Alpha-conotoxins act on postsynaptic membranes, they bind to the nicotinic acetylcholine receptors (nAChR) and thus inhibit them. This synthetic toxin blocks rat alpha-3beta-2/CHRNA3-CHRNB2 nAChRs (IC(50)=0.3 nM) and alpha-7/CHRNA7 nAChRs (IC(50)=76 nM). This synthetic toxin blocks rat alpha-3-beta-2/CHRNA3-CHRNB2 nAChRs (IC(50)=0.2 nM). Expressed by the venom duct. The cysteine framework is I (CC-C-C). Alpha4/7 pattern. Amidation at Cys-17 is important for activity, since suppression of this modification induces a 1.9-fold decrease in inhibitory potency on alpha-3-beta-2/CHRNA3-CHRNB2 nAChRs (IC(50)=0.54 nM), and a 4.8-fold decrease in inhibitory potency on alpha-7/CHRNA7 nAChRs (IC(50)=367 nM). Sulfation at Tyr-16 is important for activity, since suppression of this modification induces a 2.3-fold decrease in inhibitory potency on alpha-3-beta-2/CHRNA3-CHRNB2 nAChRs (IC(50)=0.64 nM), and a 11-fold decrease in inhibitory potency on alpha-7/CHRNA7 nAChRs (IC(50)=836 nM). Belongs to the conotoxin A superfamily.