| Class | Antiplatelet agent |
|---|---|
| Chemistry |
Thienopyridine |
| Routes of administration |
Oral |
| Absorption |
Rapidly and completely absorbed; 80% bioavailability |
| Solubility |
pKa 5.1; basically insoluble in water |
| Distribution |
VOD = 1L/kg; 98% protein-bound (mainly to albumin) |
| Metabolism |
A pro-drug: converted to an active metabolite in the liver by CYP450 enzymes |
| Elimination |
68% of the metabolites are excreted in the urine, the rest in the faeces |
| Time course of action |
Half life of the active metabolite is about 5-7 hours |
| Target receptor |
P2Y12 class of ADP receptor |
| Mechanism of action |
By inhibits the binding of ADP to the P2Y12 receptor, prasugrel prevents platelet activation, and the subsequent ADP- mediated activation of the glycoprotein GPIIb/IIIa complex. Thus, both platelet activation and platelet aggregation are affected. This effect is irreversible |
| Clinical effects |
Risk of bleeding (which is serious!), aplastic anemia, thrombocytopenia, and neutropenia |
| Literature reference |
TGA PI document |
| CICM details of understanding | Not specifically listed in the CICM syllabus |
| Mentioned around Deranged Physiology | |
| Related SAQs |