Prasugrel can cause significant, sometimes fatal, bleeding. Do not use prasugrel in patients with active pathological bleeding or a history of transient ischemic attack (TIA) or stroke.
In patients ≥75 years, prasugrel is generally not recommended because of the increased risk of fatal and intracranial bleeding and uncertain benefit, except in high-risk situations (patients with diabetes or a history of myocardial infarction [MI]) in which its effect appears to be greater and its use may be considered.
Do not start prasugrel in patients likely to undergo urgent coronary artery bypass graft (CABG) surgery. When possible, discontinue prasugrel at least 7 days prior to any surgery.
Additional risk factors for bleeding include body weight <60 kg, propensity to bleed, and concomitant use of medications that increase the risk of bleeding (eg, warfarin, heparin, fibrinolytic therapy, long-term use of nonsteroidal anti-inflammatory drugs [NSAIDs]).
Suspect bleeding in any patient who is hypotensive and has recently undergone coronary angiography, percutaneous coronary intervention (PCI), CABG, or other surgical procedures in the setting of prasugrel.
If possible, manage bleeding without discontinuing prasugrel. Discontinuing prasugrel, particularly in the first few weeks after acute coronary syndrome (ACS), increases the risk of subsequent cardiovascular events.
Note: Safety: Avoid use in patients with active bleeding or a history of stroke or transient ischemic attack. In patients who require concomitant therapeutic anticoagulation, antiplatelet selection and/or duration of therapy may differ in order to balance risks for thrombosis and bleeding (ACC [Kumbhani 2021]).
Acute coronary syndrome (non-ST-elevation myocardial infarction, unstable angina, or ST-elevation myocardial infarction) managed by percutaneous coronary intervention:
Note: For ST-elevation myocardial infarction managed with primary percutaneous coronary intervention (PCI), administer as early as possible after diagnosis. For non-ST-elevation acute coronary syndromes, administer after angiography once clinician decides to perform PCI; if PCI is not performed, use an alternative P2Y12 inhibitor (ACCF/AHA [O'Gara 2013]; AHA/ACC [Amsterdam 2014]; Montalescot 2013; Wiviott 2007). Some experts use an alternative P2Y12 inhibitor if angiography is delayed >3 hours (Cutlip 2021).
Oral:
Loading dose: 60 mg once before PCI in combination with aspirin and a parenteral anticoagulant; followed by maintenance dosing (ACCF/AHA [O’Gara, 2013]; AHA/ACC [Amsterdam 2014]).
Maintenance dose:
≥60 kg: 10 mg once daily in combination with aspirin beginning the day after PCI (ACCF/AHA [O'Gara 2013]; AHA/ACC [Amsterdam 2014]; Wiviott 2007).
East Asian descent: After 30 days, consider reducing to 5 mg once daily in patients of East Asian descent in order to decrease bleeding risk. Note: Patients of East Asian descent display a greater antiplatelet response compared to white patients. A reduced dose of prasugrel (5 mg once daily) after 30 days had a similar reduction in thrombotic events and fewer bleeding events compared to continuation of a higher maintenance dose (10 mg once daily) (Kim 2020; Levine 2014; Small 2010).
<60 kg (alternative agent): 5 mg once daily in combination with aspirin beginning the day after PCI (Erlinge 2012; manufacturer's labeling). Note: This dose adjustment is based on pharmacokinetic modeling and platelet inhibition data. Clinical efficacy has not been established. Accordingly, some experts recommend an alternative P2Y12 inhibitor in patients weighing <60 kg (Reeder 2020; Simons 2020).
Duration of therapy: Continue prasugrel plus aspirin (dual antiplatelet therapy [DAPT]) for ≥12 months unless bleeding is a major concern. If there have been no major bleeding complications after 12 months, continuation of DAPT may be considered. Reevaluate the need for DAPT at regular intervals based on bleeding and thrombotic risks. When DAPT is complete, discontinue prasugrel and continue aspirin indefinitely (ACC/AHA [Amsterdam 2014]; ACC/AHA [Levine 2016]; ACCF/AHA [O'Gara 2013]; Mauri 2014; Wiviott 2007).
Transitioning between P2Y12 inhibitors:
Note: This provides general guidance on transitioning between P2Y12 inhibitors.
Transitioning from another P2Y12 inhibitor to prasugrel:
Transitioning from clopidogrel:
≤30 days after acute coronary syndrome (ACS) or PCI: Give prasugrel 60 mg loading dose once (irrespective of timing of previous clopidogrel dose), followed the next day by 10 mg once daily (≥60 kg) or 5 mg once daily (<60 kg) (Angiolillo 2010; Angiolillo 2017; Payne 2008).
>30 days after ACS or PCI: Give prasugrel 10 mg once daily (≥60 kg) or 5 mg once daily (<60 kg) beginning 24 hours after the last dose of clopidogrel (Angiolillo 2010; Angiolillo 2017; Payne 2008).
Transitioning from ticagrelor: Give prasugrel 60 mg loading dose 12 to 24 hours after the last dose of ticagrelor, followed the next day by 10 mg once daily (≥60 kg) or 5 mg once daily (<60 kg) (Angiolillo 2014; Angiolillo 2017).
Dosage adjustment for concomitant therapy: Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.
No dosage adjustment necessary; use caution in moderate to severe impairment (patients are generally at higher risk of bleeding).
Hemodialysis: Not dialyzable (NCS/SCCM [Frontera 2016])
Mild to moderate hepatic impairment (Child-Pugh class A and B): No dosage adjustment necessary for mild-to-moderate hepatic impairment.
Severe hepatic impairment (Child-Pugh class C): There are no dosage adjustments provided in the manufacturer's labeling (has not been studied); use caution (patients are generally at higher risk of bleeding).
Patients ≥75 years of age: Use not recommended; may be considered in high-risk situations (eg, patients with diabetes or history of myocardial infarction). Refer to adult dosing.
Excipient information presented when available (limited, particularly for generics); consult specific product labeling.
Tablet, Oral:
Effient: 5 mg, 10 mg
Generic: 5 mg, 10 mg
Yes
Excipient information presented when available (limited, particularly for generics); consult specific product labeling. [DSC] = Discontinued product
Tablet, Oral:
Effient: 10 mg [DSC]
Generic: 10 mg
An FDA-approved patient medication guide, which is available with the product information and at https://www.accessdata.fda.gov/drugsatfda_docs/label/2020/022307s018lbl.pdf#page=21, must be dispensed with this medication.
Oral: Administer without regard to meals. In an emergent primary PCI setting, crushing the tablets (using a commercially available syringe crusher) and mixing with 25 mL of water led to faster absorption and a quicker, more potent antiplatelet effect seen as early as 30 minutes (Rollini 2016; Vogel 2021). In addition, according to the manufacturer, tablets may be chewed and swallowed (bitter to taste) or crushed and mixed in food or liquid (eg, applesauce, juice, water) and immediately administered by mouth or gastric tube. Administration via an enteral tube that bypasses the acidic environment of the stomach may result in reduced bioavailability of prasugrel (data on file, Daiichi Sankyo-Lilly 2012).
Acute coronary syndrome managed by percutaneous coronary intervention: To reduce the rate of thrombotic cardiovascular events (including stent thrombosis) in patients with acute coronary syndrome who are to be managed with percutaneous coronary intervention for unstable angina, non-ST-elevation myocardial infarction (MI), or ST-elevation MI.
Prasugrel may be confused with pravastatin, propranolol
Beers Criteria: Prasugrel is identified in the Beers Criteria as a potentially inappropriate medication to be used with caution in patients 75 years and older due to increased risk of bleeding in older adults; however, benefit in highest-risk older adults, such as those with prior MI or diabetes, may offset risk when used for approved indication of acute coronary syndrome to be managed by percutaneous coronary intervention (Beers Criteria [AGS 2019]).
The following adverse drug reactions and incidences are derived from product labeling unless otherwise specified.
1% to 10%:
Cardiovascular: Hypertension (8%), hypotension (4%), atrial fibrillation (3%), bradycardia (3%), peripheral edema (3%)
Central nervous system: Headache (6%), dizziness (4%), fatigue (4%), noncardiac chest pain (3%)
Dermatologic: Skin rash (3%)
Endocrine & metabolic: Hypercholesterolemia (≤7%), hyperlipidemia (≤7%)
Gastrointestinal: Nausea (5%), diarrhea (2%), gastrointestinal hemorrhage (2%)
Hematologic & oncologic: Leukopenia (3%), anemia (2%), major hemorrhage (2%), minor hemorrhage (2%), major hemorrhage (life-threatening: 1%)
Neuromuscular & skeletal: Back pain (5%), limb pain (3%)
Respiratory: Epistaxis (6%), dyspnea (5%), cough (4%)
Miscellaneous: Fever (3%)
<1%, postmarketing, and/or case reports: Abnormal hepatic function tests, anaphylaxis, angioedema, hematoma, hemoptysis, hemorrhage (requiring inotropes or transfusion), hypersensitivity reaction, intracranial hemorrhage (symptomatic), re-operation due to bleeding, thrombocytopenia, thrombotic thrombocytopenic purpura
Hypersensitivity (eg, anaphylaxis) to prasugrel or any component of the formulation; active pathological bleeding (eg, peptic ulcer, intracranial hemorrhage); prior transient ischemic attack or stroke.
Canadian labeling: Additional contraindications (not in US labeling): Severe hepatic impairment (Child-Pugh Class C).
Concerns related to adverse effects:
• Bleeding: [US Boxed Warning]: May cause significant, sometimes fatal, bleeding. Do not use prasugrel in patients with active pathological bleeding or a history of TIA or stroke. Additional risk factors for bleeding include body weight <60 kg, propensity to bleed (eg, recent trauma, recent surgery, recent or recurrent GI bleeding, active peptic ulcer disease, severe hepatic impairment, or moderate to severe renal impairment), and concomitant use of medications that increase the risk of bleeding (eg, warfarin, heparin, fibrinolytic therapy, long-term use of NSAIDs). Suspect bleeding in any patient who is hypotensive and has recently undergone coronary angiography, PCI, CABG, or other surgical procedures in the setting of prasugrel. If possible, manage bleeding without discontinuing prasugrel. Discontinuing prasugrel, particularly in the first few weeks after ACS, increases the risk of subsequent cardiovascular events. Management of bleeding episodes includes the use of PRBCs and platelet transfusion.
• Hypersensitivity: Hypersensitivity, including angioedema, has been reported, including in patients with a previous history of thienopyridine hypersensitivity. Because of structural similarities, cross-reactivity is possible among the thienopyridines (clopidogrel, prasugrel, and ticlopidine); use with caution or avoid in patients with previous history of thienopyridine hypersensitivity. Use of prasugrel is contraindicated in patients with hypersensitivity (eg, anaphylaxis) to prasugrel.
• Thrombotic thrombocytopenic purpura (TTP): Cases of TTP (usually occurring within the first 2 weeks of therapy), resulting in some fatalities, have been reported with prasugrel; urgent plasmapheresis is required.
Disease-related concerns:
• GI disease: Use with caution in patients with recent or recurrent GI bleeding or active peptic ulcer disease (patients are generally at higher risk of bleeding).
• Hepatic impairment: Use with caution in patients with severe hepatic impairment (patients are generally at higher risk of bleeding).
• Renal impairment: Use with caution in patients with moderate to severe renal impairment (patients are generally at higher risk of bleeding).
Special populations:
• Elderly: [US Boxed Warning]: In patients ≥75 years, use is generally not recommended due to increased risk of fatal and intracranial bleeding and uncertain benefit, except in high-risk situations (patients with diabetes or a history of MI) in which its effect appears to be greater and its use may be considered.
• Lower GI bleed patients: An individualized and multidisciplinary approach should be utilized to determine therapy discontinuation and management in patients with acute lower GI bleed (LGIB) who are on antiplatelet medications; risk of ongoing bleeding should be weighed with risk of thromboembolic events. In patients receiving dual antiplatelet therapy (aspirin plus P2Y12 receptor blocker [eg, clopidogrel, prasugrel, ticagrelor, ticlopidine]) or thienopyridine monotherapy, the thienopyridine should generally be resumed as soon as possible and at least within 7 days, taking into account control of bleeding and cardiovascular risk (aspirin should not be discontinued); however, dual antiplatelet therapy should not be discontinued in the 90 days post-acute coronary syndrome or 30 days post-coronary stenting (Strate 2016).
• Low-weight patients: In patients weighing <60 kg, risk of bleeding increased; consider lower maintenance dose.
• Surgical patients: [US Boxed Warning]: Do not initiate therapy in patients likely to undergo urgent CABG surgery; when possible, discontinue ≥7 days prior to any surgery; increased risk of bleeding. The American College of Chest Physicians (ACCP) recommends discontinuing prasugrel 5 days before surgery (Guyatt 2012). When urgent CABG is necessary, the ACCF/AHA suggests that it may be reasonable to perform surgery within 7 days of discontinuing prasugrel especially if the benefits of prompt revascularization outweigh the risks of bleeding (ACCF/AHA [Hillis 2011]; ACCF/AHA [O’Gara 2013]). Elective noncardiac surgery should not be performed in patients in whom dual antiplatelet therapy (DAPT) will need to be discontinued perioperatively within 30 days following bare metal stent (BMS) placement or within 12 months after drug-eluting stent (DES) placement. In patients undergoing urgent noncardiac surgery during the first 4 to 6 weeks after BMS or DES placement, continue DAPT. In patients with stents undergoing surgery that requires discontinuation of the P2Y12 inhibitor (eg, clopidogrel), continue aspirin and re-start the P2Y12 inhibitor as soon as possible after surgery (ACC/AHA [Fleisher 2014]).
Other warnings/precautions:
• Drug discontinuation: Discontinue therapy for active bleeding, elective surgery, stroke, or TIA; reinitiate therapy as soon as possible unless patient suffers stroke or TIA where subsequent use is contraindicated; if possible, manage bleeding without discontinuing therapy since premature discontinuation of treatment may cause increased risk for cardiac adverse events; lapses in treatment should be avoided.
Substrate of CYP2B6 (minor), CYP3A4 (minor); Note: Assignment of Major/Minor substrate status based on clinically relevant drug interaction potential
Abrocitinib: Agents with Antiplatelet Properties may enhance the antiplatelet effect of Abrocitinib. Management: Do not use antiplatelet drugs with abrocitinib during the first 3 months of abrocitinib therapy. The abrocitinib prescribing information lists this combination as contraindicated. This does not apply to low dose aspirin (81 mg/day or less). Risk X: Avoid combination
Acalabrutinib: May enhance the antiplatelet effect of Agents with Antiplatelet Properties. Risk C: Monitor therapy
Agents with Antiplatelet Properties (e.g., P2Y12 inhibitors, NSAIDs, SSRIs, etc.): May enhance the antiplatelet effect of other Agents with Antiplatelet Properties. Risk C: Monitor therapy
Anticoagulants: Agents with Antiplatelet Properties may enhance the anticoagulant effect of Anticoagulants. Risk C: Monitor therapy
Apixaban: Antiplatelet Agents (P2Y12 Inhibitors) may enhance the adverse/toxic effect of Apixaban. Specifically, the risk for bleeding may be increased. Management: Carefully consider risks and benefits of this combination and monitor closely; Canadian labeling recommends avoiding prasugrel or ticagrelor. Risk D: Consider therapy modification
Bemiparin: Agents with Antiplatelet Properties may enhance the anticoagulant effect of Bemiparin. Management: Avoid concomitant use of bemiparin with antiplatelet agents. If concomitant use is unavoidable, monitor closely for signs and symptoms of bleeding. Risk D: Consider therapy modification
Cangrelor: May diminish the antiplatelet effect of Prasugrel. More specifically, while the use of Cangrelor is expected to increase total platelet inhibition in patients who have previously received Prasugrel, Cangrelor is expected to decrease binding of Prasugrel metabolites to P2Y12 receptors and thus reduce the extent of irreversible platelet inhibition. Management: Avoid administration of prasugrel until cangrelor is discontinued. Risk D: Consider therapy modification
Cephalothin: Agents with Antiplatelet Properties may enhance the adverse/toxic effect of Cephalothin. Specifically, the risk for bleeding may be increased. Risk C: Monitor therapy
Collagenase (Systemic): Agents with Antiplatelet Properties may enhance the adverse/toxic effect of Collagenase (Systemic). Specifically, the risk of injection site bruising and or bleeding may be increased. Risk C: Monitor therapy
Dabigatran Etexilate: Antiplatelet Agents (P2Y12 Inhibitors) may enhance the adverse/toxic effect of Dabigatran Etexilate. Specifically, the risk of bleeding may be increased. Antiplatelet Agents (P2Y12 Inhibitors) may increase the serum concentration of Dabigatran Etexilate. Specifically, clopidogrel may increase dabigatran serum concentrations. Management: Carefully consider risks and benefits of this combination and monitor closely; Canadian labeling recommends avoiding prasugrel or ticagrelor. Risk D: Consider therapy modification
Dasatinib: May enhance the anticoagulant effect of Agents with Antiplatelet Properties. Risk C: Monitor therapy
Deoxycholic Acid: Agents with Antiplatelet Properties may enhance the adverse/toxic effect of Deoxycholic Acid. Specifically, the risk for bleeding or bruising in the treatment area may be increased. Risk C: Monitor therapy
Edoxaban: Antiplatelet Agents (P2Y12 Inhibitors) may enhance the adverse/toxic effect of Edoxaban. Specifically, the risk of bleeding may be increased. Management: Carefully consider the anticipated risks and benefits of this combination. If combined, increased monitoring for bleeding is recommended. Risk D: Consider therapy modification
Enoxaparin: Agents with Antiplatelet Properties may enhance the anticoagulant effect of Enoxaparin. Management: Discontinue antiplatelet agents prior to initiating enoxaparin whenever possible. If concomitant administration is unavoidable, monitor closely for signs and symptoms of bleeding. Risk D: Consider therapy modification
FentaNYL: May diminish the antiplatelet effect of Antiplatelet Agents (P2Y12 Inhibitors). FentaNYL may decrease the serum concentration of Antiplatelet Agents (P2Y12 Inhibitors). Risk C: Monitor therapy
Heparin: Agents with Antiplatelet Properties may enhance the anticoagulant effect of Heparin. Management: Decrease the dose of heparin or agents with antiplatelet properties if coadministration is required. Risk D: Consider therapy modification
Herbal Products with Anticoagulant/Antiplatelet Effects (eg, Alfalfa, Anise, Bilberry): May enhance the adverse/toxic effect of Agents with Antiplatelet Properties. Bleeding may occur. Risk C: Monitor therapy
Ibritumomab Tiuxetan: Agents with Antiplatelet Properties may enhance the adverse/toxic effect of Ibritumomab Tiuxetan. Both agents may contribute to impaired platelet function and an increased risk of bleeding. Risk C: Monitor therapy
Ibrutinib: May enhance the adverse/toxic effect of Agents with Antiplatelet Properties. Risk C: Monitor therapy
Icosapent Ethyl: May enhance the antiplatelet effect of Agents with Antiplatelet Properties. Risk C: Monitor therapy
Inotersen: May enhance the antiplatelet effect of Agents with Antiplatelet Properties. Risk C: Monitor therapy
Limaprost: May enhance the antiplatelet effect of Agents with Antiplatelet Properties. Risk C: Monitor therapy
Lipid Emulsion (Fish Oil Based): May enhance the adverse/toxic effect of Agents with Antiplatelet Properties. Risk C: Monitor therapy
Morphine (Systemic): May diminish the antiplatelet effect of Antiplatelet Agents (P2Y12 Inhibitors). Morphine (Systemic) may decrease the serum concentration of Antiplatelet Agents (P2Y12 Inhibitors). Management: Consider alternative anti-ischemic/analgesic therapies (eg, beta-blockers, nitroglycerin) in patients with acute coronary syndromes treated with a P2Y12 inhibitor when possible. The risks associated with other opioids are unknown. Risk D: Consider therapy modification
Multivitamins/Fluoride (with ADE): May enhance the antiplatelet effect of Agents with Antiplatelet Properties. Risk C: Monitor therapy
Multivitamins/Minerals (with ADEK, Folate, Iron): May enhance the antiplatelet effect of Agents with Antiplatelet Properties. Risk C: Monitor therapy
Multivitamins/Minerals (with AE, No Iron): May enhance the antiplatelet effect of Agents with Antiplatelet Properties. Risk C: Monitor therapy
Obinutuzumab: Agents with Antiplatelet Properties may enhance the adverse/toxic effect of Obinutuzumab. Specifically, the risk of serious bleeding-related events may be increased. Risk C: Monitor therapy
Omega-3 Fatty Acids: May enhance the antiplatelet effect of Agents with Antiplatelet Properties. Risk C: Monitor therapy
Pentosan Polysulfate Sodium: May enhance the adverse/toxic effect of Agents with Antiplatelet Properties. Specifically, the risk of bleeding may be increased by concurrent use of these agents. Risk C: Monitor therapy
Pentoxifylline: May enhance the antiplatelet effect of Agents with Antiplatelet Properties. Risk C: Monitor therapy
Prostacyclin Analogues: May enhance the antiplatelet effect of Agents with Antiplatelet Properties. Risk C: Monitor therapy
Rivaroxaban: Antiplatelet Agents (P2Y12 Inhibitors) may enhance the adverse/toxic effect of Rivaroxaban. Specifically, the risk of bleeding may be increased. Management: Carefully consider risks and benefits of this combination and monitor closely; Canadian labeling recommends avoiding prasugrel or ticagrelor. Risk D: Consider therapy modification
Salicylates: Agents with Antiplatelet Properties may enhance the adverse/toxic effect of Salicylates. Increased risk of bleeding may result. Risk C: Monitor therapy
Selumetinib: May enhance the antiplatelet effect of Agents with Antiplatelet Properties. Risk C: Monitor therapy
Telotristat Ethyl: May decrease serum concentrations of the active metabolite(s) of Prasugrel. Risk C: Monitor therapy
Thrombolytic Agents: Agents with Antiplatelet Properties may enhance the anticoagulant effect of Thrombolytic Agents. Risk C: Monitor therapy
Tipranavir: May enhance the antiplatelet effect of Agents with Antiplatelet Properties. Risk C: Monitor therapy
Urokinase: Agents with Antiplatelet Properties may enhance the anticoagulant effect of Urokinase. Risk X: Avoid combination
Vitamin E (Systemic): May enhance the antiplatelet effect of Agents with Antiplatelet Properties. Risk C: Monitor therapy
Zanubrutinib: May enhance the antiplatelet effect of Agents with Antiplatelet Properties. Risk C: Monitor therapy
Adverse events have not been observed in animal reproduction studies. Information related to use during pregnancy is limited (Tello-Montoliu 2013).
It is not known if prasugrel is excreted in breast milk. According to the manufacturer, the decision to continue or discontinue breast-feeding during therapy should take into account the risk of infant exposure, the benefits of breast-feeding to the infant, and benefits of treatment to the mother.
Hemoglobin and hematocrit periodically.
Prasugrel, an inhibitor of platelet activation and aggregation, is a prodrug that is metabolized to both active (R-138727) and inactive metabolites. The active metabolite irreversibly blocks the P2Y12 component of ADP receptors on the platelet, which prevents activation of the GPIIb/IIIa receptor complex, thereby reducing platelet activation and aggregation
Onset of action: Inhibition of platelet aggregation (IPA): Dose dependent: 60 mg loading dose: <30 minutes; median time to reach ≥20% IPA: 30 minutes (Brandt 2007).
Peak effect: Time to maximal IPA: Dose-dependent: Note: Degree of IPA based on adenosine diphosphate (ADP) concentration used during light aggregometry: 60 mg loading dose: Occurs ~4 hours post administration; Mean IPA (ADP 5 micromole/L): ~84.1%; Mean IPA (ADP 20 micromole/L): ~78.8% (Brandt 2007).
Duration of effect: Platelet aggregation gradually returns to baseline values over 5 to 9 days after discontinuation; reflective of new platelet production.
Absorption: Rapid; ≥79%.
Distribution: Active metabolite: Vd: 44 to 68 L.
Protein binding: Active metabolite: ~98%.
Metabolism: Rapid intestinal and serum metabolism via esterase-mediated hydrolysis to a thiolactone intermediate (inactive), which is then converted, via CYP450-mediated (primarily CYP3A4 and CYP2B6) oxidation, to an active metabolite (R-138727) (Farid 2007; Riley 2008).
Half-life elimination: Active metabolite: ~7 hours (range 2 to 15 hours).
Time to peak, plasma: Active metabolite: ~30 minutes; With high-fat/high-calorie meal: 1.5 hours.
Excretion: Urine (~68% inactive metabolites); feces (27% inactive metabolites).
Renal function impairment: In patients with ESRD, both Cmax and AUC0-t last of the active metabolite were approximately half that in healthy patients and in patients with moderate renal impairment.
Geriatric: The AUC of active metabolite was 19% higher in patients 75 years and older than in patients younger than 75 years.
Race: The AUC of active metabolite was approximately 19% higher in Chinese, Japanese, and Korean subjects than in white subjects.
Body weight: The AUC of the active metabolite is approximately 30% to 40% higher in subjects with a body weight of less than 60 kg compared to those weighing 60 kg or more.
Tablets (Effient Oral)
5 mg (per each): $18.36
10 mg (per each): $18.36
Tablets (Prasugrel HCl Oral)
5 mg (per each): $16.51
10 mg (per each): $16.50 - $16.51
Disclaimer: A representative AWP (Average Wholesale Price) price or price range is provided as reference price only. A range is provided when more than one manufacturer's AWP price is available and uses the low and high price reported by the manufacturers to determine the range. The pricing data should be used for benchmarking purposes only, and as such should not be used alone to set or adjudicate any prices for reimbursement or purchasing functions or considered to be an exact price for a single product and/or manufacturer. Medi-Span expressly disclaims all warranties of any kind or nature, whether express or implied, and assumes no liability with respect to accuracy of price or price range data published in its solutions. In no event shall Medi-Span be liable for special, indirect, incidental, or consequential damages arising from use of price or price range data. Pricing data is updated monthly.