Sagrada tablets 10 mg No. 28

Instructions for Sagrada tablets 10mg No. 28

Composition

active ingredient: prasugrel;

1 tablet contains prasugrel 10 mg;

Excipients: crospovidone (type A), lactose monohydrate, croscarmellose sodium, microcrystalline cellulose (E 460), sucrose stearate.

Coating mixture: Opadry II 32K230012 Orange*

* - dry coating mixture contains: hypromellose (E 464) (hydroxypropylmethylcellulose), lactose monohydrate, titanium dioxide (E 171), triacetin (E 1518), talc, iron oxide yellow (E 172), iron oxide red (E 172).

Dosage form

Film-coated tablets.

Main physicochemical properties: film-coated tablets, oval in shape with a biconvex surface and the inscription "F2" on one side.

Pharmacotherapeutic group

Antithrombotic drugs. Platelet aggregation inhibitors, except heparin. Prasugrel.

ATX code B01AC22.

Pharmacological properties

Pharmacodynamics.

Mechanism of action

Prasugrel is an inhibitor of platelet activation and aggregation through irreversible binding of its active metabolite to the P2Y12 ADP receptor on platelets. Since platelets are involved in the initiation and/or progression of thrombotic complications of atherosclerotic disease, inhibition of platelet function may result in a reduction in the incidence of cardiovascular events such as death, myocardial infarction, or stroke.

Following a 60 mg loading dose of prasugrel, inhibition of ADP-induced platelet aggregation occurs within 15 minutes with 5 μM ADP and 30 minutes with 20 μM ADP. The maximal inhibition of ADP-induced platelet aggregation by prasugrel is 83% with 5 μM ADP and 79% with 20 μM ADP, with at least 50% inhibition of platelet aggregation achieved within 1 hour in both 89% of healthy subjects and patients with stable atherosclerosis. Prasugrel-mediated inhibition of platelet aggregation shows low intersubject (9%) and intrasubject (12%) variability with both 5 μM and 20 μM ADP. The mean steady-state inhibition of platelet aggregation was 74% and 69% for 5 μM ADP and 20 μM ADP, respectively, and was achieved 3-5 days after administration of a 10 mg prasugrel maintenance dose with a 60 mg loading dose. More than 98% of subjects had ≥20% inhibition of platelet aggregation during maintenance therapy.

Platelet aggregation after cessation of prasugrel therapy gradually returns to baseline values: within 7-9 days after a single loading dose of prasugrel 60 mg and within 5 days after discontinuation of the maintenance dose at steady state.

Data on switching from one drug to another

After receiving 75 mg of clopidogrel once daily for 10 days, 40 healthy patients were switched to prasugrel 10 mg once daily, with or without a 60 mg loading dose. Similar or greater inhibition of platelet aggregation was observed with prasugrel. Switching to a 60 mg loading dose of prasugrel resulted in more rapid and potent inhibition of platelets. After a 900 mg loading dose of clopidogrel (with ASA), 56 patients with ACS received either prasugrel 10 mg once daily or clopidogrel 150 mg once daily for 14 days and then switched to clopidogrel 150 mg or prasugrel 10 mg for 14 days. Greater inhibition of platelet aggregation was observed in patients switched to prasugrel 10 mg compared with patients receiving clopidogrel 150 mg. In a study of 276 patients with ACS (acute coronary syndrome) undergoing PCI (percutaneous coronary intervention), switching from an initial loading dose of 600 mg of clopidogrel or placebo administered on admission to the hospital prior to coronary angiography to a loading dose of 60 mg of prasugrel administered at the time of percutaneous coronary intervention resulted in a similar increase in inhibition of platelet aggregation over the 72 hours of the study.

Clinical efficacy and safety

Acute coronary syndrome (ACS)

TRITON Phase 3 compared prasugrel with clopidogrel, given with acetylsalicylic acid (ASA) and other medications, according to standard of care. TRITON is a multicenter, international, randomized, double-blind, parallel-group study in 13,608 patients with ACS at moderate to high risk of developing unstable angina (UA)/non-ST-segment elevation myocardial infarction (NSTEMI) and ST-elevation myocardial infarction (STEMI) undergoing PCI.

Patients randomized to receive prasugrel (60 mg loading dose, then 10 mg once daily) or clopidogrel (300 mg loading dose, then 75 mg once daily) were treated for a median of 14.5 months (maximum 15 months, minimum 6 months). Patients also received ASA (75 mg to 325 mg once daily). The use of any thienopyridine within 5 days prior to study entry was an exclusion criterion. Other therapies, such as heparin and GPIIb/IIIa inhibitors, were administered at the discretion of the physician. Approximately 40% of patients (in each treatment group) received GPIIb/IIIa inhibitors at PCI (no information on the type of GP IIb/IIIa inhibitor used). Approximately 98% of patients (in each treatment group) received antithrombins (heparin, low molecular weight heparin, bivalirudin, or other agents) immediately at the time of PCI.

The efficacy criterion was time to first non-fatal myocardial infarction (MI), non-fatal stroke, or cardiovascular death. Analysis of the combined endpoint in the entire ACS patient population (combined population with ACS/ST elevation MI and ST elevation MI) showed a statistically significant advantage of prasugrel over clopidogrel in the ACS/ST elevation MI group (p < 0.05).

All population with GCS

Prasugrel demonstrated superior efficacy compared with clopidogrel in reducing the incidence of the primary composite endpoint as well as the incidence of secondary endpoints, including stent thrombosis (see Table 1). The benefit of prasugrel was observed within the first 3 days and was maintained through the end of the study. The superior efficacy was accompanied by an increase in major bleeding (see sections 4.4 and 4.8). The patient population was 92% Caucasian, 26% female, and 39% ≥ 65 years of age. The efficacy of prasugrel was independent of concomitant therapy, including heparin/low molecular weight heparins, bivalirudin, intravenous GPIIb/IIIa inhibitors, lipid-lowering agents, beta-blockers, and ACE inhibitors. Prasugrel efficacy was also independent of ASA dosage (75 mg to 325 mg once daily). Oral anticoagulants, non-study antiplatelet agents, and NSAIDs (long-term use) were not permitted in TRITON. In the overall ACS population, prasugrel was associated with a lower incidence of cardiovascular death, non-fatal MI, or non-fatal stroke compared with clopidogrel, regardless of baseline characteristics such as age, sex, body weight, geographic region, use of GPIIb/IIIa inhibitors, and stent type.

The benefit was primarily due to a significant reduction in non-fatal MI (see Table 1). In patients with diabetes, there was also a significant reduction in the primary and all secondary composite endpoints.

The benefits of prasugrel therapy are less pronounced in patients ≥ 75 years of age and older than in patients < 75 years of age. Patients ≥ 75 years of age had an increased risk of bleeding, including fatal bleeding (see sections 4.2, 4.8, and 4.8).

For patients ≥ 75 years with diabetes, ST-elevation MI, increased risk of stent thrombosis, or with disease recurrence, the benefit of prasugrel is more apparent.

In patients with a history of TIA or a history of ischemic stroke more than 3 months prior to initiation of prasugrel therapy, there was no reduction in the primary composite endpoint.

Table 1

Patients with outcomes in the primary TRITON analysis

In the entire ACS population, analysis of each of the secondary endpoints showed significant advantages (p<0.001) for prasugrel compared with clopidogrel. These included the incidence of definite or probable stent thrombosis at the end of the study (0.9% and 1.8%, respectively; hazard ratio 0.498; CI 0.364, 0.683); cardiovascular death, nonfatal MI, or urgent target vessel revascularization within 30 days (5.9% and 7.4%, respectively; HR 0.784; CI 0.688, 0.894); all-cause mortality, nonfatal MI, or nonfatal stroke by the end of the study (10.2% and 12.1%, respectively; HR 0.831; CI 0.751, 0.919); cardiovascular death, nonfatal MI, nonfatal stroke, or rehospitalization for ischemic heart disease by the end of the study (11.7% and 13.8%, respectively; HR 0.838; CI 0.762, 0.921). Analysis of all-cause mortality did not reveal any significant differences between prasugrel and clopidogrel in the overall ACS population (2.76% and 2.90%, respectively), in the ACS/STEMI population (2.58% and 2.41%, respectively), and in the STEMI population (3.28% and 4.31%, respectively).

Prasugrel was associated with a 50% reduction in the incidence of stent thrombosis over a 15-month follow-up period. The reduction in the incidence of stent thrombosis with prasugrel was observed both at baseline and after 30 days for both bare-metal and drug-eluting stents.

In the analysis of patients who experienced an ischemic event, prasugrel was associated with a reduction in the incidence of subsequent primary endpoints (7.8% for prasugrel and 11.9% for clopidogrel).

Although bleeding was increased with prasugrel, analysis of the composite endpoint of all-cause death, nonfatal MI, nonfatal stroke, and non-CABG-related TIMI major bleeding favored prasugrel over clopidogrel (hazard ratio 0.87, 95% CI 0.79-0.95, p = 0.004).

In the TRITON trial, for every 1000 patients taking prasugrel, there were 22 fewer patients with myocardial infarction and 5 more with TIMI major bleeding not related to CABG compared with patients taking clopidogrel.

Results of a pharmacodynamic/pharmacogenomic study in 720 Asian patients with ACS PCI demonstrated that prasugrel achieved a higher level of platelet inhibition compared with clopidogrel and that prasugrel at a loading dose of 60 mg/maintenance dose of 10 mg is an appropriate dosing regimen for Asian subjects weighing less than 60 kg and aged less than 75 years (see section 4.2).

In a 30-month study (TRILOGY-ACS) in 9326 patients with ACS ACS/STEMI BP who were treated medically without revascularization (unapproved indication), prasugrel did not significantly reduce the incidence of the composite endpoint of cardiovascular death, MI, or stroke compared with clopidogrel. The incidence of TIMI major bleeding (including life-threatening, fatal, and intracranial bleeding) was similar in patients treated with prasugrel and clopidogrel. The study blinded patients ≥75 years of age or patients weighing <60 kg (N=3022) who received 5 mg prasugrel. As in patients < 75 years of age and ≥ 60 kg receiving 10 mg prasugrel, there was no difference in the incidence of CV events between patients receiving 5 mg prasugrel and patients receiving 75 mg clopidogrel. The incidence of major bleeding was similar in patients receiving 5 mg prasugrel and patients receiving 75 mg clopidogrel. Prasugrel 5 mg had a greater antiplatelet effect than 75 mg clopidogrel. Prasugrel should be used with caution in patients over 75 years of age and in patients weighing less than 60 kg (see sections 4.2, 4.4, and 4.8).

Pediatric population

The study evaluated the use of prasugrel (n=171) compared with placebo (n=170) in patients aged 2 to 18 years with sickle cell disease to reduce vaso-occlusive crisis in a phase III study. The study did not meet any of its primary or secondary endpoints. Overall, no new safety findings were identified for prasugrel (as monotherapy in this patient population).

Pharmacokinetics.

Prasugrel is a prodrug and is rapidly metabolized in vivo to active and inactive metabolites. The area under the pharmacokinetic curve "concentration-time" (AUC) is characterized by moderate to low variability within the population (27%) and within an individual patient (19%). The pharmacokinetic parameters of prasugrel are similar in healthy volunteers, patients with stable atherosclerotic disease, and patients who have undergone PCI.

Absorption

When taken orally, prasugrel is rapidly absorbed and metabolized. The time to reach maximum concentration (Tmax) of the active metabolite in the blood serum is reached approximately 0.5 hours after administration. The AUC of the active metabolite increases in direct proportion to the therapeutic dose of the drug.

In healthy volunteers, a high-fat, high-calorie meal had no effect on the AUC of the active metabolite, but Cmax was decreased by 49% and Tmax was increased by 0.5 to 1.5 hours. Prasugrel was administered without regard to food in the TRITON study. Thus, prasugrel can be administered without regard to food intake, but administration of a loading dose on an empty stomach may provide a more rapid onset of action (see section 4.2).

Distribution

The binding of the active metabolite of prasugrel to human serum albumin is 98%.

Metabolism

Prasugrel is not detectable in plasma after oral administration. Prasugrel is rapidly hydrolyzed in the intestine to the thiolactone, which is then converted to the active metabolite, primarily by cytochrome P450 isoenzymes such as CYP3A4 and CYP2B6, and to a lesser extent by CYP2C9 and CYP2C19. The active metabolite is converted to two inactive metabolites by S-methylation or conjugation with cysteine.

In healthy volunteers, patients with stable atherosclerotic disease, and patients who had undergone coronary artery bypass grafting who took prasugrel, no effect of genetic variations in CYP2B6, CYP2C9, CYP2C19, or CYP3A5 isoenzymes on the pharmacokinetic parameters of prasugrel or inhibition of platelet aggregation was detected.

Breeding

Approximately 68% of prasugrel is excreted in the urine and approximately 27% in the feces as inactive metabolites. The half-life (T1/2) of the active metabolite is approximately 7.4 hours (range 2 to 15 hours).

Special patient groups

Elderly patients. A study conducted in healthy volunteers aged 20 to 80 years shows that the pharmacokinetics of prasugrel or inhibition of platelet aggregation are not dependent on the age of the patients. The AUC of the active metabolite is 19% higher in elderly patients (aged 75 years and older) compared with patients younger than 75 years. Prasugrel should be used with caution in patients aged 75 years and older due to the potential risk of bleeding in this population (see sections 4.4 and 4.2). In a study in patients with stable atherosclerotic disease, the AUC of the active metabolite in patients aged 75 years and older receiving 5 mg prasugrel was approximately half that in patients aged 65 years and older receiving 10 mg prasugrel, while in patients taking 5 mg prasugrel, its antiplatelet effect was reduced.

Hepatic impairment. No dose adjustment is required for patients with mild to moderate hepatic impairment (Child-Pugh class A and B). The pharmacokinetics of prasugrel and its inhibitory effect on platelet aggregation are similar in patients with mild to moderate hepatic impairment and healthy volunteers. The pharmacokinetics and pharmacodynamics of prasugrel in patients with severe hepatic impairment (Child-Pugh class C) have not been studied. Prasugrel is contraindicated in such patients (see section 4.3).

Body weight. The AUC of the active metabolite of prasugrel is approximately 30-40% higher in healthy volunteers and patients weighing less than 60 kg compared to patients weighing ≥ 60 kg. Prasugrel should be used with caution in patients weighing less than 60 kg due to the potential risk of bleeding in this population (see section 4.4). In a study in patients with stable atherosclerosis, the mean AUC of the active metabolite in patients weighing less than 60 kg receiving 5 mg prasugrel was 38% lower than in patients weighing ≥ 60 kg receiving 10 mg prasugrel, while the antiplatelet effect of 5 mg prasugrel was similar to that of 10 mg prasugrel.

Ethnicity. In clinical pharmacology studies, the AUC of the active metabolite (adjusted for body weight) was approximately 19% higher in Mongoloid subjects compared to Caucasians. No differences were found between Chinese, Japanese, and Korean subjects. Exposure in Negroids and Hispanics was comparable to that in Caucasians. No dose adjustment is required based on ethnicity.

Gender: In healthy volunteers and patients, the pharmacokinetic parameters of prasugrel do not differ between men and women.

Children and adolescents under 18 years of age: The pharmacokinetics and pharmacodynamics of prasugrel in children and adolescents have not been studied (see section 4.2).

Indication

Prasugrel in combination with acetylsalicylic acid (ASA) is indicated for the prevention of atherothrombotic events in adult patients with acute coronary syndrome, i.e. unstable angina (UA), non-ST-segment elevation myocardial infarction (NSTEMI), or ST-segment elevation myocardial infarction (ST-elevation MI) undergoing primary or delayed percutaneous coronary intervention (PCI).

The drug Sagrada® 10 mg is used in adults with a body weight of more than 60 kg and up to 75 years of age.

For more information, see the Pharmacological Properties section.

Contraindication

Hypersensitivity to the active substance or to any of the excipients of the medicinal product.

Active bleeding.

History of stroke or transient ischemic attack (TIA).

Severe hepatic impairment (Child-Pugh class C).

Interaction with other medicinal products and other types of interactions

Warfarin: The concomitant use of prasugrel with coumarin derivatives other than warfarin has not been studied. Due to the potential increased risk of bleeding, warfarin (or other coumarin derivatives) and prasugrel should be administered with caution (see section 4.4).

Nonsteroidal anti-inflammatory drugs (NSAIDs). Interaction with NSAIDs (long-term use) has not been studied. Due to the potentially increased risk of bleeding, NSAIDs (long-term use), including COX-2 inhibitors and prasugrel, should be prescribed with caution (see section 4.4).

Prasugrel may be administered concomitantly with drugs that are metabolized by cytochrome P450 enzymes (including statins) or with drugs that are inducers or inhibitors of P450 enzymes. Prasugrel may also be administered concomitantly with ASA, heparin, digoxin, and drugs that increase gastric pH, including proton pump inhibitors and H2-receptor blockers. Although prasugrel has not been studied in specific interaction studies, it has been administered concomitantly with low molecular weight heparins, bivalirudin, and GP IIb/IIIa inhibitors (information on the type of GP IIb/IIIa inhibitor used is not available) in phase 3 clinical trials without evidence of clinically significant adverse interactions.

Effects of other medicinal products on prasugrel

ASA: Prasugrel should be co-administered with ASA. Although there is a potential for an increased risk of bleeding with a pharmacodynamic interaction with ASA, the efficacy and safety of prasugrel have been demonstrated in patients receiving prasugrel co-administered with ASA.

Heparin. A single intravenous bolus dose of unfractionated heparin (100 U/kg) does not significantly alter prasugrel-mediated inhibition of platelet aggregation. Prasugrel also does not significantly alter the effect of heparin on coagulation. Therefore, both drugs can be used together. An increased risk of bleeding is possible with the simultaneous use of prasugrel and heparin.

Statins: Atorvastatin (80 mg/day) did not alter the pharmacokinetics of prasugrel or prasugrel-mediated inhibition of platelet aggregation. Therefore, statins that are substrates of CYP3A are not expected to affect the pharmacokinetics of prasugrel or prasugrel-mediated inhibition of platelet aggregation.

CYP3A inhibitors: Ketoconazole (400 mg/day), a selective and potent inhibitor of CYP3A4 and CYP3A5, did not affect prasugrel-mediated inhibition of platelet aggregation or the AUC and Tmax of the active metabolite of prasugrel, but decreased Cmax by 34% to 46%. Therefore, CYP3A inhibitors, such as antifungals, azole derivatives, HIV protease inhibitors, clarithromycin, telithromycin, verapamil, diltiazem, indinavir, ciprofloxacin, and grapefruit juice, are not expected to have a significant effect on the pharmacokinetics of the active metabolite.

Cytochrome P450 inducers: Rifampicin (600 mg/day), a potent inducer of CYP3A and CYP2B6 and an inducer of CYP2C9, CYP2C19 and CYP2C8, did not significantly alter the pharmacokinetics of prasugrel. Therefore, known inducers of CYP3A, such as rifampicin, carbamazepine and other inducers of cytochrome P450, are not expected to significantly affect the pharmacokinetics of the active metabolite.

Morphine and other opioids. Delayed and reduced effects of oral P2Y12 inhibitors, including prasugrel and its active metabolite, have been observed in patients with ACS receiving morphine. This interaction may be related to decreased gastrointestinal motility and may be applicable to other opioids. The clinical significance is unknown, but available data suggest that prasugrel may be less effective when co-administered with morphine. In patients with ACS requiring morphine and in whom rapid inhibition of P2Y12 is considered critical, the use of a parenteral P2Y12 inhibitor should be considered.

Effect of prasugrel on other medicinal products

Digoxin: Prasugrel has no clinically significant effect on the pharmacokinetics of digoxin.

Medicinal products metabolised by CYP2C9: Prasugrel does not inhibit CYP2C9 as it did not affect the pharmacokinetics of S-warfarin. Due to the potential increased risk of bleeding, warfarin and prasugrel should be administered with caution (see section 4.4).

Medicinal products metabolized by CYP2B6. Prasugrel is a weak inhibitor of CYP2B6. In healthy volunteers, prasugrel reduced the exposure of hydroxybupropion, a CYP2B6-mediated metabolite of bupropion, by 23%. This effect is likely to be of clinical concern only when prasugrel is coadministered with medicinal products for which CYP2B6 is the sole metabolic pathway and which have a narrow therapeutic window (e.g., cyclophosphamide, efavirenz).

Application features

Risk of bleeding

In the phase 3 clinical trials (TRITON), key exclusion criteria were increased risk of bleeding; anemia; thrombocytopenia; history of intracranial pathology. Patients with ACS who underwent PCI and received prasugrel and ASA showed an increased risk of major and minor bleeding according to the TIMI classification system. Therefore, the use of prasugrel in patients at increased risk of bleeding should only be considered when the benefit of preventing ischemic events outweighs the risk of major bleeding. This applies to the following patient groups:

aged 75 and over (see below);

with a tendency to bleed (e.g. due to recent trauma, recent surgery, recent or recurrent gastrointestinal bleeding, or active peptic ulcer disease);

with a body weight <60 kg (see sections “Dosage and Administration” and “Adverse Reactions”). In these patients, a maintenance dose of 10 mg is not recommended; a maintenance dose of 5 mg should be used;

with concomitant use of medications that may increase the risk of bleeding, including oral anticoagulants, clopidogrel, NSAIDs, and fibrinolytics.

In patients with active bleeding who require reversal of the pharmacological effect of prasugrel, platelet transfusion may be appropriate.

The use of prasugrel in patients aged 75 years and older is generally not recommended and should be used with caution and only after a careful individual benefit/risk assessment by the physician, demonstrating that the benefits of preventing ischemic events outweigh the risk of serious bleeding. In phase 3 clinical trials, this group of patients had a higher risk of bleeding, including fatal bleeding, compared with patients aged <75 years. If necessary, a lower maintenance dose (5 mg) should be used; a maintenance dose of 10 mg is not recommended (see sections 4.2 and 4.8).

Therapeutic experience with prasugrel is limited in patients with renal impairment, including patients with TNN, and in patients with moderate hepatic impairment. These patients may be at increased risk of bleeding. Therefore, prasugrel should be used with caution in these patients.

Patients should be advised that it may take longer than usual to stop bleeding when they are taking prasugrel (in combination with ASA) and that they should report any unusual bleeding (site or duration) to their doctor.

In a clinical trial of patients with STEMI (ACCOAST), where patients were scheduled to undergo coronary angiography within 2-48 hours of randomization, a loading dose of prasugrel administered on average 4 hours before coronary angiography increased the risk of major and minor periprocedural bleeding compared with a loading dose of prasugrel administered during PCI. Therefore, in patients with STEMI/STEMI who undergo coronary angiography within 48 hours of presentation, the loading dose should be administered at the time of PCI. (See sections 5.1, 5.2, and 4.8).

Surgery

When planning surgery or prescribing new medications, patients should inform their doctor, including dentists, about the use of prasugrel.

If the patient requires elective surgery and the antiplatelet effect is undesirable, prasugrel should be discontinued 7 days prior to surgery. Patients undergoing CABG may experience an increase in the frequency (up to 3-fold) and severity of bleeding within 7 days of prasugrel discontinuation.

The benefits and risks of using prasugrel should be carefully assessed in patients in whom coronary anatomy has not been determined and urgent CABG is possible.

Hypersensitivity, including angioedema

Cases of hypersensitivity, including angioedema, have been reported in patients taking prasugrel, including patients with a history of hypersensitivity reactions to other thienopyridines.

Thrombotic thrombocytopenic purpura (TTP)

TTP has been reported with prasugrel treatment. TTP is a serious condition that can be fatal and requires urgent treatment.

Lactose

If you have been told by your doctor that you have an intolerance to some sugars, contact your doctor before taking this medicine.

Morphine and other opioids

Reduced efficacy of prasugrel has been observed in patients taking prasugrel in combination with morphine (see section “Interaction with other medicinal products and other types of interactions”).

Use during pregnancy or breastfeeding

Clinical studies involving pregnant or breastfeeding women have not been conducted.

Pregnancy

Animal studies do not indicate direct adverse effects with respect to pregnancy, embryonic or postnatal development. Prasugrel should be used during pregnancy only if the potential benefit to the mother justifies the potential risk to the fetus.

Breastfeeding period

It is not known whether prasugrel is excreted in human milk. Animal studies have shown excretion of prasugrel in breast milk. Use of the drug is not recommended during breastfeeding.

Fertility

Prasugrel had no effect on the fertility of male and female rats when administered orally at a dose 240 times the recommended daily human maintenance dose (based on mg/m2).

Ability to influence reaction speed when driving vehicles or other mechanisms

The effect of prasugrel on the ability to drive and use machines has not been established.

Method of administration and doses

Adults.

Prasugrel is started with a single loading dose of 60 mg. A maintenance dose of 10 mg is then given daily. Patients with STEMI/STEMI who undergo coronary angiography within 48 hours of admission should receive a loading dose only at the time of PCI. Patients taking prasugrel should also receive daily ASA (75-325 mg/day).

In patients with ACS who have undergone PCI, premature discontinuation of any antiplatelet therapy, including prasugrel, may lead to an increased risk of thrombosis, myocardial infarction, or death from the underlying disease. It is recommended to continue treatment for up to 12 months unless there are indications for discontinuation of prasugrel (see sections 5.1 and 4.4).

The drug in this dosage is not used in patients over 75 years of age.

The drug in this dosage is not used in patients with a body weight of less than 60 kg.

Kidney failure.

No dose adjustment is required in patients with renal impairment, including patients with end-stage renal disease. Experience with prasugrel in patients with renal impairment is limited.

Liver failure.

No dose adjustment is required in patients with mild to moderate hepatic impairment (Child-Pugh class A and B). There is limited experience in patients with mild to moderate hepatic impairment.

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