Alpha-conotoxins act on postsynaptic membranes, they bind to the nicotinic acetylcholine receptors (nAChR) and thus inhibit them. This toxin is very potent on alpha-9-alpha-10/CHRNA9-CHRNA10 nAChR (IC(50)=4.61-12 nM for the bead isomer (I-II; III-IV), IC(50)=7-16 nM for the ribbon isomer (I-IV; II-III) and IC(50)=22.7 nM for the globular isomer (I-III; II-IV)) (PubMed:26170295, PubMed:31986036). The bead isomer also shows a weak inhibition on other nAChRs (alpha-1-beta-1-delta-epsilon/CHRNA1-CHRNB1-CHRND-CHRNE, alpha-7/CHRNA7, alpha-6/alpha-3-beta-2-beta-3 (CHRNA6/CHRNA3-CHRNB2-CHRNB3), alpha-3-beta-2/CHRNA3-CHRNB2, alpha-2-beta-2/CHRNA2-CHRNB2, alpha-6/alpha-3-beta-4 (CHRNA6/CHRNA3-CHRNB4), alpha-4-beta-2/CHRNA4-CHRNB2, alpha-4-beta-4/CHRNA4-CHRNB4, alpha-2-beta-4/CHRNA2-CHRNB4, alpha-3-beta-4/CHRNA3-CHRNB4) (PubMed:26170295, PubMed:31986036). The toxin blockade is voltage-dependent, and its binding site does not overlap with the binding site of the competitive antagonist alpha-conotoxin RgIA (PubMed:26170295). The toxin inhibits Sf9 cell growth (PubMed:22825834). Both the bead and ribbon isomers relieve pain effects in the rat chronic constriction injury (CCI) model of neuropathic pain, and in the acute pain model of tail flick test, but have no effect on motor performance (PubMed:26170295, PubMed:26706456). Expressed by the venom duct. The cysteine framework is XIV (C-C-C-C). The native disulfide bond pairing has not been studied. Three isomers may exist: the bead isomer (I-II; III-IV), the globular isomer (I-III; II-IV), the ribbon isomer (I-IV; II-III). They have all been synthesized and their activity tested (PubMed:26170295). All of them show similar potency on alpha-9-alpha-10 (CHRNA9-CHRNA10) nAChR, showing that disulfide bonds does not significantly affect their activity (PubMed:26170295). In addition, removal of disulfide bonds does not affect the activity on alpha-9-alpha-10 (CHRNA9-CHRNA10) nAChR either (PubMed:31986036). Is a promising analgesic drug candidate. It shows analgesic effect without the development of tolerance and retains its effect two weeks after drug withdrawal. This toxin (both bead (I-II; III-IV) and ribbon (I-IV; II-III) isomers) does not inhibit voltage-gated calcium channels from DRG neurons (Cav1.2/CACNA1C, Cav2.1/CACNA1A, Cav2.2/CACNA1B and Cav2.3/CACNA1E). Belongs to the conotoxin O1 superfamily.