natgillin/translations-raw huggingface dataset:
115 patienter blev randomiseret til behandling med Xeloda kombineret med irinotecan (XELIRI) og bevacizumab:
115 Patients were randomised to treatment with Xeloda combined with irinotecan (XELIRI) and bevacizumab:
I alt blev 118 patienter randomiseret til behandling med Xeloda kombineret med oxaliplatin plus bevacizumab:
Xeloda (800 mg/ m2 twice daily for two weeks followed by a 7-day rest period), irinotecan (200 mg/ m2 as a 30 minute infusion on day 1 every 3 weeks), and bevacizumab (7.5 mg/ kg as a 30 to 90 minute infusion on day 1 every 3 weeks); a total of 118 patients were randomised to treatment with Xeloda combined with oxaliplatin plus bevacizumab:
Xeloda (1000 mg/ m2 to gange daglig i to uger efterfulgt af 7 dages pause), oxaliplatin (130 mg/ m2 som en 2 timers infusion på dag 1 hver 3. uge) og bevacizumab (7, 5 mg/ m2 som en 30 til 90 minutters infusion på dag 1 hver 3. uge).
Xeloda (1000 mg/ m2 twice daily for two weeks followed by a 7-day rest period), oxaliplatin (130 mg/ m2 as a 2 hour infusion on day 1 every 3 weeks), and bevacizumab (7.5 mg/ kg as a 30 to 90 minute infusion on day 1 every 3 weeks).
Den progressionsfri overlevelse efter 6 måneder i intent- to- treat- populationen var 80% (XELIRI plus bevacizumab) versus 74% (XELOX plus bevacizumab).
Progression-free survival at 6 months in the intent-to-treat population was 80% (XELIRI plus bevacizumab) versus 74% (XELOX plus bevacizumab).
Den samlede responsrate (komplet + partiel remission) var 45% (XELOX plus bevacizumab versus 47% (XELIRI plus bevacizumab).
Overall response rate (complete response plus partial response) was 45% (XELOX plus bevacizumab) versus 47% (XELIRI plus bevacizumab).
18 Kombinationsterapi i 2. linjebehandling af metastatisk kolorektalkræft Data fra et multicenter, randomiseret, kontrolleret klinisk fase III- studie (NO16967) understøtter anvendelsen af Xeloda i kombination med oxaliplatin til 2. linjebehandling af metastatisk kolorektalkræft.
Combination therapy in second-line treatment of metastatic colorectal cancer Data from a multicentre, randomised, controlled phase III clinical study (NO16967) support the use of Xeloda in combination with oxaliplatin for the second-line treatment of metastastic colorectal cancer.
I denne undersøgelse blev 627 patienter med metastatisk kolorektalkræft, som tidligere havde modtaget behandling med irinotecan i kombination med fluoropyrimidin som 1. linje - behandling, randomiseret til behandling med XELOX eller FOLFOX- 4.
In this trial, 627 patients with metastatic colorectal carcinoma who have received prior treatment with irinotecan in combination with a fluoropyrimidine regimen as first line therapy were randomised to treatment with XELOX or FOLFOX-4.
For doseringen af XELOX og FOLFOX- 4 (uden tillæg af placebo eller bevacizumab) se tabel 6.
For the dosing schedule of XELOX and FOLFOX-4 (without addition of placebo or bevacizumab), refer to Table 6.
Det blev vist, at XELOX var non - inferior i forhold til FOLFOX- 4 med hensyn til progressionsfri overlevelse i per- protokolpopulationen og intent- to- treat- populationen (se tabel 8).
18 FOLFOX-4 in terms of progression-free survival in the per-protocol population and intent-to-treat population (see Table 8).
Resultaterne indikerer, at XELOX er ækvivalent med FOLFOX- 4 med hensyn til samlet overlevelse (se tabel 8).
The results indicate that XELOX is equivalent to FOLFOX-4 in terms of overall survival (see Table 8).
Data fra analyser efter yderligere 6 måneders follow- up fremgår også af tabel 8.
The median follow up at the time of the primary analyses in the intent- to-treat population was 2.1 years; data from analyses following an additional 6 months of follow up are also included in Table 8.
Nøgleresultater fra non- inferioritetsanalyserne af studie NO16967 PRIMÆRE ANALYSE XELOX FOLFOX- 4 (PPP *:
the non-inferiority analysis of Study NO16967 PRIMARY ANALYSIS
(97, 5% KI)
(95% CI)
388 363 MÅNEDERS YDERLIGERE FOLLOW UP
388 363
1, 07 (0, 88; 1, 31) 1, 03 (0, 87; 1, 23) HR
1.07 (0.88; 1.31) 1.03 (0.87; 1.23)
* PPP=per protokol population; ** ITT=intent- to- treat population
*PPP=per-protocol population; **ITT=intent-to-treat population
Data fra et randomiseret, kontrolleret, klinisk fase III- multicenterstudie hos patienter med fremskreden ventrikelkræft støtter anvendelsen af Xeloda som 1. linjebehandling af fremskreden ventrikelkræft (ML17032).
Data from a multicentre, randomised, controlled phase III clinical trial in patients with advanced gastric cancer supports the use of Xeloda for the first-line treatment of advanced gastric cancer (ML17032).
I dette studie blev 160 patienter randomisered til behandling med Xeloda (1000 mg/ m2 to gange dagligt i 2 uger efterfulgt af 7 dages pause) og cisplatin (80 mg/ m2 som en 2- timers infusion hver 3. uge).
In this trial, 160 patients were randomised to treatment with Xeloda (1000 mg/ m2 twice daily for 2 weeks followed by a 7-day rest period) and cisplatin (80 mg/ m2 as a 2-hour infusion every 3 weeks).
I alt blev 156 patienter randomiseret til behandling med 5- FU (800 mg/ m2 dagligt som kontinuerlig infusion på dag 1 til 5 hver 3. uge) og cisplatin (80 mg/ m2 som en 2- timers infusion på dag 1 hver 3. uge).
A total of 156 patients were randomised to treatment with 5-FU (800 mg/ m2 per day, continuous infusion on days 1 to 5 every 3 weeks) and cisplatin (80 mg/ m2 as a 2-hour infusion on day 1, every 3 weeks).
Xeloda var i kombination med cisplatin non- inferiørt i forhold til 5- FU i kombination med cisplatin med hensyn til progressionsfri overlevelse i per protokolanalysen (hazard ratio 0, 81; 95% konfidensinterval 0, 63 – 1, 04).
Xeloda in combination with cisplatin was non-inferior to 5-FU in combination with cisplatin in terms of progression-free survival in the per protocol analysis (hazard ratio 0.81; 95% CI 0.63 - 1.04).
Den mediane progressionsfrie overlevelse var 5, 6 måneder (Xeloda + cisplatin) versus 5, 0 måneder (5- FU + cisplatin).
The median progression-free survival was 5.6 months (Xeloda + cisplatin) versus 5.0 months (5-FU + cisplatin).
Resultatet for hazard ratio for varighed af overlevelse (samlet overlevelse) svarede til resultatet for hazard ratio for progressionsfri overlevelse (hazard ratio 0, 85, 95% konfidensinterval 0, 64 – 1, 13).
The hazard ratio for duration of survival (overall survival) was similar to the hazard ratio for progression-free survival (hazard ratio 0.85; 95% CI 0.64 - 1.13).
Den mediane varighed for overlevelse var 10, 5 måneder (Xeloda + cisplatin) versus 9, 3 måneder (5- FU + cisplatin).
The median duration of survival was 10.5 months (Xeloda + cisplatin) versus 9.3 months (5-FU + cisplatin).
Data fra et randomiseret fase III- multicenterstudie, der sammenlignede capecitabin med 5- FU og i kombination med enten oxaliplatin eller cisplatin til patienter med fremskreden ventrikelkræft, støtter anvendelse af Xeloda til 1. linjebehandling af fremskreden ventrikelkræft (REAL- 2).
Data from a randomised multicentre, phase III study comparing capecitabine to 5-FU and oxaliplatin to cisplatin in patients with advanced gastric cancer supports the use of Xeloda for the first-line treatment of advanced gastric cancer (REAL-2).
- ECF: epirubicin (50 mg / m2 som bolus på dag 1 hver 3. uge), cisplatin (60 mg/ m2 som en to -
- ECF: epirubicin (50 mg/ m2 as a bolus on day 1 every 3 weeks), cisplatin (60 mg/ m2 as a two
timers infusion på dag 1 hver 3. uge) og 5- FU (200 mg/ m2 dagligt givet som kontinuerlig infusion via et centralt venekateter).
hour infusion on day 1 every 3 weeks) and 5-FU (200 mg/ m2 daily given by continuous infusion via a central line).
- ECX: epirubicin (50 mg / m2 som bolus på dag 1 hver 3. uge), cisplatin (60 mg/ m2 som en to -
- ECX: epirubicin (50 mg/ m2 as a bolus on day 1 every 3 weeks), cisplatin (60 mg/ m2 as a two
timers infusion på dag 1 hver 3. uge) og Xeloda (625 mg/ m2 to gange dagligt givet kontinuerligt).
hour infusion on day 1 every 3 weeks), and Xeloda (625 mg/ m2 twice daily continuously).
- EOF: epirubicin (50 mg / m2 som bolus på dag 1 hver 3. uge), oxaliplatin (130 mg/ m2 som en to -
- EOF: epirubicin (50 mg/ m2 as a bolus on day 1 every 3 weeks), oxaliplatin (130 mg/ m2 given as
timers infusion på dag 1 hver 3. uge) og 5- FU (200 mg/ m2 dagligt givet som kontinuerlig infusion via en central linje).
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 som bolus på dag 1 hver 3. uge), oxaliplatin (130 mg/ m2 som en
- EOX: epirubicin (50 mg/ m2 as a bolus on day 1 every 3 weeks), oxaliplatin (130 mg/ m2 given as
to- timers infusion på dag 1 hver 3. uge) og Xeloda (625 mg/ m2 to gange dagligt givet kontinuerligt).
a 2 hour infusion on day 1 every three weeks), and Xeloda (625 mg/ m2 twice daily continuously).
Den primære effektanalyse i per protokolpopulationen demonstrerede non- inferioritet i samlet overlevelse for capecitabin versus 5- FU regimerne (hazard ratio 0, 86; 95% konfidensinterval 0, 8 - 0, 99) og for oxaliplatin mod cisplatinbaserede regimer (hazard ratio 0, 92; 95% konfidensinterval 0, 80 - 1, 1).
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).
Den mediane samlede overlevelse var 10, 9 måneder for de capecitabinbaserede regimer og 9, 6 måneder for de 5- FU- baserede regimer.
The median overall survival was 10.9 months in capecitabine-based regimens and 9.6 months in 5-FU based regimens.
Den mediane samlede overlevelse var 10, 0 måneder for de cisplatinbaserede regimer og 10, 4 måneder for de oxaliplatin- baserede regimer.
The median overall survival was 10.0 months in cisplatin-based regimens and 10.4 months in oxaliplatin-based regimens.
Xeloda har også været anvendt i kombination med oxaliplatin til behandling af fremskreden ventrikelkræft.
Xeloda has also been used in combination with oxaliplatin for the treatment of advanced gastric cancer.
Studier med Xeloda- monoterapi indikerer, at Xeloda har effekt i fremskreden ventrikelkræft.
Studies with Xeloda monotherapy indicate that Xeloda has activity in advanced gastric cancer.
Kolonkræft, kolorektalkræft og fremskreden ventrikelkræft, metaanalyse En metaanalyse af seks kliniske forsøg (studie SO14695, SO14796, M66001, NO16966, NO16967 og M17032) støtter, at Xeloda kan erstatte 5- FU i mono - og kombinationsbehandling af gastrointestinal kræft.
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.
Den poolede analyse omfatter 3097 patienter, som blev behandlet med regimer, som indeholdt Xeloda, og 3074 patienter, som blev behandlet med regimer, som indeholdt 5- FU.
The pooled analysis includes 3097 patients treated with Xeloda-containing regimens and 3074 patients treated with 5-FU-containing regimens.
Den mediane samlede overlevelse var 703 dage (95% konfidensinterval:
Median overall survival time was 703 days (95% CI:
671, 743) hos patienter, som blev behandlet med regimer, der indeholdt Xeloda og 683 dage (95% konfidensinterval:
671; 743) in patients treated with Xeloda-containing regimens and 683 days (95% CI:
648, 715) hos patienter, som blev behandlet med regimer, der indeholdt 5- FU.
648; 715) in patients treated with 5-FU-containing regimens.
Hazard ratio for samlet overlevelse var 0, 96 (95% konfidensinterval:
The hazard ratio for overall survival was 0.96 (95% CI:
Det indikerer, at regimer, som indeholder Xeloda, er ækvivalente med regimer, som indeholder 5- FU.
0.90; 1.02) indicating that Xeloda-containing regimens are equivalent to 5-FU-containing regimens.
Kombinationsbehandling med Xeloda og docetaxel ved lokal advanceret eller metastatisk brystkræft Data fra et randomiseret, kontrolleret, klinisk fase III- multicenterstudie støtter anvendelsen af Xeloda i kombination med docetaxel til behandling af patienter med lokal fremskreden eller metastatisk brystkræft hos hvem cytotoksisk kemoterapi, inklusive et anthracyklin, har svigtet.
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.
I dette studie randomiseredes 255 patienter til behandling med Xeloda (1250 mg/ m2 to gange dagligt i 2 uger efterfulgt af en uges pause og behandling med docetaxel 75 mg/ m2 som 1 times intravøs infusion hver 3. uge).
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).
256 patienter blev randomiseret til behandling med docetaxel alene (100 mg/ m2 som 1 times intravøs infusion hver 3. uge).
256 patients were randomised to treatment with docetaxel alone (100 mg/ m2 as a 1 hour intravenous infusion every 3 weeks).
Overlevelsen var bedre i kombinationsarmen med Xeloda + docetaxel (p = 0, 0126).
Survival was superior in the Xeloda + docetaxel combination arm (p=0.0126).
Den mediane overlevelse var 442 dage (docetaxel + Xeloda) vs.
Median survival was 442 days (Xeloda + docetaxel) vs.
De totale objektive responsrater i den totale randomiserede population (investigators vurdering) var 41, 6% (Xeloda + docetaxel) vs.
The overall objective response rates in the all-randomised population (investigator assessment) were 41.6% (Xeloda + docetaxel) vs.
Tid indtil progressiv sygdom var længere i kombinationsarmen med Xeloda + docetaxel (p < 0, 0001).
Time to progressive disease was superior in the Xeloda + docetaxel combination arm (p < 0.0001).
Den mediane tid indtil progression var 186 dage (Xeloda + docetaxel) vs.
The median time to progression was 186 days (Xeloda + docetaxel) vs.
20 Monoterapi med Xeloda efter svigt af taxaner og kemoterapi, som indeholder antracykliner, og af patienter til hvem behandling med antracykliner ikke er indiceret Data fra to kliniske multicenterstudier i fase II støtter anvendelsen af Xeloda- monoterapi hos patienter, hos hvem taxoider og et anthracyklinindeholdende kemoterapiregime har svigtet, eller hos hvem yderligere anthracyklinbehandling ikke er indiceret.
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.
I disse studier blev 236 patienter behandlet med Xeloda (1250 mg/ m2 to gange dagligt i 2 uger efterfulgt af en uges pause).
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).
De totale objektive responsrater (investigators vurdering) var 20% (første studie) og 25% (andet studie).
The overall objective response rates (investigator assessment) were 20% (first trial) and 25% (second trial).
Alle indikationer:
All indications:
Hazard ratio var 0, 59 (95% konfidensinterval 0, 54; 0, 64).
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).
5. 2 Farmakokinetiske egenskaber
20 5.2 Pharmacokinetic properties
Capecitabins farmakokinetik er undersøgt i dosisintervallet 502 – 3514 mg/ m2/ dag.
The pharmacokinetics of capecitabine have been evaluated over a dose range of 502-3514 mg/ m2/ day.
Parametrene for capecitabin, 5 ’ - deoxy- 5- fluorocytidin (5 ’ - DFCR) og 5 ’ - deoxy- 5- fluorouridin (5 ’ - DFUR) var ens på dag 1 og 14.
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.
AUC for 5- FU var 30- 35% højere på dag 14.
The AUC of 5-FU was 30%-35% higher on day 14.
Dosisreduktion af capecitabin nedsætter den systemiske eksponering for 5- FU mere end svarende til dosisproportionaliteten på grund af den aktive metabolits non- lineære farmakokinetik.
Capecitabine dose reduction decreases systemic exposure to 5-FU more than dose-proportionally, due to non-linear pharmacokinetics for the active metabolite.
Efter oral administration absorberes capecitabin hurtigt og fuldstændigt efterfulgt af en omfattende omdannelse til metabolitterne 5 ’ - DFCR og 5 ‘ - DFUR.
Absorption: after oral administration, capecitabine is rapidly and extensively absorbed, followed by extensive conversion to the metabolites, 5'-DFCR and 5'-DFUR.
Administration sammen med føde nedsætter hastigheden af capecitabinabsorptionen, men medfører kun mindre virkning på 5 ‘ - DFURs AUC og på AUC af den efterfølgende metabolit 5- FU.
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.
Efter en dosis på 1250 mg/ m2 efter indtagelse af føde var peak- plasmakoncentrationerne på dag 14 (Cmax, μg/ ml) for capecitabin, 5 ’ - DFCR, 5 ’ - DFUR, 5- FU og FBAL 4, 67; 3, 05; 12, 1; 0, 95 og 5, 46.
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.
Tiden indtil peak- plasmakoncentrationen (Tmax, timer) var 1, 50; 2, 00; 2, 00; 2, 00 og 3, 34.
The time to peak plasma concentrations (Tmax in hours) were 1.50, 2.00, 2.00, 2.00 and 3.34.
AUC0- ∞ værdierne (μg• time/ ml var 7, 75; 7, 24; 24, 6; 2, 03 og 36, 3.
The AUC0-∞ values in μ g• h/ ml were 7.75, 7.24, 24.6, 2.03 and 36.3.
54%, 10%, 62% og 10% bundet til protein, hovedsageligt til albumin.
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.
Capecitabin metaboliseres først af hepatisk carboxylesterase til 5 ’ - DFCR, som derefter omdannes til 5 ’ - DFUR af cytidindeaminase, som fortrinsvis findes i leveren og i tumorvæv.
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.
Den videre katalytiske aktivering af 5 ’ - DFUR sker derefter ved hjælp af thymidinfosforylase (ThyPase).
Further catalytic activation of 5'-DFUR then occurs by thymidine phosphorylase (ThyPase).
Den sekventielle enzymatiske biotransformation af capecitabin til 5- FU fører til højere koncentrationer inden i tumorcellerne.
The sequential enzymatic biotransformation of capecitabine to 5-FU leads to higher concentrations within tumour tissues.
For så vidt angår kolorektale tumorer synes dannelsen af 5- FU hovedsageligt at være lokaliseret til stromale tumorceller.
In the case of colorectal tumours, 5-FU generation appears to be in large part localised in tumour stromal cells.
0, 9 – 8, 0).
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).
3, 9 – 59, 9, n=8), mens forholdet mellem normalt væv og plasma var 8, 9 (spændvidde:
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).
21 5- FU nedbrydes yderligere af enzymet dihydropyrimidindehydrogenase (DPD) til det meget mindre toksiske dihydro- 5- fluoruracil (FUH2).
5-FU is further catabolised by the enzyme dihydropyrimidine dehydrogenase (DPD) to the much less toxic dihydro-5-fluorouracil (FUH2).
Dihydropyrimidinase spalter pyrimidinringen til 5- fluoro - ureidopropionsyre (FUPA).
Dihydropyrimidinase cleaves the pyrimidine ring to yield 5-fluoro-ureidopropionic acid (FUPA).
Endeligt spalter β- ureido- propionase FUPA til α- fluoro- β- alanin (FBAL), som udskilles i urinen.
Finally, β -ureido-propionase cleaves FUPA to α -fluoro-β - alanine (FBAL) which is cleared in the urine.
4. 3 og 4. 4).
Deficiency of DPD may lead to increased toxicity of capecitabine (see section 4.3 and 4.4).
Eliminationshalveringstiden (t½, timer) for capecitabin, 5 ’ - DFCR, 5 ’ - DFUR, 5- FU og FBAL var 0, 85, 1, 11, 0, 66, 0, 76 og 3, 23.
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.
95, 5% af den indgivne capecitabindosis genfandtes i urinen.
Capecitabine and its metabolites are predominantly excreted in urine; 95.5% of administered capecitabine dose is recovered in urine.
Udskillelse i fæces er minimal (2, 6%).
Faecal excretion is minimal (2.6%).
Hovedmetabolitten som udskilles i urinen er FBAL, der repræsenterer 57% af den indgivne dosis.
The major metabolite excreted in urine is FBAL, which represents 57% of the administered dose.
3% af den indgivne dosis udskilles uændret i urinen.
About 3% of the administered dose is excreted in urine as unchanged drug.
Fase I- studier, som evaluerede Xelodas effekt på enten docetaxels eller paclitaxels farmakokinetik og vice versa, viste ingen effekt af Xeloda på hverken docetaxels eller paclitaxels farmakokinetik (Cmax og AUC) og inden effekt af docetaxel eller paclitaxel på 5 ’ - DFUR’ s farmakokinetik.
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.
Farmakokinetik i specielle populationer:
Pharmacokinetics in special populations:
Efter Xeloda- behandling af 505 patienter med kolorektalkræft, som fik 1250 mg/ m2 to gange dagligt, blev der foretaget en populationsfarmakokinetisk analyse.
A population pharmacokinetic analysis was carried out after Xeloda treatment of 505 patients with colorectal cancer dosed at 1250 mg/ m2 twice daily.
Køn, tilstedeværelse eller fravær af levermetastaser ved baseline, Karnofsky Performance Status, total bilirubin, serum- albumin, ASAT og ALAT havde ingen statistisk signifikant effekt på farmakokinetikken af 5 ’ - DFUR, 5- FU og FBAL.
Gender, presence or absence of liver metastasis at baseline, Karnofsky Performance Status, total bilirubin,
Patienter med leverinsufficiens pga. levermetastaser:
Patients with hepatic impairment due to liver metastases:
I henhold til et farmakokinetisk studie på kræftpatienter med let til moderat leverinsufficiens pga. levermetastaser kan capecitabins biotilgængelighed og eksponeringen for 5- FU øges sammenlignet med patienter uden leverinsufficiens.
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.
Baseret på et farmakokinetisk studie hos kræftpatienter med let til svær nyreinsufficiens er der ingen tegn på effekt af creatininclearance på farmakokinetikken af det intakte lægemiddel og 5- FU.
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.