| Features: | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Used to treat urea cycle disorders Sodium phenylbutyrate helps remove ammonia from the body. -Phenyl-butyrate (PB)4 is an aromatic fatty acid that is converted in vivo to phenylacetate (PA) by β-oxidation in liver and kidney mitochondria. -In human body, phenylbutyrate is oxidized to phenylacetate, which is in turn conjugated with glutamine and eliminated in urine as phenylacetylglutamine, thereby mediating elimination of waste nitrogen -Phenylbutyrate is one of the first drugs encountered in cancer therapy as a histone deacetylase inhibitor (HDACI) (relatively weak compared to vorinostat (SAHA), romidepsin, etc.). -Butyric acid is one of the short-chain fatty acids produced by the gut microbiota through the fermentation of dietary fiber. Butyrate is primarily recognized for its beneficial effects in the colon and is tightly linked to gut health. -Phenylbutyrate is a derivative of butyrate that has been chemically modified by the addition of a phenyl group. This structural change increases its lipophilicity (fat solubility) and alters its metabolic fate and biological activity. This allows it to be used as a systemic drug, in contrast to the locally produced butyrate in the gut, which is rapidly metabolized by colonocytes Pathways: -Histone deacetylase (HDAC) inhibitor -ER stress inhibitor (at least in normal cell) -Can act as a chemical chaperone, helping to reduce ER stress by facilitating proper protein folding. -Modulation of NF-κB Signaling -Changes in pathways such as PI3K/Akt/mTOR and MAPK. -Some preclinical investigations have reported that treatment with phenylbutyrate leads to mitochondrial dysfunction and endoplasmic reticulum (ER) stress, both of which can result in an increase of ROS within cancer cells. Note: Sodium butyrate (NaBu) vs Sodium phenylbutyrate -Sodium butyrate is primarily a research tool with limited clinical application, whereas phenylbutyrate is used clinically -Phenylbutyrate typically exhibits improved pharmacokinetics and is more amenable to systemic use compared to sodium butyrate. -Both compounds act as HDAC inhibitors, phenylbutyrate additionally modulates ER stress and mitochondrial function, leading to potentially greater ROS production in certain cancer cells. https://www.purepba.com/shop/
|
| Source: |
| Type: |
| Protein expression of ATF, GRP78, and GADD153 which is a hall marker of ER stress. The endoplasmic reticulum (ER) stress signaling pathway plays a crucial role in maintaining cellular homeostasis and responding to various stressors, including those encountered in cancer. When cells experience stress, such as the accumulation of misfolded proteins, they activate a series of signaling pathways collectively known as the unfolded protein response (UPR). The UPR aims to restore normal function by enhancing the protein-folding capacity of the ER, degrading misfolded proteins, and, if the stress is unresolved, triggering apoptosis. The activation of ER stress pathways can contribute to resistance against chemotherapy and targeted therapies. Cancer cells may utilize the UPR to survive treatment-induced stress, making it challenging to achieve effective therapeutic outcomes. -ER stress-associated proteins include: phosphorylation of PERK, eIF2α, ATF4, CHOP and cleaved-caspase 12 |
| 2065- | PB, | TMZ, | Inhibition of Mitochondria- and Endoplasmic Reticulum Stress-Mediated Autophagy Augments Temozolomide-Induced Apoptosis in Glioma Cells |
| - | in-vitro, | GBM, | NA |
| 2076- | PB, | Sodium Butyrate Induces Endoplasmic Reticulum Stress and Autophagy in Colorectal Cells: Implications for Apoptosis |
| - | in-vitro, | CRC, | HCT116 | - | in-vitro, | CRC, | HT29 |
| 2078- | PB, | Butyrate-induced apoptosis in HCT116 colorectal cancer cells includes induction of a cell stress response |
| - | in-vitro, | CRC, | HCT116 |
Query results interpretion may depend on "conditions" listed in the research papers. Such Conditions may include : -low or high Dose -format for product, such as nano of lipid formations -different cell line effects -synergies with other products -if effect was for normal or cancerous cells
Filter Conditions: Pro/AntiFlg:% IllCat:% CanType:% Cells:% prod#:15 Target#:103 State#:% Dir#:2
wNotes=0 sortOrder:rid,rpid