TNP-ATP triethylammonium
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TNP-ATP triethylammonium is a P2X receptor antagonist with an IC50 of 0.010 μM for P2X3 and an IC50 of 0.062 μM for P2X2/3. TNP-ATP triethylammonium acts as an inhibitor of CheA autophosphorylation, with a Ki of 0.7 µM. TNP-ATP triethylammonium blocks the functional activation of P2X1-7 receptors. TNP-ATP triethylammonium attenuates hypoxia-induced IL-1β expression and release. TNP-ATP triethylammonium alleviates visceral pain, and improves hypoxia-induced cognitive impairment, insufficient myelination and neuroinflammation. Binding of TNP-ATP triethylammonium to CheA enhances the fluorescence of the TNP group. TNP-ATP triethylammonium can be used in studies related to visceral pain. NP-ATP triethylammonium can be used in studies related to hypoxia-induced insufficient myelination and cognitive decline.
For research use only. We do not sell to patients.
- Purity: 98.7%
- CAS No.: 61368-63-6
- Formula: C40H77N12O19P3
- Molecular Weight:1123.03
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Storage:
Solution, -20°C, 2 years
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Biological Activity
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Chemical Information
- Purity & Documentation
- References
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Help & FAQs
All P2X Receptor Isoforms
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Biological Activity
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P2X3 Receptor 0.010 μM (IC50) |
P2X2/3 0.062 μM (IC50) |
IL-1β |
TNP-ATP triethylammonium (3 min) potently blocks agonist-mediated activation of recombinant P2X3 receptors (IC50 = 0.010 μM) and recombinant P2X2/3 receptors (IC50 = 0.062 μM) in 1321N1 cells by inhibiting cytoplasmic calcium influx[1].
TNP-ATP triethylammonium attenuates hypoxia-induced IL-1β expression and release in vitro[2].
TNP-ATP triethylammonium binds to the dimer of E. coli CheA (H48Q mutant), with macroscopic dissociation constants of Kd1 = 0.4 µM and Kd2 = 1.8 µM[3].
TNP-ATP (0.66-9.9 µM) triethylammonium potently inhibits autophosphorylation of wild-type E. coli CheA, with a competitive inhibition constant (Ki) of 0.7 µM[3].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
TNP-ATP (1-8 mg/kg; i.p.; single dose; 2 h after hypoxia exposure) triethylammonium significantly ameliorates hypoxia-induced cognitive dysfunction, hypomyelination, neuroinflammation, and glutamate deregulation, with peak efficacy across all measured endpoints at 2 mg/kg[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:129J (adult male, 20-25 g)[1]
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Dosage:1.28 μmol/kg; 12.8 μmol/kg; 38.4 μmol/kg; 128 μmol/kg
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Administration:i.p.; single dose (3 minutes prior to acetic acid injection)
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Result:Reduced acetic acid-induced abdominal constrictions dose-dependently, with an ED50 of 6.35 μmol/kg (i.p.).
Completely abolished nociceptive behavior at 128 μmol/kg (i.p.).
Showed antinociceptive potency comparable to morphine (ED50=3 μmol/kg, i.p.), and 6-10 fold greater than suramin and PPADS, and 10 fold greater than TNP-AMP.
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Animal Model:Sprague-Dawley (postnatal day 0, either sex; male used for P30 Y-maze, P45 Morris water maze, and P60 MRI DTI testing; neonatal hypoxic brain injury model)[2]
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Dosage:1 mg/kg; 2 mg/kg; 4 mg/kg; 8 mg/kg
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Administration:i.p.; single dose; 2 h after hypoxia exposure
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Result:Reduced days needed to reach learning criterion in Y-maze test (P30 male rats) in a dose-dependent manner, with peak efficacy at 2 mg/kg (P < 0.01 vs hypoxia-only group).
Increased time spent in target quadrant and number of platform location crossings in Morris water maze test (P45 male rats) at 2 mg/kg (P < 0.05 vs hypoxia-only group), reversing hypoxia-induced spatial memory deficits.
Attenuated hypoxia-induced expansion of septum and lateral ventricles, restored destroyed myelin structure in corpus callosum (CC), and fully restored fractional anisotropy (FA) values in CC and middle corpus callosum (MCC) to normal control levels at 2 mg/kg (P < 0.01 vs hypoxia-only group) in MRI DTI scanning (P60 male rats).
Reduced hypoxia-induced elevation of IL-1β protein levels in brain tissue at 1 day post-hypoxia at 2 mg/kg (P < 0.05 vs hypoxia-only group).
Prevented hypoxia-induced glutamate elevation in periventricular zone at both 4 h and 1 day post-hypoxia at 2 mg/kg (P < 0.01 at 4 h, P < 0.05 at 1 day vs hypoxia-only group).
Chemical Information
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CAS No. 61368-63-6
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Appearance Liquid
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Molecular Weight 1123.03
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Formula C40H77N12O19P3
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Color Orange to red
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SMILES
CCN(CC)CC.CCN(CC)CC.CCN(CC)CC.CCN(CC)CC.NC1=NC=NC2=C1N=CN2[C@H](O3)[C@H](O4)[C@H](OC54C([N+]([O-])=O)=CC([N+]([O-])=O)=CC5[N+]([O-])=O)[C@H]3COP(O)(OP(OP(O)(O)=O)(O)=O)=O
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Solution, -20°C, 2 years
Purity & Documentation
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Data Sheet (276 KB)
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SDS (251 KB)
- English - EN (251 KB)
- Français - FR (251 KB)
- Deutsch - DE (251 KB)
- Norwegian - NO (251 KB)
- Español - ES (251 KB)
- Swedish - SV (251 KB)
- Italian - IT (251 KB)
- Korean - KR (251 KB)
- Portuguese - PT (251 KB)
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Handling Instructions (2659 KB)
References
[1]. Honore P, et al. TNP-ATP, a potent P2X3 receptor antagonist, blocks acetic acid-induced abdominal constriction in mice: comparison with reference analgesics. Pain. 2002 Mar;96(1-2):99-105. [Content Brief]
[2]. Xiao J, et al. TNP-ATP is Beneficial for Treatment of Neonatal Hypoxia-Induced Hypomyelination and Cognitive Decline. Neurosci Bull. 2016;32(1):99-107. [Content Brief]
[3]. Stewart RC, et al. TNP-ATP and TNP-ADP as probes of the nucleotide binding site of CheA, the histidine protein kinase in the chemotaxis signal transduction pathway of Escherichia coli. Biochemistry. 1998;37(35):12269-12279. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
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