 0, 6%), Lp( a) (- 17, 6% v prim. z 1, 1%), in razmerje Ch: hHDL (- 21, 2% v prim. z 1, 9%), bistveno pa sta se jim zvišala hHDL (18, 8% v prim. z 1, 2%) in apo A- I (11, 2% v prim. s 4, 3%), merjeno v odstotkih spremembe od izhodišča.
In general, the between-group treatment effects on all lipid parameters were consistent across all patient subgroups examined.
Na splošno so se učinki zdravljenja na parametre lipidov med skupinami skladali po vseh analiziranih podskupinah bolnikov.
Patients receiving Pelzont, nicotinic acid (prolonged-released formulation), or placebo were also taking statins (29% atorvastatin [5-80 mg], 54% simvastatin [10-80 mg], 17% other statins [2.5-180 mg] (pravastatin, fluvastatin, rosuvastatin, lovastatin)), of which 9% were also taking ezetimibe [10 mg].
Bolniki, ki so dobivali zdravilo Pelzont, nikotinsko kislino (pripravek s podaljšanim sproščanjem), ali placebo, so jemali tudi statine (29% atorvastatin [5– 80 mg], 54% simvastatin [10– 80 mg], 17% druge statine [2, 5– 180 mg] (pravastatin, fluvastatin, rosuvastatin, lovastatin)) in 9% od teh jih je jemalo tudi ezetimib [10 mg].
The placebo-adjusted LDL-C, HDL-C and TG responses appeared greater among women compared to men and appeared greater among elderly patients (≥ 65 years) compared to younger patients (< 65 years).
Za placebo korigirani odzivi hLDL, hHDL in trigliceridov so bili pri ženskah večji kot pri moških in med starejšimi bolniki (≥ 65 let) večji kot med mlajšimi (< 65 let).
In a multicentre, double-blind, 12-week factorial study, Pelzont 1000 mg/ 20 mg co-administered with simvastatin, when compared with simvastatin alone or Pelzont 1000 mg/ 20 mg alone, for 4 weeks, significantly lowered LDL-C (-44.2%, -37.4%, -8.2% respectively), TG (-25.8%, -15.7%, -18.7% respectively), TC (-27.9%, -25.8%, -4.9% respectively) and significantly increased HDL-C (19.2%, 4.2%, 12.5% respectively).
V multicentrični, dvojno slepi 12- tedenski faktorski študiji je 4- tedenska uporaba zdravila Pelzont 1000 mg/ 20 mg skupaj s simvastatinom v primerjavi s simvastatinom samim oz. z zdravilom Pelzont
Pelzont (2000 mg/ 40 mg) co-administered with simvastatin when compared with simvastatin alone or Pelzont (2000 mg/ 40 mg) alone for 12 weeks, significantly lowered LDL-C (-47.9%, -37.0%, -17.0% respectively), TG (-33.3%, -14.7%, -21.6% respectively), apo B (-41.0%, -28.8%, -17.1%
12, 5%).
11 respectively), and TC (-29.6%, -24.9%, -9.1% respectively), as well as LDL-C: HDL-C (-57.1%, -39.8%, -31.2% respectively), non-HDL-C (-45.8%, -33.4%, -18.1% respectively), and TC: HDL-C (-43.0%, -28.0%, -24.9% respectively), and significantly increased HDL-C (27.5%, 6.0%, 23.4% respectively).
6, 0% oz.
Further analysis showed Pelzont (2000 mg/ 40 mg) co-administered with simvastatin when compared with simvastatin alone significantly increased apo A-I (8.6%, 2.3% respectively) and significantly decreased Lp(a) (-19.8%, 0.0% respectively).
0, 0%).
Flushing In two large clinical trials measuring patient-reported flushing symptoms, patients taking Pelzont experienced less flushing than those taking nicotinic acid (prolonged-release formulations).
Zardevanje V dveh velikih kliničnih preskušanjih, ki sta ugotavljali simptome zardevanja po navedbi bolnikov, je bilo zardevanja manj med bolniki, ki so prejemali zdravilo Pelzont, kot med bolniki, ki so prejemali nikotinsko kislino (pripravek s podaljšanim sproščanjem).
In patients continuing in the first study (24 weeks), the frequency of moderate or greater flushing in patients treated with Pelzont declined and approached that of patients receiving placebo (see Figure 1), whereas in patients treated with nicotinic acid (prolonged-release formulation) the flushing frequency remained constant (after Week 6).
Pri bolnikih, ki so dobivali nikotinsko kislino (pripravek s podaljšanim sproščanjem), pa se pogostnost zardevanja ni spremenila (po 6. tednu).
Flushing efficacy of laropiprant has not been established past 24 weeks.
Učinkovitosti laropipranta glede zardevanja po preteklih 24 tednih niso preučevali.
Average number of days per week with moderate or greater* flushing symptoms across weeks 1-24 2 Number of Days per Week
2 Število dni na teden
Weeks on Treatment
tedni zdravljena
● Pelzont (1000 mg/ 20 mg to 2000 mg/ 40 mg at week 5) ▲ Nicotinic acid (prolonged-release 1000 mg to 2000 mg at week 5) ○ Placebo *Includes patients with moderate, severe, or extreme flushing symptoms † Dose advancement at Week 5
● Pelzont (1000 mg/ 20 mg do 2000 mg/ 40 mg 5. teden) ▲Nikotinska kislina (s podaljšanim sproščanjem, 1000 mg do 2000 mg 5. teden) ○ Placebo * Vključuje bolnike z zmernimi, hudimi ali izredno hudimi simptomi zardevanja † Povečanje odmerka 5. teden
In the second study (16 weeks) where acetylsalicylic acid was allowed, patients taking Pelzont experienced significantly fewer days per week with moderate or greater flushing compared to nicotinic acid (prolonged-release formulation taken as a 12-week multi-step 500 mg to 2000 mg titration) (p < 0.001).
V drugi študiji (16 tednov), v kateri je bilo dovoljeno uporabljati acetilsalicilno kislino, so bolniki, ki so prejemali zdravilo Pelzont, doživljali zmerno ali izrazitejše zardevanje statistično značilno manj dni na teden kot bolniki, ki so prejemali nikotinsko kislino (pripravek s podaljšanim sproščanjem, uporabljen v 12- tedenski večstopenjski titraciji od 500 mg do 2000 mg) (p < 0, 001).
Absorption Nicotinic acid Following a 2000 mg dose of nicotinic acid administered orally as two modified-release tablets of nicotinic acid/ laropiprant with food, nicotinic acid was absorbed with a median time to peak plasma concentration (Tmax) of 4 hours, a mean area under the plasma concentration-time curve (AUC0-last) of approximately 58.0 μ M·hr and a mean peak plasma concentration (Cmax) of approximately 20.2 μ M.
11 Absorpcija Nikotinska kislina Po peroralni uporabi 2. 000 mg nikotinske kisline v dveh tabletah nikotinske kisline/ laropipranta s prirejenim sproščanjem, zaužitih s hrano, je bil mediani čas do največje koncentracije nikotinske kisline v plazmi (tmax) 4 ure, povprečna površina pod krivuljo plazemske koncentracije v odvisnoti od časa (AUC0 - last) približno 58, 0 µM· h in povprečna največja koncentracija v plazmi (Cmax) približno 20, 2 µM.
Bioavailability with or without food is at least 72% based on the recovery of the nicotinic acid dose in the urine.
Biološka uporabnost nikotisnke kisline, zaužite s hrano ali brez nje, je na podlagi pojavljanja njenega odmerka v urinu vsaj 72%.
The oral bioavailability of nicotinic acid is not altered when it is taken with a high-fat meal.
Biološka uporabnost nikotinske kisline se ne spremeni, če je zaužita z mastnim obrokom.
Laropiprant Following a 40 mg dose of laropiprant administered orally as two modified-release tablets of nicotinic acid/ laropiprant with food, laropiprant is rapidly absorbed with a median Tmax of 1 hour, a mean AUC0- ∞ of approximately 13 μ M·hr, and a mean Cmax of approximately 1.6 μ M.
Laropiprant Po peroralni uporabi 40 mg laropipranta v dveh tabletah nikotinske kisline/ laropipranta s prirejenim sproščanjem, zaužitih s hrano, se laropiprant hitro absorbira; mediani tmax je 1 uro, povprečna AUC0- ∞ približno 13 µM· h in povprečna Cmax približno 1, 6 µM.
The rate and extent of absorption are not altered with a high-fat meal.
Hitrost in obseg absorpcije se z mastnim obrokom ne spremenita.
The mean absolute bioavailability of laropiprant is approximately 71% following a 40 mg dose when administered as two modified-release tablets of nicotinic acid/ laropiprant after an overnight fast.
Povprečna absolutna biološka uporabnost laropipranta po uporabi 40- mg odmerka (v obliki dveh tablet nikotinske kisline/ laropipranta s prirejenim sproščanjem na tešče po noči brez hrane) je približno 71%.
Distribution Nicotinic acid Nicotinic acid is less than 20% bound to serum proteins.
Porazdelitev Nikotinska kislina Manj kot 20% nikotinske kisline se veže na beljakovine v serumu.
Laropiprant The mean volume of distribution at steady state following a single 40 mg intravenous dose of laropiprant to healthy subjects is approximately 70 litres.
Laropiprant Pri zdravih preiskovancih je povprečni volumen porazdelitve v stanju dinamičnega ravnovesja po posamičnem 40- mg intravenskem odmerku laropipranta približno 70 litrov.
Laropiprant is highly bound (> 99%) to plasma proteins, and its binding is independent of concentration.
Laropiprant je v veliki meri (> 99%) vezan na beljakovine v plazmi in vezava ni odvisna od koncentracije.
Metabolism Nicotinic acid Nicotinic acid undergoes extensive first-pass metabolism through two pathways that are dose and dose-rate dependent.
Presnova Nikotinska kislina Nikotinska kislina je podvržena znatni presnovi prvega prehoda po dveh poteh, ki sta odvisni od odmerka in odmerka na čas.
In humans, nicotinamide is further predominantly metabolised to N-methylnicotinamide (MNA) and to N-methyl-2-pyridone-5-carboxamide (2PY).
Pri človeku se nikotinamid nato presnovi v glavnem v N- metilnikotinamid (MNA) in N- metil- 2- piridon- 5- karboksamid (2PY).
With low doses of nicotinic acid or lower rates of absorption, the first pathway predominates.
Med uporabo majhnih odmerkov nikotinske kisline oz. pri majhni hitrosti absorpcije prevladuje prva pot.
At higher doses or higher rates of absorption, the NAD pathway is saturable, and an increasing fraction of the oral dose reaches the bloodstream unchanged as nicotinic acid.
Med uporabo večjih odmerkov oz. pri večji hitrosti absorpcije pa se NAD- pot nasiti in vse večji delež peroralnega odmerka pride v krvni obtok kot nespremenjena nikotinska kislina.
The glycine conjugation pathway is not saturated across the clinically relevant dose range, based on the dose-proportional increase in the plasma concentrations of NUA from 1000 mg to 2000 mg.
Pot konjugacije z glicinom pa se v celotnem razponu klinično pomembnih odmerkov ne nasiti, če presojamo na podlagi odmerku sorazmernega porasta koncentracije nikotinurične kisline v plazmi od odmerka 1000 mg do 2000 mg.
In in vitro studies, nicotinic acid and its metabolites did not inhibit CYP1A2, CYP2B6, CYP2C9, CYP2C19, CYP2D6, CYP2E1, or CYP3A4-mediated reactions or UGT1A1-mediated 3-glucuronidation of estradiol.
V študijah in vitro nikotinska kislina in njeni presnovki niso zavrli reakcij, ki potekajo s CYP1A2, CYP2B6, CYP2C9, CYP2C19, CYP2D6, CYP2E1 ali CYP3A4, in tudi ne 3- glukuronidacije estradiola, ki poteka z UGT1A1.
13 Laropiprant Laropiprant is metabolised primarily via acyl glucuronidation, with a smaller component of oxidative metabolism, followed by excretion of the glucuronide into faeces (via bile) and urine.
Laropiprant Laropiprant se presnovi predvsem z acilglukuronidacijo, z manjšim deležem oksidativne presnove; temu sledi izločanje glukuronida v blatu (z žolčem) in urinu.
In vitro studies have shown that the acyl glucuronide conjugate of laropiprant had at least a 65-fold reduced affinity for DP1 as compared to laropiprant; thus, it is not expected to contribute to the overall DP1 activity of laropiprant.
Po študijah in vitro ima acilglukuronidni konjugat laropipranta vsaj 65- krat manjšo afiniteto za DP1 kot laropiprant, zato ni pričakovati, da bi prispeval k celotni DP1- aktivnosti laropipranta.
The major component (73% of radioactivity) in faeces is laropiprant (comprising unabsorbed active substance and/ or hydrolysed glucuronic acid conjugate).
Glavna snov (73% radioaktivnosti) v blatu je laropiprant (obsega neabsorbirano zdravilo in/ ali hidrolizirani konjugat z glukuronsko kislino).