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| Clinical data | |
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| Trade names | Alloferin |
| Other names | Ro 4-3816, diallylnortoxiferine |
| AHFS/Drugs.com | International Drug Names |
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| Pharmacokinetic data | |
| Metabolism | not metabolized |
| Elimination half-life | 2–4 hours |
| Excretion | 70–90% unchanged in urine 1.3 mL/kg/min |
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| CompTox Dashboard (EPA) | |
| ECHA InfoCard | 100.035.648 |
| Chemical and physical data | |
| Formula | C44H50N4O2+2 |
| Molar mass | 666.910 g·mol−1 |
| 3D model (JSmol) | |
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Alcuronium chloride (formerly marketed as Alloferin) 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, 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 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 alcuronium.
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. It also has a more rapid onset of action, and is ~1.5 times as potent as tubocurarine. The pharmacological action of alcuronium is readily reversed by neostigmine, and it produces little histamine release. The major disadvantage of alcuronium is that it elicits a vagolytic effect produced by a selective atropine-like blockade of cardiac muscarinic receptors.
Effects
- Cardiovascular system: histamine release and blockage of the sympathetic ganglia including adrenal medulla could cause hypotension
- Respiratory system: apnea due to phrenic blockage but bronchoconstriction can occur from the histamine release
- Central nervous system: no effect on intraocular pressure
- Autonomic ganglion blockade can cause a 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
See also
Further reading
- 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. S2CID 534003.
- 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. S2CID 23053191.
- 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.