Potent and selective KV1.3 channel blocker (IC50 values are 0.0019 and 0.65 nM for KV1.3 and KV1.1, respectively). Inhibits CD4+ CCR7- T cell activation. Ameliorates rat experimental autoimmune encephalomyelitis, in a model for multiple sclerosis.
(Modifications: Disulfide bridge: 7 - 27, 13 - 32, 17 - 34)
|Storage||Store at -20°C|
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
All Tocris products are intended for laboratory research use only.
|Solubility||Soluble to 2 mg/ml in water|
Preparing Stock Solutions
The following data is based on the product molecular weight 4071.86. Batch specific molecular weights may vary from batch to batch due to solvent 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||0.25 mL||1.23 mL||2.46 mL|
|5 mM||0.05 mL||0.25 mL||0.49 mL|
|10 mM||0.02 mL||0.12 mL||0.25 mL|
|50 mM||0 mL||0.02 mL||0.05 mL|
References are publications that support the biological activity of the product.
Han et al (2008) Structural basis of a potent peptide inhibitor designed for KV1.3 channel, a therapeutic target of autoimmune disease. J.Biol.Chem. 283 19058 PMID: 18480054
Li et al (2012) Selective inhibition of CCR7(-) effector memory T cell activation by a novel peptide targeting Kv1.3 channel in a rat experimental autoimmune encephalomyelitis model. J.Biol.Chem. 287 29479 PMID: 22761436
If you know of a relevant reference for ADWX 1, please let us know.
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Keywords: ADWX 1, ADWX 1 supplier, ADWX1, KV1.3, potassium, channels, blockers, CD4+, CCR7-, T-cell, autoimmune, encephalomyelitis, multiple, sclerosis., Voltage-Gated, Potassium, Channels, 4812, Tocris Bioscience
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Literature in this Area
Tocris offers the following scientific literature in this area to showcase our products. We invite you to request* or download your copy today!
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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.
Peripheral sensitization is the reduction in the threshold of excitability of sensory neurons that results in an augmented response to a given external stimulus. This poster outlines the excitatory and inhibitory signaling pathways involved in modulation of peripheral sensitization. The role of ion channels, GPCRs, neurotrophins, and cytokines in sensory neurons are also described.