Sodium 4-phenylbutyrate (TriButyrate), a transcriptional regulator, reversibly inhibits class I and II histone deacetylases (HDACs )resulting in a global increase in gene expression, decreased cellular proliferation, increased cell differentiation, and the induction of apoptosis in susceptible tumor cell populations.

In G93A transgenic ALS mice, Phenylbutyrate improves clinical symptoms and increases survival. It induces the expression of NF-κB p50 in G93A mice, while reducing the expression of cytochrome c and caspases. Additionally, in transgenic mouse models of Huntington's disease (HD), Phenylbutyrate elevates brain protein acetylation levels and reduces histone methylation levels.

In prostate cancer cells, Phenylbutyrate induces apoptosis by diminishing the expression levels of the cell apoptosis antagonist Bcl-X(L), the double-strand break repair protein DNA-dependent protein kinase, the prostate progression marker Caveolin-1, and the angiogenesis promoter Vascular Endothelial Growth Factor, thereby weakening their activity.