Upon treatment with ACY-775, a clear enhancement of the acetylation of α-tubulin is visible, while histone acetylation remains unaltered. Acetylation of α-tubulin is visualized by immunofluorescence and the intensity in the neurites of the neurons is quantified and normalized to the length of the fluorescent signal. In vehicle-treated DRG neurons, acetylated α-tubulin is already present. Upon treatment with ACY-775, the signal intensity of acetylated α-tubulin increases significantly. A significant increase in motility of mitochondria and also the total number of mitochondria within the neurites are observed compared with vehicle-treated DRG neurons. A significantly higher number of retrogradely transport mitochondria is observed in DRG neurons treated with ACY-775 compared with vehicle-treated cells [1].

Biodistribution profiles of ACY-775 are examined after acute dosing at 5 or 50?mg/kg over 2?h. At t=30?min after acute 50?mg/kg injection, respective plasma levels of ACY-775 is 1359?ng/mL (4.1?μM). Elimination from the plasma is rapid, with a plasmatic half-life of 12?min and a concentration below 10?ng/mL after 2?h. When ACY-775 (50?mg/kg) is administered repeatedly in wild-type mice at 24?h, 4?h, and 30?min before killing, significant increases in α-tubulin acetylation are observed in all tested brain regions [2].