CP 339818 hydrochloride
Potent, non-peptide KV1.3 channel antagonist that preferentially binds to the C-type inactivated state of the channel (IC50 ~ 200 nM). Inhibits KV1.4 with an IC50 of ~ 300 nM. Selective over KV1.1, KV1.2, KV1.5, KV1.6, KV3.1-4, and KV4.2.
|Storage||Store at RT|
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 20 mM in water|
Preparing Stock Solutions
The following data is based on the product molecular weight 340.89. 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||2.93 mL||14.67 mL||29.33 mL|
|5 mM||0.59 mL||2.93 mL||5.87 mL|
|10 mM||0.29 mL||1.47 mL||2.93 mL|
|50 mM||0.06 mL||0.29 mL||0.59 mL|
References are publications that support the biological activity of the product.
Jager et al (1998) Regulation of mammalian Shaker-related K+ channels: evidence for non-conducting closed and non-conducting inactivated. J.Physiol. 506 291 PMID: 9490854
Nguyen et al (1996) Novel nonpeptide agents potently block the C-type inactivated conformation of Kv1.3 and suppress T cell activation. Mol.Pharmacol. 50 1672 PMID: 8967992
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1 Citation for CP 339818 hydrochloride
Citations are publications that use Tocris products. Selected citations for CP 339818 hydrochloride include:
Meredith et al (2015) Kv1 channels and neural processing in vestibular calyx afferents. J Neurosci 9 85 PMID: 26082693
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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.