α3β2 nachr

UB 165 fumarate is an agonist of the nAChR, a partial agonist of the α4β2 subtype, and a full agonist of the α3β2 subtype, with a Ki value of 0.27 nM for binding to [3H]-nicotine measured in rat brain.

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.

α7 nAchR-JAK2-STAT3 agonist 1 is a potent inhibitor of the α7 nAchR-JAK2-STAT3 pathway that acts on nitric oxide (NO) (IC50: 0.32 μM). It has demonstrated positive effects on iNOS, IL-1β, and IL-1β in murine macrophages RAW264.7, and inhibited the expression of iNOS, IL-1β, and IL-6 in mouse macrophages. Additionally, α7 nAchR-JAK2-STAT3 agonist 1 suppressed LPS-induced NO release, NF-κB activation, and cytokine production, making it useful for studying sepsis.

α-Conotoxin ImI is a conotoxin that has been found inC. imperialisand has receptor antagonist and anticancer activities.1It is a peptide antagonist of homomeric α7 nicotinic acetylcholine receptors (nAChRs; IC50= 220 nM). α-Conotoxin ImI is selective for α7 nAChRs over α2β2, α3β2, α4β2, α2β4, α3β4, α4β4, and α1β1γδ subunit-containing nAChRs at 5 μM but does inhibit homomeric α9 nAChRs (IC50= 1,800 nM). Administration of paclitaxel in micelles containing α-conotoxin ImI decreases tumor growth in an MCF-7 mouse xenograft model.2Intracerebroventricular, but not intraperitoneal, administration of α-conotoxin ImI (20 nmol/animal) induces seizures in rats.3 1.Johnson, D.S., Martinez, J., Elgoyhen, A.B., et al.α-Conotoxin ImI exhibits subtype-specific nicotinic acetylcholine receptor blockade: Preferential inhibition of homomeric α7 and α9 receptorsMol. Pharmacol.48(2)194-199(1995) 2.Mei, D., Lin, Z., Fu, J., et al.The use of α-conotoxin ImI to actualize the targeted delivery of paclitaxel micelles to α7 nAChR-overexpressing breast cancerBiomaterials4252-65(2015) 3.McIntosh, J.M., Yoshikami, D., Mahe, E., et al.A nicotinic acetylcholine receptor ligand of unique specificity, α-conotoxin ImIJ. Biol. Chem.269(24)16733-16739(1994)

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.

LtIA-F, a novel fluorescent analogue of LtIA, provides extensive pharmacological tools for investigating the structure-function relationship, distribution, and ligand-binding domain of the α3β2 nAChR subtype.

α-Conotoxin PIA TFA is an nAChR (nicotinic acetylcholine receptor) antagonist that primarily targets nAChR subtypes containing α6 and α3 subunits, exhibiting significantly higher selectivity for α6/α3β2β3 nAChR than α3β2 nAChR, and may be used for Parkinson's disease and schizophrenia.

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].

NS3861 fumarate is an agonist of nicotinic acetylcholine receptors (nAChRs), acting as a partial agonist at α3β4 nAChR and binding with high affinity to heteromeric α3β4 nAChR, with binding Ki values of 0.62, 25, 7.8, 55 nM for α3β4, α3β2, α4β4, α4β2, respectively[1].

NS3861 is an agonist of nicotinic acetylcholine receptors (nAChRs) that binds with high affinity to heteromeric α3β4 and α4β2 nAChRs, displaying β-subunit preference and no activation at α4-containing receptors. The maximal efficacy of NS3861 depends on the ligand-binding domain, and a serine to threonine substitution in the principal subunit may explain the lack of activation at α4-containing receptors.