The first and only oral antiplatelet (OAP) in a chemical class called cyclo-pentyl-triazolo-pyrimidine (CPTP)1
BRILINTA binds to the ADP P2Y12 receptor
The active metabolites of thienopyridines directly block the ADP receptor. Ticagrelor binds to an area on the P2Y12 receptor distinct from the ADP binding site.1
BRILINTA reversibly binds to the ADP P2Y12 receptor and prevents ADP from binding. This prevents the signal transduction and platelet activation that can lead to pathologic thrombus formation.2
The reversible binding allows ticagrelor to redistribute to new platelets as they are formed.1
It is not known how pharmacology or chemical class correlates to clinical efficacy or safety results.
There are no adequate, well-controlled, head-to-head clinical trials comparing BRILINTA and thienopyridines in patients with acute ischemic stroke or high-risk CAD without a history of MI or stroke.
The central role of platelets in thrombus formation
The pathophysiology of a thrombus includes atherosclerotic plaque rupture, platelet adhesion, activation, and aggregation leading to various degrees of thrombosis and occlusion, and ultimately, myocardial infarction or stroke.3
Plaque rupture signals nearby platelets to adhere to the injury site. Adhesion triggers platelet activation.3
Activated platelets change shape and express receptors that release the potent platelet agonist ADP, leading to initial thrombus formation.3,4
Activated platelets aggregate at the active lesion site, leading to growth of thrombus.3
- Husted S, van Giezen JJ. Ticagrelor: the first reversibly binding oral P2Y12 receptor antagonist. Cardiovasc Ther. 2009;27(4):259-274.
- BRILINTA® (ticagrelor) [package insert]. Wilmington, DE: AstraZeneca Pharmaceuticals LP; 2021.
- Vorchheimer DA, Becker R. Platelets in atherothrombosis. Mayo Clin Proc. 2006;81(1):59-68.
- Dorsam RT, Kunapuli SP. Central role of the P2Y12 receptor in platelet activation. J Clin Invest. 2004;113(3):340-345.