Compounds in my other articles are similar to this one(5-Methoxy-2-[[(4-methoxy-3,5-dimethyl-2-pyridyl)methyl]thio]benzimidazole)Synthetic Route of C17H19N3O2S, you can compare them to see their pros and cons in some ways,such as convenient, effective and so on.
Synthetic Route of C17H19N3O2S. Aromatic compounds can be divided into two categories: single heterocycles and fused heterocycles. Compound: 5-Methoxy-2-[[(4-methoxy-3,5-dimethyl-2-pyridyl)methyl]thio]benzimidazole, is researched, Molecular C17H19N3O2S, CAS is 73590-85-9, about Role of CYP3A4 in the regulation of the aryl hydrocarbon receptor by omeprazole sulphide. Author is Gerbal-Chaloin, Sabine; Pichard-Garcia, Lydiane; Fabre, Jean-Michel; Sa-Cunha, Antonio; Poellinger, Lorenz; Maurel, Patrick; Daujat-Chavanieu, Martine.
Cross-talk between nuclear receptors involved in the control of drug metabolism is being increasingly recognized as a source of drug side effects. Omeprazole is a well known activator of the aryl hydrocarbon receptor (AhR). We investigated the regulation of AhR by omeprazole-sulfide, a degradation metabolite of omeprazole, using CYP1A mRNA induction, reporter gene assay, receptor DNA binding, ligand binding, nuclear translocation, trypsin digests, and drug metabolism anal. in mouse Hepa-1c1c7, human HepG2 cells and primary human hepatocytes. Omeprazole-sulfide is a pure antagonist of AhR in Hepa-1c1c7 and HepG2 hepatoma cell lines. In Hepa-1c1c7 cells, omeprazole-sulfide is a ligand of AhR, inhibits AhR activation to a DNA-binding form, induces a specific pattern of AhR trypsin digestion and inhibits AhR nuclear translocation and subsequent degradation in response to 2,3,7,8-tetrachlorodibenzo-p-dioxin. However, in highly differentiated primary human hepatocytes treated with rifampicin an agonist of the pregnane X receptor (PXR), omeprazole-sulfide behaves as an agonist of AhR. Inhibition of drug metabolizing enzymes by ketoconazole restores the antagonist effect of omeprazole-sulfide. Metabolic LC/MS anal. reveals that omeprazole-sulfide (AhR antagonist) is efficiently converted to omeprazole (AhR activator) by cytochrome P 450 CYP3A4, a target gene of PXR, in primary human hepatocytes but not in hepatoma cells in which PXR is not expressed. This report provides the first evidence for a cross-talk between PXR/CYP3A4 and AhR. In addition, it clearly shows that conclusions drawn from experiments carried out in cell lines may lead to erroneous in vivo predictions in man.
Compounds in my other articles are similar to this one(5-Methoxy-2-[[(4-methoxy-3,5-dimethyl-2-pyridyl)methyl]thio]benzimidazole)Synthetic Route of C17H19N3O2S, you can compare them to see their pros and cons in some ways,such as convenient, effective and so on.
Reference:
Ether – Wikipedia,
Ether | (C2H5)2O – PubChem