α3β2 nachr

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.

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 Vc1.1 TFA is a peptide isolated from Conus victoriae and a selective nAChR antagonist that inhibits α3α5β2, α3β2 and α3β4, reversing mechanical allodynia in neuropathic pain models and can be used to study neuropathic chronic pain. α-Conotoxin Vc1.1 TFA inhibits human dorsal root ganglion nerve excitability and mouse colon nociception via GABA(B) receptors.

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]

α-Conotoxin PeIA is an analgesic that inhibits nAChRs α6β4, α9α10, and α3β2, and potently inhibits the N-type calcium channel through GABAB receptor activation [1] [2] [3].

α-Conotoxin GID is a paralytic peptide neurotoxin that selectively antagonizes nAChR with IC50 values of 5 nM (α7), 3 nM (α3β2), and 150 nM (α4β2). This small, disulfide-rich peptide has potential for chronic pain inhibition. The presence of a C-terminal carboxylate is crucial, as substitution with a C-terminal carboxamide results in loss of activity against α4β2 nAChR. Derived from species of the genus Conus [1] [2] [3].

α-Conotoxin BuIA is a paralytic peptide neurotoxin that acts as a competitive antagonist of nicotinic acetylcholine receptors (nAChR), with inhibitory concentration 50 (IC50) values of 0.258 nM for α6 α3β2, 1.54 nM for α6 α3β4, and 5.72 nM for α3β2. It serves to differentiate between nAChRs containing the β2- and β4-subunits and selectively inhibits αxβ2 nAChRs, exhibiting a potency hierarchy of α6>α3>α2>α4 [1].

κ-Bungarotoxin (κ-Bgt) is a selective, potent antagonist of α3β2 neuronal nicotinic acetylcholine receptors, characterized by slow reversibility and an IC50 of 2.30 nM [1].

α-Conotoxin LtIA, an α3β2 nAChR blocker with an IC50 value of 9.8 nM, is derived from Conus litteratus venom and is utilized in researching neurological diseases, including Parkinson's disease and pain [1].