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RX BIN: 015558RX PCN: HTGroup ID: DDN6600Card Holder ID: DDN6600
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2019 Price of Effient

$26.2830 tablets/10 mg
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Prasugrel volume of distribution

Prasugrel is extensively (>= 79%) and rapidly absorbed with peak plasma concentrations occurring within 30 minutes. Prasugrel may be administered without regard to food as exposure (AUC) is not affected by meals; however, peak plasma concentrations may be decreased and time to peak plasma concentrations may be increased following a high fat, high caloric meal. After oral absorption, hydrolysis by intestinal carboxylesterases and subsequent oxidation by hepatic cytochrome P450 enzymes, primarily CYP3A4 and CYP2B6 and to a lesser extent CYP2C9 and CYP2C19, convert prasugrel into the active metabolite. The active metabolite is 98% bound to human albumin and has an estimated volume of distribution ranging from 44—68 L. The active metabolite has an elimination half live of approximately 7 hours (range 2—15 hours) with clearance occurring via a secondary metabolism to two inactive compounds. These inactive compounds are then excreted in the urine (68%) and feces (27%).

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What is Prasugrel

Prasugrel, a thienopyridine derivative, is a platelet activation and aggregation inhibitor structurally and pharmacologically related to clopidogrel and ticlopidine. Similar to clopidogrel, prasugrel is a prodrug that requires enzymatic transformation in the liver to its active metabolite, R-138727. R-138727 irreversibly binds to P2Y12 type ADP receptors on platelets thus preventing activation of the GPIIb/IIIa receptor complex. As a result, inhibition of ADP-mediated platelet activation and aggregation occurs. Prasugrel was developed by Daiichi Sankyo Co. and is currently marketed in the United States and Canada in cooperation with Eli Lilly and Company for acute coronary syndromes planned for percutaneous coronary intervention (PCI). FDA approved in 2009.

Prasugrel mechanism of action

Prasugrel is an thienopyridine and a prodrug which inhibits ADP receptors by irreversibly acting on the P2Y12 receptor on platelets. The active metabolite of prasugrel prevents binding of adenosine diphosphate (ADP) to its platelet receptor, impairing the ADP-mediated activation of the glycoprotein GPIIb/IIIa complex. Prasugrel is proposed to have a similar mechanism of action to clopidogrel.

Dosage forms of Prasugrel

Tabletoral10 mg
Tablet, film coatedoral10 mg/1
Tablet, film coatedoral5 mg/1

Prescription Generics


International Brands



Effient Prasugrel


Eli Lilly and Company

CAS number






Affected organisms

Humans and other mammals

Indication of Prasugrel

Indicated in combination with acetylsalicylic acid (ASA) to prevent atherothrombotic events in patients with acute coronary syndrome (ACS) who are to be managed with percutaneous coronary intervention (PCI). May be used in patients with unstable angina (UA), non-ST elevation myocardial infarction (NSTEMI), ST-elevation myocardial infarction (STEMI) who are to be managed with PCI. Prasugrel is not recommended in patients 75 years of age or greater, those that weigh60kg, and patients with a history of stroke or transient ischemic attack due to increased risk of fatal and intracranial bleeding.

Toxicity of Prasugrel

LD50 (rat) 1,000 – 2,000 mg/kg; LD50 (rabbit) 1,000 mg/kg

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What is Effient?

Effient – antiplatelet drug with the active ingredient prasugrel. It is an antagonist of the P2Y12 class of receptors for adenosine diphosphate, which causes its inhibition of platelet activation and aggregation. Inhibition of platelet function involved in the development of atherosclerotic complications reduces the risk of cardiovascular complications (including myocardial infarction, stroke, death from a cardiovascular cause).

After receiving a loading dose (60 mg) of prasugrel, after 1 hour, inhibition of aggregation of not less than 50% of platelets is achieved. The subsequent use of a maintenance dose (10 mg) for 3-5 days provides for the suppression of aggregation of about 70% of platelets and an equilibrium state. With the abolition of Effient, platelet aggregation gradually (after taking a loading dose – after 7–9 days, maintaining the dose in an equilibrium state – 5 days) returns to baseline values. After previous treatment with clopidogrel (75 mg per day), switching to prasugrel does not cause significant changes in the inhibition of platelet aggregation.

When comparing prasugrel and clopidogrel, an analysis of the results of a clinical study on the efficacy and safety of their use in combination therapy with acetylsalicylic acid and other drugs showed a statistical superiority of prasugrel in patients with acute coronary syndrome (ACS) with the risk of developing unstable stenocardia or myocardial infarction without lifting the segment ST or myocardial infarction with ST segment elevation during percutaneous coronary intervention. The criterion of effectiveness in this case was the period before the onset of death, the first case of nonfatal heart attack or stroke from a cardiovascular cause. Effient demonstrated higher efficacy in lowering the frequency of the onset of the primary combined endpoint and the frequency of the secondary endpoints, including stent thrombosis. The advantage of prasugrel was noted throughout the study period.

The superior effect is accompanied by an increase in the frequency of major bleeding (any intracranial hemorrhage or bleeding with the presence of clinical manifestations, accompanied by a decrease in hemoglobin of more than 5 g / dL). The therapeutic effect of prasugrel is not affected by age, gender, body weight, ethnicity, concomitant therapy [including bivalirudin, heparin, intravenous (iv) administration of glycoprotein IIb / IIIa receptor platelet blockers, hypolipidemic agents, beta-blockers, angiotensin inhibitor inhibitors, inhibitors angiotensin inhibitor ACE), acetylsalicylic acid in a dose of from 75 to 325 mg once a day].

The main advantage is a significant reduction in the incidence of nonfatal myocardial infarction, and in diabetes mellitus, a reduction in the incidence of primary and secondary combined endpoints. Patients aged 75 years and older have less pronounced benefits of prasugrel than patients younger than 75 years. All patients with acute coronary syndrome comparative analysis showed a significant benefit of prasugrel over clopidogrel in the incidence of diagnosed or possible stent thrombosis, death from cardiovascular causes, nonfatal myocardial infarction, nonfatal stroke, rehospitalization due to coronary ischemic events or urgent revascularization target vessel for 30 days.

In terms of the incidence of death for all causes in patients with ACS, there is no significant difference between prasugrel and clopidogrel. When using prasugrel, there was a 50% reduction in thrombosis of metal stents with or without a drug coating over a long (more than a year) follow-up period.