KV7.2/7.3 activator (EC50 = 0.38 μM). Decreases neuronal excitability in CA1 hippocampal neurons. Exhibits anticonvulsive properties in amygdala-kindled rats, a model for complex partial seizures.
|Storage||Store at +4°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.
|Solvent||Max Conc. mg/mL||Max Conc. mM|
Preparing Stock Solutions
The following data is based on the product molecular weight 267.11. 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||3.74 mL||18.72 mL||37.44 mL|
|5 mM||0.75 mL||3.74 mL||7.49 mL|
|10 mM||0.37 mL||1.87 mL||3.74 mL|
|50 mM||0.07 mL||0.37 mL||0.75 mL|
References are publications that support the biological activity of the product.
Amato et al (2011) N-Pyridyl and Pyrimidine Benzamides as KCNQ2/Q3 Potassium Channel Openers for the Treatment of Epilepsy. ACS Med.Chem.Lett. 2 481
Boehlen et al (2013) The new KCNQ2 activator 4-Chlor-N-(6-chlor-pyridin-3-yl)-benzamid displays anticonvulsant potential. Br.J.Pharmacol. 168 1182 PMID: 23176257
If you know of a relevant reference for ICA 110381, please let us know.
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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!
*Please note that Tocris will only send literature to established scientific business / institute addresses.
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.