Koo,

Brilinta (ticagrelor) is used in combo with aspirin as dual antiplatelet therapy (DAPT). It was one of the arms in the Framework for Addressing Residual CVD Risk that I posted last week. Brilinta antagonizes the P2Y12 platelet receptors and therefore prevents the binding of adenosine diphosphate (ADP) to the P2Y12 receptor and inhibits platelet activation.

Apabetalone has been shown in gene expression and protein analyses to affect targets related to thrombosis/platelet activation. The DAPT therapies are often associated with increased risk of major bleeding. I don't think any bleeding concerns have been reported with apabetalone. My guess is that DAPT therapy has a much stronger effect on platelet/thrombosis endpoints than apabetalone. The beauty of apabetalone is that it seems to "cool" pathways (i.e. thrombosis, inflammation, coagulation, metabolism, complement, vascular calcification, etc), but does not strongly shut down/inhibit these processes, which could elicit undesirable side effects.

http://www.atherosclerosis-journal.com/article/S0021-9150(16)30341-0/fulltext

https://www.sciencedirect.com/science/article/pii/S2468024917304576

http://atvb.ahajournals.org/content/36/Suppl_1/A163