Sugammadex Mechanism — FRCA Primary MCQ

Instant feedback + full explanation. One question, done properly.

EasyPharmacology - NeuromuscularSugammadex MechanismFRCA Primary

Which mechanism primarily accounts for reversal of rocuronium-induced neuromuscular blockade by sugammadex?

Educational content. Not a substitute for clinical judgement or local policy.

Reveal the answer and explanation

Correct answer: A — Forming a plasma complex with rocuronium that reduces free drug

Sugammadex is a modified gamma-cyclodextrin and selective relaxant binding agent. It forms a complex with rocuronium in plasma, lowering the free rocuronium concentration and reducing the amount available to occupy nicotinic acetylcholine receptors at the neuromuscular junction. Redistribution of rocuronium away from the effect site then reverses blockade. Sugammadex does not increase acetylcholine release or directly activate nicotinic receptors. Unlike neostigmine, it does not inhibit acetylcholinesterase and therefore does not reverse blockade by increasing synaptic acetylcholine. It also does not act as a competitive nicotinic-receptor ligand. Thus, plasma complex formation with rocuronium is the distinguishing mechanism.

Reference: Dr. Reddy's Laboratories (UK) Ltd. Sugammadex 100 mg/ml Solution for Injection, Summary of Product Characteristics, section 5.1 Pharmacodynamic properties, updated 1 July 2026. https://www.medicines.org.uk/emc/product/14949/smpc