natgillin/translations-raw huggingface dataset:
- ECX: epirubicin (50 mg/ m2 as a bolus on day 1 every 3 weeks), cisplatin (60 mg/ m2 as a two
1. dan vsake 3 tedne) in 5- FU (200 mg/ m2 na dan v kontinuirani infuziji skozi centralni venski kateter); ECX: epirubicin (50 mg/ m2 kot bolus 1. dan vsake 3 tedne), cisplatin (60 mg/ m2 v 2- urni
- EOF: epirubicin (50 mg/ m2 as a bolus on day 1 every 3 weeks), oxaliplatin (130 mg/ m2 given as
infuziji 1. dan vsake 3 tedne) in Xeloda (625 mg/ m2 dvakrat na dan neprekinjeno); EOF: epirubicin (50 mg/ m2 kot bolus 1. dan vsake 3 tedne), oksaliplatin (130 mg/ m2 v 2- urni
a 2 hour infusion on day 1 every three weeks), and 5-FU (200 mg/ m2 daily given by continuous infusion via a central line).
-
- EOX: epirubicin (50 mg/ m2 as a bolus on day 1 every 3 weeks), oxaliplatin (130 mg/ m2 given as
infuziji 1. dan vsake tri tedne) in 5- FU (200 mg/ m2 na dan v kontinuirani infuziji skozi centralni venski kateter); EOX: epirubicin (50 mg/ m2 kot bolus 1. dan vsake 3 tedne), oksaliplatin (130 mg/ m2 v 2- urni
a 2 hour infusion on day 1 every three weeks), and Xeloda (625 mg/ m2 twice daily continuously).
infuziji 1. dan vsake tri tedne) in Xeloda (625 mg/ m2 dvakrat na dan neprekinjeno).
19 The primary efficacy analyses in the per protocol population demonstrated non-inferiority in overall survival for capecitabine- vs 5-FU-based regimens (hazard ratio 0.86; 95% CI 0.8 - 0.99) and for oxaliplatin- vs cisplatin-based regimens (hazard ratio 0.92; 95% CI 0.80 - 1.1).
Analiza primarne učinkovitosti pri populaciji po protokolu je za celokupno preživetje dokazala, da so sheme osnovane na kapecitabinu neinferiorne shemam osnovanim na 5- FU (razmerje ogroženosti 0, 86; 95 -% interval zaupanja 0, 80−0, 99), sheme osnovane na oksaliplatinu pa neinferiorne shemam osnovanim na cisplatinu (razmerje ogroženosti 0, 92; 95 -% interval zaupanja 0, 80−1, 10).
The median overall survival was 10.9 months in capecitabine-based regimens and 9.6 months in 5-FU based regimens.
Mediana celokupnega preživetja je bila 10, 9 meseca pri shemah osnovanih na kapecitabinu in 9, 6 meseca pri shemah, osnovanih na 5- FU.
The median overall survival was 10.0 months in cisplatin-based regimens and 10.4 months in oxaliplatin-based regimens.
Mediana celokupnega preživetja je bila 10, 0 meseca pri shemah osnovanih na cisplatinu in 10, 4 meseca pri shemah, osnovanih na oksaliplatinu.
Xeloda has also been used in combination with oxaliplatin for the treatment of advanced gastric cancer.
Zdravilo Xeloda se za zdravljenje napredovalega raka želodca uporablja tudi v kombinaciji z oksaliplatinom.
Studies with Xeloda monotherapy indicate that Xeloda has activity in advanced gastric cancer.
Študije s samostojnim zdravljenjem z zdravilom Xeloda kažejo na to, da je zdravilo Xeloda učinkovito pri napredovalem raku želodca.
Colon, colorectal and advanced gastric cancer: meta-analysis A meta-analysis of six clinical trials (studies SO14695, SO14796, M66001, NO16966, NO16967, M17032) supports Xeloda replacing 5-FU in mono- and combination treatment in gastrointestinal cancer.
Meta analiza šestih kliničnih preskušanj (študije SO14695, SO14796, M66001, NO16966, NO16967, M17032) podpira zamenjavo 5- FU z zdravilom Xeloda pri zdravljenju raka prebavil, samostojno ali v kombinaciji z drugimi zdravili.
The pooled analysis includes 3097 patients treated with Xeloda-containing regimens and 3074 patients treated with 5-FU-containing regimens.
Skupna analiza je zajela 3097 bolnikov, katerih zdravljenje je vključevalo zdravilo Xeloda, in 3074 bolnikov, katerih zdravljenje je vključevalo 5- FU.
648; 715) in patients treated with 5-FU-containing regimens.
Mediana celokupnega preživetja je bila pri bolnikih, katerih zdravljenje je vključevalo zdravilo Xeloda, 703 dni (95 -% interval zaupanja; 671; 743); pri bolnikih, katerih zdravljenje je vključevalo 5- FU, pa 683 dni (95 -% interval zaupanja; 648; 715).
0.90; 1.02) indicating that Xeloda-containing regimens are equivalent to 5-FU-containing regimens.
Razmerje ogroženosti za celokupno preživetje je bilo 0, 96 (95 -% interval zaupanja; 0, 90; 1, 02), kar kaže, da je zdravljenje, ki vključuje zdravilo Xeloda, enakovredno zdravljenju, ki vključuje 5- FU.
Breast cancer:
Rak dojk:
Combination therapy with Xeloda and docetaxel in locally advanced or metastatic breast cancer Data from one multicentre, randomised, controlled phase III clinical trial support the use of Xeloda in combination with docetaxel for treatment of patients with locally advanced or metastatic breast cancer after failure of cytotoxic chemotherapy, including an anthracycline.
Kombinirano zdravljenje z zdravilom Xeloda in docetakselom pri lokalno napredovali ali metastatski obliki raka dojk Podatki kontroliranega, randomiziranega, multicentričnega kliničnega preskušanja faze III podpirajo uporabo zdravila Xeloda v kombinaciji z docetakselom za zdravljenje lokalne napredovale ali metastatske oblike raka dojk po neuspeli citotoksični antraciklinski kemoterapiji.
In this trial, 255 patients were randomised to treatment with Xeloda (1250 mg/ m2 twice daily for 2 weeks followed by 1-week rest period and docetaxel 75 mg/ m2 as a 1 hour intravenous infusion every 3 weeks).
255 bolnikov, randomizirano vključenih v preskušanje, je prejemalo zdravljenje z zdravilom Xeloda (1250 mg/ m2 dvakrat na dan 2 tedna, sledil je enotedenski premor, in docetaksel 75 mg/ m2 v obliki enourne intravenske infuzije vsake 3 tedne).
256 patients were randomised to treatment with docetaxel alone (100 mg/ m2 as a 1 hour intravenous infusion every 3 weeks).
256 bolnikov, randomizirano vključenih v preskušanje, je prejemalo le docetaksel (100 mg/ m2 v obliki enourne intravenske infuzije vsake 3 tedne).
Survival was superior in the Xeloda + docetaxel combination arm (p=0.0126).
Daljše preživetje je bilo v skupini bolnikov, ki je prejemala kombinirano zdravljenje zdravila Xeloda in docetaksela (p = 0, 0126).
352 days (docetaxel alone).
Mediana preživetja v skupini, ki je prejemala zdravilo Xeloda in docetaksel, je bila 442 dni, v skupini, ki je jemala le docetaksel, pa 352 dni.
29.7% (docetaxel alone); p = 0.0058.
Celokupni objektivni odziv celotne vključene populacije je bil po oceni raziskovalca 41, 6% v skupini, ki je jemala zdravilo Xeloda in docetaksel, ter 29, 7% v skupini, ki je jemala le docetaksel (p = 0, 0058).
Time to progressive disease was superior in the Xeloda + docetaxel combination arm (p < 0.0001).
Mediana časa do
128 days (docetaxel alone).
21 napredovanja bolezni v skupini, ki je jemala zdravilo Xeloda in docetaksel, je bila 186 dni, v skupini, ki je jemala le docetaksel, pa 128 dni.
Monotherapy with Xeloda after failure of taxanes, anthracycline containing chemotherapy, and for whom anthracycline therapy is not indicated Data from two multicentre phase II clinical trials support the use of Xeloda monotherapy for treatment of patients after failure of taxanes and an anthracycline-containing chemotherapy regimen or for whom further anthracycline therapy is not indicated.
Samostojno zdravljenje z zdravilom Xeloda po neuspešnem zdravljenju s kemoterapijo, ki je vključevala taksane in antracikline ter zdravljenje bolnikov, za katere antraciklini niso indicirani Podatki dveh multicentričnih kliničnih preskušanj faze II podpirajo samostojno uporabo zdravila Xeloda za zdravljenje bolnikov po neuspelem zdravljenju s taksani in neuspelem zdravljenju z antraciklinsko kemoterapijo ter pri bolnikih, kjer antraciklini niso indicirani.
In these trials, a total of 236 patients were treated with Xeloda (1250 mg/ m2 twice daily for 2 weeks followed by 1-week rest period).
V preskušanjih je bilo 236 bolnikov zdravljenih z zdravilom Xeloda (odmerek 1250 mg/ m2 dvakrat na dan 2 tedna, sledi en teden premora).
The overall objective response rates (investigator assessment) were 20% (first trial) and 25% (second trial).
Celotni objektivni odziv po oceni raziskovalca je bil v prvem preskušanju 20 -%, v drugem pa 25 -%.
A meta-analysis of 13 clinical trials with data from over 3800 patients treated with Xeloda monotherapy or Xeloda in combination with different chemotherapy regimens in multiple indications (colon, colorectal, gastric and breast cancer) showed that patients on Xeloda who developed hand-foot syndrome (HFS) had a longer overall survival compared to patients who did not develop HFS: median overall survival 29.0 months (95% CI 26.0; 31.6) vs 15.9 months (95% CI 15.0; 17.0) with a hazard ratio of 0.59 (95% CI 0.54; 0.64).
Vse indikacije Meta- analiza 13 kliničnih preskušanj s podatki od več kot 3800 bolnikov, zdravljenih s kapecitabinom samim ali v kombinaciji z različnimi shemami kemoterapije pri več indikacijah (rak kolona, kolorektalni rak, rak želodca in rak dojk) je pokazala, da so imeli bolniki, pri katerih se je razvil sindrom roka- noga, daljše celokupno preživetje v primerjavi z bolniki, ki niso imeli tega sindroma; mediana celokupnega preživetja je bila 29, 0 meseca (95 -% interval zaupanja; 26, 0; 31, 6) v primerjavi s 15, 9 meseca (95 -% interval zaupanja 15, 0; 17, 0) z razmerjem ogroženosti 0, 59 (95 -% interval zaupanja; 0, 54; 0, 64).
20 5.2 Pharmacokinetic properties
5. 2 Farmakokinetične lastnosti
The pharmacokinetics of capecitabine have been evaluated over a dose range of 502-3514 mg/ m2/ day.
Farmakokinetiko kapecitabina so ocenjevali v odmerkih od 502 do 3514 mg/ m2/ dan.
The parameters of capecitabine, 5'-deoxy-5-fluorocytidine (5'-DFCR) and 5'-deoxy-5-fluorouridine (5'-DFUR) measured on days 1 and 14 were similar.
Parametri kapecitabina, 5´- deoksi- 5- fluorocitidina (5´- DFCR) in 5´- deoksi- 5- fluorouridina (5´- DFUR), ki so jih izmerili prvi in štirinajsti dan, so bili podobni.
The AUC of 5-FU was 30%-35% higher on day 14.
AUC 5- FU je bila od 30 do 35% višja štirinajstega dne.
Capecitabine dose reduction decreases systemic exposure to 5-FU more than dose-proportionally, due to non-linear pharmacokinetics for the active metabolite.
Če zmanjšamo odmerek kapecitabina, se sistemska izpostavljenost 5- FU zaradi nelinearne farmakokinetike aktivnega presnovka zmanjša bolj kot sorazmerno z odmerkom.
Absorption: after oral administration, capecitabine is rapidly and extensively absorbed, followed by extensive conversion to the metabolites, 5'-DFCR and 5'-DFUR.
Absorpcija: po peroralnem zaužitju se kapecitabin absorbira hitro in v velikem obsegu, nato pa se v velikem obsegu pretvori v presnovka 5´- DFCR in 5´- DFUR.
Administration with food decreases the rate of capecitabine absorption, but only results in a minor effect on the AUC of 5'-DFUR, and on the AUC of the subsequent metabolite 5-FU.
Jemanje s hrano zmanjša hitrost absorpcije kapecitabina, kar pa ima le neznaten vpliv na AUC 5´- DFUR in na AUC presnovka 5- FU.
At the dose of 1250 mg/ m2 on day 14 with administration after food intake, the peak plasma concentrations (Cmax in µg/ ml) for capecitabine, 5'-DFCR, 5'-DFUR, 5-FU and FBAL were 4.67, 3.05, 12.1, 0.95 and 5.46 respectively.
Pri odmerku 1250 mg/ m2 ob jemanju po obroku so bile na 14. dan največje plazemske koncentracije (Cmax v μg/ ml) za kapecitabin, 5´- DFCR, 5´- DFUR, 5- FU in FBAL 4, 67; 3, 05; 12, 1; 0, 95 in 5, 46.
The time to peak plasma concentrations (Tmax in hours) were 1.50, 2.00, 2.00, 2.00 and 3.34.
Časi do dosega največje plazemske koncentracije (Tmax v urah) so bili 1, 50; 2, 00; 2, 00; 2, 00 in 3, 34.
The AUC0-∞ values in μ g• h/ ml were 7.75, 7.24, 24.6, 2.03 and 36.3.
Vrednosti AUC0- ∞ v μg• h/ ml so znašale 7, 75; 7, 24; 24, 6; 2, 03 in 36, 3.
Protein binding: in vitro human plasma studies have determined that capecitabine, 5'-DFCR, 5'-DFUR and 5-FU are 54%, 10%, 62% and 10% protein bound, mainly to albumin.
Vezava na proteine: študije in vitro na človeški plazmi so pokazale, da se na proteine (v glavnem na albumin) veže 54% kapecitabina, 10% 5´- DFCR, 62% 5´- DFUR in 10% 5- FU.
Metabolism: capecitabine is first metabolised by hepatic carboxylesterase to 5'-DFCR, which is then converted to 5'-DFUR by cytidine deaminase, principally located in the liver and tumour tissues.
Presnova: kapecitabin se najprej pretvori z jetrno karboksilesterazo v 5´- DFCR, ta pa se prek citidin deaminaze, ki se nahaja v jetrih in tumorskih tkivih, naprej pretvori v 5´- DFUR.
The sequential enzymatic biotransformation of capecitabine to 5-FU leads to higher concentrations within tumour tissues.
Postopna encimska biotransformacija kapecitabina v 5- FU daje večje koncentracije v tumorskih tkivih.
In the case of colorectal tumours, 5-FU generation appears to be in large part localised in tumour stromal cells.
Pri kolorektalnih tumorjih je generacija 5- FU močno lokalizirana v tumorskih stromalnih celicah.
Following oral administration of capecitabine to patients with colorectal cancer, the ratio of 5-FU concentration in colorectal tumours to adjacent tissues was 3.2 (ranged from 0.9 to 8.0).
Po peroralnem zaužitju kapecitabina je pri bolnikih s kolorektalnim rakom razmerje koncentracij 5- FU v kolorektalnih tumorjih znašalo v primerjavi s sosednjimi tkivi 3, 2 (območje 0, 9 do 8, 0).
The ratio of 5-FU concentration in tumour to plasma was 21.4 (ranged from 3.9 to 59.9, n=8) whereas the ratio in healthy tissues to plasma was 8.9 (ranged from 3.0 to 25.8, n=8).
Razmerje koncentracij 5- FU v tumorjih v primerjavi s plazmo je bilo 21, 4 (območje 3, 9 do 59, 9, n = 8), razmerje med zdravimi tkivi in plazmo pa 8, 9 (območje 3, 0 do 25, 8, n = 8).
5-FU is further catabolised by the enzyme dihydropyrimidine dehydrogenase (DPD) to the much less toxic dihydro-5-fluorouracil (FUH2).
22 5- FU se nadalje presnovi z encimom dihidropirimidin dehidrogenazo (DPD) v precej manj toksični dihidro- 5- fluorouracil (FUH2).
Dihydropyrimidinase cleaves the pyrimidine ring to yield 5-fluoro-ureidopropionic acid (FUPA).
Dihidropirimidinaza cepi pirimidinski obroč, pri čemer nastane 5 - fluoro- ureidopropionska kislina (FUPA).
Finally, β -ureido-propionase cleaves FUPA to α -fluoro-β - alanine (FBAL) which is cleared in the urine.
Na koncu beta- ureido- propionaza cepi FUPA v alfa- fluoro - beta- alanin (FBAL), ki se izloči z urinom.
Deficiency of DPD may lead to increased toxicity of capecitabine (see section 4.3 and 4.4).
Pomanjkanje DPD lahko vodi do povečane toksičnosti kapecitabina (glejte poglavji 4. 3 in 4. 4).
Elimination: the elimination half-life (t1/ 2 in hours) of capecitabine, 5'-DFCR, 5'-DFUR, 5-FU and FBAL were 0.85, 1.11, 0.66, 0.76 and 3.23 respectively.
Izločanje: razpolovne dobe izločanja (t1/ 2 v urah) kapecitabina, 5´- DFCR, 5´- DFUR, 5- FU in FBAL so bile 0, 85; 1, 11; 0, 66; 0, 76 in 3, 23.
Faecal excretion is minimal (2.6%).
Kar 95, 5% zaužitega odmerka kapecitabina se izloči z urinom, z blatom pa le 2, 6% odmerka.
The major metabolite excreted in urine is FBAL, which represents 57% of the administered dose.
Glavni presnovek, ki se izloča z urinom, je FBAL, katerega delež je 57% zaužitega odmerka.
About 3% of the administered dose is excreted in urine as unchanged drug.
Približno 3% kapecitabina se izločijo nespremenjeni.
Phase I studies evaluating the effect of Xeloda on the pharmacokinetics of either docetaxel or paclitaxel and vice versa showed no effect by Xeloda on the pharmacokinetics of docetaxel or paclitaxel (Cmax and AUC) and no effect by docetaxel or paclitaxel on the pharmacokinetics of 5’ -DFUR.
Prav tako niso pokazale vplivov docetaksela ali paklitaksela na farmakokinetiko 5´- DFUR.
A population pharmacokinetic analysis was carried out after Xeloda treatment of 505 patients with colorectal cancer dosed at 1250 mg/ m2 twice daily.
Farmakokinetika pri posebnih skupinah: populacijsko farmakokinetično študijo so opravili po zdravljenju 505 bolnikov s kolorektalnim rakom, ki so prejemali 1250 mg/ m2 zdravila Xeloda dvakrat na dan.
21 serum albumin, ASAT and ALAT had no statistically significant effect on the pharmacokinetics of 5'-DFUR, 5-FU and FBAL.
Spol, prisotnost ali odsotnost zasevkov v jetrih, splošno bolnikovo stanje, celokupni bilirubin, serumski albumin, AST in ALT niso statistično značilno vplivali na farmakokinetiko 5´- DFUR, 5- FU in FBAL.
According to a pharmacokinetic study in cancer patients with mild to moderate liver impairment due to liver metastases, the bioavailability of capecitabine and exposure to 5-FU may increase compared to patients with no liver impairment.
Bolniki z jetrno okvaro zaradi zasevkov v jetrih: glede na farmakokinetično študijo pri bolnikih z rakom, ki imajo blago ali zmerno jetrno okvaro zaradi zasevkov v jetrih, je biološka uporabnost kapecitabina in izpostavljenost 5- FU lahko povečana v primerjavi z bolniki brez okvare.
Based on a pharmacokinetic study in cancer patients with mild to severe renal impairment, there is no evidence for an effect of creatinine clearance on the pharmacokinetics of intact drug and 5-FU.
Bolniki z ledvično okvaro: glede na farmakokinetično študijo pri bolnikih, ki imajo blago do hudo ledvično okvaro, ni dokazov za vpliv kreatininskega očistka na farmakokinetiko zdravila in 5- FU.
Creatinine clearance was found to influence the systemic exposure to 5’ -DFUR (35% increase in AUC when creatinine clearance decreases by 50%) and to FBAL (114% increase in AUC when creatinine clearance decreases by 50%).
Kreatininski očistek je vplival na sistemsko izpostavljenost 5´- DFUR (35 -% povečanje AUC, kreatininski očistek zmanjšan za 50%) in FBAL (114 -% povečanje AUC in padec kreatinskega očistka za 50%).
Based on the population pharmacokinetic analysis, which included patients with a wide range of ages (27 to 86 years) and included 234 (46%) patients greater or equal to 65, age has no influence on the pharmacokinetics of 5'-DFUR and 5-FU.
Starejši bolniki: na osnovi podatkov populacijske farmakokinetične študije, ki je zajela bolnike z velikim razponom v letih (27 do 86 let) in 234 bolnikov (46%), starih 65 let ali starejših, so ugotovili, da starost ne vpliva na farmakokinetiko 5´- DFUR in 5- FU.
The AUC of FBAL increased with age (20% increase in age results in a 15% increase in the AUC of FBAL).
AUC za FBAL je z leti naraščala (20 -% povečanje v letih daje 15 -% povečanje AUC za FBAL).
Following oral administration of 825 mg/ m2 capecitabine twice daily for 14 days, Japanese patients (n=18) had about 36% lower Cmax and 24% lower AUC for capecitabine than Caucasian patients (n=22).
Etnični dejavniki: po peroralnem dajanju 825 mg/ m2 kapecitabina dvakrat na dan 14 dni so japonski bolniki (n = 18) imeli približno 36% nižjo Cmax in 24% nižjo AUC kapecitabina kakor kavkaški bolniki (n = 22).
Japanese patients had also about 25% lower Cmax and 34% lower AUC for FBAL than Caucasian patients.
Japonski bolniki so imeli v primerjavi s kavkaškimi bolniki prav tako približno 25% nižjo Cmax in 34% nižjo AUC za FBAL.
No significant differences occurred in the exposure to other metabolites (5'-DFCR, 5'-DFUR, and 5-FU).
Značilnih razlik v izpostavljenosti drugim presnovkom (5´- DFCR, 5´- DFUR in 5- FU) ni bilo.
Skin toxicity, characterised by degenerative/ regressive changes, was observed with capecitabine.
Opazili so tudi toksični učinek kapecitabina na kožo, znan kot degenerativne/ regresivne spremembe.
Cardiovascular toxicity (e. g.
Kapecitabin ni toksično učinkoval na jetra in centralni živčni sistem.
PR- and QT-interval prolongation) was detectable in cynomolgus monkeys after intravenous administration (100 mg/ kg) but not after repeated oral dosing (1379 mg/ m2/ day).
Toksično delovanje na srce in ožilje (podaljšanje intervalov PR in QT) so opazili pri opicah cynomolgus po intravenskem dajanju (100 mg/ kg), po večkratnem peroralnem dajanju (1379 mg/ m2/ dan) pa ne.
A two-year mouse carcinogenicity study produced no evidence of carcinogenicity by capecitabine.
23 Dveletna študija pri miših ni pokazala kancerogenega delovanja kapecitabina.
In addition, during a 13-week study, atrophic and degenerative changes occurred in reproductive organs of male mice; however these effects were reversible after a drug-free period.
Med 13- tedensko študijo so se pri mišjih samcih pojavile atrofične in degenerative spremembe na reproduktivnih organih, ki so po prenehanju jemanja kapecitabina izginile.
In monkeys, abortion and embryolethality were observed at high doses, but there was no evidence of teratogenicity.
Dokazov o teratogenosti ni bilo.
Capecitabine was not mutagenic in vitro to bacteria (Ames test) or mammalian cells (Chinese hamster V79/ HPRT gene mutation assay).
Kapecitabin in vitro pri bakterijah (Amesov test) ali celicah sesalcev (kitajski hrček V79/ HPRT, metoda genske mutacije) ni bil mutagen.
However, similar to other nucleoside analogues (ie, 5-FU), capecitabine was clastogenic in human lymphocytes (in vitro) and a positive trend occurred in mouse bone marrow micronucleus tests (in vivo).
Podobno kakor drugi nukleozidni analogi, kot je 5- FU, je bil kapecitabin v človeških limfocitih klastogen (in vitro), mikronukleozni test (in vivo) v celicah kostnega mozga miši pa je imel pozitivno tendenco.
Tablet core: anhydrous lactose, croscarmellose sodium, hypromellose, microcrystalline cellulose, magnesium stearate.
Jedro tablete: brezvodna laktoza, premrežen natrijev karmelozat, hipromeloza, mikrokristalna celuloza, magnezijev stearat.
Tablet coating: hypromellose, titanium dioxide (E171), yellow and red iron oxide (E172), talc.
Filmska obloga: hipromeloza, titanov dioksid (E171), rumeni in rdeči železov oksid (E172), smukec.
PVC/ PVDC blisters
PVC/ PVDC pretisni omoti.
60 film-coated tablets (6 blisters of 10 tablets)
60 filmsko obloženih tablet (6 pretisnih omotov po 10 tablet).
02 February 2001 Date of first renewal:
2. februar 2001 Datum prve obnove:
02 February 2006
2. februar 2006
Detailed information on this medicinal product is available on the website of the European Medicines Agency (EMEA) http: / /www. emea. europa. eu/.
Podrobne informacije o zdravilu so objavljene na spletni strani Evropske agencije za zdravila (EMEA) http: // www. emea. eu. int /.
500 mg capecitabine.
500 mg kapecitabina
52 mg anhydrous lactose.
52 mg brezvodne laktoze.
Peach film-coated tablet of biconvex, oblong shape with the marking ‘ 500’ on the one side and ‘ Xeloda’ on the other side.
Filmsko obložene tablete so breskove barve, bikonveksne in podolgovate oblike z oznako “ 500 ” na eni strani in “ Xeloda ” na drugi strani.
Recommended posology (see section 5.1):
26 Priporočeno odmerjanje (glejte poglavje 5. 1):
Monotherapy Colon, colorectal and breast cancer Given as single agent, the recommended starting dose for Xeloda in the adjuvant treatment of colon cancer, in the treatment of metastatic colorectal cancer or of locally advanced or metastatic breast cancer is 1250 mg/ m2 administered twice daily (morning and evening; equivalent to 2500 mg/ m2 total daily dose) for 14 days followed by a 7-day rest period.
Samostojno zdravljenje Rak kolona in kolorektalni rak ter rak dojk Priporočeni začetni odmerek zdravila Xeloda za samostojno adjuvantno zdravljenje raka kolona, metastatskega kolorektalnega raka ali lokalno napredovalega ali metastatskega raka dojk je 1250 mg/ m2 dvakrat na dan (zjutraj in zvečer; celokupni dnevni odmerek znaša 2500 mg/ m2) 14 dni, sledi 7- dnevni premor.
25 Combination therapy Colorectal and gastric cancer In combination treatment, the recommended starting dose of Xeloda should be reduced to 800 – 1000 mg/ m2 when administered twice daily for 14 days followed by a 7-day rest period, or to 625 mg/ m2 twice daily when administered continuously (see section 5.1).
Zdravljenje s kombinacijo zdravil Kolorektalni rak in rak želodca Pri zdravljenju s kombinacijo zdravil je treba priporočeni začetni odmerek zdravila Xeloda zmanjšati na 800 do 1000 mg/ m2, kadar ga dajemo dvakrat na dan 14 dni, čemur sledi 7- dnevni premor, ali na 625 mg/ m2 dvakrat na dan, če ga dajemo neprekinjeno (glejte poglavje 5. 1).
Number of 150 mg
Preglednica 1.
500 mg administration (mg)
Enkratni Enkratni odmerek Enkratni odmerek odmerek (mg) 150 mg 500 mg (mg) (mg)
Number of 150 mg
27 Preglednica 2.
Patients taking Xeloda should be informed of the need to interrupt treatment immediately if moderate or severe toxicity occurs Doses of Xeloda omitted for toxicity are not replaced.
Opuščenih odmerkov zdravila Xeloda zaradi toksičnosti ne nadomeščamo.
27 Table 3 Xeloda Dose Reduction Schedule (3-weekly Cycle or Continuous Treatment)
z zdravilom Xeloda (3- tedenski cikli
-4th appearance • Grade 3
2. pojav 3. pojav
Not
•
applicable
Stopnja 3