Alpha-conotoxins act on postsynaptic membranes, they bind to the nicotinic acetylcholine receptors (nAChR) and thus inhibit them. The toxin with a disulfide connectivity C1-C2, C3-C4 (shown in the sequence annotation) block the rat nicotinic acetylcholine receptor (AChR) alpha-9-alpha-10/CHRNA9-CHRNA10 with an IC(50) of 1.2 uM, whereas the one with C1-C3, C2-C4 shows a lower activity with an IC(50) of 3.9 uM. Expressed by the venom duct. The cysteine framework is XXIV (C-CC-C). The 3 possibles disulfide-bond connectivities isomers have been synthesized: (C1-C2, C3-C4), (C1-C3, C2-C4), and (C1-C4, C2-C3). The 3 disulfide isomers are poorly structured in aqueous solution. The toxin (with connectivity C1-C2, C3-C4) does not have inhibitory effect on alpha-2-beta-4/CHRNA2-CHRNB4, alpha-3-beta-2/CHRNA3-CHRNB2, alpha-3-beta-4/CHRNA3-CHRNB4, alpha-4-beta-2/CHRNA4-CHRNB2, alpha-4-beta-4/CHRNA4-CHRNB4 and alpha-7/CHRNA7. The toxin (with connectivity C1-C4, C2-C3) does not have inhibitory effect on alpha-9-alpha-10/CHRNA9-CHRNA10 (PubMed:23382933). Belongs to the conotoxin B superfamily.