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ML 252 is a potent and selective inhibitor of KV7.2 voltage-gated potassium channels (IC50 = 70 nM), which displays >40-fold selectivity for KV7.2 over KV7.1 channels (IC50 = 2.9 μM for KV7.1). ML 252 is the (S)-enantiomer, and is more potent than the (R)-enantiomer or racemic mixture (IC50 values are 944 and 160 nM, respectively). ML 252 displays selectivity for KV7.2 over a panel of >68 GPCRs, ion channels and transporters; inhibits melatonin MT1 receptor 60% at 10 μM. ML 252 is brain penetrant.
ML 252 is also offered as part of the Tocriscreen 2.0 Max. Find out more about compound libraries available from Tocris.
|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 308.43. 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||3.24 mL||16.21 mL||32.42 mL|
|5 mM||0.65 mL||3.24 mL||6.48 mL|
|10 mM||0.32 mL||1.62 mL||3.24 mL|
|50 mM||0.06 mL||0.32 mL||0.65 mL|
References are publications that support the biological activity of the product.
Cheung et al (2012) Discovery of a series of 2-phenyl-N-(2-(pyrrolidin-1-yl)phenyl)acetamides as novel molecular switches that modulate modes of KV7.2 (KCNQ2) channel pharmacology: identification of (S)-2-phenyl-N-(2-(pyrrolidin-1-yl)phe J.Med.Chem. 55 6975 PMID: 22793372
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Tocris offers the following scientific literature in this area to showcase our products. We invite you to request* 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.