Ac1 weakly inhibits N-methyl-D-aspartate receptor subunit 2B (NR2B) (IC(50)=8.22 uM). In vivo, shortens sleep latency and extends sleep time after lateral brain administration. Is more potent than Ac1-O6P for these effects. Also has an analgesic activity similar to that of Ac1-O6P. Ac1-O6P has no or very weak activity on voltage-gated channels and receptors tested. In vivo, shortens sleep latency and extends sleep time after lateral brain administration. Is less potent than Ac1 for these effects. Also has an analgesic activity similar to that of Ac1. Expressed by the venom duct. Ac1-O6P is hydroxylated once at Pro-60, whereas Ac1 is hydroxylated at both Pro-57 and Pro-60. Trp-64 is supposed to be a D-amino acid in Ac1-O6P. Hydroxylation at Pro-57 is important for activity on N-methyl-D-aspartate receptors, since Ac1 is 5-fold more potent than Ac1 on NR2A/GRIN2A and NR2B/GRIN2B N-methyl-D-aspartate (NMDA) receptors. Synthetic peptides with carboxylated glutamate residues instead of Glu-61 and Trp-65, with an optional amidation of Thr-66 show a higher analgesic activity than morphine. Hydroxylated at Pro-57 (Ac1). Not hydroxylated at Pro-57 (Ac1-O6P). The mature peptide does not contain cysteine residue. Ac1 has no or very weak activity on voltage-gated sodium channel, voltage-gated potassium channel, voltage-gated calcium channels, and NR2A/GRIN2A N-methyl-D-aspartate (NMDA) receptors. Ac1-O6P has no or very weak activity on voltage-gated sodium channel, voltage-gated potassium channel, voltage-gated calcium channels, NR2A/GRIN2A and NR2B/GRIN2B N-methyl-D-aspartate (NMDA) receptors. Belongs to the conotoxin A superfamily.