Scriptaid (287383-59-9) inhibits histone deacetylases (HDAC) 1 and 3 (IC₅₀~0.6 μM) and HDAC8 (IC₅₀~1 μM) and is less toxic compared to trichostatin A.^1,2 Induces cell cycle arrest and epigenetic changes in colon cancer cells.³ Together with DRB-inhibition of RNA synthesis, scriptaid enhances gene reprogramming in somatic cell nuclear transfer (SCNT) embryos.⁴ Increases exercise endurance in mice.⁵

References/Citations
1) Su et al. (2000), A novel histone deacetylase inhibitor identified by high-throughput transcriptional screening of a compound library; Cancer Res., 60 3137
2) Huber et al. (2011), Inhibitors of histone deacetylases: correlation between isoform specificity and reactivation of HIV type 1 (HIV-1) from latently infected cells; J. Biol. Chem., 286 22211
3) Lee et al. (2008), Histone deacetylase inhibitor scriptaid induces cell cycle arrest and epigenetic change in colon cancer cells; J. Oncol., 33 767
4) Rissi et al. (2019), Inhibition of RNA synthesis during Scriptaid exposure enhances gene reprogramming in SCNT embryos; Reproduction, 157 123
5) Huang et al. (2020), Scriptaid/exercise-induced lysine acetylation is another type of posttranslational modification occurring in titin; J. Appl. Physiol., 128 276