natgillin/translations-raw huggingface dataset:
Når nedsat virus- RNA- suppression opstod, var det typisk forbundet med erstatning af cirkulerende følsomme virus med resistente virusvarianter.
When loss of viral RNA suppression occurred, it was typically associated with replacement of circulating susceptible virus with resistant viral variants.
Mindst 11 aminosyresteder i proteasen er blevet associeret med indinavirresistens:
At least eleven amino acid sites in the protease have been associated with indinavir resistance:
L10, K20, L24, M46, I54, L63, I64, A71, V82, I84 og L90.
L10, K20, L24, M46, I54, L63, I64, A71, V82, I84, and L90.
F. eks. kunne ingen enkeltsubstition eller substitutionspar skabe målelig (≥fire gange) indinavirresistens, og resistensniveauet var afhængig af måden flere substitutioner kombineredes på.
For example, no single substitution or pair of substitutions was capable of engendering measurable (≥ four– fold) resistance to indinavir, and the level of resistance was dependent on the ways in which multiple substitutions were combined.
Generelt skyldtes højere resistensniveauer imidlertid co- ekspression af et større antal substitutioner ved de 11 identificerede positioner.
In general, however, higher levels of resistance resulted from the co– expression of greater numbers of substitutions at the eleven identified positions.
Blandt patienter der oplevede viral RNA rebound under monoterapi med indinavir, 800 mg hver 8 time, sås der hos de fleste patienter kun substitution i 3 af disse positioner:
Among patients experiencing viral RNA rebound during indinavir monotherapy at 800 mg q8h, substitutions at only three of these sites were observed in the majority of patients:
V82 (til A eller F), M46 (til I eller L) og L10 (til I eller R).
V82 (to A or F), M46 (to I or L), and L10 (to I or R).
Derfor bør behandling
It should be noted that the decrease in suppression of viral RNA levels was seen more frequently when therapy with indinavir was initiated at doses lower than the recommended oral dose of 2.4 g/ day.
20 med indinavir initieres ved den anbefalede dosis for at øge suppressionen af virusreplikation og dermed hæmme udviklingen af resistent virus.
Therefore, therapy with indinavir should be initiated at the recommended dose to increase suppression of viral replication and therefore inhibit the emergence of resistant virus.
I en sammenlignende undersøgelse, gav kombinationsbehandling med nukleosidanaloger (trippelterapi med zidovudin plus didanosin) beskyttelse mod selektion af virus med mindst en resistensassocieret aminosyresubstitution over for både indinavir (fra 13/ 24 til 2/ 20 ved behandlingsuge 24) og over for nukleosidanalogerne (fra 10/ 16 til 0/ 20 ved behandlingsuge 24).
20 associated amino acid substitution to both indinavir (from 13/ 24 to 2/ 20 at therapy week 24) and to the nucleoside analogues (from 10/ 16 to 0/ 20 at therapy week 24).
Krydsresistens Isolater fra HIV- 1 patienter med nedsat følsomhed overfor indinavir udviste varierende mønstre og grader af krydsresistens overfor serier af forskellige HIV- proteasehæmmere, inklusive ritonavir og saquinavir.
Cross resistance HIV− 1 patient isolates with reduced susceptibility to indinavir expressed varying patterns and degrees of cross– resistance to a series of diverse HIV PIs, including ritonavir and saquinavir.
Fuldstændig krydsresistens fandtes mellem indinavir og ritonavir, medens krydsresistens over for saquinavir varierede mellem isolaterne.
Complete cross− resistance was noted between indinavir and ritonavir; however, cross− resistance to saquinavir varied among isolates.
Mange af de protease- aminosyresubstitutioner, som er fundet at være associeret med resistens over for ritonavir og saquinavir, er også forbundet med resistens over for indinavir.
Many of the protease amino acid substitutions reported to be associated with resistance to ritonavir and saquinavir were also associated with resistance to indinavir.
Voksne Behandling med indinavir alene eller i kombination med andre antiretrovirale stoffer (dvs. nukleosidanaloger) er indtil nu dokumenteret at reducere den virale belastning og at øge CD4 - lymfocytter hos patienter med CD4- celletal < 500 celler/ mm 3.
Adults Treatment with indinavir alone or in combination with other antiretroviral agents (i. e., nucleoside analogues) has so far been documented to reduce viral load and increase CD4 lymphocytes in patients with CD4 cell counts below 500 cells/ mm3.
I en publiceret undersøgelse blev 20 HIV- inficerede patienter med upåviselig virusbelastning i plasma (< 200 kopier/ ml), og som fik indinavir 800 mg hver 8. time, skiftet over til indinavir/ ritonavir 400/ 100 mg hver 12. time i et åbent, cross- over design.
In one published study, 20 HIV-infected patients with undetectable plasma viral load (< 200 copies / ml) receiving indinavir 800 mg every 8 hours were switched in an open, cross-over design to indinavir/ ritonavir 400/ 100 mg every 12 hours.
Virusbelastningen forblev < 200 kopier/ ml i 48 uger hos alle patienterne.
Viral load remained < 200 copies/ mL for 48 weeks in all patients.
En anden publiceret undersøgelse vurderede effekt og sikkerhed for indinavir/ ritonavir 400/ 100 mg hver 12. time hos 40 antiretroviralt naive patienter.
Another published study evaluated the efficacy and safety of indinavir/ ritonavir 400/ 100 mg every 12 hours in 40 antiretroviral-naïve patients.
Ved uge 4 var indinavirs Cmin 500 ng/ ml med væsentlig variabilitet i minimumsværdien (5- 8100 ng/ ml).
At week 4, the indinavir Cmin was 500 ng/ mL with substantial trough variability (range 5 to 8100 ng/ mL).
Ved analyse af intent- to- treat havde 65% af patienterne HIV RNA < 400 kopier/ ml, og 50% havde en virusbelastning på < 50 kopier/ ml; ved analyse af on- treatment havde 96% af disse HIV RNA < 400 kopier/ ml, og 74% havde en virusbelastning på < 50 kopier/ ml.
By intent to treat analysis 65% of patients had HIV RNA < 400 copies/ mL and 50% had viral load < 50 copies/ mL; by on-treatment analysis 96% of patients had HIV RNA < 400 copies/ mL and 74% had viral load < 50 copies/ mL.
I denne åbne ikke - randomiserede undersøgelse med én arm blev patienterne behandlet med stavudin og lamivudin plus indinavir/ ritonavir 400/ 100 mg hver 12. time.
In this open label non- randomized single arm study, patients were treated with stavudine and lamivudine plus indinavir/ ritonavir 400/ 100 mg every 12 hours.
I analyserne af intent- to- treat og on- treatment var andelen af patienter med HIV RNA < 50 kopier/ ml henholdsvis 68, 8% og 88, 7% ved uge 96.
In the intent to treat and on treatment analyses the proportion of patients with HIV RNA of < 50 copies/ mL was 68.8% and 88.7%, respectively, at week 96.
Indinavir alene eller i kombination med nukleosidanaloger (zidovudin/ stavudin og lamivudin) har vist at forsinke den kliniske progressionsrate sammenlignet med nukleosidanaloger og yder en vedvarende effekt på viralmængden og CD4- tallet.
Indinavir alone or in combination with nucleoside analogues (zidovudine/ stavudine and lamivudine) has been shown to delay clinical progression rate compared with nucleoside analogues and to provide a sustained effect on viral load and CD4 count.
Hos patienter der havde modtaget zidovudin, reducerede yderligere behandling med en kombination af indinavir, zidovudin og lamivudin sammenlignet med lamivudin og zidovudin sandsynligheden for AIDS- definerede sygdomme eller død (ADID) efter 48 uger fra 13% til 7%.
In zidovudine experienced patients, indinavir, zidovudine and lamivudine in combination compared with lamivudine added to zidovudine reduced the probability of AIDS defining illness or death (ADID) at 48 weeks from 13% to 7%.
6% med indinavir alene eller i kombination med zidovudin.
Similarly, in antiretroviral naive patients, indinavir with and without zidovudine compared with zidovudine alone reduced the probability of ADID at 48 weeks from 15% with zidovudine alone to approximately 6% with indinavir alone or in combination with zidovudine.
Effekten på viralmængden var betydeligt mere udtalt hos patienter behandlet med indinavir i kombination med nukleosidanaloger, men andelen af patienter med serumviral RNA under grænsen for kvantifikation (500 kopier/ ml) varierede undersøgelserne imellem ved uge 24 fra 40% til mere end
Effects on viral load were consistently more pronounced in patients treated with indinavir in combination with nucleoside analogues, but the proportion of patients with serum viral RNA below the limit of quantification (500 copies/ ml) varied between studies, at week 24 from 40% to more than 80%.
Denne andel synes at forblive stabil over længerevarende follow- up perioder.
This proportion tends to remain stable over prolonged periods of follow– up.
Ligeledes synes effekten på CD4- celletal at være mere udtalt hos patienter behandlet med indinavir i kombination med nukleosidanaloger sammenlignet med indinavir alene.
Similarly, effects on CD4 cell count tend to be more pronounced in patients treated with indinavir in combination with nucleoside analogues compared with indinavir alone.
Denne effekt er vedvarende i undersøgelser, også efter længerevarende follow- up perioder.
Within studies, this effect is sustained also after prolonged periods of follow– up.
Pædiatriske patienter To kliniske undersøgelser med 41 pædiatriske patienter (i alderen 4- 15 år) er designet til at karakterisere indinavirs sikkerhed, antiretroviral aktivitet og farmakokinetik i kombination med stavudin og lamivudin.
Paediatric patients Two clinical trials in 41 paediatric patients (4 to 15 years of age) were designed to characterise the safety, antiretroviral activity, and pharmacokinetics of indinavir in combination with stavudine and
I én undersøgelse var andelen af patienter med plasmaviral RNA under 400 kopier/ ml 60% i uge 24, middelstigningen i CD4- celletal var 242 celler/ mm3, og middelstigningen af CD4- celletal var, angivet i procent, 4, 2%.
In one study, at week 24, the proportion of patients with plasma viral RNA below 400 copies/ ml was 60%; the mean increase in CD4 cell counts was 242 cells/ mm3; and the mean increase in percent CD4 cell counts was 4.2%.
I uge 60 var andelen af patienter med plasmaviral RNA under 400 kopier/ ml 59%.
At week 60, the proportion of patients with plasma viral RNA below 400 copies/ ml was 59%.
I en anden undersøgelse var andelen af patienter med plasmaviral RNA under 400 kopier/ ml 59% i uge 16, middelstigningen i CD4- celletal var 73 celler/ mm3, og middelstigningen af CD4- celletal var, angivet i procent, 1, 2%.
In another study, at week 16, the proportion of patients with plasma viral RNA below 400 copies/ ml was 59%; the mean increase in CD4 cell counts was 73 cells/ mm3; and the mean increase in percent CD4 cell counts was 1.2%.
I uge 24 var andelen af patienter med plasmaviral RNA under 400 kopier/ ml 60%.
At week 24, the proportion of patients with plasma viral RNA below 400 copies/ ml was 60%.
Absorption Indinavir absorberes hurtigt i fastende tilstand med 0, 8 times varighed ± 0, 3 time (middelværdi ± S. D.) til maksimalt plasmaniveau nås.
Absorption Indinavir is rapidly absorbed in the fasted state with a time to peak plasma concentration of 0.8 hours ± 0.3 hours (mean ± S. D.).
Ved dosisintervallet 200- 800 mg var øgningen i plasmakoncentrationerne større end dosisproportional.
A greater than dose– proportional increase in indinavir plasma concentrations was observed over the 200 – 800 mg dose range.
Ved doser mellem 800 mg og 1000 mg er afvigelsen fra dosisproportionalitet mindre udtalt.
Between 800– mg and 1,000– mg dose levels, the deviation from dose– proportionality is less pronounced.
Som resultat af den korte halveringstid 1, 8 ± 0, 4 timer, sås kun minimal stigning i plasmakoncentrationer efter gentagne doser.
As a result of the short half– life, 1.8 ± 0.4 hours, only a minimal increase in plasma concentrations occurred after multiple dosing.
65% af en enkelt 800 mg dosis af indinavir (90% CI, 58- 72%).
The bioavailability of a single 800– mg dose of indinavir was approximately 65% (90% CI, 58 – 72%).
15. 550 nM, 8. 720 nM og 8. 880 nM.
Following a dosage regimen of 800 mg every 8 hours, measured peak plasma concentrations (Cmax) after morning, afternoon and evening doses were 15,550 nM, 8,720 nM and 8,880 nM, respectively.
220 nM, 210 nM og 370 nM.
Corresponding plasma concentrations at 8 hours post dose were 220 nM, 210 nM and 370 nM, respectively.
Relevansen af disse fund for ritonavir- boostet indinavir kendes ikke.
The relevance of these findings for ritonavir boosted indinavir is unknown.
Ved steady state efter et dosisregime på 800 mg, hver 8. time, opnåede HIV- seropositive patienter i en undersøgelse geometriske middelværdier af:
At steady state following a dosage regimen of 800 mg every 8 hours, HIV– seropositive adult patients in one study achieved geometric means of:
AUC0- 8 timer på 27813 nM · t, (90% konfidensinterval = 22185, 34869), maksimale plasmakoncentrationer på 11144 nM (90% konfidensinterval = 9192, 13512) og plasmakoncentrationer 8 timer efter dosering på 211 nM (90% konfidensinterval = 163, 274).
AUC0-8h of 27,813 nM*h (90% confidence interval = 22,185, 34,869), peak plasma concentrations 11,144 nM (90% confidence interval = 9,192, 13,512) and plasma concentrations at 8 hours post dose 211 nM (90% confidence interval = 163, 274).
Virkning af mad Ved steadystate efter et dosisregime på 800 mg/ 100 mg indinavir/ ritonavirterapi hver 12. time i kombination med et fedtfattigt måltid, opnåedes i en undersøgelsefølgende geometriske middelværdier:
Food effect At steady state following a dosage regimen of 800 mg/ 100 mg of indinavir/ ritonavir every 12 hours with a low-fat meal, healthy volunteers in one study achieved geometric means:
plasmakoncentrationer 12 timer efter dosering på 2274 nM (90% konfidensinterval = 1701, 3042) hos raske frivillige.
AUC0-12h 116,067 nM*h (90% confidence interval = 101,680, 132,490), peak plasma concentrations 19001 nM (90% confidence interval = 17,538, 20,588), and plasma concentrations at 12 hours post dose 2274 nM (90% confidence interval = 1,701, 3,042).
Farmakokinetisk analyse i den ene af undersøgelserne blev udført på 19 af patienterne med gennemsnitligt AUC0- 12t, Cmax og Cmin på henholdsvis 25421 nM* h (21489- 36236 nM* h), 5758 nM (5056- 6742 nM) og 239 (169- 421 nM) for indinavir.
Pharmacokinetic analysis in one study was performed on nineteen of the patients, with a median (range) indinavir AUC 0-12hr, Cmax, and Cmin of 25421 nM*h (21489-36236 nM*h), 5758 nM (5056-6742 nM) and 239 (169-421 nM), respectively.
I HIV- inficerede pædiatriske patienter, gav et dosisregimen af indinavir hårde kapsler, 500 mg/ m2 hver 8. time AUC0- 8 timer værdier på 27412 nM* t, maksimale plasmakoncentrationer på 12182 nM og plasmakoncentrationer på 122 nM 8 timer efter dosering.
In HIV− infected paediatric patients, a dosage regimen of indinavir hard capsules, 500 mg/ m2 every 8 hours, produced AUC0– 8hr values of 27,412 nM*h, peak plasma concentrations of 12,182 nM, and plasma concentrations at 8 hours post dose of 122 nM.
22 dosis på 800 mg hver 8. time; man bør være opmærksom på at plasmakoncentrationerne 8 timer efter dosering var lavere.
The AUC and peak plasma concentrations were generally similar to those previously observed in HIV– infected adults receiving the recommended dose of 800 mg every 8 hours; it should be observed that the plasma concentrations 8 hours post dose were lower.
Der er vist at den systemiske eksponering for indinavir under graviditet er relativt formindsket (PACTG 358.
During pregnancy, it has been demonstrated that the systemic exposure of indinavir is relevantly decreased (PACTG 358.
Middel indinavir plasma AUC 0- 8 timer ved 30- 32 ugers gestation (n = 11) var 9231 nM* timer, hvilket er 74% (95% konfidensinterval:
The mean indinavir plasma AUC0-8hr at week 30-32 of gestation (n=11) was 9,231 nM∗ hr, which is 74% (95% CI:
50%, 86%) lavere end hvad der blev set 6 uger efter fødslen.
50%, 86%) lower than that observed 6 weeks postpartum.
Seks af disse 11 patienter (55%) havde middel indinavir plasmakoncentrationer 8 timer efter doseringen (Cmin) under assaygrænsen for pålidelig kvantificering.
The pharmacokinetics of
4. 6).
22 indinavir in these 11 patients at 6 weeks postpartum were generally similar to those observed in non-pregnant patients in another study (see section 4.6).
80% i AUC og 86% reduktion i Cmax.
Administration of indinavir with a meal high in calories, fat, and protein resulted in a blunted and reduced absorption with an approximate 80% reduction in AUC and an 86% reduction in Cmax.
Administration sammen med lette måltider (f. eks. tørt ristet brød med syltetøj eller marmelade, æblejuice og kaffe med skummetmælk eller fedtfri mælk og sukker eller cornflakes med skummetmælk eller fedtfri mælk og sukker) resulterede i en plasmakoncentration sammenlignelig med de tilsvarende fastende værdier.
Administration with light meals (e. g., dry toast with jam or fruit conserve, apple juice, and coffee with skimmed or fat– free milk and sugar or corn flakes, skimmed or fat– free milk and sugar) resulted in plasma concentrations comparable to the corresponding fasted values.
I HIV- inficerede pædiatriske patienter var indinavirs farmakokinetiske parametre i æblemos:
In HIV– infected paediatric patients, the pharmacokinetic parameters of indinavir in apple sauce were:
AUC0- 8 timer på 26980 nM* t; maksimal plasmakoncentration på 13711 nM og plasmakoncentration på 146 nM 8 timer efter dosering.
AUC0– 8hr of 26,980 nM*h; peak plasma concentration of 13,711 nM; and plasma concentration at 8 hours post dose of 146 nM.
Distribution Indinavir bindes ikke i udstrakt grad til humane plasmaproteiner (39% ubundet).
Distribution Indinavir was not highly bound to human plasma proteins (39% unbound).
Biotransformation Der er fundet 7 hovedmetabolitter og de metaboliske veje er vist at være glukoronidering ved pyridin - nitrogenatomet, pyridin- N- oxidation med og uden 3 ’ - hydroxylering på indanringen, 3 ’ - hydroxylering af indan, p- hydroxylering af phenylmethylgruppen, og N- depyridomethylering med og uden 3 ’ - hydroxylering.
Biotransformation Seven major metabolites were identified and the metabolic pathways were identified as glucuronidation at the pyridine nitrogen, pyridine– N– oxidation with and without 3’– hydroxylation on the indane ring, 3’– hydroxylation of indane, p– hydroxylation of phenylmethyl moiety, and N– depyridomethylation with and without the 3’– hydroxylation.
Analyser af plasma - og urinprøver, fra personer som fik indinavir, viste at indinavirmetabolitter har ringe proteinasehæmmende aktivitet.
Analysis of plasma and urine samples from subjects who received indinavir indicated that indinavir metabolites had little proteinase inhibitory activity.
Elimination I dosisintervallet 200- 1000 mg administreret til både raske frivillige og HIV- smittede patienter, fandtes lidt større end dosisproportional stigning af indinavir i urinen.
Elimination Over the 200– 1,000– mg dose range administered in both volunteers and HIV infected patients, there was a slightly greater than dose– proportional increase in urinary recovery of indinavir.
Den renale clearance (116 ml/ min) af indinavir er koncentrationsuafhængig i det kliniske dosisinterval.
Renal clearance (116 ml/ min) of indinavir is concentration– independent over the clinical dose range.
Mindre end 20% af indinavir udskilles renalt.
Less than 20% of indinavir is excreted renally.
Den gennemsnitlige urinudskillelse af uomdannet lægemiddel efter administration af enkeltdoser givet i fastende tilstand var 10, 4% efter en 700 mg dosis og 12% efter en 1000 mg dosis.
Mean urinary excretion of unchanged drug following single dose administration in the fasted state was 10.4% following a 700– mg dose, and 12.0% following a 1,000– mg dose.
Indinavir blev hurtigt elimineret med en halveringstid på 1, 8 timer.
Indinavir was rapidly eliminated with a half– life of 1.8 hours.
Der er ingen klinisk signifikante forskelle i indinavirs farmakokinetik hos HIV- seropositive kvinder sammenlignet med HIV- seropositive mænd.
There are no clinically significant differences in the pharmacokinetics of indinavir in HIV seropositive women compared to HIV seropositive men.
60% højere gennemsnitlig AUC efter en 400 mg dosis.
Patients with mild– to– moderate hepatic insufficiency and clinical evidence of cirrhosis had evidence of decreased metabolism of indinavir resulting in approximately 60% higher mean AUC following a 400– mg dose.
2, 8 timer.
The mean half– life of indinavir increased to approximately 2.8 hours.
23 5. 3 Prækliniske sikkerhedsdata
5.3 Preclinical safety data
Krystallerne er ikke blevet sat i forbindelse med lægemiddelinduceret renal skade.
The crystals have not been associated with drug– induced renal injury.
Forhøjet thyroideavægt og thyroidal follikelcellehyperplasi som følge af forhøjet thyroxinclearance sås hos rotter behandlet med indinavir i doser ≥ 160 mg/ kg/ dag.
An increase in thyroidal weight and thyroidal follicular cell hyperplasia, due to an increase in thyroxine clearance, was seen in rats treated with indinavir at doses ≥ 160 mg/ kg/ day.
Forhøjet levervægt forekom hos rotter behandlet med indinavir i doser ≥ 40 mg/ kg/ dag og blev ledsaget af hepatocellulær hypertrofi ved doser ≥ 320 mg/ kg/ dag.
An increase in hepatic weight occurred in rats treated with indinavir at doses ≥ 40 mg/ kg/ day and was accompanied by hepatocellular hypertrophy at doses ≥ 320 mg/ kg/ day.
Den maksimale, ikke- letale, orale dosis indinavir var mindst 5000 mg/ kg hos rotter og mus, den højeste dosis undersøgt i akutte toksicitetsundersøgelser.
The maximum non– lethal oral dose of indinavir was at least 5,000 mg/ kg in rats and mice, the highest dose tested in acute toxicity studies.
Rotteundersøgelser indikerer at optagelsen i hjernevæv er begrænset, distributionen ind og ud af det lymfatiske system er hurtig og ekskretionen i mælk fra diegivende rotter er ekstensiv.
23 Studies in rats indicated that uptake into brain tissue was limited, distribution into and out of the lymphatic system was rapid, and excretion into the milk of lactating rats was extensive.
Mutagenicitet Indinavir havde ikke nogen mutagen eller genotoksisk aktivitet i undersøgelser med og uden metabolisk aktivering.
Mutagenicity Indinavir did not have any mutagenic or genotoxic activity in studies with or without metabolic activation.
2- 3 gange højere end klinisk eksposition.
Carcinogenicity No carcinogenicity was noted in mice at the maximum tolerated dose, which corresponded to a systemic exposure approximately 2 to 3 times higher than the clinical exposure.
Reproduktion Der blev udført reproduktionsundersøgelser med rotter, kaniner og hunde (ved doser der gav systemisk eksponering sammenlignelig med eller lidt større end human eksponering), og disse viste ingen tegn på teratogenicitet.
Developmental Toxicity Developmental toxicity studies were performed in rats, rabbits and dogs (at doses which produced systemic exposures comparable to or slightly greater than human exposure) and revealed no evidence of teratogenicity.
Der sås ingen virkninger på embryo/ føtaloverlevelse eller føtalvægt hos rotter og kaniner.
In rats and rabbits, no effects on embryonic/ foetal survival or foetal weights were observed.
Hos hunde sås lille stigning i resorptioner, dog var alle fostre hos medicinbehandlede dyr levedygtige og incidencen af levende fostre hos medicinbehandlede dyr svarede til kontrolgruppens.
In dogs, a slight increase in resorptions was seen; however, all foetuses in medication– treated animals were viable, and the incidence of live foetuses in medication– treated animals was comparable to that in controls.
Kapselindhold:
Capsule content
- vandfri lactose
- anhydrous lactose
- magnesiumstearat
- magnesium stearate
- gelatine
- gelatin
- titandioxid (E171)
- titanium dioxide (E 171)
- siliciumdioxid
- silicon dioxide
- natriumlaurilsulfat.
- sodium lauryl sulphate
Titandioxid (E 171), indigocarmin (E 132) og jernoxid (E 172).
- printing ink: titanium dioxide (E 171), indigo carmine (E 132), and iron oxide (E 172).
24 3 år.
3 years
HDPE- beholder med polypropylenlåg og folielukning, indeholdende 180 kapsler.
HDPE bottles with a polypropylene cap and a foil induction cap containing 180 capsules.