Sodium phenylbutyrate, an HDAC (histone deacetylase) inhibitor, has been shown to cause cellular differentiation, growth arrest, and apoptosis in certain cells. Sodium phenylbutyrate has been reported to cause cell growth arrest at the G1 phase and induce apoptosis through activation of JNK. Studies suggest that Sodium Phenylbutyrate also acts as a chemical chaperone by causing a reduction of the load of mutant and mislocated proteins retained in the endoplasmic reticulum (ER). Other experiments have noted that Sodium Phenylbutyrate demonstrates neuroprotective capabilities by attenuating infarction volume, apoptosis, hemispheric swelling and improving neurological status in a murine model of hypoxia-ischemia. Moreover, this agent has been shown to suppress ER-mediated apoptosis by initiating factor 2α phosphorylation, caspase-12 activation, and CCAAT/enhancer-binding protein homologous protein induction.
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