Entinostat is a benzamide derivative that inhibits histone deacetylase 1 (HDAC1); entinostat exhibits anticancer chemotherapeutic, anti-metastatic, and neuroprotective properties. In vitro, entinostat increases transcription of E-cadherin and decreases transcription of N-cadherin, decreasing tubulin-based microtentacles, reversing epithelial-to-mesenchymal transition (EMT) and inhibiting cell migration. In cellular and animal models, this compound upregulates natural killer cell activating receptor NKG2D, increasing the ability of natural killer cells to destroy cancer cells. Additionally, entinostat downregulates cellular FLICE-inhibiting protein (c-FLIP), increasing caspase activation and inducing apoptosis in animal models. Inhibition of HDAC1 in the nucleus accumbens (NAcc) inhibits cocaine-induced plasticity and behavioral changes in rodent models. Entinostat also decreases amyloid-β (Aβ) deposition in the hippocampus and cortex of animal models.