Prasugrel 5mg tablets
Requires a prescription from a doctor or prescriber
Prasugrel, a thienopyridine derivative, is a platelet activation and aggregation inhibitor structurally and pharmacologically related to clopidogrel and ticlopidine.
Official documents, adverse reaction reporting, and safety monitoring
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Official medicine documents
Safety monitoring data
Yellow Card reports
The MHRA Yellow Card scheme collects reports of suspected side effects from healthcare professionals and patients. View the Drug Analysis Profile (iDAP) for real-world adverse reaction data.
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Suspected adverse reactions reported for Prasugrel
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Submit a Yellow Card report to the MHRA
Data from the MHRA Yellow Card scheme. A reported reaction does not necessarily mean the medicine caused it. Contains public sector information licensed under the Open Government Licence v3.0.
EudraVigilance
The European Medicines Agency (EMA) collects suspected adverse reaction reports from across the EU/EEA through the EudraVigilance system. Search for safety data on this medicine.
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Suspected adverse reactions reported for Prasugrel
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Learn about EU pharmacovigilance and safety monitoring
EudraVigilance data is published by the European Medicines Agency (EMA). A suspected adverse reaction is not necessarily caused by the medicine.
18 branded products available
MHRA licensed products
View all licensed products for Prasugrel on the MHRA register
Efient 5mg tablets
Efient 5mg tablets
Prasugrel 5mg tablets
Prasugrel 5mg tablets
Prasugrel 5mg tablets
Prasugrel 5mg tablets
Prasugrel 5mg tablets
Prasugrel 5mg tablets
Prasugrel 5mg tablets
Prasugrel 5mg tablets
Prasugrel 5mg tablets
Prasugrel 5mg tablets
This is the NHS Drug Tariff indicative price used for reimbursement purposes. It may not reflect the price paid by patients or pharmacies.
View full Drug TariffSource: NHS Drug Tariff via NHSBSA. Derived from dm+d VMPP (Virtual Medicinal Product Pack) pricing data. Contains public sector information licensed under the Open Government Licence v3.0.
WHO defined daily dose (DDD)
10 mg
Not a recommended dose. The DDD is the assumed average maintenance dose per day for a drug used for its main indication in adults. It is a statistical measure used for research and comparison purposes only.
Source: WHO Collaborating Centre for Drug Statistics Methodology, distributed via the NHS dm+d supplementary BNF/ATC mapping files (NHSBSA). Contains public sector information licensed under the Open Government Licence v3.0.
Therapeutically similar medicines
Similarity is based on WHO Anatomical Therapeutic Chemical (ATC) classification and on a factual NHS dm+d therapeutic-grouping code prefix. Source data: NHS dm+d via TRUD (OGL v3.0), WHO ATC/DDD Index.
NHS prescribing volume and spending trends
Guidelines from the National Institute for Health and Care Excellence
NICE clinical guidance(8)
Prasugrel with percutaneous coronary intervention for treating acute coronary syndromes (TA317)
Acute coronary syndromes (NG185)
Coronary revascularisation: Cangrelor (ESNM63)
Ticagrelor for the treatment of acute coronary syndromes (TA236)
Rivaroxaban for preventing adverse outcomes after acute management of acute coronary syndrome (TA335)
Spartan RX point-of-care CYP2C19 test to guide treatment in acute coronary syndrome (MIB223)
Ticagrelor for preventing atherothrombotic events after myocardial infarction (TA420)
Head injury: assessment and early management (NG232)
Source: National Institute for Health and Care Excellence (NICE). Contains public sector information licensed under the Open Government Licence v3.0.
Check stock at pharmacies and supply information
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Supply & safety information
Official UK regulator monitoring and safety alerts
Pharmacy links redirect to the retailer's own search and do not represent real-time stock levels. Shortage and safety information sourced from MHRA drug safety updates (gov.uk, Crown Copyright under OGL v3.0).
Codes for healthcare professionals and prescribing systems
These codes are used by healthcare IT systems and prescribers to identify this medicine.
NHS UK identifiers
Browse tools
SNOMED CT and dm+d codes from NHS TRUD (Technology Reference data Update Distribution), licensed under the Open Government Licence v3.0. BNF code shown is the factual mapping value distributed by NHS Business Services Authority (NHSBSA) in the dm+d supplementary file under OGL v3.0; it is not affiliated with, nor licensed from, the publishers of the British National Formulary. ATC codes from the WHO Collaborating Centre for Drug Statistics Methodology (whocc.no).
Active and completed clinical studies from ClinicalTrials.gov
Source: ClinicalTrials.gov, a database of the U.S. National Library of Medicine (NLM), National Institutes of Health (NIH). Data accessed via ClinicalTrials.gov API v2. Trial information is provided for research purposes and does not constitute medical advice.
Academic studies and reviews for this medicine's active substance
Showing all 30 studies.
Reviews & meta-analyses: 1 · Randomised trials: 6 · 2007–2026
Showing all 30 studies, sorted by most relevant.
M. Gimbel, Khalid Qaderdan, L. Willemsen, et al.
Lancet, 2020
- Prasugrel Hydrochloride
- Clopidogrel
- Ticagrelor
Hyo‐Soo Kim, Jeehoon Kang, D. Hwang, et al.
Lancet, 2020
- Prasugrel Hydrochloride
- Dual Anti-Platelet Therapy
- Aspirin
R. Shah, Aimen Shafiq, Mohammad Hamza, et al.
The American journal of cardiology, 2023
- Myocardial Infarction
- Thrombosis
- Stroke
Stefanie Schüpke, F. Neumann, M. Menichelli, et al.
The New England journal of medicine, 2019
- Prasugrel Hydrochloride
- Ticagrelor
- Coronary Thrombosis
Youngwoo Jang, Sang-Don Park, J. Lee, et al.
EuroIntervention : journal of EuroPCR in collaboration with the Working Group on Interventional Cardiology of the European Society of Cardiology, 2025
- Prasugrel Hydrochloride
- Dual Anti-Platelet Therapy
- Aspirin
N. Krüger, J. Krefting, Thorsten Kessler, et al.
JAMA Network Open, 2024
- Prasugrel Hydrochloride
- Ticagrelor
- Germany
Importance: In patients with acute coronary syndrome (ACS) undergoing invasive treatment, ticagrelor and prasugrel are guideline-recommended P2Y12 receptor inhibitors. The ISAR-REACT5 randomized clinical trial demonstrated superiority for prasugrel, although concerns were raised about the generalizability of some underpowered subgroup analyses. Objectives: To emulate a randomized clinical trial evaluating the safety and effectiveness of ticagrelor vs prasugrel under the conditions of routine care in individuals with ACS planned to undergo an invasive treatment strategy. Design, Setting, and Participants: This new-user cohort study included secondary data from a German statutory health insurance claims database between January 2012 and December 2021, using 1:1 propensity score nearest-neighbor matching to emulate ISAR-REACT5. Individuals with ACS receiving either ticagrelor or prasugrel treatment after hospital discharge were followed up for 1 year. Eligibility criteria closely emulated those of ISAR-REACT5 and included age of 18 years or older and cardiovascular risk factors. Data were analyzed from May 2023 to May 2024. Exposure: Outpatient prescription of ticagrelor or prasugrel. Main Outcomes and Measures: The primary end point was the composite of all-cause mortality, myocardial infarction (MI), or stroke within 1 year of outpatient treatment initiation. Secondary end points included individual components of the primary end point and stent thrombosis. The safety end point was major bleeding. A Cox proportional hazards regression model was fitted to the overall cohort. Results: Of 17 642 propensity score-matched individuals (mean [SD] age, 63.1 [10.9] years; 73.9% male), 8821 received ticagrelor and 8821 received prasugrel. Agreement was met in 11 of 12 predefined agreement metrics when comparing the results with ISAR-REACT5. The primary composite end point of all-cause mortality, MI, or stroke occurred in 815 individuals (9.2%) receiving ticagrelor and 663 (7.5%) receiving prasugrel (hazard ratio [HR], 1.24; 95% CI, 1.12-1.37). Myocardial infarction (HR, 1.20; 95% CI, 1.06-1.36) and stroke (HR, 1.33; 95% CI, 1.02-1.74) each occurred significantly more often in the ticagrelor group. Analysis of all-cause mortality (HR, 1.27; 95% CI, 0.99-1.64), stent thrombosis (HR, 1.11; 95% CI, 0.89-1.30), and major bleeding (HR, 1.12; 95% CI, 0.96-1.32) revealed no significant differences between treatment groups. Subgroup analysis showed that prasugrel was associated with the primary composite end point in fewer individuals with ST-segment elevation MI (338 of 4941 [6.8%] vs 451 of 4852 [9.3%]). Conclusions and Relevance: This cohort study found that prasugrel was associated with lower rates of all-cause mortality, MI, or stroke compared with ticagrelor in individuals with ACS undergoing an invasive treatment strategy in routine care, particularly in individuals with ST-segment elevation MI. The findings suggest that carefully designed database studies can complement and extend findings from randomized clinical trials, informing guidelines and clinical decision-making.
Abstract licence: CC BY
Bangalore S, Sinha SK, Singh R, et al.
2026
- Prasugrel Hydrochloride
- Ticagrelor
- Coronary Artery Disease
Salman Nikfarjam, Yasaman Borghei, Arsalan Salari, et al.
Research in Cardiovascular Medicine, 2023
Abstract Background: Reperfusion can be done through primary percutaneous coronary intervention (PPCI) and thrombolytic administration. Patients with myocardial infarction should receive antiplatelet drugs from the P2Y12 receptor inhibitor category (such as ticagrelor, prasugrel, and clopidogrel). Based on recent researches, effectiveness of ticagrelor versus clopidogrel is still debatable. Methods: A total of 128 patients who underwent PPCI, divided into two groups (Zyllt ® group (600 mg received as a loading dose, maintenance with dose of 75 mg daily)) and Ticora ® group (180 mg as a loading dose, maintenance with dose of 90 mg twice). Both the groups received aspirin 80 mg daily, too. They were followed up after 3 months. Results: In this study, 86.9% were men, and there was no significant difference in terms of gender and age in 2 groups. Risk factors, type of myocardial infraction (MI), number of involved and infarct-related arteries, and presence of complications and their type were not statistically different in groups ( P > 0.05). Among all complications, only one person had dyspnea in the Ticora group, one patient in the Ticora group, and 3 patients in the Zyllt group had chest pain. The difference in “TIMI Score” during Time was significant ( P = 0.037). Conclusion: Our study shows no difference between ticagrelor and clopidogrel after PPCI in patients with MI in terms of risk factors, type of MI, number of involved and infarct-related arteries, and presence of complications and their type, in two studied groups.
Abstract licence: CC BY-NC-SA
S. Wiviott, E. Braunwald, C. Mccabe, et al.
The New England journal of medicine, 2007
- Prasugrel Hydrochloride
- Clopidogrel
- Aspirin
S. Savonitto, Luca A. Ferri, L. Piatti, et al.
Circulation, 2018
- Prasugrel Hydrochloride
- Clopidogrel
- Hemorrhage
Sources: aggregated from Europe PMC (EMBL-EBI), OpenAlex, Crossref, PubMed and other open scholarly databases. Retracted articles are excluded. Study information is provided for research purposes and does not constitute medical advice.
Pharmacology and chemical data from DrugBank
Key facts
Drug status
Approved
Major interactions
152 found
Half-life
7.4 hours
Mechanism
Prasugrel is an thienopyridine and a prodrug which inhibits ADP receptors by irr…
Food interactions
2 warnings
Human targets
1 target
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
79%
Half-life
7.4 hours
Protein binding
98%
Volume of distribution
44-68L
Metabolism
Elimination
68%
Clearance
112 - 166 L/h
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Known interactions with other medications. Always consult a healthcare professional.
Showing 50 of 1379 interactions
How the body processes this drug — absorption, distribution, metabolism, and elimination
Prasugrel may be administered with or without food.
The active metabolite is further metabolized by S-methylation or cysteine conjugation to two inactive metabolites.
Unlike clopidogrel, transformation of prasugrel to its active metabolite does not appear to be affected by cytochrome P450 polymorphisms.
Proteins and enzymes this drug interacts with in the body
Enzymes involved in drug metabolism — important for understanding drug interactions
Proteins that carry this drug through the body
PMID:19021548
Major calcium and magnesium transporter in plasma, binds approximately 45% of circulating calcium and magnesium in plasma (By similarity).
Potentially has more than two calcium-binding sites and might additionally bind calcium in a non-specific manner (By similarity). The shared binding site between zinc and calcium at residue Asp-273 suggests a crosstalk between zinc and calcium transport in the blood (By similarity). The rank order of affinity is zinc > calcium > magnesium (By similarity).
Binds to the bacterial siderophore enterobactin and inhibits enterobactin-mediated iron uptake of E.coli from ferric transferrin, and may thereby limit the utilization of iron and growth of enteric bacteria such as E.coli .
PMID:6234017
Does not prevent iron uptake by the bacterial siderophore aerobactin PMID:6234017
ATC B01AC22
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
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Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Linked compound data from DrugBank Open Data (CC BY-NC 4.0)
Prasugrel
Additional database identifiers
Drugs Product Database (DPD)
20588
ChemSpider
5293653
HUGO Gene Nomenclature Committee (HGNC)
HGNC:18124
GenAtlas
P2RY12
GeneCards
P2RY12
GenBank Gene Database
AF313449
GenBank Protein Database
12083902
Guide to Pharmacology
328
UniProt Accession
P2Y12_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1864
GeneCards
CES2
Guide to Pharmacology
3298
UniProt Accession
EST2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2637
GenAtlas
CYP3A4
GeneCards
CYP3A4
GenBank Gene Database
M18907
Guide to Pharmacology
1337
UniProt Accession
CP3A4_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2615
GeneCards
CYP2B6
GenBank Gene Database
M29874
GenBank Protein Database
181296
Guide to Pharmacology
1324
UniProt Accession
CP2B6_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2623
GenAtlas
CYP2C9
GeneCards
CYP2C9
GenBank Gene Database
AY341248
Guide to Pharmacology
1326
UniProt Accession
CP2C9_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2621
GeneCards
CYP2C19
GenBank Gene Database
M61854
GenBank Protein Database
181344
Guide to Pharmacology
1328
UniProt Accession
CP2CJ_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:399
GenAtlas
ALB
GeneCards
ALB
GenBank Gene Database
V00494
GenBank Protein Database
28590
UniProt Accession
ALBU_HUMAN
DrugBank citations
If you use DrugBank data in your research, please cite the following publications:
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Structured knowledge from the free knowledge base
Wikipedia article
drug that acts as a platelet inhibitor and is used to prevent formation of blood clots.
Read on WikipediaATC classifications (Wikidata)
Linked open data from Wikidata (Q416232), a free and open knowledge base operated by the Wikimedia Foundation. Data is available under the Creative Commons CC0 1.0 Public Domain Dedication.