Ticagrelor's pharmacological advantage over clopidogrel includes all EXCEPT:

• A Ticagrelor binds reversibly to P2Y12 ADP receptor at a site distinct from ADP, allowing more predictable and consistent antiplatelet effect
• B Ticagrelor has a more rapid onset of action compared to clopidogrel
• C Ticagrelor inhibits adenosine uptake via ENT1 transporter, contributing to dyspnoea as a side effect
• D Ticagrelor is a prodrug requiring CYP2C19 activation, eliminating the CYP2C19 *2 poor metaboliser problem seen with clopidogrel ✓

Explanation

Ticagrelor is NOT a prodrug — it is active as administered, which is the key pharmacological advantage. Clopidogrel (and prasugrel) require CYP2C19-mediated hepatic activation; CYP2C19 *2 or *3 loss-of-function alleles (poor metabolisers, ~30% of Asians) significantly reduce active metabolite formation and platelet inhibition. Ticagrelor's direct activity eliminates this pharmacogenomic variability. Additionally, ticagrelor binds reversibly to an allosteric site on P2Y12 (not the ADP binding site), provides more rapid and consistent platelet inhibition, and inhibits adenosine reuptake (ENT1), which causes the characteristic dyspnoea side effect (20% incidence) through adenosine accumulation.

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

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Written and medically reviewed by the StethoPrep medical team.