Pharmacodynamics<unk>  is a modified γ-cyclodextrin, with a lipophilic core and a hydrophilic periphery. This gamma cyclodextrin has been modified from its natural state by placing eight carboxyl thio ether groups at the sixth carbon positions. These extensions extend the cavity size allowing greater encapsulation of the rocuronium molecule. These negatively charged extensions electrostatically bind to the quaternary nitrogen of the target as well as contribute to the aqueous nature of the cyclodextrin.<unk> 's binding encapsulation of rocuronium is one of the strongest among cyclodextrins and their guest molecules. The rocuronium molecule (a modified steroid) bound within<unk> 's lipophilic core, is rendered unavailable to bind to the acetylcholine receptor at the neuromuscular junction. Schematic diagram of<unk>  encapsulating a rocuronium molecule 160px Left: Schematic of a<unk>  molecule encapsulating a rocuronium molecule.Right: Space-filling model of a<unk>  sodium molecule in the same orientation.<unk> , unlike neostigmine, does not inhibit acetylcholinesterase so cholinergic effects are not produced and co-administration of an antimuscarinic agent (glycopyrronium bromide or atropine) is not needed.<unk>  might therefore be expected to have fewer adverse effects than the traditional reversal agents. When muscle relaxant with rapid onset and short duration of action is required, there has been little choice apart from succinylcholine but this drug has important contraindications; for example, it can trigger malignant hyperthermia in susceptible individuals, it has a prolonged duration of action in patients with pseudocholinesterase deficiency and it causes an increase in plasma potassium concentration which is dangerous in some circumstances. Rocuronium has a comparably quick onset in high dose (0.6 mg kg−1 to 1 mg kg−1) and can be rapidly reversed with<unk>  (16 mg kg−1), so this drug combination offers an alternative to suxamethonium. 'Recurarisation', a phenomenon of recurrence of neuromuscular block, may occur where the reversal agents wear off before a neuromuscular blocking drug is completely cleared. This is very unusual with all but the longest acting neuromuscular blocking drugs (such as gallamine, pancuronium or tubocurarine). It has been demonstrated to occur only rarely with<unk> , and only when insufficient doses were administered. The underlying mechanism is thought to be related to redistribution of relaxant after reversal. It may occur for a limited range of<unk>  doses which are sufficient for complex formation with relaxant in the central compartment, but insufficient for additional relaxant returning to central from peripheral compartments.<unk>  has been shown to have affinity for two other aminosteroid neuromuscular blocking agents, vecuronium and pancuronium. Although<unk>  has a lower affinity for vecuronium than for rocuronium, reversal of vecuronium is still effective because fewer vecuronium molecules are present in vivo for equivalent blockade: vecuronium is approximately seven times more potent than rocuronium.<unk>  encapsulates with a 1:1 ratio and therefore will adequately reverse vecuronium as there are fewer molecules to bind compared to rocuronium. Shallow pancuronium blockade has been successfully reversed by<unk>  in phase III clinical trials.
Sugammadex
Eptazocine
Pentazocine
Iopentol
Fomepizole
Etomidate
Neostigmine
Bremazocine