Prasugrel
Regulatory sources consulted
- openfda-label-2ddfdce2-a7ba-b612-e063-6294a90a0ce3
- ema-epar-EMEA/H/C/000984
- aemps-cima-84066
- ansm-bdpm-64503651
- PubMed PMID:35094598 ↗
- PubMed PMID:36065676 ↗
- PubMed PMID:39382876 ↗
- PubMed PMID:40888723 ↗
- OpenFDA · B01AC22
- RxNorm rxcui 613391 ↗
Approved indications
- Prevention of atherothrombotic events in adult patients with acute coronary syndrome (i.e. unstable angina, non-ST-segment-elevation myocardial infarction [UA / NSTEMI] or ST-segment-elevation myocardial infarction [STEMI]) undergoing primary or delayed percutaneous coronary intervention (PCI).
Contraindications
Absolute
- Active pathological bleeding (e.g., peptic ulcer, intracranial hemorrhage).
- History of prior transient ischemic attack (TIA) or stroke.
- Severe hepatic impairment (Child-Pugh Class C).
- Hypersensitivity to prasugrel or any component of the product.
Clinical warnings
- Boxed warning · BLEEDING RISK: Can cause significant, sometimes fatal, bleeding. Do not use in patients with active pathological bleeding or a history of TIA or stroke. Generally not recommended in patients ≥75 years of age. Discontinue at least 7 days prior to any surgery (including CABG). Additional risk factors include body weight <60 kg, concomitant use of NSAIDs or anticoagulants. — FDA
- Major warning · Thrombotic Thrombocytopenic Purpura (TTP): TTP has been reported with the use of prasugrel. It is a serious condition that requires prompt treatment. — EMA SPC
- Hypersensitivity including angioedema: Hypersensitivity reactions have been reported. Monitoring is recommended in patients with a known allergy to other thienopyridines (e.g., clopidogrel). — EMA SPC
Drug interactions
- HighWarfarinB01AA03
Mechanism: Pharmacodynamic synergism; increased antithrombotic effect and bleeding risk.
Recommendation: Coadministration increases the risk of bleeding. Use with extreme caution if unavoidable.
FDA label
- ModerateNSAIDs (chronic use)M01A
Mechanism: Pharmacodynamic synergism; increased risk of bleeding, especially gastrointestinal.
Recommendation: Chronic coadministration should be undertaken with caution.
FDA label
- ModerateOpioids (e.g., Morphine)N02A
Mechanism: Delayed gastric emptying, which delays and reduces the absorption and effect of prasugrel's active metabolite.
Recommendation: In ACS patients requiring opioids, consider the use of a parenteral antiplatelet agent.
FDA labelPMID:36065676
Adverse events
Common (≥1%)
bleeding · hematoma · epistaxis · bruising · hematuria · anemia
Rare but serious
intracranial hemorrhage · thrombotic thrombocytopenic purpura (TTP) · angioedema · fatal bleeding
Pregnancy and lactation
No data in pregnant women. Due to bleeding risk, use should consider the benefit/risk balance. Not studied in lactation; it is unknown if excreted in human milk.
Recent literature (PubMed)
Meta-análisis en red de 15 ECA (35,326 pacientes) con SCA post-ICP. Comparó duraciones cortas de DAPT vs 12 meses. DAPT de 1 mes seguido de monoterapia con inhibidor P2Y12 (prasugrel/ticagrelor) redujo el sangrado mayor (RR 0.47) sin aumentar los eventos cardiovasculares (MACCE), aunque los intervalos de confianza para MACCE fueron amplios. Este hallazgo apoya estrategias de DAPT más cortas para reducir el riesgo hemorrágico en pacientes seleccionados.
Ensayo aleatorizado (3410 pacientes con SCA post-ICP) que comparó monoterapia con inhibidor P2Y12 potente (prasugrel/ticagrelor) iniciada precozmente vs DAPT por 12 meses. La monoterapia no alcanzó la no inferioridad para el combinado de muerte, IM, ACV o revascularización urgente, pero redujo significativamente el sangrado mayor o clínicamente relevante (2.0% vs 4.9%). Se observó una mayor tasa de trombosis de stent en el grupo de monoterapia (12 vs 4 pacientes).
Revisión sobre la farmacología de los antiplaquetarios. Destaca interacciones clave, como la de los opioides (morfina) con los inhibidores P2Y12 orales, que resulta en un efecto antiplaquetario atenuado debido a la absorción retardada y reducida. Discute la importancia de la alta reactividad plaquetaria residual en el SCA y estrategias para superarla, como el uso de agentes parenterales.
Revisión de la literatura sobre agentes antiplaquetarios para la prevención primaria y secundaria del ACV isquémico. Se centra principalmente en aspirina y clopidogrel. Menciona a prasugrel en el contexto de agentes disponibles, pero confirma que su uso principal no es la prevención del ACV, donde está contraindicado si hay antecedentes.