Prescription Required
Manufacturer
APOTEX CORP
SKU
60505464203

prasugrel 5 mg tablet (generic effient)

Generic
Out of Stock

Uses

Acute Coronary Syndromes

Patients Undergoing Percutaneous Coronary Intervention

Prasugrel hydrochloride is used in combination with aspirin for the reduction of thrombotic cardiovascular events (e.g., stent thrombosis, myocardial infarction [MI]) in patients with acute coronary syndrome (ACS) undergoing percutaneous coronary intervention (PCI). Prasugrel is used in patients with unstable angina or non-ST-segment-elevation MI (NSTEMI) undergoing PCI and in patients with ST-segment-elevation MI (STEMI) managed with primary or nonprimary/delayed (i.e., after medical treatment for STEMI) PCI.

Dual-drug antiplatelet therapy with a P2Y12 platelet adenosine diphosphate (ADP)-receptor antagonist (e.g., clopidogrel, prasugrel, ticagrelor) and aspirin is part of the current standard of care in patients with ACS. The American Heart Association (AHA), the American College of Cardiology Foundation (ACCF), the Society for Cardiovascular Angiography and Interventions (SCAI), and the American College of Chest Physicians (ACCP) recommend antiplatelet therapy with a P2Y12-receptor antagonist (clopidogrel, prasugrel, or ticagrelor) in conjunction with aspirin for treatment and secondary prevention in patients with ACS. These experts generally recommend ticagrelor or clopidogrel as the P2Y12-receptor antagonist in patients with ACS who are treated medically without stent placement; because prasugrel has been studied principally in patients undergoing planned PCI, recommendations for the use of this drug are restricted to that population. In patients undergoing PCI with stent placement (bare-metal or drug-eluting), a loading dose of ticagrelor, clopidogrel, or prasugrel is recommended, followed by maintenance therapy with one of these agents for at least 12 months (unless the risk of bleeding outweighs the anticipated net benefit of therapy); aspirin should be continued indefinitely in such patients. There is some evidence suggesting that a longer duration of dual antiplatelet therapy (for more than 12 months) may be beneficial in some patients with drug-eluting stents to reduce the risk of late stent thrombosis and other cardiovascular events, but such prolonged therapy may be associated with an increased risk of bleeding and other adverse effects.(See Discontinuance of Therapy under Warnings/Precautions: Warnings, in Cautions.)

Current ACCF/AHA guidelines make no recommendations regarding the P2Y12-receptor antagonist of choice in patients with ACS. Unlike clopidogrel, genetic polymorphism of the cytochrome P-450 (CYP) 2C19 isoenzyme does not appear to affect the pharmacodynamic or clinical response to prasugrel; therefore, some experts recommend the use of prasugrel as an alternative to clopidogrel in patients who are identified as potential poor metabolizers of clopidogrel. In preclinical and early clinical studies, prasugrel inhibited platelet aggregation more potently and rapidly than standard or higher dosages of clopidogrel and was associated with less interpatient variability in antiplatelet effects. Such improved inhibition of platelet aggregation was associated with reduced ischemic events (e.g., reductions in stent thrombosis and MI) in a large prospective randomized study of patients with ACS undergoing PCI; however, these benefits were accompanied by an increased risk of bleeding. When considering the use of prasugrel over other P2Y12-receptor antagonists, clinicians should balance the anticipated greater benefits with prasugrel against the increased risk of bleeding, and also consider the patient populations in whom the drugs have been used. Some evidence suggests that certain patient populations (e.g., those with diabetes or previous MI) are more likely to benefit from prasugrel's greater inhibition of platelet aggregation, while others (e.g., geriatric patients, those with low body weight or history of stroke/transient ischemic attack [TIA]) may experience harm.

Because of the substantial risk of serious bleeding, prasugrel should not be initiated in patients who are likely to undergo urgent coronary artery bypass grafting (CABG); when possible, therapy with the drug should be discontinued at least 7 days prior to any surgery.(See Bleeding, under Warnings/Precautions: Warnings, in Cautions.) In addition, prasugrel should not be used in patients with a history of TIA or stroke.(See Cautions: Contraindications.)

The current indication for prasugrel is based principally on results of a multicenter, randomized, double-blind parallel group study (Trial to Assess Improvement in Therapeutic Outcomes by Optimizing Platelet Inhibition with Prasugrel-Thrombolysis in Myocardial Infarction [TRITON-TIMI 38]) comparing efficacy and safety of prasugrel and clopidogrel in 13,608 patients with moderate- to high-risk ACS undergoing planned PCI. Patients with unstable angina or NSTEMI were eligible if they had ischemic manifestations lasting 10 minutes or more within 72 hours prior to randomization, a TIMI risk score of at least 3, and either ST-segment deviation of at least 1 mm or elevated levels of a cardiac biomarker of necrosis; patients with STEMI were enrolled within 12 hours of symptom onset if primary PCI was planned or within 14 days after receiving medical treatment for STEMI (nonprimary/delayed PCI). Patients received either clopidogrel (300-mg loading dose followed by 75 mg daily) or prasugrel (60-mg loading dose followed by 10 mg daily) for 6-15 months. The loading dose of the study drug was administered anytime between randomization and 1 hour after the patient was transferred from the cardiac catheterization laboratory; most patients (approximately 75%) received the study drug after the first coronary guidewire was placed or within 1 hour of PCI. Patients were required to receive concomitant treatment with aspirin 75-325 mg daily; other standard therapies (e.g., heparin, platelet glycoprotein [GP] IIb/IIIa-receptor inhibitors) were given at the discretion of the treating clinician. Most patients (94%) received at least one intracoronary stent.

Treatment with prasugrel resulted in a 19% relative reduction in the composite primary end point of cardiovascular death, nonfatal MI, or nonfatal stroke compared with clopidogrel; such benefits were apparent within 3 days and persisted throughout the duration of the study (median 14.5 months). The reduction in the primary end point was largely driven by a substantial reduction in MI (new or recurrent) with little or no difference in the incidence of stroke or cardiovascular death (other than from MI) between groups. Reductions in the rate of stent thrombosis and urgent target-vessel revascularization also favored prasugrel. Stent thrombosis was substantially reduced with prasugrel in patients who received at least one intracoronary stent irrespective of the stent type (bare-metal or drug-eluting).

The benefit of prasugrel in reducing ischemic events in the TRITON-TIMI 38 study was accompanied by an increased risk of bleeding. Major and minor bleeding complications, including life-threatening and fatal bleeding, occurred more frequently in patients receiving prasugrel compared with clopidogrel.(See Bleeding under Warnings/Precautions: Warnings, in Cautions.) When efficacy and bleeding end points were combined, the net clinical benefit (defined as death from any cause, nonfatal MI, nonfatal stroke, or non-CABG-related nonfatal TIMI major hemorrhage) favored prasugrel over clopidogrel in the overall study population, but not in all subgroups. In post hoc analyses, patients 75 years of age or older, those weighing less than 60 kg, and those with previous stroke or TIA were identified as subgroups experiencing no net clinical benefit and possibly harm with such therapy. In patients with diabetes mellitus, however, a trend towards greater efficacy of prasugrel compared with nondiabetics was noted without a relative increase in major bleeding. Results of such subgroup analyses should be considered exploratory and should be interpreted with caution.

The prasugrel dosage regimen used in the TRITON-TIMI 38 study (60-mg loading dose, 10 mg daily maintenance dosage) has been shown to produce substantially greater and more consistent inhibition of platelet aggregation than that produced by a clopidogrel loading dose of 600 mg and maintenance dosage of 150 mg daily, dosages higher than current FDA-labeled loading and maintenance dosages. In addition, while it is generally recommended that antiplatelet agents be administered promptly upon presentation or diagnosis in patients with ACS, administration of prasugrel and clopidogrel in the TRITON-TIMI 38 study was delayed until after coronary anatomy was determined to be appropriate for PCI. Therefore, this study does not provide information on the comparative efficacy and safety of clopidogrel and prasugrel in dosages that provide equivalent inhibition of platelet aggregation, nor does it directly address the potential effects on efficacy of routine pretreatment with clopidogrel or prasugrel before diagnostic cardiac catheterization.

Increased risk of bleeding is a concern in patients receiving antiplatelet agents who require urgent CABG. Because most patients with ACS are managed without CABG, pretreatment with prasugrel may be considered prior to performing diagnostic coronary angiography in patients who are not likely to undergo CABG. The potential benefits of pretreatment should be balanced against the risk of surgical bleeding in patients who may subsequently require CABG.

Dosage and Administration

Administration

Prasugrel hydrochloride is administered orally without regard to meals. Dosage of prasugrel hydrochloride is expressed in terms of prasugrel.

Dosage

Acute Coronary Syndromes

Patients Undergoing PCI

For the reduction of thrombotic cardiovascular events in patients with an acute coronary syndrome (ACS) undergoing percutaneous coronary intervention (PCI), the manufacturer recommends a loading dose of 60 mg of prasugrel, followed by 10 mg once daily. Aspirin (75-325 mg daily) should be given concomitantly. The majority of patients in the TRITON-TIMI 38 study received the loading dose of prasugrel after the first coronary guidewire was placed or within 1 hour of PCI. The American College of Cardiology Foundation (ACCF) and the American Heart Association (AHA) recommend that the loading dose of prasugrel be initiated as soon as possible or at the time of PCI in patients with ST-segment-elevation myocardial infarction (STEMI) undergoing primary PCI. Experts state that a prasugrel loading dose of 60 mg is reasonable in patients undergoing delayed PCI after initial thrombolytic therapy who did not previously receive a loading dose of clopidogrel; prasugrel should not be administered sooner than 24 hours after a fibrin-specific thrombolytic agent.

A prasugrel maintenance dosage of 5 mg daily may be considered in patients weighing less than 60 kg, although safety and efficacy of this lower dosage has not been established.(See Bleeding under Warnings/Precautions: Warnings, in Cautions.)

The optimum duration of prasugrel therapy has not been determined. However, in patients undergoing PCI with stent implantation, premature discontinuance of any antiplatelet therapy (i.e., aspirin, a P2Y12-receptor antagonist) increases the risk of stent thrombosis, myocardial infarction, and death; therefore, long-term (e.g., at least 12 months) dual antiplatelet therapy is recommended in such patients unless the risk of bleeding outweighs the anticipated net benefit.

Adjunctive Antithrombotic Therapy

Adjunctive antithrombotic therapy with daily aspirin (e.g., 75-325 mg) is recommended in all patients with ACS, including those undergoing PCI. For additional information on the dosage of aspirin used as adjunctive antithrombotic therapy in the management of ACS, .

Discontinuance in Patients Undergoing Invasive Procedures

Thienopyridines, including prasugrel, should be discontinued prior to elective surgery. In patients who require elective coronary artery bypass grafting (CABG), discontinuance of prasugrel therapy is recommended at least 7 days prior to surgery. Prasugrel should not be initiated in those who are likely to undergo emergent CABG. To minimize the risk of adverse cardiac events, thienopyridines, including prasugrel, and other antiplatelet therapy should be resumed as soon as possible after temporary discontinuance of therapy for adverse effects or invasive procedures.(See Discontinuance of Therapy under Warnings/Precautions: Warnings, in Cautions.)

Special Populations

No dosage adjustment necessary in patients with renal impairment.

No dosage adjustment necessary in patients with mild to moderate hepatic impairment (Child-Pugh Class A and B). Not studied in patients with severe hepatic disease.

Not known whether dosage adjustments based on age, weight or other patient characteristics will maintain effectiveness of prasugrel while decreasing risk of bleeding.

Cautions

Contraindications

Presence of active pathological bleeding (e.g., peptic ulcer, intracranial hemorrhage).

History of transient ischemic attack (TIA) or stroke.

Warnings/Precautions

Warnings

Bleeding

Use of prasugrel is associated with a risk of serious, sometimes fatal bleeding. Major bleeding (defined as intracranial hemorrhage or clinically overt bleeding associated with a decline in hemoglobin concentration of at least 5 g/dL) and minor bleeding (defined as overt bleeding with a decrease in hemoglobin concentration of at least 3 g/dL but less than 5 g/dL) were more frequent in patients receiving prasugrel versus clopidogrel in the TRITON-TIMI 38 study. Major hemorrhage not related to coronary artery bypass grafting (CABG) occurred in 2.4% of patients receiving prasugrel compared with 1.8% of those receiving clopidogrel; this included higher rates of life-threatening and fatal bleeding. Life-threatening bleeding occurred mostly at GI, intracranial, retroperitoneal, or puncture sites. CABG-related major bleeding occurred in 13.4% of patients receiving prasugrel versus 3.2% of those receiving clopidogrel.(See Bleeding Related to Coronary Artery Bypass Grafting under Warnings/Precautions: Warnings, in Cautions.) Subgroup analysis indicated that patients 75 years of age or older, those weighing less than 60 kg, and those with prior stroke or TIA had higher rates of bleeding than patients without these characteristics. Additional risk factors for bleeding include recent trauma, recent surgery (e.g., CABG), recent or recurrent GI bleeding, active peptic ulcer disease, severe hepatic impairment, and concurrent use of drugs that increase risk of bleeding (e.g., oral anticoagulants, sustained use of nonsteroidal anti-inflammatory agents, thrombolytic agents).

Prasugrel should not be used in patients who are actively bleeding and/or who have a history of stroke or TIA. The drug also should not be initiated in those who are likely to undergo emergent CABG. Bleeding should be suspected in any patient who is hypotensive and has recently undergone coronary angiography, percutaneous coronary intervention (PCI), CABG, or any other surgical procedure, even if there are no overt manifestations of bleeding. Risk of bleeding appears to be highest in the first several days of therapy. If possible, bleeding should be managed without discontinuing prasugrel; premature discontinuance is associated with an increased risk of subsequent cardiovascular events.(See Discontinuance of Therapy under Warnings/Precautions: Warnings, in Cautions.) If bleeding occurs, platelet transfusions may be given to restore homeostasis; however, such transfusions may be less effective within 6 hours of a loading dose or 4 hours of a maintenance dose. Withholding a dose of prasugrel is unlikely to resolve a bleeding episode or prevent bleeding associated with an invasive procedure because of the drug's prolonged inhibitory effects on platelet aggregation.

Cerebrovascular Events

In the TRITON-TIMI 38 study, patients with a history of TIA or ischemic stroke had no evidence of a clinical benefit from prasugrel and a strong trend towards a higher rate of major bleeding compared with clopidogrel. In this subgroup, a higher incidence of stroke was observed during treatment with prasugrel compared with clopidogrel (6.5 or 1.2%, respectively). In patients without such a history, the incidence of stroke was similar (0.9 or 1%, respectively) between treatment groups. Strokes occurring in patients receiving prasugrel were both thrombotic and hemorrhagic, while those reported with clopidogrel were all thrombotic. Based on these findings, prasugrel should not be initiated in patients with a history of stroke or TIA and generally should be discontinued in those who experience an adverse cerebrovascular event during therapy.

Bleeding Related to Coronary Artery Bypass Grafting

Risk of bleeding is increased in patients receiving prasugrel who undergo CABG.(See Bleeding under Warnings/Precautions: Warnings, in Cautions.) CABG-related major and minor bleeding events occurred more frequently in patients receiving prasugrel than with clopidogrel in the TRITON-TIMI 38 study (14.1 versus 4.5%, respectively). Bleeding was reported in 26.7 or 5% of those who received prasugrel or clopidogrel, respectively, within 3 days prior to CABG. Although the bleeding risk decreased in both groups when the last dose of study drug was given 4-7 days prior to surgery, the incidence of bleeding remained comparatively higher in the prasugrel-treated group (11.3 versus 3.4%, respectively). Prasugrel should not be initiated in patients who are likely to undergo urgent CABG. In patients scheduled for CABG, prasugrel should be discontinued at least 7 days prior to surgery. CABG-related bleeding may be treated with blood product transfusions (e.g., packed red blood cells, platelets); however, platelet transfusions within 6 hours of a loading dose or 4 hours of a maintenance dose of prasugrel may be less effective in restoring homeostasis.

Discontinuance of Therapy

Prasugrel should be discontinued in patients who develop active bleeding, stroke, or TIA during therapy.(See Cautions: Contraindications.) The drug also should be discontinued prior to elective surgery to minimize risk of bleeding, but should be reinitiated postoperatively as soon as possible (e.g., once adequate hemostasis has been established).

In general, treatment with a thienopyridine derivative should not be discontinued prematurely, particularly in the first few weeks after an acute coronary syndrome (ACS), because of the subsequent increased risk of cardiovascular events. Premature discontinuance of any antiplatelet therapy (e.g., thienopyridine derivative, aspirin) in patients undergoing PCI and coronary artery stent placement has been associated with an increased risk of stent thrombosis, myocardial infarction (MI), and/or death. Because of the risk of late stent thrombosis and other cardiovascular events in patients with drug-eluting stents, experts recommend at least 12 months of dual antiplatelet therapy in such patients. Some evidence suggests that an even longer duration of dual antiplatelet therapy (for more than 12 months) may be beneficial in some patients with drug-eluting stents. Preliminary results of the DAPT (Dual Antiplatelet Therapy) study, a randomized, placebo-controlled, double-blind study, found that patients who received 30 months of dual antiplatelet therapy (aspirin plus clopidogrel or prasugrel) following placement of a drug-eluting stent had substantially reduced rates of stent thrombosis and major adverse cardiovascular and cerebrovascular events compared with those who received 12 months of dual antiplatelet therapy. However, the longer duration of therapy was associated with a higher incidence of moderate to severe bleeding and also an unexpected finding of an increased rate of noncardiovascular mortality (principally related to trauma or cancer). In November 2014, FDA issued a drug safety communication to alert health care professionals about these findings. At this time, the FDA has not reached any conclusions about the results of the DAPT study and is continuing to evaluate the information as well as other available data. FDA currently believes that the benefits of prasugrel continue to outweigh its potential risks when used appropriately according to the manufacturer's prescribing information; patients should continue to take prasugrel as directed and clinicians should not change their current prescribing practices at this time.

Patients should be advised to never stop prasugrel without first consulting their prescribing clinician, even if instructed by another health-care professional (e.g., dentist) to stop such therapy. Prior to scheduling an invasive procedure, patients should inform their clinicians (including dentists) that they currently are taking prasugrel, and clinicians performing the invasive procedure should consult with the prescribing clinician before discontinuing prasugrel therapy. If prasugrel must be temporarily discontinued because of an adverse event, therapy should be reinstituted as soon as possible.

Thrombotic Thrombocytopenic Purpura

Thrombotic thrombocytopenic purpura (TTP) has been reported rarely with use of thienopyridine derivatives, sometimes after brief exposure (less than 2 weeks). TTP is a potentially fatal condition that is characterized by thrombocytopenia, microangiopathic hemolytic anemia (schistocytes on peripheral blood smear), neurologic findings, renal dysfunction, and fever. Urgent treatment (e.g., plasmapheresis) is required in patients who develop TTP.

Specific Populations

Pregnancy

Category B.

Lactation

Prasugrel metabolites are distributed into milk in rats; not known whether the drug is distributed into milk in humans. The drug should be used in nursing women only if the anticipated benefits to the mother outweigh potential risks to the infant.

Pediatric Use

Safety and efficacy have not been established in pediatric patients.

Geriatric Use

Geriatric patients, particularly those 75 years of age and older, appear to be at greater risk of bleeding (including fatal bleeding) with prasugrel therapy compared with younger patients. In the TRITON-TIMI 38 trial, about 39% of patients were 65 years of age or older and 13% were 75 years of age or older. Risk of bleeding increased with advancing age in both prasugrel and clopidogrel treatment groups. Among patients 75 years of age or older, fatal bleeding was more common with prasugrel than with clopidogrel (1 or 0.1%, respectively); symptomatic intracranial hemorrhage also was reported more frequently with prasugrel (0.8 or 0.3%, respectively). Mean exposure to the active metabolite of prasugrel is approximately 19% higher in patients 75 years or older compared with younger patients. Prasugrel generally should be avoided in patients 75 years of age or older because of a higher risk of bleeding and uncertain efficacy, but use may be considered in certain patients with high-risk conditions (e.g., diabetes, previous MI) in whom a greater net clinical benefit has been demonstrated.

Hepatic Impairment

Pharmacokinetics of prasugrel's active metabolite and its inhibition of platelet aggregation are similar in patients with mild to moderate hepatic impairment (Child-Pugh Class A and B) and healthy individuals. The pharmacokinetics and pharmacodynamics of the drug have not been specifically studied in patients with severe hepatic impairment; however, such patients generally are at higher risk of bleeding.

Renal Impairment

Pharmacokinetics of prasugrel's active metabolite and its inhibition of platelet aggregation in patients with moderate renal impairment (creatinine clearance of 30-50 mL/minute) are similar to that observed in healthy individuals. In patients with end-stage renal impairment, exposure to the active metabolite was decreased to about half that of healthy individuals and those with moderate renal impairment.

Low Body Weight

In the TRITON-TIMI 38 study, patients with low body weight (less than 60 kg) had an increased exposure to the active metabolite of prasugrel and an increased risk of bleeding. Clearance of prasugrel's active metabolite appears to increase exponentially with increasing body weight.(See Bleeding under Warnings/Precautions: Warnings, in Cautions.)

Common Adverse Effects

Bleeding, including life-threatening and fatal bleeding events, was the most commonly reported adverse effect in the TRITON-TIMI 38 study. Other nonhemorrhagic treatment-related adverse effects reported in at least 2.5% of patients in the TRITON-TIMI 38 study included hypertension, hypercholesterolemia/hyperlipidemia, headache, back pain, dyspnea, nausea, dizziness, cough, hypotension, fatigue, noncardiac chest pain, atrial fibrillation, bradycardia, leukopenia (white blood cells less than 4000/mm), rash, pyrexia, peripheral edema, extremity pain, and diarrhea.

Drug Interactions

Drugs Affecting Gastric Acidity

May be used concomitantly with proton pump inhibitors and histamine H2-receptor antagonists. Maximum plasma concentrations of the active metabolite of prasugrel are decreased by 14 or 29% with ranitidine or lansoprazole, respectively, but systemic exposure of this metabolite is unaffected. In a pharmacokinetic study in healthy adults, concomitant daily administration of a single loading dose of prasugrel 60 mg with lansoprazole 30 mg decreased systemic exposure and peak plasma concentrations of prasugrel's active metabolite but did not affect inhibition of platelet aggregation.

Drugs Affecting or Metabolized by Hepatic Microsomal Enzymes

Prasugrel is metabolized by the cytochrome P-450 (CYP) microsomal enzyme system, principally by isoenzymes 3A4 and 2B6, and to a lesser extent by isoenzymes 2C9 and 2C19. In vitro studies indicate that prasugrel is not likely to inhibit CYP isoenzymes 1A2, 2C9, 2C19, 2D6, and 3A or induce CYP isoenzymes 1A2 or 3A. Prasugrel is a weak inhibitor of CYP2B6.

Clinically important drug interactions mediated by CYP isoenzymes are considered unlikely with prasugrel. Studies have shown that if one of the CYP isoenzymes involved in the metabolism of prasugrel is inhibited, others remain capable of forming the active metabolite. CYP3A4 inhibitors such as verapamil, diltiazem, indinavir, ciprofloxacin, clarithromycin, and grapefruit juice are not expected to have a substantial effect on the pharmacokinetics of prasugrel's active metabolite. In healthy individuals receiving prasugrel, concomitant administration of ketoconazole (a potent inhibitor of CYP3A4) decreased maximum concentrations of prasugrel's active metabolite by 34-46%, but did not alter systemic exposure or degree of inhibition of platelet aggregation. Similarly, CYP3A4 inducers (e.g., rifampin, carbamazepine) are not expected to substantially alter the pharmacokinetic or pharmacodynamic response to prasugrel; concomitant administration of rifampin, a potent inducer of CYP3A4 and CYP2B6, did not affect formation of the active prasugrel metabolite nor its ability to inhibit platelet aggregation. Concomitant administration of prasugrel and drugs principally metabolized by CYP2B6 (e.g., halothane, cyclophosphamide, propofol, nevirapine) may increase plasma concentrations and exposure of the concomitant drug; however, clinically important interactions are not expected because of weak inhibition of CYP2B6.

Digoxin

May be administered concomitantly. Prasugrel is not an inhibitor of the P-glycoprotein transport system and is not expected to affect clearance of digoxin.

HMG-CoA Reductase Inhibitors (Statins)

May be used concomitantly without dosage adjustments. Coadministration of prasugrel and atorvastatin 80 mg daily had little effect on exposure to the active prasugrel metabolite and no effect on inhibition of platelet aggregation.

Nonsteroidal Anti-inflammatory Agents

Increased risk of bleeding with concomitant long-term use of aspirin or other nonsteroidal anti-inflammatory agents (NSAIAs).

Thrombolytic Agents

Increased risk of bleeding with concomitant use.

Warfarin

Increased risk of bleeding in patients receiving concomitant therapy with warfarin. Bleeding time substantially prolonged with concomitant administration of a single 15-mg dose of warfarin.

Other Antiplatelet or Antithrombotic Agents

The manufacturer states that prasugrel may be administered concomitantly with aspirin, heparin, and GP IIb/IIIa-receptor inhibitors. Concomitant use of prasugrel and aspirin 150 mg daily increased bleeding time compared with use of either drug alone, but inhibition of platelet aggregation was not altered. In a study in healthy individuals, concomitant use of prasugrel and aspirin 325 mg daily resulted in greater inhibition of platelet aggregation, but the combination was well tolerated; no clinically important bleeding events occurred. When a single IV dose of unfractionated heparin sodium 100 units/kg was given concomitantly with prasugrel, bleeding time was increased without any associated changes in coagulation or inhibition of platelet aggregation.

Although evidence from drug interaction studies generally is lacking, increased risk of bleeding is likely with concomitant use of prasugrel and other antiplatelet or antithrombotic agents; caution is advised.

Write Your Own Review
You're reviewing:PRASUGREL 5 MG TABLET (Generic Effient)
Your Rating