qanastek/EMEA-V3 huggingface dataset:
No studies on the effects on ability to drive and use machines have been performed.
Ma sarux studji dwar l- effetti fuq il- ħila biex issuq jew tħaddem magni.
Prasugrel is expected to have no or negligible influence on the ability to drive and use machines.
Huwa mistenni li prasugrel ma jkollu l- ebda jew ftit li xejn effett fuq il- ħila biex issuq u tħaddem magni.
Safety in patients with acute coronary syndrome undergoing PCI was evaluated in one clopidogrel- controlled study (TRITON) in which 6741 patients were treated with prasugrel (60 mg loading dose and 10 mg once daily maintenance dose) for a median of 14.5 months (5802 patients were treated for over 6 months, 4136 patients were treated for more than 1 year).
F' studju wieħed ikkontrollat bi clopidogrel (TRITON) ġiet ivvalutata s- sigurtà f' pazjenti b' sindromu koronarju akut ittrattati b' PCI fejn 6741 pazjent ġie kkurat b' prasugrel (doża ta ’ kkargar ta '60 mg u doża ta' manteniment ta '10 mg darba kuljum) għal medjan ta' 14. 5 xhur (5802 pazjenti ġew ikkurati għal aktar minn 6 xhur, 4136 pazjent ġie kkurati għal aktar minn sena).
The rate of study drug discontinuation due to adverse events was 7.2% for prasugrel and 6.3% for clopidogrel.
Ir- rata tat- twaqqif tal- mediċina taħt studju minħabba avvenimenti avversi kienet ta '7. 2% għal prasugrel u 6. 3% għal clopidogrel.
Of these, bleeding was the most common adverse reaction for both drugs leading to study drug discontinuation (2.5% for prasugrel and 1.4% for clopidogrel).
Minn dawn, il - fsada kienet ir- reazzjoni avversa l- aktar komuni għaż- żewġ mediċini li waslet għat- twaqqif tal- mediċina taħt studju( 2. 5% għal prasugrel u 1. 4% għal clopidogrel).
Bleeding
Fsada
Non-Coronary Artery Bypass Graft (CABG) related bleeding In TRITON, the frequency of patients experiencing a non-CABG related bleeding event is shown in Table 1.
Fsada relatata ma 'trapjant ta' bypass ta 'arterja li mhijiex koronarja (non- CABG) F' TRITON, il- frekwenza ta' pazjenti li esperjenzaw avveniment ta 'fsada relatata ma' non- CABG tidher f' Tabella 1.
The incidence of Non-CABG-related TIMI major bleeding, including life-threatening and fatal, as well as TIMI minor bleeding, was statistically significantly higher in subjects treated with prasugrel compared to clopidogrel in the UA/ NSTEMI and All ACS populations.
L- inċidenza ta 'fsada maġġuri skont TIMI relatata ma' non- CABG, fosthom dik ta 'theddid għall- ħajja u fatali, kif ukoll fsada minuri skont TIMI, kienet statistikament ogħla b' mod sinifikanti f' suġġetti kkurati b' prasugrel meta mqabbel ma' clopidogrel f' UA/ NSTEMI u l- popolazzjonijiet tal - Pazjenti Kollha b' ACS.
No significant difference was seen in the STEMI population.
Ma ġietx innutata l- ebda differenza sinifikanti fil- popolazzjoni STEMI.
The most common site of spontaneous bleeding was the gastrointestinal tract (1.7% rate with prasugrel and 1.3% rate with clopidogrel); the most frequent site of provoked bleeding was the arterial puncture site (1.3% rate with prasugrel and 1.2% with clopidogrel).
Is- sit l - aktar komuni ta 'fsada spontanja kien l- apparat gastro- intestinali (rata ta' 1. 7% b' prasugrel u rata ta '1. 3% b' clopidogrel); l- aktar sit frekwenti ta' fsada pprovokata kien is- sit tat- titqib arterjali (rata ta '1. 3% b' prasugrel u rata ta' 1. 2% b' clopidogrel).
Incidence of Non-CABG related bleedinga (% Patients) Event
Inċidenza ta 'fsada relatata ma' Non- CABG a (% ta 'Pazjenti) Avveniment
All ACS
Pazjenti Kollha b' ACS
Prasugrelb Clopidogrel b +ASA
Prasugrelb Clopidogrelb Prasugrelb Clopidogrelb +ASA +ASA +ASA +ASA
Prasugrelb +ASA
Prasugrelb Clopidogrelb +ASA +ASA
TIMI major bleedingc
Fsada maġġuri skont TIMI c
2.2 1.7
2. 2
2.2
1. 6
1.6
2. 2
2.2 2.0
2. 0
Life-threateningd Fatal Symptomatic ICHe
Ta 'theddid għall - ħajjad
1.3 0.8 0.3 0.1 0.3 0.3
0. 1 0. 3
1.3 0.3 0.3
0. 3 0. 3
0.8 0.1 0.3
0. 1 0. 3
1.2 0.4 0.2
0. 4 0. 2
1.0 0.1 0.2
0. 1 0. 2
Requiring inotropes
Ħtieġa ta ’ inotropes
0.3 0.1
0. 1
Requiring surgical intervention
Ħtieġa ta ’ intervent kirurġiku
0.3 0.3
0. 3
Requiring transfusion (≥ 4 units)
Ħtieġu ta ’ trasfużjoni (≥4 unitajiet)
0.7 0.5
0. 5
TIMI minor bleeding f
Fsada minuri skont TIMI f
2.4 1.9
2. 4
2.3
1. 9
1.6
2. 3
2.7
1. 6
2.6
2. 7
6 d Life-threatening bleeding is a subset of TIMI major bleeding and includes the types indented below.
2. 6
Patients may be counted in more than one row. e ICH=intracranial haemorrhage. f Clinically overt bleeding associated with a fall in haemoglobin of ≥ 3 g/ dL but < 5 g/ dL.
Il- pazjenti jistgħu jiġu magħduda f' aktar minn ringiela waħda. e ICH= emorraġija fir- ras. f Fsada li tidher klinikament u assoċċjata ma 'waqa' ta 'emoglobina ta' ≥3 g/ dL iżda < 5 g/ dL.
Patients ≥ 75 years old In the phase 3 clinical trial, non-CABG-related TIMI major or minor bleeding rates for patients in two age groups were as follows:
Pazjenti ≥ 75 sena Fl- istudju kliniku ta 'fażi 3, ir- rati ta' fsada maġġuri jew minuri skont TIMI relatata ma 'non- CABG għall - pazjenti f' żewġ gruppi ta' etajiet kienu kif ġej:
≥ 75 years (N=1785) < 75 years (N=11672)
≥75 sena (N=1785) < 75 sena (N=11672)
9.0% (1.0% fatal) 3.8% (0.2% fatal)
9. 0% (1. 0% fatali) 3. 8% (0. 2% fatali)
6.9% (0.1% fatal) 2.9% (0.1% fatal)
6. 9% (0. 1% fatali) 2. 9% (0. 1% fatali)
Patients < 60 kg
Pazjenti < 60 kg
In the phase 3 clinical trial, non-CABG-related TIMI major or minor bleeding rates for patients in two weight groups were as follows:
Fl- istudju kliniku ta 'fażi 3, ir- rati ta' fsada maġġuri jew minuri skont TIMI relatata ma 'non- CABG għall - pazjenti f' żewġ gruppi ta' piżijiet kienu kif ġej:
Weight
Piż
10.1% (0% fatal) 4.2% (0.3% fatal)
10. 1% (0% fatali) 4. 2% (0. 3% fatali)
6.5% (0.3% fatal) 3.3% (0.1% fatal)
6. 5% (0. 3% fatali) 3. 3% (0. 1% fatali)
In patients ≥ 60 kg and age < 75 years, non-CABG-related TIMI major or minor bleeding rates were 3.6% for prasugrel and 2.8% for clopidogrel; rates for fatal bleeding were 0.2% for prasugrel and 0.1% for clopidogrel.
F' pazjenti ≥60 kg u età < 75 sena, ir- rati ta 'fsada maġġuri jew minuri skont TIMI relatata ma' non- CABG kienu ta '3. 6% għal prasugrel u 2. 8% għal clopidogrel; ir- rati ta' fsada fatali kienu ta '0. 2% għal prasugrel u 0. 1% għal clopidogrel.
CABG-related bleeding In the phase 3 clinical trial, 437 patients underwent CABG during the course of the study.
Fsada relatata ma 'CABG Fl- istudju kliniku ta' fażi 3, 437 pazjent saritilhom CABG matul l- istudju.
Of those patients, the rate of CABG-related TIMI major or minor bleeding was 14.1% for the prasugrel group and 4.5% in the clopidogrel group.
Minn dawk il- pazjenti, ir- rata ta 'fsada maġġuri jew minuri skont TIMI relatata ma' CABG kienet ta '14. 1% għall- grupp ta' prasugrel u 4. 5% fil- grupp ta 'clopidogrel.
The higher risk for bleeding events in subjects treated with prasugrel persisted up to 7 days from the most recent dose of study drug.
L- ogħla riskju ta 'avvenimenti ta' fsada f' suġġetti kkurati b' prasugrel ippersista sa 7 ijiem mid- doża l- aktar riċenti tal- mediċina studjata.
For patients who received their thienopyridine within 3 days prior to CABG, the frequencies of TIMI major or minor bleeding were 26.7% (12 of 45 patients) in the prasugrel group, compared with 5.0% (3 of 60 patients) in the clopidogrel group.
7 fi żmien 3 ijiem qabel CABG, il- frekwenzi ta 'fsada maġġuri jew minuri skont TIMI kienu ta' 26. 7% (12 minn 45 pazjent) fil- grupp ta 'prasugrel, meta mqabbel ma' 5. 0% (3 minn 60 pazjent) fil- grupp ta 'clopidogrel.
For patients who received their last dose of thienopyridine within 4 to 7 days prior to CABG, the frequencies decreased to 11.3% (9 of 80 patients) in the prasugrel group and 3.3% (3 of 90 patients) in the clopidogrel group.
Għall- pazjenti li rċevew l- aħħar doża ta 'thienopyridine fi żmien 4 sa 7 ijiem qabel CABG, il - frekwenzi naqsu għal 11. 3% (9 minn 80 pazjent) fil- grupp ta' prasugrel u 3. 3% (3 minn 90 pazjent) fil - grupp ta 'clopidogrel.
Beyond 7 days after drug discontinuation, the observed rates of CABG-related bleeding were similar between treatment groups (see section 4.4).
Wara 7 ijiem mit- twaqqif tal- mediċina, ir- rati osservati ta 'fsada relatata ma' CABG kienu simili bejn il- gruppi ta 'kura (ara sezzjoni 4. 4).
Adverse Reactions Table 2 summarises haemorrhagic and non-haemorrhagic adverse reactions in TRITON classified by frequency and system organ class.
Reazzjonijiet avversi Tabella 2 tiġbor fil- qosor ir- reazzjonijiet avversi emorraġiċi u mhux emorraġiċi fi TRITON ikklassifikati skont il- frekwenza u s- sistema ta 'klassifika ta' l- organi.
Frequencies are defined as follows:
Il- frekwenzi huma ddefiniti kif ġej:
Very common (≥ 1/ 10); common (≥ 1/ 100 to < 1/ 10); uncommon (≥ 1/ 1000 to < 1/ 100); rare (≥ 1/ 10,000 to < 1/ 1,000); very rare (< 1/ 10,000); not known (cannot be estimated from the available data).
Komuni ħafna (≥ 1/ 10); komuni (≥ 1/ 100 to < 1/ 10); mhux komuni (≥ 1/ 1000 sa ≤ 1/ 100); rari (≥ 1/ 10, 000 sa ≤1/ 1, 000); rari ħafna (≤ 1/ 10, 000); mhux magħruf (ma tistax tittieħed stima mid- data disponibbli).
Haemorrhagic and Non-haemorrhagic adverse reactions System Organ Class Blood and Lymphatic System disorders
Reazzjonijiet avversi emorraġiċi u mhux emorraġiċi Sistema ta 'klassifika ta' l- organi
Common Anaemia
Komuni
Eye disorders Vascular Disorders
Disturbi fl- għajnejn Disturbi vaskulari
Eye haemorrhage
Emorraġija fl- għajnejn
Haemoptysis
Sogħla bid- demm
Gastrointestinal haemorrhage
Emorraġija gastro- intestinali
Retroperitoneal haemorrhage Rectal haemorrhage Haematochezia
Emorraġija retroperitonali Emorraġija fir- rektum Demm fl- ippurgar Fsada mill- ħanek
7 Gingival bleeding Skin and subcutaneous tissue disorders Renal and urinary disorders
Disturbi fil- ġilda u fit - tessuti ta ’ taħt il- ġilda Disturbi fil- kliewi u fis - sistema urinarja
Rash Ecchymosis Haematuria
Raxx Ekimożi Ematurja
Vessel puncture site haematoma Puncture site haemorrhage
Ematoma fis- sit tat- titqib ta 'l- arterja Emorraġija fis- sit tat- tiqib
Injury, poisoning and procedural complications
Korriment, avvelenament u komplikazzjonijiet ta ’ xi proċedura
Contusion
Tbenġil
Post-procedural haemorrhage
Emorraġija wara l- proċedura
Subcutaneous haematoma
Ematoma taħt il- ġilda
In patients with or without a history of TIA or stroke, the incidence of stroke in the phase 3 clinical trial was as follows (see section 4.4):
F' pazjenti li għandhom jew li m’ għandhomx passat ta 'TIA jew puplesija, l- inċidenza ta' puplesija fl - istudju kliniku ta 'fażi 3 kienet kif ġej (ara sezzjoni 4. 4):
History of TIA or stroke
Passat ta 'TIA jew puplesija
Yes (N=518)
Iva (N=518)
6.5% (2.3% ICH*)
6. 5% (2. 3% ICH *)
1.2% (0% ICH*)
1. 2% (0% ICH *)
No (N=13090)
Le (N=13090) ICH=emorraġija fir- ras.
0.9% (0.2% ICH*)
0. 9% (0. 2% ICH *)
1.0% (0.3% ICH*)
1. 0% (0. 3% ICH *)
* ICH=intracranial haemorrhage.
4. 9 Doża eċċessiva
Overdose of Efient may lead to prolonged bleeding time and subsequent bleeding complications.
Doża eċċessiva ta 'Efient tista' twassal għal ħin imtawwal ta 'fsada u kumplikazzjonijiet konsegwenti ta' fsada.
No data are available on the reversal of the pharmacological effect of prasugrel; however, if prompt correction of prolonged bleeding time is required, platelet transfusion and/ or other blood products may be considered.
M' hemmx tagħrif dwar kif l- effett farmakoloġiku ta 'prasugrel jista' jitreġġa 'lura; madanakollu, jekk tkun meħtieġa korrezzjoni fil- pront tal- ħin imtawwal ta' fsada, tista 'tiġi kkunsidrata trasfużjoni ta' plejtlits u/ jew l- użu ta 'prodotti tad- demm oħra.
ATC code:
Għadu mhux stabbilit Kodiċi ATC:
Not yet assigned.
Għadu mhux stabbilit.
Pharmacodynamics Prasugrel is an inhibitor of platelet activation and aggregation through the irreversible binding of its active metabolite to the P2Y12 class of ADP receptors on platelets.
Farmakodinamika Prasugrel huwa inibitur ta 'l- attivazzjoni u l- aggregazzjoni tal- plejtlits permezz ta' rbit irriversibbli tal - metabolit attiv tiegħu mal- klassi P2Y12 tar- riċetturi ADP fuq il- plejtlits.
Since platelets participate in the initiation and/ or evolution of thrombotic complications of atherosclerotic disease, inhibition of platelet function can result in the reduction of the rate of cardiovascular events such as death, myocardial infarction, or stroke.
Billi l- plejtlits jipparteċipaw fil - bidu u/ jew fl- iżvilupp ta 'kumplikazzjonijiet trombotiċi ta' mard aterosclerotiku, l- inibizzjoni tal- funzjoni tal- plejtlits tista 'tirriżulta fit- tnaqqis tar- rata ta' avvenimenti kardjovaskulari bħall- mewt, infart mijokardijaku, jew puplesija.
Following a 60 mg loading dose of prasugrel, inhibition of ADP-induced platelet aggregation occurs at 15 minutes with 5 µM ADP and 30 minutes with 20 µM ADP.
Wara doża ta ’ kkargar ta '60 mg prasugrel, inibizzjoni ta' aggregazzjoni ta 'plejtlits stimulata minn ADP seħħet wara 15- il minuta b' 5 µM ADP u 30 minuta b' 20 µM ADP.
The maximum inhibition by prasugrel of ADP-induced platelet aggregation is 83% with 5 µM ADP and 79% with 20 µM ADP, in both cases with 89% of healthy subjects and patients with stable atherosclerosis achieving at least 50% inhibition of platelet aggregation by 1 hour.
L- inibizzjoni massima permezz ta 'prasugrel ta' aggregazzjoni ta 'plejtlits stimulata minn ADP hija ta' 83% b' 5 µM ADP u ta '79% b' 20 µM ADP, fiż- żewġ każijiet b' 89% tas- suġġetti b' saħħithom u pazjenti b' aterosklerosi li kellhom mill- anqas 50% inibizzjoni ta' aggregazzjoni ta 'plejtlits f' siegħa.
Prasugrel-mediated inhibition of platelet aggregation exhibits low between-subject (12%) and within-subject (9%) variability with both 5 µM and 20 µM ADP.
L- inibizzjoni ta 'aggregazzjoni ta' plejtlits permezz ta 'prasugrel turi varjabbilità baxxa bejn is- suġġetti (12%) u fis- suġġetti (9%) kemm b' 5 µM u b' 20 µM ADP.
Mean steady-state inhibition of platelet aggregation was 74% and 69% respectively for 5 µM ADP and 20 µM ADP, and was achieved following 3 to 5 days of administration of the 10 mg prasugrel maintenance dose preceded by a 60 mg loading dose.
Steady state medju tal- inibizzjoni ta 'aggregazzjoni ta' plejtlits kien ta '74% u 69% rispettivament għal 5 µM ADP u 20 µM ADP, u ntlaħaq wara li ngħatat id- doża ta' manteniment ta '10 mg prasugrel għal 3 sa 5 ijiem wara d- doża ta ’ kkargar ta' 60 mg.
More than 98% of subjects had ≥ 20% inhibition of platelet aggregation during maintenance dosing.
Aktar minn 98% tas- suġġetti kellhom ≥20% inibizzjoni ta 'aggregazzjoni ta' plejtlits waqt id- dożaġġ ta 'manteniment.
Platelet aggregation gradually returned to baseline values after treatment in 7 to 9 days after administration of a single 60 mg loading dose of prasugrel and in 5 days following discontinuation of maintenance dosing at steady-state.
L- aggregazzjoni ta 'plejtlits reġgħet lura bil- mod għall- valuri fil- linja bażi wara l- kura f' 7 sa 9 ijiem wara li ngħatat doża waħda ta ’ kkargar ta' 60 mg prasugrel u f' 5 ijiem wara t- twaqqif tad- dożaġġ ta 'manteniment fi steady state.
Following administration of 75 mg clopidogrel once daily for 10 days, 40 healthy subjects were switched to prasugrel 10 mg once daily with or without a loading dose of 60 mg.
Wara li ngħatat 75 mg clopidogrel darba kuljum għal 10 ijiem, 40 suġġett b' saħħtu nqalbu għal prasugrel 10 mg darba kuljum bid- doża ta ’ kkargar ta '60 mg jew mingħajrha.
Similar or higher inhibition of platelet aggregation was observed with prasugrel.
Inibizzjoni simili jew ogħla ta 'aggregazzjoni ta' plejtlits ġiet osservata b' prasugrel.
Switching directly to prasugrel 60 mg loading dose resulted in the most rapid onset of higher platelet inhibition.
It- taqlib dirett għal prasugrel b' doża ta ’ kkargar ta '60 mg wassal għall- aktar mod mgħaġġel ta ’ inibizzjoni aktar għolja ta' plejtlits.
Following administration of a 900 mg loading dose of clopidogrel (with ASA), 56 subjects with ACS were treated for 14 days with either prasugrel 10 mg once daily or clopidogrel 150 mg once daily, and then switched to either clopidogrel 150 mg or prasugrel 10 mg for another 14 days.
Wara li ngħatat doża ta ’ kkargar ta '900 mg clopidogrel (ma' ASA), 56 suġġett b' ACS ġew ikkurati għal 14- il ġurnata jew b' prasugrel 10 mg darba kuljum jew b' clopidogrel 150 mg darba kuljum, u mbagħad inqalbu jew għal clopidogrel 150 mg jew prasugrel 10 mg għal 14- il ġurnata oħra.
Higher inhibition of platelet aggregation was observed in patients switched to prasugrel 10 mg compared with those treated with clopidogrel 150 mg.
Ġiet osservata inibizzjoni ogħla ta 'aggregazzjoni ta' plejtlits fil- pazjenti li nqalbu għal 10 mg prasugrel meta mqabbel ma 'dawk ikkurati b' 150 mg clopidogrel.
No data are available on switching from a clopidogrel loading dose directly to a prasugrel loading dose.
M' hemmx tagħrif dwar meta taqleb minn doża ta ’ kkargar ta 'clopidogrel direttament għal doża ta ’ kkargar ta' prasugrel.
Efficacy and Safety in Acute Coronary Syndrome (ACS) The phase 3 TRITON study compared Efient (prasugrel) with clopidogrel, both co-administered with ASA and other standard therapy.
L- Effikaċja u s- Sigurtà fis- Sindromu Koronarju Akut (ACS) L- istudju TRITON ta 'fażi 3 qabbel Efient (prasugrel) ma' clopidogrel, it- tnejn li huma ngħataw flimkien ma 'ASA u terapija oħra standard.
TRITON was a 13,608 patient, multicentre international, randomised, double blind, parallel group study.
TRITON b' 13, 608 pazjenti kien studju tat- tip internazzjonali b' ħafna ċentri, randomised, double blind, b' grupp parallel.
Patients had ACS with moderate to high risk UA, NSTEMI, or STEMI and were managed with PCI.
Il- pazjenti kellhom ACS b' UA, NSTEMI, jew STEMI ta 'riskju moderat jew għoli u ġew ittrattati b' PCI.
Patients with UA/ NSTEMI within 72 hours of symptoms or STEMI between 12 hours to 14 days of symptoms were randomised after knowledge of coronary anatomy.
Pazjenti b' UA/ NSTEMI fi żmien 72 siegħa tas- sintomi jew STEMI bejn 12- il siegħa u 14- il ġurnata tas - sintomi ġew magħżulin b' mod arbitrarju wara li ġiet magħrufa l- anatomija koronarja.
Patients with STEMI within 12 hours of symptoms and planned for primary PCI could be randomised without knowledge of coronary anatomy.
Pazjenti b' STEMI fi żmien 12– il siegħa tas- sintomi u li kellhom ippjanat PCI setgħu jiġu magħżula b' mod arbitrarju mingħajr ma tkun magħrufa l- anatomija koronarja.
For all patients, the loading dose could be administered anytime between randomisation and 1 hour after the patient left the catheterisation lab.
Għall- pazjenti kollha, id- doża ta ’ kkargar setgħet tingħata f' kull ħin bejn li tingħata b' mod arbitrarju u siegħa minn mindu l- pazjent jitlaq mil- laboratorju ta ’ katetirizzazzjoni
Patients randomised to receive prasugrel (60 mg loading dose followed by 10 mg once daily) or clopidogrel (300 mg loading dose followed by 75 mg once daily) were treated for a median of 14.5 months (maximum of 15 months with a minimum of 6 months follow-up).
9 Pazjenti magħżulin b' mod arbitrarju biex jirċievu prasugrel (b' doża ta 'kkargar ta ’ 60 mg segwita b' 10 mg darba kuljum) jew clopidogrel (b' doża ta ’ kkargar ta' 300 mg segwita b' 75 mg darba kuljum) ġew ikkurati għal medjan ta '14. 5 xhur (massimu ta' 15- il xahar u segwiti wara l- kura għal minimu ta '6 xhur).
Patients also received ASA (75 mg to 325 mg once daily).
Il - pazjenti rċevew ukoll ASA (75 mg sa 325 mg darba kuljum).
Use of any thienopyridine within 5 days before enrolment was an exclusion criterion.
L- użu ta 'xi thienopyridine fi żmien 5 ijiem qabel ir- reġistrazzjoni kien kriterju ta' esklużjoni.
Other therapies, such as heparin and GPIIb/ IIIa inhibitors, were administered at the discretion of the physician.
Terapiji oħra, bħal eparina u inibituri ta 'GPIIb/ IIIa, ingħataw skont id- deċiżjoni ta' l- ispeċjalista.
Approximately 40% of patients (in each of the treatment groups) received GPIIb/ IIIa inhibitors in support of PCI (no information available regarding the type of GP IIb/ IIIa inhibitor used).
Madwar 40% tal- pazjenti (f' kull grupp ta 'kura) irċevew inibitur ta' GPIIb/ IIIa bħala sostenn għal PCI (m' hemmx tagħrif dwar it- tip ta 'inibitur GPIIb/ IIIa li ntuża).
Approximately 98% of patients (in each of the treatment groups) received antithrombins (heparin, low molecular weight heparin, bivalirudin, or other agent) directly in support of PCI.
Madwar 98% tal- pazjenti (f' kull grupp ta 'kura) irċevew sustanzi kontra thrombin (eparina, eparina b' piż molekulari baxx, bivalirudin, jew sustanza oħra) direttament bħala sostenn għal PCI.
The trial’ s primary outcome measure was the time to first occurrence of cardiovascular (CV) death, non-fatal myocardial infarction (MI), or non-fatal stroke.
Ir- riżultat primarju li bih ġie mkejjel l- istudju kien iż- żmien biex ikun hemm l- ewwel okkorrenza ta 'mewt karjovaskulari (CV), infart mijikardijaku (MI) mhux fatali, jew puplesija mhux fatali.
Analysis of the composite endpoint in the All ACS population (combined UA/ NSTEMI and STEMI cohorts) was contingent on showing statistical superiority of prasugrel versus clopidogrel in the UA/ NSTEMI cohort (p < 0.05).
L- analiżi tar- riżultat finali kompost fil- popolazzjoni tal- Pazjenti Kollha b' ACS (gruppi ta ’ UA/ NSTEMI kkombinati u STEMI) kienet kontinġenti fit- turija ta 'superjorità statistika ta' prasugrel kontra clopidogrel fil- grupp ta ’ UA/ NSTEMI (p < 0. 05).
All ACS population:
Il- popolazzjoni tal- Pazjenti Kollha b' ACS:
Efient showed superior efficacy compared to clopidogrel in reducing the primary composite outcome events as well as the pre-specified secondary outcome events, including stent thrombosis (see Table 3).
Efient wera effikaċja superjuri meta mqabbel ma 'clopidogrel fit- tnaqqis tal- avvenimenti primarji komposti riżultanti kif ukoll tal- avvenimenti sekondarji riżultanti speċifikati minn qabel, fosthom it- trombożi minn stent (ara Tabella 3).
The benefit of prasugrel was apparent within the first 3 days and it persisted to the end of study.
Il- benefiċċju ta 'prasugrel deher fl- ewwel 3 ijiem u ppersista sa l- aħħar ta' l- istudju.
The superior efficacy was accompanied by an increase in major bleeding (see sections 4.4 and 4.8).
L- effikaċja superjuri kienet akkumpanjata ma 'żieda fi fsada maġġuri (ara sezzjonijiet 4. 4 u 4. 8).
The patient population was 92% Caucasian, 26% female, and 39% ≥ 65 years of age.
Il- poplazzjoni tal- pazjenti kienet ta '92% Kawkasi, 26% femminili, u 39% ≥65 sena.
The benefits associated with prasugrel were independent of the use of other acute and long-term cardiovascular therapies, including heparin/ low molecular weight heparin, bivalirudin, intravenous GPIIb/ IIIa inhibitors, lipid-lowering medicinal products, beta-blockers, and angiotensin converting enzyme inhibitors.
Il- benefiċċji assoċjati ma 'prasugrel kienu indipendenti mill- użu ta' terapiji oħra kardjovaskulari akuti u għat- tul, fosthom eparina / eparina b' piż molekulari baxx, bivalirudin, inibituri ta 'GPIIb/ IIIa li jingħataw ġol- vini, prodotti mediċinali li jbaxxu l- lipidi, imblokkaturi tar - riċetturi beta, u inibituri ta' l- enzim li jikkonverti angiotensin.
The efficacy of prasugrel was independent of the ASA dose (75 mg to 325 mg once daily).
L- effikaċja ta 'prasugrel kienet indipendenti mid- doża ta' ASA (75 mg sa 325 mg darba kujum).
The use of oral anticoagulants, non-study antiplatelet medicinal products and chronic NSAIDs was not allowed in TRITON.
F' TRITON ma kienx permess l- użu ta 'sustanzi kontra l- koagulazzjoni li jittieħdu mill- ħalq, prodotti mediċinali kontra l- plejtlits mhux ta' l- istudju u NSAIDs kroniċi.
In the All ACS population, prasugrel was associated with a lower incidence of CV death, non-fatal MI, or non-fatal stroke compared to clopidogrel, regardless of baseline characteristics such as age, sex, body weight, geographical region, use of GPIIb/ IIIa inhibitors, and stent type.
Fil- popolazzjoni tat- Pazjenti Kollha b' ACS, prasugrel kien assoċjat ma 'inċidenza aktar baxxa ta' mewt CV, MI mhux fatali, jew puplesija mhux fatali meta mqabbel ma 'clopidogrel, mingħajr kunsiderazzjoni tal- karateristiċi bażilari bħall- età, is- sess, il- piż tal- ġisem, ir- reġjun ġeografiku, l- użu ta' inibituri ta 'GPIIb/ IIIa, it- tip ta' stent.
The benefit was primarily due to a significant decrease in non-fatal MI (see table 3).
Il- benefiċċju prinċipalment seħħ minħabba tnaqqis sinifikanti f' MI mhux fatali (ara tabella 3).
Subjects with diabetes had significant reductions in the primary and all secondary composite endpoints.
Suġġetti bid- dijabete kellhom tnaqqis sinifikanti fir- riżultati finali komposti primarji u fis- sekondarji kollha.
9 The observed benefit of prasugrel in patients ≥ 75 years was less than that observed in patients < 75 years.
Il- benefiċċju ta 'prasugrel li ġie osservat f' pazjenti ≥ 75 sena kien anqas minn dak osservat f' pazjenti < 75 sena.
Patients ≥ 75 years were at increased risk of bleeding, including fatal (see sections 4.2, 4.4, and 4.8).
Pazjenti ≥ 75 sena kellhom riskju ogħla ta ’ fsada inkluża dik fatali (ara sezzjonijiet 4. 2, 4. 4 u 4. 8).
Patients ≥ 75 years in whom the benefit with prasugrel was more evident included those with diabetes, STEMI, higher risk of stent thrombosis, or recurrent events.
Pazjenti ≥ 75 li fihom il- benefiċċju ta ’ prasugrel kien aktar evidenti kienu jinkludu dawk bid- dijabete, b’ STEMI, f’ riskju ogħla ta ’ trombożi fl- istent jew li kellhom avveniment rikorrenti.
Patients with a history of TIA or a history of ischaemic stroke more than 3 months prior to prasugrel therapy had no reduction in the primary composite endpoint.
Pazjenti b' passat ta 'TIA jew b' passat ta' puplesija iskemika aktar minn 3 xhur qabel it- terapija b' prasugrel ma kellhomx tnaqqis fir- riżultat finali primarju kompost.
Patients with Outcome Events in TRITON Primary Analysis
Pazjenti b’ Avvenimenti li Seħħew fl- Analiżi Primarja TRITON
Outcome Events
Avvenimenti li Seħħew
+ ASA
Prasugrel + ASA (N=6813)
+ASA
Clopidogrel +ASA (N=6795)
(95% CI)
Proporzjon ta 'Periklu (HR) (95% CI)
value
valur p
Primary Composite Outcome Events Cardiovascular (CV) death, non fatal MI, or non fatal stroke Primary Individual Outcome Events
Avvenimenti Primarji Komposti li Seħħew Mewt kardjovaskulari (CV), MI mhux fatali, jew puplesija mhux fatali Avvenimenti Primarji Individwali li Seħħew
9.4
9. 4
11.5
11. 5
0.812 (0.732, 0.902)
0. 812 (0. 732, 0. 902)
CV death Nonfatal MI Nonfatal stroke
Mewt CV MI mhux fatali Puplesija mhux fatali
2.0 7.0 0.9
2. 0 7. 0 0. 9
2.2 9.1 0.9
2. 2 9. 1 0. 9
0.886 (0.701, 1.118) 0.757 (0.672, 0.853) 1.016 (0.712, 1.451)
0. 886 (0. 701, 1. 118) 0. 757 (0. 672, 0. 853) 1. 016 (0. 712, 1. 451)
0.307 < 0.001 0.930
0. 307 < 0. 001 0. 930
UA/ NSTEMI Primary Composite Outcome Events
UA/ NSTEMI Avvenimenti Primarji Komposti li Seħħew
CV death, nonfatal MI, or nonfatal stroke CV death Nonfatal MI Nonfatal stroke STEMI Primary Composite Outcome Events
Mewt CV MI mhux fatali Puplesija mhux fatali
0.820 (0.726, 0.927) 0.979 (0.732,1.309) 0.761 (0.663,0.873) 0.979 (0.633,1.513)
Mewt kardjovaskulari, MI mhux fatali, jew puplesija mhux fatali
0.002 0.885 < 0.001 0.922
0. 793 (0. 649, 0. 968)
CV death, nonfatal MI, or nonfatal stroke CV death Nonfatal MI Nonfatal stroke
Mewt CV MI mhux fatali Puplesija mhux fatali
9.8 2.4 6.7 1.2
2. 4 6. 7 1. 2
12.2 3.3 8.8 1.1
3. 3 8. 8 1. 1
0.793 (0.649, 0.968) 0.738 (0.497,1.094) 0.746 (0.588,0.948) 1.097 (0.590,2.040)
0. 738 (0. 497, 1. 094) 0. 746 (0. 588, 0. 948) 1. 097 (0. 590, 2. 040)
0.019 0.129 0.016 0.770
0. 129 0. 016 0. 770
In the All ACS population, analysis of each of the secondary endpoints showed a significant benefit (p < 0.001) for prasugrel versus clopidogrel.
Fil- poplazzjoni tal- Pazjenti Kollha b' ACS, l- analiżi ta 'kull riżultat finali sekondarju wera benefiċċju sinifikanti (p < 0. 001) għal prasugrel kontra clopidogrel.
These included definite or probable stent thrombosis at study end (0.9% vs 1.8%; HR 0.498; CI 0.364, 0.683); CV death, nonfatal MI, or urgent target vessel revascularisation through 30 days (5.9% vs 7.4%; HR 0.784; CI 0.688,0.894); all cause death, nonfatal MI, or nonfatal stroke through study end (10.2% vs 12.1%; HR 0.831; CI 0.751, 0.919); CV death, nonfatal MI, nonfatal stroke or rehospitalisation for cardiac ischaemic event through study end (11.7% vs 13.8%; HR 0.838; CI 0.762, 0.921).
Dawn inkludew trombożi ċerta jew probabbli fl- istent fl- aħħar tal- istudju (0. 9% kontra 1. 8%; HR 0. 498; CI 0. 364, 0. 683); mewt CV, MI mhux fatali, jew rivaskularizzazzjoni tal- vina/ arterja mira tul 30 ġurnata (5. 9% kontra 7. 4%; HR 0. 784; CI 0. 688, 0. 894); mewt mill- kawżi kollha, MI mhux fatali, jew puplesija mhux fatali tul l- aħħar ta 'l- istudju (10. 2% kontra 12. 1%; HR 0. 831; CI 0. 751, 0. 919); mewt CV, MI mhux fatali, puplesija mhux fatali jew dħul lura l- isptar minħabba avveniment iskemiku kardijaku tul l- aħħar tal- istudju (11. 7% kontra 13. 8%; HR 0. 838; CI 0. 762, 0. 921).
Analysis of all cause death did not show any significant difference between prasugrel and clopidogrel in the All ACS population (2.76% vs 2.90%), in the UA/ NSTEMI population (2.58% vs 2.41%), and in the STEMI population (3.28% vs 4.31%).
Analiżi tal - mewt mill- kawżi kollha ma wriet ebda differenza sinifikanti bejn prasugrel u clopidogrel fil- poplazzjoni tal- Pazjenti Kollha b' ACS (2. 7% vs 2. 9%), fil- popolazzjoni UA/ NSTEMI (2. 58% vs 2. 41%) u fil - popolazzjoni STEMI (3. 28% vs 4. 31%).
Prasugrel was associated with a 50% reduction in stent thrombosis through the 15 month follow-up period.
Prasugrel gie assoċjat ma 'tnaqqis ta' 50% ta 'trombożi fl- istent tul il- perijodu ta' 15- il xahar ta 'studju ta' wara l- kura.
The reduction in stent thrombosis with Efient was observed both early and beyond 30 days for both bare metal and drug eluting stents.
It- tnaqqis fit- trombożi fl- istent b' Efient ġie osservat kemm mill- ewwel kif ukoll wara 30 ġurnata bl- istents tal- metal mhux miksi u wkoll bi stents miksija b' mediċina.
In an analysis of patients who survived an ischaemic event, prasugrel was associated with a reduction in the incidence of subsequent primary endpoint events (7.8% for prasugrel vs 11.9% for clopidogrel).
F' analiżi ta 'pazjenti li baqgħu ħajjin wara avveniment iskemiku, prasugrel ġie assoċjat ma' tnaqqis fl - inċidenza ta 'avvenimenti ta ’ riżultati finali primarji sussegwenti (7. 8% għal prasugrel kontra 11. 9% għal clopidogrel).
Although bleeding was increased with prasugrel, an analysis of the composite endpoint of death from any cause, nonfatal myocardial infarction, nonfatal stroke, and non-CABG-related TIMI major haemorrhage favoured Efient compared to clopidogrel (Hazard ratio, 0.87; 95% CI, 0.79 to 0.95; p=0.004).
Għalkemm bi prasugrel żdiedet il- fsada, analiżi tar- riżultat finali kompost ta 'mewt minn kull kawża, infart mijokardijaku mhux fatali, puplesija mhux fatali, emorraġija maġġuri skont TIMI relatata ma' non - CABG iffavorixxit Efient meta mqabbel ma 'clopidogrel (Proporzjon ta' periklu, 0. 87; 95% CI, 0. 79 sa 0. 95; p=0. 004).
In TRITON, for every 1000 patients treated with Efient, there were 22 fewer patients with myocardial infarction, and 5 more with non– CABG-related TIMI major haemorrhages, compared with patients treated with clopidogrel.
F' TRITON, għal kull 1000 pazjent ikkurat b' Efient, kien hemm 22 pazjent anqas b' infart
10 5.2 Pharmacokinetic properties
5. 2 Tagħrif farmakokinetiku
Prasugrel is a prodrug and is rapidly metabolised in vivo to an active metabolite and inactive metabolites.
Prasugrel huwa prodrug u jiġi metabolizzat malajr in vivo f' metabolit attiv u metaboliti inattivi.
The active metabolite’ s exposure (AUC) has moderate to low between-subject (27%) and within-subject (19%) variability.
L - espożizzjoni (AUC) tal- metabolit attiv għandha varjabbilità bejn is- suġġetti (27%) u fis- suġġetti (19%) minn moderata għal baxxa.
Prasugrel’ s pharmacokinetics are similar in healthy subjects, patients with stable atherosclerosis, and patients undergoing percutaneous coronary intervention.
Il- farmakokinetika ta 'prasugrel hija simili f' suġġetti b' saħħithom, pazjenti b' aterosklerosi stabbli, u pazjenti li għaddejjin minn intervent koronarju minn ġol- ġilda.
Absorption The absorption and metabolism of prasugrel are rapid, with peak plasma concentration (Cmax) of the active metabolite occurring in approximately 30 minutes.
Assorbiment L- assorbiment u l- metaboliżmu ta 'prasugrel huma mgħaġġlin, bl- ogħla konċentrazzjoni fil- plażma (Cmax) tal- metabolit attiv iseħħ f' madwar 30 minuta.
The active metabolite’ s exposure (AUC) increases proportionally over the therapeutic dose range.
L- espożizzjoni (AUC) tal- metabolit attiv tiżdied proporzjonalment fuq l- iskala tad- doża terapewtika.
In a study of healthy subjects, AUC of the active metabolite was unaffected by a high fat, high calorie meal, but Cmax was decreased by 49% and the time to reach Cmax (Tmax) was increased from 0.5 to 1.5 hours.
Fi studju b' suġġetti b' saħħithom, AUC tal- metabolit attiv ma ġiex affettwat b' ikla b' ħafna xaħam u ħafna kaloriji, iżda Cmax naqas b' 49% u l- ħin biex intlaħaq Cmax (Tmax) żdied minn 0. 5 għal 1. 5 sigħat.
Efient was administered without regard to food in TRITON.
F' TRITON, Efient ingħata mingħajr kunsiderazzjoni għall- ikel.
Therefore, Efient can be administered without regard to food; however, the administration of prasugrel loading dose in the fasted state may provide most rapid onset of action (see section 4.2).
Għaldaqstant, Efient jista 'jingħata mingħajr kunsiderazzjoni għall- ikel; madanakollu, il- bidu l- aktar mgħaġġel ta' l- azzjoni jista 'jseħħ b' għoti tad- doża tal- bidu bl- ogħla qawwa ta' prasugrel fl- istat ta 'sawm (ara sezzjoni 4. 2).
Distribution Active metabolite binding to human serum albumin (4% buffered solution) was 98%.
Distribuzzjoni L- irbit tal- metabolit attiv ma 'l- albumina fis- serum uman (soluzzjoni bafferjata ta' 4%) kien ta '98%.
Metabolism Prasugrel is not detected in plasma following oral administration.
Metaboliżmu Wara t- teħid mill- ħalq prasugrel ma jiġix osservat fil- plażma.
It is rapidly hydrolysed in the intestine to a thiolactone, which is then converted to the active metabolite by a single step of cytochrome P450 metabolism, primarily by CYP3A4 and CYP2B6 and to a lesser extent by CYP2C9 and CYP2C19.
Huwa jiġi idrolizzat b' mod rapidu fil - musrana f' thiolactone li b' pass wieħed tal- metaboliżmu ta 'ċitokromu P450 jinbidel fil- metabolit attiv, prinċipalment minn CYP3A4 u CYP2B6 u anqas minn CYP2C9 u CYP2C19.
The active metabolite is further metabolised to two inactive compounds by S- methylation or conjugation with cysteine.
Il- metabolit attiv jerġa 'jiġi metabolizzat f' żewġ kompożizzjonijiet inattivi b' S- metilazzjoni jew konjugazzjoni ma' cysteine.
In healthy subjects, patients with stable atherosclerosis, and patients with ACS receiving Efient, there was no relevant effect of genetic variation in CYP3A5, CYP2B6, CYP2C9, or CYP2C19 on the pharmacokinetics of prasugrel or its inhibition of platelet aggregation.
F' suġġetti b' saħħithom, pazjenti b' aterosklerosi stabbli, u pazjenti b' ACS li jirċievu Efient, ma kienx hemm effett rilevanti ta 'varjazzjoni ġenetika f' CYP3A5, CYP2B6, CYP2C9, jew CYP2C19 fuq il - farmakokinetika jew l- inibizzjoni ta' l- aggregazzjoni ta 'plejtlits ta' prasugrel.
Elimination Approximately 68% of the prasugrel dose is excreted in the urine and 27% in the faeces, as inactive metabolites.
Eliminazzjoni Madwar 68% tad- doża ta 'prasugrel titneħħa fl- awrina u 27% fl- ippurgar, bħala metaboliti inattivi.
The active metabolite has an elimination half-life of about 7.4 hours (range 2 to 15 hours).
Il - metabolit attiv għandu half- life ta 'l- eliminazzjoni ta madwar 7. 4 sigħat (f' skala minn 2 sa 15- il siegħa).
Special Populations:
Popolazzjonijiet speċjali:
In a study of healthy subjects between the ages of 20 and 80 years, age had no significant effect on pharmacokinetics of prasugrel or its inhibition of platelet aggregation.
Fi studju ta 'suġġetti b' saħħithom b' etajiet bejn l- 20 u t- 80 sena, l- età ma kellix effett sinifikanti fuq il- farmakokinetika jew l- inibizzjoni ta' l- aggregazzjoni ta 'plejtlits ta' prasugrel.
In the large phase 3 clinical trial, the mean estimated exposure (AUC) of the active metabolite was 19% higher in very elderly patients (≥ 75 years of age) compared to subjects < 75 years of age.
Fi studju kliniku kbir ta 'fażi 3, l- espożizzjoni medja stmata (AUC) tal- metabolit attiv kienet 19% ogħla f' pazjenti anzjani ħafna (≥75 sena) meta mqabbel ma' suġġetti < 75 sena.
Prasugrel should be used with caution in patients ≥ 75 years of age due to the potential risk of bleeding in this population (see sections 4.2 and 4.4).
Prasugrel għandu jintuża b' kawtela f' pazjenti ta '≥ 75 sena minħabba r- riskju potenzjali ta' fsada f' din il- popolazzjoni (ara sezzjonijiet 4. 2 u 4. 4).
No dose adjustment is necessary for patients with mild to moderate impaired hepatic function (Child Pugh Class A and B).
Mhux meħtieġ li jsir aġġustament fid- doża għal pazjenti b' indeboliment ħafif jew moderat tal- funzjoni tal- fwied (Child Pugh Klassi A u B).
Pharmacokinetics of prasugrel and its inhibition of platelet aggregation were similar in subjects with mild to moderate hepatic impairment compared to healthy subjects.
Il- farmakokinetika u l- inibizzjoni ta 'l - aggregazzjoni ta' plejtlits ta 'prasugrel kienu simili f' suġġetti b' indeboliment tal- fwied ħafif jew moderat meta mqabbel ma' suġġetti b' saħħithom.
Pharmacokinetics and pharmacodynamics of prasugrel in patients with severe hepatic impairment have not been studied.
Ma ġewx studjati l- farmakokinetika u l- farmakodinamika ta 'prasugrel f' pazjenti b' indeboliment qawwi tal- fwied.
3).
Prasugrel m' għandux jintuża f' pazjenti b' indeboliment tal- fwied qawwi (ara sezzjoni 4. 3).
No dosage adjustment is necessary for patients with renal impairment, including patients with end stage renal disease (ESRD).
Mhux meħtieġ li jsir aġġustament fid- doża għal pazjenti b' indeboliment tal -
Pharmacokinetics of prasugrel and its inhibition of platelet aggregation are similar in patients with moderate renal impairment (GFR 30- < 50 ml/ min/ 1.73m2) and healthy subjects.
12 kliewi, inklużi pazjenti b' mard tal- kliewi fl- aħħar stadju (ESRD).
Prasugrel-mediated inhibition of platelet aggregation was also
Il- farmakokinetika u l- inibizzjoni ta 'l - aggregazzjoni ta' plejtlits ta 'prasugrel kienu simili f' suġġetti b' indeboliment tal- kliewi moderat (GFR 30 - < 50 ml/ min/ 1. 73m2) u f' suġġetti b' saħħithom.
11 similar in patients with ESRD who required haemodialysis compared to healthy subjects, although Cmax and AUC of the active metabolite decreased 51% and 42%, respectively, in ESRD patients.
L- inibizzjoni ta 'aggregazzjoni ta' plejtlits permezz ta 'prasugrel kienet simili wkoll f' pazjenti b' ESRD li kellhom bżonn dijaliżi tad- demm meta mqabbel ma' suġġetti b' saħħithom, għalkemm Cmax u AUC tal- metabolit attiv naqsu 51% u 42%, rispettivament, f' pazjenti b' ESRD.
The mean exposure (AUC) of the active metabolite of prasugrel is approximately 30 to 40% higher in healthy subjects and patients with a body weight of < 60 kg compared to those weighing ≥ 60 kg.
L- espożizzjoni medja (AUC) tal- metabolit attiv ta 'prasugrel hija madwar 30 sa 40% ogħla f' suġġetti b' saħħithom u pazjenti b' piż tal- ġisem ta' < 60 kg ikkomparaw ma 'dawk li jiżnu ≥60 kg.
Prasugrel should be used with caution in patients with a body weight of < 60 kg due to the potential risk of bleeding in this population (see section 4.4).
Prasugrel għandu jintuża b' kawtela f' pazjenti b' piż tal- ġisem < 60 kg minħabba r- riskju potenzjali ta 'fsada f' din il- popolazzjoni (ara sezzjoni 4. 4).
Ethnicity:
Etniċità:
In clinical pharmacology studies, after adjusting for body weight, the AUC of the active metabolite was approximately 19% higher in Chinese, Japanese, and Korean subjects compared to that of Caucasians, predominantly related to higher exposure in Asian subjects < 60 kg.
Fi studji tal- farmakoloġija klinika, wara l- aġġustament għall- piż tal- ġisem, AUC tal- metabolit attiv kien madwar 19% ogħla f' suġġetti Ċiniżi, Ġappuniżi u Koreani meta mqabbel ma 'dak tal- Kawkażi, il- biċċa l- kbira relatat ma' espożizzjoni ogħla f' suġġetti Asjatiċi < 60 kg.
There is no difference in exposure among Chinese, Japanese, and Korean subjects.
M' hemmx differenza fl - espożizzjoni bejn suġġetti Ċiniżi, Ġappuniżi u Koreani.
Exposure in subjects of African and Hispanic descent is comparable to that of Caucasians.
L- espożizzjoni f' suġġetti ta 'dixxendenza Afrikana u Spanjola jew Latin- Amerikana hija komparabbli ma' dik tal- Kawkażi.
No dose adjustment is recommended based on ethnicity alone.
Mhux irrakkomandat li jsir aġġustament fid- doża fuq il- bażi ta 'etniċità biss.
In healthy subjects and patients, the pharmacokinetics of prasugrel are similar in men and women.
F' suġġetti u pazjenti b' saħħithom, il- farmakokinetika ta 'prasugrel hija simili fl- irġiel u fin- nisa.
Pharmacokinetics and pharmacodynamics of prasugrel have not been evaluated in a paediatric population (see section 4.2).
Il- farmakokinetika u l- farmakodinamika ta 'prasugrel ma ġewx stmati fil- popolazzjoni pedjatrika (ara sezzjoni 4. 2).
Non-clinical data reveal no special hazard for humans based on conventional studies of safety pharmacology, repeat-dose toxicity, genotoxicity, carcinogenic potential, or toxicity to reproduction.
Informazzjoni mhux klinika, magħmula fuq studji konvenzjonali ta ’ sigurtà farmakoloġika, effett tossiku minn dożi ripetuti, effett tossiku fuq il- ġeni, riskju ta ’ kanċer, effett tossiku fuq is- sistema riproduttiva, ma turi l- ebda periklu speċjali għall- bnedmin.
Effects in non-clinical studies were observed only at exposures considered sufficiently in excess of the maximum human exposure indicating little relevance to clinical use.
Fi studji mhux kliniċi, effetti dehru biss wara esponimenti meqjusa ferm aktar għolja mill- massimu ta ’ l- esponimenti lill- bnedmin, li juru ftit li xejn rilevanza għall - użu kliniku.
Embryo-foetal developmental toxicology studies in rats and rabbits showed no evidence of malformations due to prasugrel.
Studji tossikoloġiċi fuq l- iżvilupp tal- embriju/ fetu fil- firien u l- fniek ma wrew ebda evidenza ta ’ malformazzjonijiet minħabba prasugrel.
At a very high dose (> 240 times the recommended daily human maintenance dose on a mg/ m2 basis) that caused effects on maternal body weight and/ or food consumption, there was a slight decrease in offspring body weight (relative to controls).
Meta ngħatat doża għolja ħafna (> 240 darba d- doża rakkomandata ta ’ manteniment ta ’ kuljum fil- bniedem fuq bażi ta ’ mg/ m2) li kkawżat effetti fuq il- piż tal- ġisem matern u / jew il- konsum tal- ikel, kien hemm tnaqqis żgħir fil- piż tal- frieħ (meta mqabbel ma ’ dawk użati bħala kontroll).
In pre- and post-natal rat studies, maternal treatment had no effect on the behavioural or reproductive development of the offspring at doses up to an exposure 240 times the recommended daily human maintenance dose (based on mg/ m2).
F’ studji ta ’ qabel u wara t- tqala fil- firien, il- kura li ngħatat lil omm ma kellha ebda effett fuq l- iżvilupp tal- imġiba u tas- sistema riproduttiva fil- frieħ f’ dożi sa esponiment ta ’ 240 darba d- doża rakkomandata ta ’ manteniment ta ’ kuljum fil- bniedem (fuq bażi ta ’ mg/ m2).
No compound-related tumours were observed in a 2-year rat study with prasugrel exposures ranging to greater than 75 times the recommended therapeutic exposures in humans (based on plasma exposures to the active and major circulating human metabolites).
Ma ġewx osservati tumuri kkawżati mill- prodott f’ studju fil- firien li dam sentejn b’ esponimenti għal prasugrel li waslu sa aktar minn 75 darba l- esponimenti terapewtiċi rakkomandati fil- bnedmin (bbażati fuq l- esponimenti fil- plażma għall- metaboliti umani attivi u maġġuri li jkunu qed jiċċirkolaw).
There was an increased incidence of tumours (hepatocellular adenomas) in mice exposed for 2 years to high doses (> 75 times human exposure), but this was considered secondary to prasugrel-induced enzyme-induction.
Kien hemm żieda fl- inċidenza ta ’ tumuri (adenomas epatoċellulari) fil- ġrieden esposti għal sentenjn għal dożi għoljin (> 75 darba l- esponiment fil- bniedem) iżda din kienet ikkunsidrata bħala sekondarja għal dawk ikkawżati minn enzimi li fuqhom jaħdem prasugrel.
The rodent-specific association of liver tumours and drug-induced enzyme induction is well documented in the literature.
L- assoċjazzjoni speċifika bejn l- annimali gerriema u t- tumuri fil- fwied u l- attivazzjoni tal- enzimi kkawżati mill- prodott mediċinali huma magħrufa sew fil - letteratura.
The increase in liver tumours with prasugrel administration in mice is not considered a relevant human risk.
Iż- żieda fit- tumuri tal- fwied fil- ġrieden mogħtija prasugrel mhijiex ikkunsidrata bħala riskju rilevanti fil- bniedem.
Tablet Core:
Qalba tal- pillola:
Microcrystalline cellulose Mannitol (E421) Croscarmellose sodium Hypromellose (E464) Magnesium stearate
Microcrystalline cellulose Mannitol (E421) Croscarmellose sodium Hypromellose (E464) Magnesium stearate
12 Film-Coat:
Kisja tal- pillola:
Lactose monohydrate Hypromellose (E464) Titanium dioxide (E171) Triacetin (E1518) Iron oxide yellow (E172) Talc
Lactose monohydrate Hypromellose (E464) Titanium dioxide (E171) Triacetin (E1518) Iron oxide isfar (E172) Talc
This medicinal product does not require any special temperature storage conditions.
Dan il- prodott mediċinali m’ għandux bżonn l- ebda kundizzjoni ta 'temperatura speċjali għall- ħażna.
Store in the original package to protect from air and moisture.
Aħżen fil- pakkett oriġinali sabiex tilqa ’ mill- arja u mill- umdità.
Aluminium foil blisters in cartons of 14, 28, 30 (x1), 56, 84, 90 (x1) and 98 tablets.
Folji tal- fojl tal- aluminju f’ pakketti ta ’ 14, 28, 30 (x1), 56, 84, 90 (x1) u 98 pillola.
< {DD month YYYY} >
14 {JJ xahar SSSS}
Efient 10 mg film-coated tablets.
Efient 10 mg pilloli miksija b' rita.
Each tablet contains 10 mg prasugrel (as hydrochloride).
Kull pillola fiha 10 mg prasugrel (bħala hydrochloride).
Each tablet contains 2.1 mg lactose.
Kull pillola fiha 2. 1 mg lactose.
Beige and double-arrow shaped tablets, debossed with “ 10 mg” on one side and “ 4759” on the other.
Pilloli beġ f' forma ta 'vleġġa doppja, b' “ 10 mg ” imnaqqxa fuq naħa waħda u “ 4759 ” imnaqqxa fuq in - naħa l- oħra.
Patients ≥ 75 years of age have greater sensitivity to bleeding and higher exposure to the active metabolite of prasugrel (see sections 4.4, 4.8, 5.1 and 5.2).
L- evidenza
The evidence for the 5 mg dose is based only on pharmacodynamic/ pharmacokinetic analyses and no clinical data currently exist on the safety of this dose in the patients age group ≥ 75 years.
16 għad- doża ta ’ 5 mg hija bbażata biss fuq l- analiżi farmakodinamika/ farmakokinetika u f’ dan il- mument ma jeżisti ebda tagħrif kliniku dwar is- sigurtà ta ’ din id- doża fil- grupp ta età ta ’ pazjenti ≥ 75 sena.
Patients weighing < 60 kg Efient should be given as a single 60 mg loading dose and then continued at a 5 mg once daily dose.
Pazjenti li jiżnu < 60 kg Efient għandu jingħata bħala doża waħda ta ’ kkargar ta '60 mg u mbagħad jitkompla b' doża ta' 5 mg darba kuljum.
14 The 10 mg maintenance dose is not recommended.
Id- doża ta '10 mg mhix irrakkomandata.
For patients with active bleeding for whom reversal of the pharmacological effects of Efient is required, platelet transfusion may be appropriate.
17 F’ pazjenti b’ fsada attiva li jkollhom bżonn il- maqlub tal- effetti farmakoloġiċi ta ’ Efient, tista ’ tkun xierqa it- trasfużjoni bil- plejtlits.
In the phase 3 clinical trial these patients were at greater risk of bleeding, including fatal 15 bleeding, compared to patients < 75 years of age.
Fl- istudju kliniku ta 'fażi 3 dawn il- pazjenti kienu f' riskju akbar ta' fsada, inkluża fsada fatali, meta mqabbel ma 'pazjenti < 75 sena.
Efient can be concomitantly administered with medicinal products metabolised by cytochrome P450 enzymes (including statins), or medicinal products that are inducers or inhibitors of cytochrome P450 enzymes.
18 Efient jista 'jingħata flimkien ma' prodotti mediċinali li jiġu mmetabolizzati minn enzimi ta 'ċitokromu P450 (fosthom statins), jew prodotti mediċinali li huma stimulanti jew inibituri ta' l- enzimi ta 'ċitokromu P450.
Medicinal products metabolised by CYP2B6: prasugrel is a weak inhibitor of CYP2B6.
19 Prodotti mediċinali mmetabolizzati minn CYP2B6: prasugrel huwa inibitur dgħajjef ta 'CYP2B6.