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Clinical data
AHFS/Drugs.comInternational Drug Names
ATC code
Pharmacokinetic data
Metabolismnot metabolized
Excretion70–90% unchanged in urine 1.3ml/kg/min t1/2 2–4 hours
CAS Number
PubChem CID
E number{{#property:P628}}
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Chemical and physical data
Molar mass666.894 g/mol
3D model (JSmol)
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]


Alcuronium is a neuromuscular blocking (NMB) agent, alternatively referred to as a skeletal muscle relaxant. It is a semi-synthetic substance prepared from C-toxiferine I,[1] a bis-quaternary alkaloid obtained from Strychnos toxifera. C-toxiferine I itself has been tested for its pharmacological action and noted to be a very long acting neuromuscular blocking agent[2] For a formal definition of the durations of actions associated with NMB agents, see page for gantacurium. The replacement of both the N-methyl groups with N-allyl moieties yielded N,N-diallyl-bis-nortoxiferine, now recognized as alcuornium (and at one time marketed as the proprietary agent called Alloferin).

Inclusion of the allylic functions presented an enhanced potential area of biotransformation, and thus alcuronium is observed to have a much shorter duration of neuromuscular blocking action than its parent C-toxiferine I.[3] It also has a more rapid onset of action, and is ~1.5 times as potent as tubocurarine.[4] The pharmacological action of alcuronium is readily reversed by neostigmine, and it produced little histamine release.[5] The major disadvantage of alcuronium is that it elicits a vagolytic effect produced by a selective atropoine-like blockade of cardiac muscarinic receptors.[4][6][7]


  • Cardiovascular system: histamine release and blockage of the sympathetic ganglia including adrenal medulla could cause hypotension
  • Respiratory: apnea due to phrenic blockage but bronchoconstriction can occur from the histamine release
  • Central nervous system: no effect on intraoccular pressure
  • Autonomic ganglion blockade can cause decrease in gut motility

Special points

  • Duration of action prolonged in states of low potassium, calcium and protein, also in states of high magnesium and acidosis.
  • Pharmaceutically incompatible with thiopentone
  • Infusion can cause fixed dilated pupils


  1. Foldes FF (1954). Br. J. Anaesth. 26: 394. doi:10.1093/bja/26.6.394. Missing or empty |title= (help)
  2. Waser PG (1950). Helv. Physiol. Pharmacol. Acta. 8: 342. Missing or empty |title= (help)
  3. Martin-Smith M (1971), In: Ariens EJ (ed.), "Drug Design". Vol. 2. Academic Press. New York and London. pp.453-530.
  4. 4.0 4.1 Speight TM, Avery GS (1972). Drugs. 4: 163. doi:10.2165/00003495-197204030-00002. Missing or empty |title= (help)
  5. Thompson MA (1980). Br. J. Hosp Med. 23: 153. Missing or empty |title= (help)
  6. Coleman AJ, Downing JW, Leary WP, Moyes DG, Styles M. (1972). "The immediate cardiovascular effects of pancuronium, alcuronium and tubocurarine in man". Anaesthesia. 27 (4): 415–22. doi:10.1111/j.1365-2044.1972.tb08247.x. PMID 4264060.
  7. Hughes R, Chapple DJ. (1976). Br. J. Anaesth. 48: 59. doi:10.1093/bja/48.2.59. Missing or empty |title= (help)
  • Zahn K, Eckstein N, Tränkle C, Sadée W, Mohr K (2002). "Allosteric modulation of muscarinic receptor signaling: alcuronium-induced conversion of pilocarpine from an agonist into an antagonist". J Pharmacol Exp Ther. 301 (2): 720–8. doi:10.1124/jpet.301.2.720. PMID 11961078.
  • Maass A, Mohr K (1996). "Opposite effects of alcuronium on agonist and on antagonist binding to muscarinic receptors". Eur J Pharmacol. 305 (1–3): 231–4. doi:10.1016/0014-2999(96)00240-3. PMID 8813558.
  • Jakubík J, Tucek S (1994). "Protection by alcuronium of muscarinic receptors against chemical inactivation and location of the allosteric binding site for alcuronium". J Neurochem. 63 (5): 1932–40. doi:10.1046/j.1471-4159.1994.63051932.x. PMID 7931349.
  • Proska J, Tucek S (1994). "Mechanisms of steric and cooperative actions of alcuronium on cardiac muscarinic acetylcholine receptors". Mol Pharmacol. 45 (4): 709–17. PMID 8183250.