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Biological Activity for A 803467
A 803467 is a selective blocker of NaV1.8 channels (IC50 values are 8, 2450, 6740, 7340 and 7380 nM for hNaV1.8, hNaV1.3, hNaV1.7, hNaV1.5 and hNaV1.2 channels respectively). Shows no significant activity against TRPV1, P2X2/3, CaV2.2 and KCNQ2/3 channels. Antinociceptive; potently attenuates mechanical allodynia in two models of neuropathic pain following i.p. administration.
Compound Libraries for A 803467
Technical Data for A 803467
|Storage||Store at +4°C|
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
Tocris products are intended for laboratory research use only, unless stated otherwise.
Solubility Data for A 803467
|Solvent||Max Conc. mg/mL||Max Conc. mM|
Preparing Stock Solutions for A 803467
The following data is based on the product molecular weight 357.79. Batch specific molecular weights may vary from batch to batch due to the degree of hydration, which will affect the solvent volumes required to prepare stock solutions.
|Concentration / Solvent Volume / Mass||1 mg||5 mg||10 mg|
|1 mM||2.79 mL||13.97 mL||27.95 mL|
|5 mM||0.56 mL||2.79 mL||5.59 mL|
|10 mM||0.28 mL||1.4 mL||2.79 mL|
|50 mM||0.06 mL||0.28 mL||0.56 mL|
References for A 803467
References are publications that support the biological activity of the product.
Rush and Cummins (2007) Painful research: identification of a small-molecule inhibitor that selectively targets NaV1.8 sodium channels. Mol.Interv. 7 192 PMID: 17827438
McGaraughty et al (2008) A selective NaV1.8 sodium channel blocker, A-803467 [5-(4-chlorophenyl-N-(3,5-dimethoxyphenyl)furan-2-carboxamide], attenuates spinal neuronal activity in neuropathic rats. J.Pharmacol.Exp.Ther. 324 1204 PMID: 18089840
Kort et al (2008) Discovery and biological evaluation of 5-Aryl-2-furfuramides, potent and selective blockers of the Nav1.8 sodium channel with efficacy in models of neuropathic and inflammatory pain. J.Med.Chem. 51 407 PMID: 18176998
Jarvis et al (2007) A-803467, a potent and selective NaV1.8 sodium channel blocker, attenuates neuropathic and inflammatory pain in the rat. Proc.Natl.Acad.Sci. 104 8520
If you know of a relevant reference for A 803467, please let us know.
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Keywords: A 803467, A 803467 supplier, Selective, NaV18, blockers, Sodium, Channels, voltage-gated, voltage-dependent, Na+, A803467, Voltage-gated, 2976, Tocris Bioscience
7 Citations for A 803467
Citations are publications that use Tocris products. Selected citations for A 803467 include:
Bladen (2012) Common mechanisms of drug interactions with sodium and T-type calcium channels. Mol Pharmacol 82 481 PMID: 22695716
Schuelert and McDougall (2012) Involvement of Nav 1.8 sodium ion channels in the transduction of mechanical pain in a rodent model of osteoarthritis. Arthritis Res Ther 14 R5 PMID: 22225591
Curtright et al (2015) Modeling nociception in zebrafish: a way forward for unbiased analgesic discovery. PLoS One 10 e0116766 PMID: 25587718
Stone et al (2013) Attenuation of autonomic reflexes by A803467 may not be solely caused by blockade of NaV 1.8 channels. Nat Med 543 177 PMID: 23523647
Mascanfroni et al (2015) Metabolic control of type 1 regulatory T cell differentiation by AHR and HIF1-α. Biol Open 21 638 PMID: 26005855
Liu et al (2014) Functional upregulation of nav1.8 sodium channels on the membrane of dorsal root Ganglia neurons contributes to the development of cancer-induced bone pain. PLoS One 9 e114623 PMID: 25503076
Wu et al (2016) CXCL13/CXCR5 enhances sodium channel Nav1.8 current density via p38 MAP kinase in primary sensory neurons following inflammatory pain Scientific Reports 6 34836 PMID: 27708397
Do you know of a great paper that uses A 803467 from Tocris? Please let us know.
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Literature in this Area
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Epilepsy is a brain disease that affects 60 million people globally. More than 20 anti-seizure drugs are currently available, but these do not address the underlying causes of the condition. This poster summarizes current knowledge about the development of the condition and highlights some approaches that have disease-modifying effects in proof-of-concept studies.