Decamethonium is a depolarizing neuromuscular blocking agent. It is a partial agonist of muscle-type nicotinic acetylcholine receptors (nAChRs). Decamethonium activates α1β1-containing adult mouse muscle-type nAChRs expressed in X. laevis oocytes with an EC50 value of 40 μM using voltage clamp electrophysiology. It is also a nondepolarizing antagonist of neuronal-type nAChRs, inhibiting mouse α7-, α3β2-, α3β4-, and α4β2-containing receptors with IC50 values of 7.4, 405, 28, and 59 μM, respectively. Decamethonoium is a competitive antagonist of α4β2-containing nAChRs expressed in SH-EP1 cells (IC50 = 52 μM for the human receptor). It also inhibits electric eel acetylcholinesterase (AChE) and blocks electrically-evoked tibialis muscle twitches in anesthetized cats with ED95 values of 35 and 70 μg/kg for cats under chloralose and ether anesthesia, respectively. Formulations containing decamethonium have been used to induce paralysis during anesthesia.
Syncurine (GlaxoSmithKline).
Decamethonium was one of the first neuromuscular blocking agents to be synthesized. An SAR study on a series of bis-quaternary ammonium
compounds with varying numbers of methylene groups separating the nitrogen atoms demonstrated that maximal neuromuscular blockade
occurred with 10 to 12 unsubstituted methylene groups. Activity diminished as the number of carbons was either decreased or increased. The
compound with six methylene groups, hexamethonium, is a nicotinic antagonist at autonomic ganglia (ganglionic blocking agent). All the
compounds in this series that possessed neuromuscular blocking activity also caused depolarization of the postjunctional membrane.
Crystals derived from methanol and acetone.
ACUTE/CHRONIC HAZARDS: When heated to decomposition DECAMETHONIUM BROMIDE emits very toxic fumes.
Flash point data for DECAMETHONIUM BROMIDE are not available. DECAMETHONIUM BROMIDE is probably combustible.
