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Description

A cell permeable, benzylsulfonamide that inhibits SIRT2 activity (IC50= 12.5 µ,M through enzymatic assay) by targeting the SIRT2 nicotinamide binding site, but may also target SIRT1 and SIRT3 (IC50 >40 µ,M) with much less potency. Western analysis illustrates that treatment with AK-1 (>25 µ,M) leads to an increase in acetylated tubulin. AK-1 (1 to 10 µ,M) is shown to rescue neuronal dysfunction in two in vivo models of Huntington's Disease (HD) in Dropshila and Caenorhabditis elegans. It also demonstrates recovery of neuronal toxicity in a primary model of HD from 1µ,M to 4 µ,M similar to that of genetic SIRT2 inhibition, and also correlates with the negative regulation of sterol biosynthesis.