a-conotoxin mii

α-Conotoxin MII is a highly potent and selective competitive antagonist for α3β2 subunit-containing nicotinic receptors (IC50 = 0.5 - 3.5 nM at α3β2 expressed in Xenopus oocytes). Also potently blocks β3-containing neuronal nicotinic receptors. Displays >

α-Conotoxin MII acetate is a 16-amino acid peptide from the venom of the marine snail Conus magus. α-Conotoxin MII acetate potently blocks nicotinic acetylcholine receptors composed of α3β2 subunits, with an IC50 of 0.5 nM. α-Conotoxin MII acetate potently blocks β3-containing neuronal nicotinic acetylcholine receptors.

AT-1001 is an α3β4 nAChR partial agonist. AT-1001 attenuates stress-induced reinstatement of nicotine seeking in a rat model of relapse and induces minimal withdrawal in dependent rats. AT-1001 also potently and reversibly blocks epibatidine-induced inward currents in HEK cells transfected with α3β4 nAChR. Importantly, AT-1001 potently and dose-dependently blocks nicotine self-administration in rats, without affecting food responding. When tested in a nucleus accumbens (NAcs) synaptosomal preparation, AT-1001 inhibits nicotine-induced [³H]dopamine release poorly and at significantly higher concentrations compared with mecamylamine and conotoxin MII.

α-Conotoxin MII TFA (α-CTxMII TFA), a peptide of 16 amino acids derived from Conus magus venom, selectively inhibits nicotinic acetylcholine receptors (nAChRs) composed of α3β2 subunits with an IC50 of 0.5 nM and effectively targets β3-containing neuronal nicotinic receptors. [1] [2] [3]