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GX 201 is a potent and selective Nav1.7 blocker (IC50 = 3.2 nM). Exhibits 10x selectivity for Nav1.7 over Nav1.1, Nav1.2, and Nav1.6 channels. Displays prolonged residency time on the Nav1.7 channel. Chronic dosing increases compound potency ~10-fold and provides efficacy that persists after the compound has cleared from plasma. Suppresses neuropathic pain in a mouse diabetic neuropathy model. Analgesic.
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|Storage||Store at -20°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.
|Solvent||Max Conc. mg/mL||Max Conc. mM|
The following data is based on the product molecular weight 563. 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||1.78 mL||8.88 mL||17.76 mL|
|5 mM||0.36 mL||1.78 mL||3.55 mL|
|10 mM||0.18 mL||0.89 mL||1.78 mL|
|50 mM||0.04 mL||0.18 mL||0.36 mL|
References are publications that support the biological activity of the product.
Shields et al (2018) Insensitivity to pain upon adult-onset deletion of NaV1.7 or its blockade with selective inhibitors J.Neurosci. 38 10180 PMID: 30301756
Banker et al (2018) Selective NaV1.7 antagonists with long residence time show improved efficacy against inflammatory and neuropathic pain. Cell Rep. 24 3133 PMID: 30231997
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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.