Prasugrel (trade name Effient in the US, Australia and India, and Efient in the EU) is a drug used to prevent formation of blood clots. It is a platelet inhibitor and an irreversible antagonist of P2Y12 ADP receptors and is of the thienopyridine drug class. It was developed by Daiichi Sankyo Co. and produced by Ube and currently marketed in the United States in cooperation with Eli Lilly and Company.

Prasugrel racemic.svg
Clinical data
Trade namesEffient, Efient
License data
  • US: B (No risk in non-human studies)
  • B
Routes of
ATC code
Legal status
Legal status
Pharmacokinetic data
Protein bindingActive metabolite: ~98%
Elimination half-life~7 h (range 2 h to 15 h)
ExcretionUrine (~68% inactive metabolites); feces (27% inactive metabolites)
CAS Number
PubChem CID
ECHA InfoCard100.228.719 Edit this at Wikidata
Chemical and physical data
Molar mass373.442 g/mol g·mol−1
3D model (JSmol)
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Prasugrel was approved for use in Europe in February 2009,[1] and in the US in July 2009, for the reduction of thrombotic cardiovascular events (including stent thrombosis) in people with acute coronary syndrome (ACS) who are to be managed with percutaneous coronary intervention (PCI).[2]

Medical usesEdit

Prasugrel is used in combination with low dose aspirin to prevent thrombosis in patients with ACS, including unstable angina pectoris, non-ST elevation myocardial infarction (NSTEMI), and ST elevation myocardial infarction (STEMI), who are planned for treatment with PCI. In studies, prasugrel was more effective than the related clopidogrel but also caused more bleeding. Overall mortality was the same.[1][3]

Prasugrel does not change the risk of death when given to people who have had a STEMI[citation needed] or NSTEMI. Prasugrel does however increase the risk of bleeding and may decrease the risk of further cardiovascular problems. Thus routine use in NSTEMI patients is of questionable value.[4]


Prasugrel should not be given to patients 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).[5]

Adverse effectsEdit

Adverse effects include:[6]

  • 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


As opposed to clopidogrel, proton pump inhibitors do not reduce the antiplatelet effects of prasugrel and hence it is relatively safe to use these medications together.[7]


Mechanism of actionEdit

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. Compared to clopidogrel, prasugrel inhibits adenosine diphosphate–induced platelet aggregation more rapidly, more consistently, and to a greater extent than do standard and higher doses of clopidogrel in healthy volunteers and in patients with coronary artery disease, including those undergoing PCI.[8] 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.[9][10] Unlike clopidogrel, prasugrel is effective in most individuals, although several cases have been reported of decreased responsiveness to prasugrel.[11]


Prasugrel produces inhibition of platelet aggregation to 20 μM or 5 μM ADP, as measured by light transmission aggregometry.[12] 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.[6]


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).[13][14] 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.

Further readingEdit

U.S. National Center for Biotechnology Information: Medical Genetics Summaries - Prasugrel Therapy and CYP Genotype


  • US 5288726  claims prasugrel compound; expired on 14 Apr 2017
  • US 6693115  claims hydrochloride salt of prasugrel; will expire on 3 Jul 2021


  1. ^ a b "European Public Assessment Report for Efient" (PDF). EMA. 2009.
  2. ^ Baker WL, White CM (2009). "Role of prasugrel, a novel P2Y(12) receptor antagonist, in the management of acute coronary syndromes". American Journal of Cardiovascular Drugs. 9 (4): 213–229. doi:10.2165/1131209-000000000-00000. PMID 19655817.CS1 maint: uses authors parameter (link)
  3. ^ "Arzneimittelinformation der Arzneimittelkommission der deutschen Ärzteschaft (AkdÄ): Efient (Prasugrel)" (PDF) (in German). 16 April 2009. pp. 30–44.
  4. ^ Bellemain-Appaix, A; Kerneis, M; O'Connor, SA; Silvain, J; Cucherat, M; Beygui, F; Barthelemy, O; Collet, J-P; Jacq, L; Bernasconi, F; Montalescot, G (2014). "Reappraisal of thienopyridine pretreatment in patients with non-ST elevation acute coronary syndrome: a systematic review and meta-analysis". BMJ. 349: g6269–g6269. doi:10.1136/bmj.g6269. PMC 4208629. PMID 25954988.
  5. ^ "Effient (prasugrel hydrochloride) Prescribing Information". FDA. September 2011.
  6. ^ a b Efient: Highlights of prescribing information
  7. ^ John, Jinu; Koshy S (2012). "Current Oral Antiplatelets: Focus Update on Prasugrel". Journal of american board of family medicine. 25: 343–349. doi:10.3122/jabfm.2012.03.100270. PMID 22570398.
  8. ^ Wiviott SD, Braunwald E, McCabe CH, et al. (2007). "Prasugrel versus clopidogrel in patients with acute coronary syndromes". N Engl J Med. 357 (20): 2001–15. doi:10.1056/NEJMoa0706482.
  9. ^ "FDA Announces New Boxed Warning on Plavix: Alerts patients, health care professionals to potential for reduced effectiveness" (Press release). Food and Drug Administration (United States). March 12, 2010. Retrieved March 13, 2010.
  10. ^ "FDA Drug Safety Communication: Reduced effectiveness of Plavix (clopidogrel) in patients who are poor metabolizers of the drug". Drug Safety and Availability. Food and Drug Administration (United States). March 12, 2010. Retrieved March 13, 2010.
  11. ^ Silvano M, et al. (2011). "A case of resistance to clopidogrel and prasugrel after percutaneous coronary angioplasty". J Thromb Thrombolysis. 31 (2): 233–4. doi:10.1007/s11239-010-0533-x. PMID 21088983.
  12. ^ O'Riordan, Michael. "Switching from clopidogrel to prasugrel further reduces platelet function". Retrieved 1 April 2011.
  13. ^ Rehmel, J. L. F. (24 January 2006). "INTERACTIONS OF TWO MAJOR METABOLITES OF PRASUGREL, A THIENOPYRIDINE ANTIPLATELET AGENT, WITH THE CYTOCHROMES P450". Drug Metabolism and Disposition. 34 (4): 600–607. doi:10.1124/dmd.105.007989.
  14. ^ Kurokawa, T.; Fukami, T.; Yoshida, T.; Nakajima, M. (30 December 2015). "Arylacetamide Deacetylase is Responsible for Activation of Prasugrel in Human and Dog". Drug Metabolism and Disposition. 44 (3): 409–416. doi:10.1124/dmd.115.068221.