Nicotinic anthelmintic
Pyrantel pamoate
Nicotinic acetylcholine at nematode neuromuscular junctions, causing spastic paralysis.
Primary Mechanism of Action
Clinical / Scientific
Pyrantel opens L-subtype nicotinic receptors on nematode muscle, depolarizing the neuromuscular junction. Spastic paralysis prevents attachment in the gut; the poorly absorbed pamoate salt keeps action largely intraluminal.
Pathway Targets
Nematode nAChR
Scientific explanation
Agonism causing depolarizing neuromuscular blockade.
Pathway Convergence
Clinical / Scientific
Target → pathway → downstream effect → biological consequence. This is a mechanistic map, not a treatment claim.
Spastic paralysis
Target to downstream effect: nAChR agonism → Persistent depolarization → Loss of attachment in the intestine
Mechanistically Relevant Repurposed & Adjunctive Applications
Intestinal nematodes
EstablishedMechanistic rationale
Established for labelled pinworm and other susceptible intestinal nematode infections.
Mechanistic Application Matrix
| Biological Target | Mechanism | Potential Relevance | Evidence Level |
|---|---|---|---|
| nAChR | Agonism | Nematode locomotion / attachment | Established mechanism |
In Plain Language
Pyrantel overstimulates worm muscle receptors so the worm stiffens and cannot hang onto the intestinal wall.
Compounds Sharing Pathways
Other library compounds whose structured pathway data overlap this ingredient. Shared pathways are not combination recommendations.
Nematode nAChR
Mechanistic information is provided for scientific and educational purposes. Discussion of biological pathways or investigational applications does not establish clinical efficacy or constitute individualized medical advice.