Mechanism of Action (MoA) for BRIDION® (sugammadex)
BRIDION works differently than neostigmine by directly encapsulating, binding, and thus inactivating rocuronium or vecuronium.1-3
After intravenous injection, BRIDION distributes through the plasma and binds to the neuromuscular blocking agents rocuronium or vecuronium to form a complex.3 BRIDION does not affect the release or breakdown of acetylcholine.2
- The reduction of free rocuronium available in the blood plasma creates a concentration gradient with the neuromuscular junction.2
- As a result, there is a shift of rocuronium into the plasma, where it is encapsulated by BRIDION.2
- This process reduces the amount of neuromuscular blocking agent available to bind to nicotinic cholinergic receptors in the neuromuscular junction, resulting in the reversal of neuromuscular blockade.
- The process is similar for vecuronium.
- The elimination half-life of BRIDION for adults with normal renal function is approximately 2 hours, with over 90% excreted within 24 hours, primarily in urine.
- NMB = neuromuscular blockade
- NMBA = neuromuscular blocking agent
- NMJ = neuromuscular junction
- Claudius C, Fuchs-Buder T. Neuromuscular monitoring. In: Gropper MA, ed. Miller’s Anesthesia. 9th ed. Elsevier; 2020:1354-1372.
- Bom A, Hope F, Rutherford S, et al. Preclinical pharmacology of sugammadex. J Crit Care. 2009;24(1):29-35.
- Gijsenbergh F, Ramael S, Houwing N, et al. First human exposure of Org 25969, a novel agent to reverse the action of rocuronium bromide. Anesthesiology. 2005;103(4):695-703.
- Bom A, Bradley M, Cameron K, et al. A novel concept of reversing neuromuscular block: chemical encapsulation of rocuronium bromide by a cyclodextrin-based synthetic host. Angew Chem Int Ed Engl. 2002;41(2):266-270.