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A3109

Sigma-Aldrich

A-803467

≥98% (HPLC)

Synonyme(s) :

5-4(-Chlorophenyl)-N-(3,5-dimethoxyphenyl)furan-2-carboxamide

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About This Item

Formule empirique (notation de Hill):
C19H16NO4Cl
Numéro CAS:
944261-79-4
Poids moléculaire :
357.79
Numéro MDL:
MFCD10574689
Code UNSPSC :
12352200
ID de substance PubChem :
329770815
Nomenclature NACRES :
NA.77

Pureté

≥98% (HPLC)

Forme

powder

Couleur

white to tan

Solubilité

DMSO: >10 mg/mL

Auteur

Abbott

Température de stockage

room temp

Chaîne SMILES 

COc1cc(NC(=O)c2ccc(o2)-c3ccc(Cl)cc3)cc(OC)c1

InChI

1S/C19H16ClNO4/c1-23-15-9-14(10-16(11-15)24-2)21-19(22)18-8-7-17(25-18)12-3-5-13(20)6-4-12/h3-11H,1-2H3,(H,21,22)

Clé InChI

VHKBTPQDHDSBSP-UHFFFAOYSA-N

Description générale

A-803467 inhibits spontaneous and evoked action potentials in sensory neurons. It exhibits antinociceptive effects. A-803467 decreases the firing in spinal dorsal horn neurons in vivo.
The small molecule A-803467 is a potent and selective Nav1.8 sodium channel blocker. Nav1.8 is a tetrodotoxin-resistant (TTX-R) sodium channel that contributes to pain sensation by transmitting pain stimuli in peripheral sensory neurons; blockage of this channel by A-803467 reduces pain with varying effectiveness in a number of different models. A-803467 has been used to further understand the role of Nav1.8 in transmitting pain stimuli and also can be used as an analgesic.

Actions biochimiques/physiologiques

A-803467 blocks Nav1.8 in both half-maximal inactive and resting states with an IC50 of 8 nM and IC50 of 79 nM, respectively. A-803467 is over 100-fold more selective vs. human Nav1.2, 1.3, 1.5 and 1.7.

Caractéristiques et avantages

This compound was developed by Abbott. To browse the list of other pharma-developed compounds and Approved Drugs/Drug Candidates, click here.

Code de la classe de stockage

11 - Combustible Solids

Classe de danger pour l'eau (WGK)

WGK 3

Point d'éclair (°F)

Not applicable

Point d'éclair (°C)

Not applicable

Certificats d'analyse (COA)

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Sigma-Aldrich

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Voltage-gated sodium channels in nociceptive neurons are attractive targets for novel pain therapeutics. Although drugs that target voltage-gated sodium channels have proven value as pain therapeutics, the drugs that are currently available are non-specific sodium channel inhibitors, which limit their
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Accumulating myelin abnormalities and conduction slowing occur in peripheral nerves during aging. In mice deficient of myelin protein P0, severe peripheral nervous system myelin damage is associated with ectopic expression of Nav1.8 voltage-gated Na(+) channels on motor axons aggravating the
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Sodium Channels

Voltage-gated sodium channels are present in most excitable cell membranes and play an important role in generating action potentials.

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