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Trade namesEffient, Efient
  • (RS)-5-[2-Cyclopropyl-1-(2-fluorophenyl)-2-oxoethyl]-4,5,6,7-
    tetrahydrothieno[3,2-c]pyridin-2-yl acetate
Clinical data
Drug classPlatelet inhibitor (P2Y12)[1]
Main usesPrevent blood clots with percutaneous coronary intervention (PCI)[2]
Side effectsBleeding, thrombotic thrombocytopenic purpura, angioedema[1]
  • AU: B1
  • US: N (Not classified yet)
Routes of
By mouth
External links
License data
Legal status
  • AU: S4 (Prescription only)
  • UK: POM (Prescription only)
  • US: ℞-only
  • EU: Rx-only
Protein bindingActive metabolite: ~98%
Elimination half-life~7 h (range 2 h to 15 h)
ExcretionUrine (~68% inactive metabolites); feces (27% inactive metabolites)
Chemical and physical data
Molar mass373.44 g·mol−1
3D model (JSmol)
  • CC(=O)Oc1cc2c(s1)CCN(C2)C(c3ccccc3F)C(=O)C4CC4
  • InChI=1S/C20H20FNO3S/c1-12(23)25-18-10-14-11-22(9-8-17(14)26-18)19(20(24)13-6-7-13)15-4-2-3-5-16(15)21/h2-5,10,13,19H,6-9,11H2,1H3 checkY

Prasugrel, sold under the brand name Effient and Efient, is a medication used to prevent blood clots in people with acute coronary syndrome (ACS) who getting percutaneous coronary intervention (PCI).[2] It is used together with aspirin.[2] It is taken by mouth.[2]

Common side effects include bleeding.[1] Other side effects may include thrombotic thrombocytopenic purpura and angioedema.[1] It is a platelet inhibitor of the P2Y12 platelet adenosine diphosphate (ADP)-receptor inhibitor type.[1]

Prasugrel was approved for use in Europe and the United States in 2009.[2][3] It is available as a generic medication.[4] In the United Kingdom 4 weeks of medication costs the NHS about £6 as of 2021.[4] This amount in the United States is about 30 USD.[5] It is no longer available in Canada as of 2020.[6]

Medical uses

Prasugrel is used in combination with low dose aspirin to prevent thrombosis in people with acute coronary syndrome, including unstable angina pectoris, non-ST elevation myocardial infarction (NSTEMI), and ST elevation myocardial infarction (STEMI), who are planned for treatment with PCI. Prasugrel is associated with a higher bleeding risk compared to clopidogrel but has demonstrated superiority in reducing the composite endpoint of death, recurrent myocardial infarctions and stroke.[7]

Prasugrel does not change the risk of death when given to people who have had a STEMI or NSTEMI.[8] Prasagrel does however increase the risk of bleeding and may decrease the risk of further cardiovascular problems.[8] Thus routine use is of questionable value.[8]

Given the risk of bleeding, prasugrel should not be used in people who are older than 75 years, who have low body weight or a history of transient ischemic attacks or strokes.[7][9] The initiation of prasugrel before coronary angiography outside the context of primary PCI is not recommended.[10][11][9]


It is taken at a dose of 60 mg initially followed by 10 mg per day.[2] In those who weight less than 60 kg the dose is 5 mg per day.[2]


Prasugrel should not be given to people with active pathological bleeding, such as peptic ulcer or a history of transient ischemic attack or stroke, because of higher risk of stroke (thrombotic stroke and intracranial hemorrhage).[12]

Side effects

Photographs of person with prasugrel-induced hypersensitivity skin reaction. A: exanthema on both forearms and hands. (A) shows exanthema on both forearms and hands after 5 days of prasugrel exposure. B: exanthema on the anterior chest and abdominal wall. (B) shows exanthema on anterior chest and abdominal wall.

Side effects include:[13]

  • Cardiovascular: Hypertension (8%), hypotension (4%), atrial fibrillation (3%), bradycardia (3%), noncardiac chest pain (3%), peripheral edema (3%), thrombotic thrombocytopenic purpura (TTP)
  • Central nervous system: Headache (6%), dizziness (4%), fatigue (4%), fever (3%), extremity pain (3%)
  • Dermatologic: Rash (3%)
  • Endocrine and metabolic: Hypercholesterolemia/hyperlipidemia (7%)
  • Gastrointestinal: Nausea (5%), diarrhea (2%), gastrointestinal hemorrhage (2%)
  • Hematologic: Leukopenia (3%), anemia (2%)
  • Neuromuscular and skeletal: Back pain (5%)
  • Respiratory: Epistaxis (6%), dyspnea (5%), cough (4%)
  • Hypersensitivity, including angioedema


Prasugrel has a low potential for interactions. It may, for example, be used with proton pump inhibitors to reduce the risk of gastrointestinal bleeding without loss of its antiplatelet effect.[14][15][16][17]


Mechanism of action

Prasugrel is a member of the thienopyridine class of ADP receptor inhibitors, like ticlopidine (trade name Ticlid) and clopidogrel (trade name Plavix). These agents reduce the aggregation ("clumping") of platelets by irreversibly binding to P2Y12 receptors. Prasugrel inhibits platelet aggregation more rapidly, more consistently, and to a greater extent than clopidogrel.[18][19] The TRITON-TIMI 38 study compared prasugrel with clopidogrel, and showed that prasugrel reduced rates of ischaemic events, but increased bleeding risk. Overall mortality rates were similar for each drug.[20]

Clopidogrel, unlike prasugrel, was issued a black box warning from the FDA on March 12, 2010, as the estimated 2–14% of the US population who have low levels of the CYP2C19 liver enzyme needed to activate clopidogrel may not get the full effect. Tests are available to predict if a patient would be susceptible to this problem or not.[21][22] Unlike clopidogrel, prasugrel is effective in most individual with the exception in patients over the age of 75, weight under 60 kg, and patients with a history of stroke or TIA due to increased risk of bleeding,[23][24] although several cases have been reported of decreased responsiveness to prasugrel.[25] It has been suggested that the decreased responsiveness observed in prasugrel is likely due to its low but significant frequency of High Platelet Reactivity (HPR).[26]


Prasugrel produces inhibition of platelet aggregation to 20 μM or 5 μM ADP, as measured by light transmission aggregometry.[27] Following a 60-mg loading dose of the drug, about 90% of patients had at least 50% inhibition of platelet aggregation by one hour. Maximum platelet inhibition was about 80%. Mean steady-state inhibition of platelet aggregation was about 70% following three to five days of dosing at 10 mg daily after a 60-mg loading dose. Platelet aggregation gradually returns to baseline values over five to 9 days after discontinuation of prasugrel, this time course being a reflection of new platelet production rather than pharmacokinetics of prasugrel. Discontinuing clopidogrel 75 mg and initiating prasugrel 10 mg with the next dose resulted in increased inhibition of platelet aggregation, but not greater than that typically produced by a 10-mg maintenance dose of prasugrel alone. Increasing platelet inhibition could increase bleeding risk. The relationship between inhibition of platelet aggregation and clinical activity has not been established.[13]


The reaction of prasugrel (top left) to its active metabolite (R-138727, top right). The two structures at the bottom represent the inactive thiolactone; they are tautomers of each other.

Prasugrel is a prodrug and is rapidly metabolized by carboxylesterase 2 in the intestine and carboxylesterase 1 in the liver to a likewise inactive thiolactone, which is then converted by CYP3A4 and CYP2B6, and to a minor extent by CYP2C9 and CYP2C19, to a pharmacologically active metabolite (R-138727).[28][29] R-138727 has an elimination half-life of about 7 hours (range 2 h to 15 h). Healthy subjects, patients with stable atherosclerosis, and patients undergoing PCI show similar pharmacokinetics.


Prasugrel has one chiral atom. It is used in racemic form as the hydrochloride salt, which is a white powder.

Society and culture

It was developed by Daiichi Sankyo Co. and produced by Ube and marketed in the United States in cooperation with Eli Lilly and Company.


The drug was introduced to clinical practice in Canada in 2010 [30] but was subsequently withdrawn by the manufacturer in 2020 as a "business decision".[6]


  1. 1.0 1.1 1.2 1.3 1.4 "DailyMed - PRASUGREL- prasugrel hydrochloride tablet, film coated". Archived from the original on 30 October 2021. Retrieved 29 October 2021.
  2. 2.0 2.1 2.2 2.3 2.4 2.5 2.6 "Efient". Archived from the original on 26 February 2021. Retrieved 29 October 2021.
  3. "Prasugrel Monograph for Professionals". Archived from the original on 27 February 2021. Retrieved 29 October 2021.
  4. 4.0 4.1 BNF 81: March-September 2021. BMJ Group and the Pharmaceutical Press. 2021. p. 230. ISBN 978-0857114105.
  5. "Prasugrel Prices, Coupons & Patient Assistance Programs". Archived from the original on 19 April 2021. Retrieved 29 October 2021.
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  9. 9.0 9.1 Chew, Derek P; Scott, Ian A; Cullen, Louise; French, John K; Briffa, Tom G; Tideman, Philip A; Woodruffe, Stephen; Kerr, Alistair; Branagan, Maree; Aylward, Philip EG (August 2016). "National Heart Foundation of Australia and Cardiac Society of Australia and New Zealand: Australian clinical guidelines for the management of acute coronary syndromes 2016". Medical Journal of Australia. 205 (3): 128–133. doi:10.5694/mja16.00368. PMID 27465769. S2CID 13014429.
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External links

External sites: