Icotrokinra may act as an agonist of the neurotransmitter γ-aminobutyric acid (GABA), interfering with GABA-mediated central nervous system synaptic transmission, thereby leading to nerve paralysis and death of the parasite; at the same time, it can also activate glutamate-gated chloride ion channels expressed on nematode neurons and pharyngeal muscle cells, prompting neurons or muscle cells to maintain a hyperpolarized or depolarized state, thereby causing paralysis and death of the parasite.