TMEM16A/B calcium-activated chloride channel (CaCC) blocker. Inhibits ATP-induced mucin secretion and metacholine-induced airway smooth muscle contraction in vitro.
|Storage||Store at +4°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 424.08. 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||2.36 mL||11.79 mL||23.58 mL|
|5 mM||0.47 mL||2.36 mL||4.72 mL|
|10 mM||0.24 mL||1.18 mL||2.36 mL|
|50 mM||0.05 mL||0.24 mL||0.47 mL|
References are publications that support the biological activity of the product.
Huang et al (2012) Calcium-activated chloride channel TMEM16A modulates mucin secretion and airway smooth muscle contraction. Proc.Natl.Acad.Sci.U.S.A. 109 16354 PMID: 22988107
Gallos et al (2013) Functional expression of the TMEM16 family of calcium-activated chloride channels in airway smooth muscle. Am.J.Physiol.Lung Cell Mol.Physiol. 305 625 PMID: 23997176
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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.
Programmed Cell Death Poster
There are two currently recognized forms of programmed cell death: apoptosis and necroptosis. This poster summarizes the signaling pathways involved in apoptosis, necroptosis and cell survival following death receptor activation, and highlights the influence of the molecular switch, cFLIP, on cell fate.