It looks like 4-phenylbutyrate (sodium phenylbutyrate) was used to lower copper induced ER STRESS in this study (human) https://pubmed.ncbi.nlm.nih.gov/27502587/ Sodium phenylbutyrate is a sodium salt of an aromatic fatty acid, made up of an aromatic ring and butyric acid (butyrate). I had mentioned zinc and sodium butyrate earlier in studies also have known effects to lower ER Stress so they may work well to try together and are needed for numerous other functions related to ME/CFS that are additionally dysregulated. HDAC inhibitors (Butyrate is one) blocked GRP78 release by inducing its aggregation in the ER. GRP78 increases WASF3 levels. https://www.nature.com/articles/srep30406 Butyrate inhibits histone deacetylase activity (HDAC) https://www.ncbi.nlm.nih.gov/pubmed/12840228 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6333934/ TUDCA has also been mentioned perhaps in tandem with zinc.Am I stupid or can you easily put together this relyvrio yourself using freely available nutritional supplements? Is it sodium phenylbutyrate?
A drug approach to target a pathway hopefully will work great in some cases as they would have an effect on all downstream areas of that specific pathway, but sometimes they cant replace all the functions of the missing nutrient as well as other pathways that may require that nutrient. A recent work previously highlighted the ability of butyrate to enhance the expression of AhR-dependent genes through its histone deacetylase inhibitor (HDACi) properties. We confirmed the butyrate-activating role at the transcriptional level on AhR-dependent genes in Caco-2 and HT-29 cell lines. Interestingly, other HDAC inhibitors that could enhance AhR-dependent gene expression were unable to mimic the butyrate dependent-activation of the AhR reporter system so butyrate worked beyond just its hdac inhibition in that case where the HDAC inhibition alone could be replaced with a drug for example. https://www.nature.com/articles/s41598-018-37019-2