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AK 7 is a selective SIRT2 inhibitor (IC50 = 15.5 μM); displays no effect on SIRT1 or SIRT3. Decreases neuronal cholesterol levels; improves motor function and ameliorates brain atrophy in a mouse model of Huntington's disease. Brain penetrant.
AK 7 is also offered as part of the Tocriscreen 2.0 Max, Tocriscreen Antiviral Library and Tocriscreen Epigenetics Library. Find out more about compound libraries available from Tocris.
|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|
The following data is based on the product molecular weight 437.35. 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||2.29 mL||11.43 mL||22.86 mL|
|5 mM||0.46 mL||2.29 mL||4.57 mL|
|10 mM||0.23 mL||1.14 mL||2.29 mL|
|50 mM||0.05 mL||0.23 mL||0.46 mL|
References are publications that support the biological activity of the product.
Chopra et al (2012) The sirtuin inhibitor AK-7 is neuroprotective in Huntington's disease mouse models. Cell Rep. 2 1492 PMID: 23200855
Taylor et al (2011) A brain-permeable small molecule reduces neuronal cholesterol by inhibiting activity of sirtuin 2 deacetylase. ACS Chem.Biol. 6 540 PMID: 21370928
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Keywords: AK 7, AK 7 supplier, AK7, SIRT2, sirtuin, inhibitors, inhibits, Huntingdon's, disease, selective, reduces, neuronal, cholesterol, Class, III, HDACs, (Sirtuins), 4754, Tocris Bioscience
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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.
Rheumatoid arthritis (RA) is a chronic destructive inflammatory autoimmune disease that results from a breakdown in immune tolerance, for reasons that are as yet unknown. This poster summarizes the pathology of RA and the inflammatory processes involved, as well as describing some of the epigenetic modifications associated with the disease and the potential for targeting these changes in the discovery of new treatments.