Omeprazole magnesium 

Omeprazole (H 16868) magnesium is an orally active H⁺,K⁺-ATPase inhibitor and a proton pump inhibitor. Omeprazole magnesium competitively inhibits CYP2C19, CYP3A4, and CYP2C9 activity. Omeprazole magnesium inhibits gastric acid secretion and can be used for acid-related gastrointestinal disorders. Omeprazole magnesium inhibits pancreatic cancer cell proliferation, induces apoptosis, autophagosome accumulation (elevated LC3-I and LC3-II levels), oxidative stress, and cytogenetic imbalance, modulates lysosomal transport, reduces inflammatory cytokines. Omeprazole magnesium alters small intestinal morphology and magnesium absorption, and induces gastric mucosa morphologic changes. Omeprazole magnesium aslo has neuroprotective and antibacterial effects^{[1][2][3][4][5]}.

Omeprazole magnesium (15 min) competitively inhibits CYP2C9 activity in pooled human liver microsomes with a K_i of 16.4 μM^[1].
Omeprazole magnesium (20 min) competitively inhibits CYP2C19 activity in pooled human liver microsomes with a K_i of 2.4-6.2 μM μM^[1].
Omeprazole magnesium (15 min) does not significantly inhibit CYP2D6 activity in pooled human liver microsomes, with an IC₅₀ >200 μM^[1].
Omeprazole magnesium (15 min) competitively inhibits CYP3A4 activity in pooled human liver microsomes with a K_i of 41.9 μM^[1].
Omeprazole magnesium (0-200 μg/mL; 4 days) inhibits proliferation of MiaPaCa-2, ASPC-1, Panc-1, Colo357, PancTu-1, and Panc89 human pancreatic cancer cell lines in a dose-dependent manner with IC₅₀ values ranging from 9.1 to 42.4 μg/mL^[2].
Omeprazole magnesium (80 μg/mL; 30 min-24 ) does not cause consistent intralysosomal pH changes in MiaPaCa-2 and ASPC-1 human pancreatic cancer cell lines, but increases acidity in ASPC-1 cells and decreases acidity in MiaPaCa-2 cells after 24 hours of incubation at 80 μg/mL^[2].
Omeprazole magnesium (80-160 μg/mL; 24 h) induces accumulation of early autophagic markers (phagophores and autophagosomes) in MiaPaCa-2 and ASPC-1 human pancreatic cancer cell lines, and induces apoptosis in ASPC-1 cells^[2].
Omeprazole magnesium (80 μg/mL; 24 h) accumulates intracellularly in MiaPaCa-2 and ASPC-1 human pancreatic cancer cell lines, and induces changes in fatty acid and phospholipid metabolism^[2].
Omeprazole magnesium (80 μg/mL; 24 h) alters the distribution of lysosomal markers and reduces Golgi complex marker expression in MiaPaCa-2 human pancreatic cancer cells, indicating disruption of the lysosomal transport pathway without accumulating in lysosomes or the Golgi complex^[2].
Omeprazole magnesium (40-160 μg/mL; 24 h) induces autophagy in a dose-dependent manner with elevated LC3-I and LC3-II levels, and impairs autophagosome turnover in MiaPaCa-2 and ASPC-1 human pancreatic cancer cell lines^[2].
Omeprazole magnesium (80 μg/mL; 6-24 h) alters gene expression in ASPC-1 and MiaPaCa-2 human pancreatic cancer cell lines, downregulating bad and survivin and upregulating mdr-1 in ASPC-1 cells^[2].
Omeprazole magnesium (80 μg/mL; 24 h) activates autophagy via upregulation of Atg12 in MiaPaCa-2 and ASPC-1 human pancreatic cancer cell lines, and upregulates pro-apoptotic Puma in ASPC-1 cells^[2].
Omeprazole magnesium generate sulfone, sulfite
and hydroxy-omeprazole, compounds that can generate more oxidative damage ^[3].
Omeprazole magnesium exerts toxicogenic effects in Allium cepa plant cells, as well as Saccharomyces cerevisiae and murine Sarcoma 180 cells^[3].
Omeprazole magnesium (200-300 mg/L) results in a
dose-dependent inhibition of E.faecalis at time zero^[6].
Omeprazole magnesium (200 mg/L) inhibits S. aureus at both time zero and 2 h^[6].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Omeprazole (20 mg/kg; s.c.; daily; 12-24 weeks) magnesium in male Sprague-Dawley rats induces small intestinal inflammation, villous atrophy, tight junction narrowing, and systemic magnesium deficiency with hypomagnesemia^[4].
Omeprazole magnesium prevents Oxaliplatin (HY-17371)-induced peripheral neuropathy in Rattus norvegicus^[5].
Omeprazole magnesium reduces the levels of the inflammatory cytokines, tumor necrosis factor-α, interleukin-1β, and interleukin-6, in sciatic nerve-ligated mice^[5].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

713.12

C₃₄H₃₆MgN₆O₆S₂

95382-33-5

COC1=CC=C2[N]3=C([N-]C2=C1)[S](CC(N=CC(C)=C4OC)=C4C)=[O][Mg+2]35[N](C6=CC=C7OC)=C([N-]C6=C7)[S](CC(N=CC(C)=C8OC)=C8C)=[O]5

Room temperature in continental US; may vary elsewhere.

Please store the product under the recommended conditions in the Certificate of Analysis.

• [1]. Li XQ, et al. Comparison of inhibitory effects of the proton pump-inhibiting drugs omeprazole, esomeprazole, lansoprazole, pantoprazole, and rabeprazole on human cytochrome P450 activities. Drug Metab Dispos. 2004;32(8):821-827.  [Content Brief]

  [2]. Udelnow A, et al. Omeprazole inhibits proliferation and modulates autophagy in pancreatic cancer cells. PLoS One. 2011;6(5):e20143.

  [3]. da Mata AMOF, et al. Evaluation of mutagenesis, necrosis and apoptosis induced by omeprazole in stomach cells of patients with gastritis. Cancer Cell Int. 2022;22(1):154. Published 2022 Apr 18.

  [4]. Chamniansawat S, et al. Ultrastructural intestinal mucosa change after prolonged inhibition of gastric acid secretion by omeprazole in male rats. Anat Sci Int. 2021;96(1):142-156.

  [5]. Mori Y, et al. Class effects of proton pump inhibitors in preventing oxaliplatin-induced peripheral neurotoxicity. J Pharmacol Sci. 2025;159(4):279-282.

  [6]. Jonkers D, et al. Omeprazole inhibis growth of Gram-positive and Gram-negative bacteria including Helicobacter pylori in vitro[J]. Journal of Antimicrobial Chemotherapy, 1996, 37(1): 145-150.