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Potent and selective TMEM16A (Anoctamin-1; ANO1) blocker (IC50 = 77 nM). Displays no effect on ANO2 activity (at 10 μM). Also exhibits no effect on intracellular calcium signaling or CFTR and ENaC channel activity (at 30 μM).
|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 332.78. 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 mL||15.02 mL||30.05 mL|
|5 mM||0.6 mL||3 mL||6.01 mL|
|10 mM||0.3 mL||1.5 mL||3 mL|
|50 mM||0.06 mL||0.3 mL||0.6 mL|
References are publications that support the biological activity of the product.
Seo et al (2016) Ani9, a novel potent small-molecule ANO1 inhibitor with negligible effect on ANO2. PLoS One 11 e0155771 PMID: 27219012
If you know of a relevant reference for Ani 9, please let us know.
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Keywords: Ani 9, Ani 9 supplier, Ani9, Potent, TMEM16A, Anoctamin-1, blockers, transmembrane, protein, 16A, CaCC, blocks, calcium-activated, chloride, channels, ANO1, Ca2+-Activated, Chloride, Channels, 6076, Tocris Bioscience
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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.
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.