Alpha-conotoxins act on postsynaptic membranes, they bind to the nicotinic acetylcholine receptors (nAChR) and thus inhibit them. This toxin specifically blocks mammalian neuronal nAChR of the alpha-7/CHRNA7, alpha-3-beta-2/CHRNA3-CHRNB2 (IC(50)=370 nM) and alpha-4-beta-2/CHRNA4-CHRNB2 subtypes. VxXXB inhibits alpha-7/CHRNA7 and alpha-3-beta-2/CHRNA3-CHRNB2 nAChR subtypes with the highest efficiency, followed by VxXXA and VxXXC. VxXXB and VxXXC inhibit the alpha-4-beta-2/CHRNA4-CHRNB2 nAChR subtype more efficiently than VxXXA. Homodimer or pseudo-homodimer. Three dimers exist: homodimer of VxXXA, pseudo-homodimer of both VxXXA and [hydroxyPro-74]VxXXA and homodimer of [hydroxyPro-74]VxXXA. These three components exist in a 1:2:1 ratio. Expressed by the venom duct. The cysteine framework is XX (C-CC-C-CC-C-C-C-C). Contains 5 disulfide bonds. VxXXA stands for the form with the Pro-55 hydroxylated. A second major form has both Pro-55 and Pro-74 hydroxylated. The two major forms VxXXA and [hydroxyPro-74]VxXXA exist in a 1:1 ratio. Minor forms are [hydroxyPro-70,hydroxyPro-74]VxXXA and [Pro-55]VxXXA. With hydroxyPro-55. With hydroxyPro-55 and hydroxyPro-74. Belongs to the conotoxin D superfamily.