2. Signaling Pathways
  3. Membrane Transporter/Ion Channel
    Neuronal Signaling
  4. nAChR
  5. nAChR Antagonist

nAChR Antagonist

nAChR Antagonists (62):

Cat. No. Product Name Effect Purity
  • HY-N2332A
    Methyllycaconitine citrate
    		Antagonist 99.58%
    Methyllycaconitine citrate is a specific antagonist of α7 neuronal nicotinic acetylcholine receptor (α7nAChR) with blood-brain barrier permeability.
  • HY-P5188A
    Waglerin-1
    		Antagonist
    Waglerin-1, a 22-amino acid peptide, is a competitive antagonist of the muscle nicotinic receptor (nAChR).
  • HY-P1050A
    COG 133 TFA
    		Antagonist 99.39%
    COG 133 TFA is a fragment of Apolipoprotein E (APOE) peptide. COG 133 TFA competes with the ApoE holoprotein for binding the LDL receptor, with potent anti-inflammatory and neuroprotective effects. COG 133 TFA is also a nAChR antagonist with an IC50 of 445 nM.
  • HY-P1264
    α-Bungarotoxin
    		Antagonist ≥99.0%
    α-Bungarotoxin is a competitive antagonist at nicotinic acetylcholine receptors (nAChRs). α-Bungarotoxin, a selective α7 receptor blocker, blocks α7 currents with an IC50 of 1.6 nM and has no effects on α3β4 currents at concentrations up to 3 μM.
  • HY-B0567
    Dequalinium Chloride
    		Antagonist 99.91%
    Dequalinium chloride is an Apamin (HY-P0256)-sensitive potassium channel selective blocker. Dequalinium chloride is a cationic, lipophilic mitochondrial poison. Dequalinium chloride is also an antagonist pf α7 nAChR, and an anti-microbial antiseptic agent with a broad bactericidal and fungicidal activity.
  • HY-13596
    Cisatracurium besylate
    		Antagonist ≥98.0%
    Cisatracurium besylate (51W89) is a nondepolarizing neuromuscular blocking agent, antagonizing the action of acetylcholine by inhibiting neuromuscular transmission.
  • HY-B0569
    Hexamethonium Bromide
    		Antagonist 99.91%
    Hexamethonium Bromide is a non-selective ganglionic nicotinic-receptor antagonist (nAChR) antagonist, with mixed competitive and noncompetitive activity. Hexamethonium Bromide has anti-hypertensive activity. Hexamethonium Bromide attenuates sympathetic activity and blood pressure in spontaneously hypertensive animal models.
  • HY-107670
    Dihydro-β-erythroidine hydrobromide
    		Antagonist 99.84%
    Dihydro-β-erythroidine (DHβE) hydrobromide is a potent, orally active, and competitive antagonist of neuronal nAChRs. Dihydro-β-erythroidine hydrobromide shows selectivity for α4β4 and α4β2 nAChRs, with IC50s of 0.19 and 0.37 μM, respectively. Antidepressant-like activities.
  • HY-B0429
    Pancuronium dibromide
    		Antagonist ≥98.0%
    Pancuronium dibromide, a bis-quaternary steroid, is a neuromuscular relaxant. Pancuronium dibromide inhibits neuromuscular transmission by competing with acetylcholine for binding sites on nACh receptors. Pancuronium dibromide also inhibits cardiac muscarinic receptors and has a sympathomimetic action.
  • HY-B0743A
    Pipecuronium bromide
    		Antagonist 98.71%
    Pipecuronium bromide is a potent long-acting nondepolarizing steroidal neuromuscular blocking agent (NMBA), and a bisquaternary ammonium compound. Pipecuronium bromide is a powerful competitive nAChR antagonist with a Kd of 3.06 μM.
  • HY-P1269A
    α-Conotoxin AuIB TFA
    		Antagonist
    α-Conotoxin AuIB TFA, a potent and selective α3β4 nicotinic acetylcholine receptor (nAChR) antagonist, blocks α3β4 nAChRs expressed in Xenopus oocytes with an IC50 of 0.75 μM.
  • HY-106901AS
    Asoxime-d4 dichloride
    		Antagonist
    Asoxime-d4 (dichloride) is the deuterium labeled Asoxime dichloride. Asoxime dichloride (HI-6) is an antagonist to acetylcholine receptors (AChRs) including the nicotinic receptor, α7 nAChR. Asoxime dichloride involves in modulating immunity response. Asoxime dichloride (HI-6) can be used as an antigen and improves vaccination efficacy in the nervous system[1].
  • HY-137231B
    (S)-UFR2709 hydrochloride
    		Antagonist 98.10%
    (S)-UFR2709 (hydrochloride) is a competitive nAChR antagonist and displays higher affinity for α4β2 nAChRs than for α7 nAChRs. (S)-UFR2709 (hydrochloride) decreases anxiety and reduces ethanol consumption and ethanol preference in alcohol-preferring rats. (S)-UFR2709 (hydrochloride) acts as an anxiolytic agent and can be used for the study of nicotine addiction.
  • HY-107672
    MG624
    		Antagonist
    MG624 is a potent and selective neuronal α7 nAChR antagonist with a Ki of 106 nM.
  • HY-P1268A
    α-Conotoxin PIA TFA
    		Antagonist 99.05%
    α-Conotoxin PIA TFA is a nicotinic acetylcholine receptor (nAChR) antagonist that targets nAChR subtypes containing α6 and α3 subunits. α-Conotoxin PIA has the potential for the research of Parkinson’s disease, and schizophrenia。
  • HY-101347
    Chlorisondamine diiodide
    		Antagonist ≥98.0%
    Chlorisondamine (diiodide) is a potent nicotinic acetylcholine receptor (nAChR) antagonist and a ganglion blocker. Chlorisondamine antagonizes some of nicotine's central actions in a potent, long-lasting and pharmacologically selective way.
  • HY-152170
    bPiDI
    		Antagonist 99.65%
    bPiDI is a novel selective α6β2 nicotinic receptor antagonist. bPiDI inhibits nicotine-evoked striatal dopamine (DA) release through an interaction with α6β2-containing nAChRs.
  • HY-136146
    SUVN-911
    		Antagonist 99.40%
    SUVN-911 is a potent, selective, brain penetrated and orally bioavailable neuronal nicotinic acetylcholine α4β2 receptor antagonist, with a Ki of 1.5 nM. SUVN-911 has antidepressant activity.
  • HY-P5149
    αC-Conotoxin PrXA
    		Antagonist 98.44%
    αC-Conotoxin PrXA is a paralytic peptide neurotoxin and a competitive nAChR antagonist, with IC50s of 1.8 nM (α1β1εδ, adult) and 3.0 nM (α1β1γδ, fetal), respectively. αC-Conotoxin PrXA competes with α-bungarotoxin at the α/δ and α/γ subunit interfaces of the nAChR, shows high specificity against neuromuscular nAChR.
  • HY-145298
    Dicloromezotiaz
    		Antagonist 98.65%
    Dicloromezotiaz is a potent insecticide acting on nicotinic acetylcholine receptors (nAChRs). Dicloromezotiaz can be used to control a broad range of lepidoptera.