Ticagrelor differs from clopidogrel in that it does NOT require metabolic activation and is reversible. It acts by:

• A Irreversible covalent binding to P2Y12 ADP receptor
• B Reversible, non-competitive allosteric binding to P2Y12 ADP receptor ✓
• C Irreversible inhibition of COX-1 in platelets preventing TXA2 synthesis
• D Competitive antagonism of the GP IIb/IIIa fibrinogen receptor on activated platelets

Explanation

Ticagrelor is a cyclopentyltriazolopyrimidine that binds to a distinct allosteric site on P2Y12, not the ADP binding site, making the interaction non-competitive and reversible. Unlike clopidogrel and prasugrel (thienopyridines), ticagrelor does not require hepatic bioactivation by CYP2C19, thus its effect is not affected by CYP2C19 polymorphisms. Its reversibility means platelet function recovers faster after discontinuation (~3 days vs ~7 days for clopidogrel). Ticagrelor also inhibits adenosine reuptake and causes dyspnoea as a side effect.

Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.