Omeprazole sulfide

Omeprazole sulfide (Ufiprazole) is a metabolic degradation product of Omeprazole (HY-B0113). Omeprazole sulfide acts as a modulator of AhR. Omeprazole sulfide in cells with low CYP3A4 expression, functions as an AhR antagonist; however, in cells with high CYP3A4 expression, it is rapidly metabolized to Omeprazole, thereby acting as an AhR agonist. Omeprazole sulfide exhibits antibacterial activity when conjugated with silver nanoparticles (AgNPs). Omeprazole sulfide can be used in research on acid suppression and bacterial infections^[1][2]. In Vitro: Omeprazole sulfide (100 μM; 30 min) induces a unique conformational change in mouse AhR, resulting in a trypsin digestion pattern distinct from that of unliganded or agonist-bound receptors in Hepa-1c1c7 cell cytoplasmic extracts^[1].
Omeprazole sulfide (15 μM; 2 h) blocks AhR-mediated nuclear translocation of mouse AhR in Hepa-1c1c7 cells^[1].
Omeprazole sulfide (15 μM; 5.5 h) blocks TCDD-mediated degradation of mouse AhR and inhibits TCDD-induced CYP1A1 protein expression in Hepa-1c1c7 cells^[1].
Omeprazole sulfide (5-50 μM; 8 h) acts as an AhR antagonist in mouse Hepa-1c1c7 and human HepG2 hepatocellular carcinoma cells, and inhibits TCDD-induced CYP1A1 mRNA expression in a concentration-dependent manner, with an inhibition rate of over 80% after treatment with 50 μM for 8 h^[1].
Omeprazole sulfide (1-100 μM; 16 h) inhibits ligand-induced AhR transcriptional activity in mouse Hepa-1c1c7 and human HepG2 hepatocellular carcinoma cells, with an IC₅₀ value of 1 to 10 μM after 16 h of incubation^[1].
Omeprazole sulfide (1-50 μM; 8 h) inhibits agonist-induced conversion of mouse AhR to its DNA-binding form in cytoplasmic extracts of Hepa-1c1c7 cells, with complete inhibition achieved after treatment at 50 μM for 8 h^[1].
Omeprazole sulfide (3-50 μM; 8 h) acts as an AhR agonist in freshly seeded primary human hepatocytes and induces CYP1A1 mRNA expression^[1].
Omeprazole sulfide (5-60 μM; 8 h) switches from an AhR antagonist to an agonist in primary human hepatocytes depending on cellular metabolic capacity: it acts as an antagonist in low-metabolism control cells or ketoconazole-treated cells, whereas it functions as an agonist in rifampicin-pretreated cells with induced CYP3A4 activity^[1].
Omeprazole sulfide forms stable spherical Ag@OMPS nanoparticles, which inhibit the growth of tested Gram-positive and Gram-negative bacterial strains, producing measurable inhibition zones with a maximum diameter of 5 mm^[2].