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Potent voltage-dependent NaV1.8 channel blocker (IC50 = 11 nM in recombinant human NaV1.8 channels). Reduces tactile allodynia in neuropathic rat models. 3- and 28-fold more potent at NaV1.8 channels compared to NaV1.2 and NaV1.7 channels respectively.
|Storage||Store at RT|
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.
|Solvent||Max Conc. mg/mL||Max Conc. mM|
Preparing Stock Solutions
The following data is based on the product molecular weight 480.99. 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|
|0.5 mM||4.16 mL||20.79 mL||41.58 mL|
|2.5 mM||0.83 mL||4.16 mL||8.32 mL|
|5 mM||0.42 mL||2.08 mL||4.16 mL|
|25 mM||0.08 mL||0.42 mL||0.83 mL|
References are publications that support the biological activity of the product.
Zhang et al (2010) A-887826 is a structurally novel, potent and voltage-dependent NaV1.8 sodium channel blocker that attenuates neuropathic tactile allodynia in rats. Neuropharmacology 59 201 PMID: 20566409
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Keywords: A 887826, A 887826 supplier, A887826, sodium, channel, blocker, blocks, NaV1.8, voltage-dependent, ion, channels, antiallodynic, Voltage-gated, Sodium, Channels, 4249, Tocris Bioscience
1 Citation for A 887826
Citations are publications that use Tocris products. Selected citations for A 887826 include:
Cho et al (2013) Injury-induced HDAC5 nuclear export is essential for axon regeneration. Nat Chem Biol 155 894 PMID: 24209626
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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.