Target intelligence / Profile preview

Bungarus candidus Venom Neurotoxins

Molecular classification
Three-finger toxins (3FTx), Phospholipase A2 enzymes (PLA2), Kunitz-type serine protease inhibitors, Neurotoxin, Enzyme
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Overview

Bungarus candidus (Malayan krait) venom contains a complex mixture of neurotoxins, primarily three-finger toxins (3FTxs) and phospholipase A2 enzymes (PLA2s), that induce rapid and severe neuromuscular paralysis. β-bungarotoxins act presynaptically to irreversibly damage motor nerve terminals, while α-neurotoxins act postsynaptically to block nicotinic acetylcholine receptors. This leads to flaccid paralysis and respiratory failure, potentially resulting in death if untreated. Antivenom is the primary treatment, but its effectiveness is limited once significant paralysis develops. The venom also contains other components like L-amino acid oxidase (LAAO), hyaluronidase, and acetylcholinesterase that contribute to the overall toxicity.

Other names
Malayan Krait Venom NeurotoxinsBungarus candidus toxinsβ-bungarotoxinsα-neurotoxinsBucandin
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Mechanism of action

Presynaptic: Blocks acetylcholine release by damaging nerve terminals (β-bungarotoxins). Postsynaptic: Competitively inhibits nicotinic acetylcholine receptors (α-neurotoxins).

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Biological functions

NeurotoxicityNeuromuscular blockadeAcetylcholine receptor inhibitionPhospholipid hydrolysisSynaptic vesicle depletion
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Disease associations

EnvenomationParalysisRespiratory failure
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Safety considerations

Rapid onset of flaccid paralysisRespiratory failureIrreversible presynaptic damageLimited efficacy of antivenom after paralysis onset
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Interacting drugs

Antivenom

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