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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 |
| ATC code | |
| Pharmacokinetic data | |
| Metabolism | not metabolized |
| Eliminationhalf-life | 2–4 hours |
| Excretion | 70–90% unchanged in urine 1.3 mL/kg/min |
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| CAS Number | |
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| UNII | |
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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 asAlloferin) is aneuromuscular blocking (NMB) agent, alternatively referred to as a skeletalmuscle relaxant. It is a semi-synthetic substance prepared from C-toxiferine I,[1] abis-quaternary alkaloid obtained fromStrychnos 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 forgantacurium. The replacement of both theN-methyl groups withN-allyl moieties yieldedN,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.[3] It also has a more rapid onset of action, and is ~1.5 times as potent astubocurarine.[4] The pharmacological action of alcuronium is readily reversed byneostigmine, and it produces littlehistamine release.[5] The major disadvantage of alcuronium is that it elicits a vagolytic effect produced by a selectiveatropine-like blockade of cardiacmuscarinic receptors.[4][6][7]
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