| Class | Antiplatelet agent |
|---|---|
| Chemistry |
Nucleoside (adenosine) analog |
| Routes of administration |
Oral |
| Absorption |
Incompletely absorbed (about 60% of the dose is recovered in the faeces); erratic bioavailability, 25-65% |
| Solubility |
pKa 12.9; basically insoluble in water |
| Distribution |
VOD = 1.2L/kg; 99.8% protein-bound |
| Metabolism |
Extensively metabolised by hepatic CYP3A enzymes; only one active metabolite (but the parent drug itself has pharmacological activity) |
| Elimination |
Inactive metabolites are renally excreted; the main active metabolite undergoes biliary excretion |
| Time course of action |
Half-life is about 7-8.5 hrs; |
| Target receptor |
P2Y12 class of ADP receptor |
| Mechanism of action |
By inhibits the binding of ADP to the P2Y12 receptor, ticagrelor reversibly prevents platelet activation, and the subsequent ADP- mediated activation of the glycoprotein GPIIb/IIIa complex. Thus, both platelet activation and platelet aggregation are affected. |
| Clinical effects |
Risk of bleeding (which is serious!), aplastic anemia, thrombocytopenia, and neutropenia, also some kind of unexplainable dyspnoea |
| Literature reference |
TGA PI document |
| CICM details of understanding | Level 3 |
| Mentioned around Deranged Physiology | |
| Related SAQs |
Question 3 from thw second paper of 2013 (mechanism) Question 5 from the second paper of 2010 (mechanism) |