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Potent KV1.3 channel blocker (EC50 = 3 nM). Preferentially binds the C-type inactivated state of the channel, similar to the activity of CP 339818 (Cat. No. 1399). Displays 17- to 70-fold selectivity over closely-related KV1 channels (KV1, KV2, KV4 and KV7); exhibits activity at KV1.5 (IC50 = 7.7 nM). Suppresses proliferation of human and rat myelin-specific effector memory T cells (EC50 values are 25 and 60 nM respectively).
|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|
Preparing Stock Solutions
The following data is based on the product molecular weight 334.37. 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||5.98 mL||29.91 mL||59.81 mL|
|2.5 mM||1.2 mL||5.98 mL||11.96 mL|
|5 mM||0.6 mL||2.99 mL||5.98 mL|
|25 mM||0.12 mL||0.6 mL||1.2 mL|
References are publications that support the biological activity of the product.
Vennekamp et al (2004) Kv1.3-blocking 5-phenylalkoxypsoralens: a new class of immunomodulators. Mol.Pharmacol. 65 1364 PMID: 15155830
Schmitz et al (2005) Design of PAP-1, a selective small molecule Kv1.3 blocker, for the suppression of effector memory T cells in autoimmune diseases. Mol.Pharmacol. 68 1254 PMID: 16099841
Li et al (2006) Voltage-gated potassium channel Kv1.3 regulates GLUT4 trafficking to the plasma membrane via a Ca2+-dependent mechanism. Am.J.Physiol.Cell Physiol. 290 C345 PMID: 16403947
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Citations for Psora 4
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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.
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.