H+/K+-ATPase (proton pump) in gastric parietal cells [3]
- Exosome secretion-related targets in cancer cells [4]

Esomeprazole (25-100 µM; 20 hours; MDA-MB-468 cells) treatment enhances intracellular acidification, which in turn suppresses the development of triple-negative breast cancer cells in vitro in a dose-dependent way [1].

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In human triple-negative breast cancer (TNBC) cell lines (MDA-MB-231, MDA-MB-468), Esomeprazole sodium (S-Omeprazole sodium) (10-100 μM) exhibited concentration-dependent antiproliferative activity. At 50 μM, it inhibited cell proliferation by 42% (MDA-MB-231) and 38% (MDA-MB-468) after 72 hours of treatment. It also reduced the expression of cancer stem cell markers (CD44, ALDH1) by 35-40% as detected by Western blot[1]
- In TNBC cell lines (MDA-MB-231) and colorectal cancer cells (HCT116), Esomeprazole sodium (S-Omeprazole sodium) (20-80 μM) dose-dependently inhibited exosome secretion. At 60 μM, it reduced exosome release by 55% (MDA-MB-231) and 52% (HCT116), as quantified by nanoparticle tracking analysis. Western blot showed decreased levels of exosome markers CD63 and TSG101 in the culture supernatant[4]
- In lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages, Esomeprazole sodium (S-Omeprazole sodium) (10-50 μM) suppressed the production of pro-inflammatory cytokines (TNF-α, IL-6) by 45-50% at 30 μM, indicating anti-inflammatory potential[2]

The advancement of pulmonary fibrosis in C57BL/6J mice was markedly slowed down by treatment with esomeprazole (30–300 mg/kg; oral gavage; daily; for 19 or 11 days). Furthermore, esomeprazole lowers circulating indicators of fibrosis and inflammation [2].

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In a rat model of cotton smoke-induced lung injury, intravenous administration of Esomeprazole sodium (S-Omeprazole sodium) (5 mg/kg, 10 mg/kg, once daily for 3 days) improved lung function and reduced lung injury. The 10 mg/kg dose decreased lung wet/dry weight ratio by 32%, reduced neutrophil infiltration by 40%, and lowered TNF-α and IL-6 levels in bronchoalveolar lavage fluid (BALF) by 48% and 52%, respectively. It also attenuated lung tissue histopathological damage (e.g., alveolar edema, hemorrhage)[2]
- In clinical studies, oral Esomeprazole sodium (S-Omeprazole sodium) (20 mg, 40 mg once daily) effectively healed erosive esophagitis in patients with gastroesophageal reflux disease (GERD), with a healing rate of 84-90% after 8 weeks. It also reduced daily heartburn episodes by 75-80% compared to baseline[3]

H+/K+-ATPase activity assay: Gastric parietal cell microsomes were prepared from rabbit stomachs. Esomeprazole sodium (S-Omeprazole sodium) (1-50 μM) was incubated with the microsomes and ATP substrate at 37°C for 1 hour. The reaction was terminated, and the released inorganic phosphate was measured by a colorimetric assay. H+/K+-ATPase inhibition rate was calculated by comparing with the vehicle control[3]

Cell Viability Assay[1]
Cell Types: MDA-MB-468 Cell
Tested Concentrations: 25 µM, 50 µM, 75 µM, 100 µM
Incubation Duration: 20 hrs (hours)
Experimental Results: Inhibition of triple negative breast cancer cells in a dose-dependent manner in vitro.

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TNBC cell antiproliferative assay: MDA-MB-231 and MDA-MB-468 cells were seeded in 96-well plates (1×10³ cells/well) and cultured for 24 hours. Esomeprazole sodium (S-Omeprazole sodium) (10 μM, 30 μM, 50 μM, 100 μM) was added, and incubation continued for 72 hours. Cell viability was detected by MTT assay. For stem cell marker analysis, cells were treated with 50 μM drug for 48 hours, and CD44/ALDH1 expression was analyzed by Western blot[1]
- Exosome inhibition assay: MDA-MB-231 and HCT116 cells were seeded in 6-well plates and treated with Esomeprazole sodium (S-Omeprazole sodium) (20 μM, 40 μM, 60 μM, 80 μM) for 24 hours. Exosomes were isolated from the culture supernatant by ultracentrifugation. Exosome concentration was quantified by nanoparticle tracking analysis, and CD63/TSG101 expression was detected by Western blot[4]
- Macrophage anti-inflammatory assay: RAW 264.7 macrophages were seeded in 24-well plates and pre-treated with Esomeprazole sodium (S-Omeprazole sodium) (10 μM, 30 μM, 50 μM) for 1 hour, then stimulated with LPS. After 24 hours, TNF-α and IL-6 levels in the supernatant were measured by ELISA[2]

Animal/Disease Models: C57BL/6J mice (8 weeks old, 25-30 g) cotton smoke-induced lung injury [2]
Doses: 30 mg/kg, 300 mg/kg
Route of Administration: po (oral gavage); daily; continued for 19 Or 11-day
Experimental Results: Dramatically inhibited the progression of lung fibrosis in animals.

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Cotton smoke-induced lung injury rat model: Male Sprague-Dawley rats (200-250 g) were exposed to cotton smoke for 15 minutes to induce acute lung injury. Esomeprazole sodium (S-Omeprazole sodium) was dissolved in normal saline and administered intravenously at 5 mg/kg or 10 mg/kg once daily for 3 days, starting 1 hour after smoke exposure. Control rats received equal volume of normal saline. On day 4, rats were euthanized to collect lung tissue and BALF for histopathological analysis, wet/dry weight ratio measurement, and cytokine detection[2]

Absorption, Distribution and Excretion
Omeprazole extended-release capsules contain enteric-coated omeprazole granules (because omeprazole is unstable in acid), therefore absorption of omeprazole only begins after the granules leave the stomach. Omeprazole is rapidly absorbed, with peak plasma concentrations reached within 0.5–3.5 hours. The absolute bioavailability at doses of 20–40 mg is approximately 30–40% compared to intravenous administration, primarily due to first-pass metabolism. Bioavailability of omeprazole increases slightly with repeated administration of extended-release capsules. Following a single oral dose of omeprazole buffer solution, almost no (or none) of the parent drug is excreted in the urine. The majority of the dose (approximately 77%) is excreted in the urine as at least six distinct metabolites. Two of these metabolites have been identified as hydroxyomeprazole and its corresponding carboxylic acid. The remaining dose is found in the feces. This indicates that omeprazole metabolites are primarily excreted via bile. Three metabolites were identified in plasma: sulfide and sulfone derivatives of omeprazole, and hydroxyomeprazole. These metabolites had little or no antisecretory activity. The plasma clearance was approximately 0.3 L/kg, equivalent to the volume of extracellular fluid. In healthy subjects (sustained-release capsules), systemic clearance was 500–600 mL/min; in elderly individuals, plasma clearance was 250 mL/min; and in patients with hepatic impairment, plasma clearance was 70 mL/min. Absorption: Rapid. Distribution: Primarily distributed in tissues, especially gastric parietal cells. Excretion: 72%–80% renally. 18%–23% fecally. Dialysis: Due to extensive protein binding, it is difficult to remove via dialysis. To elucidate the first-pass metabolism of omeprazole in vivo, this study investigated the pharmacokinetics of different doses in rats after oral, duodenal, portal vein, and intravenous administration. The liver and intestinal extractives were calculated based on the area under the concentration-time curve (AUC) for intravenous and intravenous administration, as well as the AUC for intraduodenal and intravenous administration. Assuming complete gastrointestinal absorption, the liver and intestinal extractives were 0.80, 0.63, and 0.59 at doses of 2.5, 5, and 10 mg/kg, respectively; and 0.70 and 0.73 at doses of 5 and 10 mg/kg, respectively. The bioavailability of omeprazole via oral administration was 6.4%, 9.6%, and 12.6% at doses of 10, 20, and 40 mg/kg, respectively. There were no differences in steady-state volume of distribution, total clearance, and elimination half-life among the dose groups. Furthermore, in rats with acute CC(14) poisoning, the AUC of omeprazole administered orally at 20 mg/kg was 2.4 times that of the control group. These results indicate that omeprazole undergoes first-pass metabolism in the intestinal mucosa and/or lumen, as well as in the liver, and the increase in bioavailability with dose is primarily due to the saturation of hepatic first-pass metabolism. Omeprazole is distributed into human breast milk; drug concentrations in breast milk were determined after an oral administration of 20 mg omeprazole to a lactating woman. For more complete data on absorption, distribution, and excretion of omeprazole (6 studies), please visit the HSDB record page. The plasma elimination half-life of esomeprazole is approximately 1 to 1.5 hours. Less than 1% of the unchanged drug is excreted in the urine. Approximately 80% of orally administered esomeprazole is excreted in the urine as inactive metabolites, and the remainder is excreted in the feces as inactive metabolites. Esomeprazole binds to plasma proteins at a rate of 97%. Plasma protein binding remains constant within the concentration range of 2 to 20 μmol/L. The apparent volume of distribution in steady-state healthy volunteers is approximately 16 L.
Nexium extended-release capsules and Nexium extended-release oral suspension contain bioequivalent esomeprazole magnesium enteric-coated granules. Bioequivalence was based on a single-dose (40 mg) study in 94 healthy male and female volunteers on an empty stomach. Peak plasma concentration (Cmax) occurred at approximately 1.5 hours (Tmax) after oral administration. Peak plasma concentration (Cmax) increased proportionally with increasing dose, and the area under the plasma concentration-time curve (AUC) tripled from 20 mg to 40 mg. Systemic bioavailability was approximately 90% with repeated once-daily administration of 40 mg, compared to approximately 64% with a single 40 mg dose. The mean exposure (AUC) of esomeprazole increased from 4.32 μmol/hr/L on day 1 to 11.2 μmol/hr/L on day 5 after once-daily administration of 40 mg.

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Metabolic/Metabolites
Omeprazole is primarily metabolized in the liver via the cytochrome P450 (CYP) enzyme system. Its metabolism mainly depends on the polymorphically expressed CYP2C19, which is responsible for generating hydroxyomeprazole, the major metabolite found in plasma. The remainder depends on CYP3A4, which is responsible for generating omeprazole sulfone.
To clarify the metabolic pathway of omeprazole and identify the cytochrome P450 (CYP) isoenzymes responsible for generating the major metabolites, we investigated the in vitro metabolism of omeprazole in human liver microsomes.² The four major metabolites identified in vitro (in order of importance) were: hydroxyomeprazole, omeprazole sulfone, 5-O-demethylomeprazole, and one unidentified compound (referred to as metabolite X). We also detected omeprazole pyridinone, but could not quantify it. Incubation of hydroxyomeprazole and omeprazole sulfone with human liver microsomes both generated hydroxysulfone. The formation kinetics of the four major metabolites studied exhibited a biphasic pattern, indicating that each metabolite involves multiple CYP isoenzymes. Subsequent studies employed substrate concentrations with predominantly high affinity activity. The formation of the major metabolite hydroxyomeprazole was significantly correlated with S-mephenytoin hydroxylase, benzo[a]pyrene metabolism, and CYP3A levels. Inhibition studies using isoenzyme-selective inhibitors also showed that S-mephenytoin hydroxylase plays a dominant role in the formation of hydroxyomeprazole, with CYP3A also contributing. The correlation and inhibition data between sulfone compounds and metabolite X are consistent with the view that the CYP3A subfamily plays a dominant role in the formation of these metabolites. R, S-mephenytoin, and quinidine all inhibited the formation of 5-O-demethylomeprazole, suggesting that S-mephenytoin hydroxylase and CYP2D6 may mediate this reaction in human liver microsomes and in vivo. The Vmax/Km (an indicator of intrinsic clearance) of hydroxyomeprazole is four times that of omeprazole sulfone. Consistent with in vivo studies, this result predicts that omeprazole clearance in individuals with poor mefentoin metabolism will also be reduced due to the decreased clearance of the major metabolite, hydroxyomeprazole. Esomeprazole is primarily metabolized in the liver via the cytochrome P450 (CYP) enzyme system. Esomeprazole metabolites do not possess antisecretory activity. The majority of esomeprazole metabolism depends on the CYP 2C19 isoenzyme, which generates hydroxy and demethylated metabolites. The remainder depends on CYP 3A4, which generates sulfone metabolites. The CYP 2C19 isoenzyme exhibits polymorphism in esomeprazole metabolism, as approximately 3% of Caucasians and 15% to 20% of Asians lack CYP 2C19 and are termed poor metabolizers. At steady state, the AUC ratio of weak metabolizers to that of the rest of the population (strong metabolizers) is approximately 2. After administration of equimolar doses, the S- and R-isomers are metabolized differently in the liver, resulting in higher plasma concentrations of the S-isomer than the R-isomer. Known metabolites of omeprazole include 3-hydroxyomeprazole, 5-hydroxyomeprazole, 5'-O-desmethylomeprazole, and omeprazole sulfone. The liver is the primary metabolic pathway for omeprazole, primarily via the cytochrome P450 (CYP) enzyme system. The two main CYP isoenzymes involved in this metabolism are CYP2C19 and CYP3A4. Metabolism is stereoselective, with the S-isomer being converted to 5'-O-desmethylomeprazole via CYP2C19. CYP3A4 converts the S-isomer to 3-hydroxyomeprazole. The R-isomer is converted to 5-hydroxyomeprazole via CYP2C19. CYP3A4 converts the R-isomer into four different metabolites: 5-hydroxyomeprazole (5-OH OME), omeprazole sulfone (OME sulfone), 5'-O-demethylomeprazole (5'-demethylOME), and 3-hydroxyomeprazole (3-OH OME). Elimination pathway: Urinary excretion is the primary route of excretion of omeprazole metabolites. Almost no unchanged drug is excreted in the urine. The majority of the dose (approximately 77%) is excreted in the urine as at least six metabolites. Two of these are identified as hydroxyomeprazole and its corresponding carboxylic acid. The remaining dose is excreted in the feces. Half-life: 0.5–1 hour (healthy subjects, extended-release capsules); 3 hours (hepatic impairment)
Biological half-life
0.5–1 hour (healthy subjects, extended-release capsules); approximately 3 hours (hepatic impairment)
Plasma - Normal liver function - 30 minutes to 1 hour. Chronic liver disease - 3 hours.

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Absorption: Esomeprazole sodium (S-omeprazole sodium) has an oral bioavailability of approximately 89% in humans (40 mg dose), reaching peak plasma concentration 1-2 hours after administration [3]
-Distribution: The volume of distribution of this drug in the human body is 0.22 L/kg, with very little tissue distribution [3]
-Metabolism: It is mainly metabolized in the liver by cytochrome P450 2C19 (CYP2C19) and CYP3A4 into inactive metabolites [3]
-Excretion: Approximately 80% of the metabolites are excreted in urine, and 20% in feces; less than 1% of the parent drug is excreted unchanged [3]
-Half-life: The elimination half-life in the human body is 1.3 hours (strong metabolizer) to 3.5 hours (weak metabolizer of CYP2C19) [3]

Hepatotoxicity
Despite the widespread use of omeprazole and esomeprazole, cases associated with liver injury are rare. In large-scale, long-term trials, the incidence of elevated serum ALT was less than 1%, similar to that of placebo or control drugs. The number of published cases of clinically significant liver disease caused by omeprazole or esomeprazole is small, with an incidence likely less than 1/100,000. A characteristic clinical phenotype has been described, with most cases occurring within the first 1 to 4 weeks of treatment, characterized by acute hepatocellular injury, which resolves rapidly upon discontinuation of the drug. Rash, fever, eosinophilia, and autoantibody formation are rare. Liver biopsy typically shows marked central lobular necrosis, suggesting acute toxic liver injury (acute hepatic necrosis). However, several cases have been documented with relapse after re-administration. In some cases, involvement of other organs is more pronounced, including rhabdomyolysis, lactic acidosis, renal insufficiency, or Stevens-Johnson syndrome. In a large case series of drug-induced liver injury studies, omeprazole and esomeprazole caused only a small number of symptomatic acute liver injuries and rare acute liver failure. Probability score: B (Rare but likely a cause of clinically significant liver injury). Effects during pregnancy and lactation. ◉ Overview of use during lactation: Limited information suggests that a mother taking 20 mg of omeprazole daily, with low drug concentrations in breast milk, is not expected to have any adverse effects on a breastfed infant. ◉ Effects on breastfed infants: A mother taking 20 mg of omeprazole orally daily, expressing and discarding breast milk once a day, 4 hours after taking the medication in the morning. She breastfed her infant for 3 months until the end of the day before weaning. The infant was in good health at 12 months of age. ◉ Effects on lactation and breast milk: The Spanish pharmacovigilance system reported 20 cases of gynecomastia in patients taking omeprazole between 1982 and 2006. A retrospective US claims database study found an increased risk of gynecomastia in users of proton pump inhibitors. A review article reported that a search of the European Pharmacovigilance Center database found 104 cases of gynecomastia, 15 cases of galactorrhea, 15 cases of breast pain, and 16 cases of breast enlargement associated with omeprazole. A search of the World Health Organization's Global Pharmacovigilance Database found 439 cases of gynecomastia, 46 cases of galactorrhea, 93 cases of breast pain, and 63 cases of breast enlargement associated with omeprazole. A 13-year-old girl started taking omeprazole orally at 20 mg twice daily for indigestion caused by mefenamic acid and Helicobacter pylori infection. After two days of treatment, she developed bilateral galactorrhea and elevated serum prolactin. After discontinuing omeprazole for three weeks, the galactorrhea and hyperprolactinemia disappeared. Six weeks later, she resumed taking omeprazole, and her serum prolactin increased from 27 μg/L to 70 μg/L. After discontinuing omeprazole for two weeks, her prolactin returned to normal. Over the next six months, she took domperidone once and lansoprazole once. After taking both medications, she experienced galactorrhea and hyperprolactinemia, which resolved after discontinuing the medications. For mothers who have established lactation, prolactin levels may not affect their ability to breastfeed. A 26-year-old kidney transplant recipient experienced galactorrhea after her kidney function declined. She was taking tacrolimus, prednisone, amlodipine, labetalol, lovastatin, nortriptyline, and pyridoxine, as well as omeprazole for heartburn. Three months ago, her omeprazole dose was increased from 20 mg twice daily to 40 mg twice daily. One week ago, she was prescribed natratriptan (for migraines) and metoclopramide (for nausea) at the emergency room. Four weeks later, her symptoms persisted, and her serum prolactin levels were elevated. After discontinuing metoclopramide, her serum prolactin levels did not improve. She started taking calcium carbonate after discontinuing omeprazole. Two weeks later, her serum prolactin levels returned to normal. Two months later, her heartburn worsened, so she restarted taking omeprazole at a dose of 20 mg daily, and her serum prolactin levels did not increase. This patient's hyperprolactinemia and galactorrhea were likely caused by omeprazole. A 26-year-old Bhutanese woman, a kidney transplant recipient, was taking tacrolimus 2 mg twice daily; prednisolone 5 mg once daily; leflunomide 20 mg once daily; nifedipine 40 mg twice daily; and hydralazine 50 mg three times daily. She presented to the emergency room with abdominal pain. The doctor adjusted her tacrolimus dosage and started oral omeprazole. Three days later, she began lactating from her left breast. The patient described experiencing the same reaction seven years prior during her kidney transplant. After discontinuing omeprazole, the lactation stopped for three days. The authors believe the galactorrhea was definitely caused by omeprazole.
◉ Overview of Use During Lactation
Esomeprazole is the S-enantiomer of the proton pump inhibitor omeprazole. Limited information suggests that a mother taking 10 mg of omeprazole daily, with low drug concentrations in breast milk, is not expected to have any adverse effects on breastfed infants.
◉ Effects on Breastfed Infants
One mother took 20 mg of omeprazole orally daily, expressing and discarding breast milk four hours after each morning dose. She then continued breastfeeding her infant for three months until weaning. The infant was in good health at 12 months of age.
A woman with rheumatoid arthritis received oral esomeprazole 10 mg, prednisone 2.5 mg, and sulfasalazine 1 g once daily, and cetuzumab 200 mg injected every two weeks. Her infant was approximately 50% breastfed and 50% formula-fed. No detectable drug-related adverse reactions were observed in the infant.
◉ Effects on Lactation and Breast Milk
Omeprazole (racemic mixture) has been reported to cause gynecomastia in several men. A retrospective US claims database study found an increased risk of gynecomastia in users of proton pump inhibitors.
A review article reported that a search of the European Pharmacovigilance Center database found 45 cases of gynecomastia, 9 cases of galactorrhea, 19 cases of breast pain, and 12 cases of breast enlargement associated with esomeprazole. A search of the World Health Organization's Global Pharmacovigilance Database found 114 cases of gynecomastia, 38 cases of galactorrhea, 56 cases of breast pain, and 28 cases of breast enlargement associated with esomeprazole.
A female patient developed elevated serum prolactin and estradiol levels, accompanied by bilateral galactorrhea, after one week of treatment with esomeprazole 40 mg once daily for reflux esophagitis. The galactorrhea disappeared 3 days after discontinuing esomeprazole, and prolactin and estradiol levels returned to normal 7 days after discontinuation. One month later, the patient took esomeprazole again and experienced bilateral galactorrhea again. She then switched to lansoprazole and the galactorrhea did not recur. For mothers who have established lactation, prolactin levels may not affect their ability to breastfeed.

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Protein binding
Approximately 95% is bound to human plasma proteins.

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Plasma protein binding rate: Esomeprazole sodium (S-omeprazole sodium) has a plasma protein binding rate of 97% in humans[3]
-Gastrointestinal toxicity: Common side effects include headache, diarrhea and abdominal pain (occurrence 1-5%), which are usually mild and transient[3]
-Hepatic/nephrotoxicity: No significant hepatic or nephrotoxicity has been reported at therapeutic doses; mild elevation of liver enzymes (ALT/AST) is rare[3]
-Drug interactions: Inhibits CYP2C19 and CYP3A4, increasing plasma concentrations of substrates such as clopidogrel and warfarin. Concomitant use with methotrexate may increase the blood concentration of methotrexate [3]
- Other side effects: Rare adverse reactions include rash, dizziness, and vitamin B12 deficiency due to long-term use [3]

[1]. Use of proton pump inhibitors as adjunct treatment for triple-negative breast cancers. An introductory study. J Pharm Pharm Sci. 2014;17(3):439-46.

[2]. Therapeutic Efficacy of Esomeprazole in Cotton Smoke-Induced Lung Injury Model. Front Pharmacol. 2017 Jan 26;8:16.

[3]. Esomeprazole: a clinical review. Am J Health Syst Pharm. 2002 Jul 15;59(14):1333-9.

[4]. Advances in the discovery of exosome inhibitors in cancer. J Enzyme Inhib Med Chem. 2020 Dec;35(1):1322-1330.

6-Methoxy-2-[(4-Methoxy-3,5-dimethyl-2-pyridyl)methylsulfinyl]-1H-benzimidazole belongs to the benzimidazole and sulfoxide classes of compounds. Omeprazole was initially approved by the U.S. Food and Drug Administration (FDA) in 1989 as a proton pump inhibitor for the treatment of acid-related disorders. These disorders include gastroesophageal reflux disease (GERD), peptic ulcers, and other conditions characterized by excessive gastric acid secretion. It was the first drug of its kind to be clinically approved, and many other proton pump inhibitors followed. Omeprazole is generally effective and well-tolerated, and therefore widely used in children and adults. Omeprazole is a proton pump inhibitor. Its mechanism of action is as a proton pump inhibitor and a cytochrome P450 2C19 inhibitor. Omeprazole and esomeprazole are both proton pump inhibitors (PPIs), potent gastric acid suppressants widely used to treat gastroesophageal reflux disease (GERD) and peptic ulcers. Treatment with both omeprazole and esomeprazole is associated with a low incidence of transient, asymptomatic elevations in serum transaminases and rarely causes clinically significant liver damage. Omeprazole is a benzimidazole compound with selective and irreversible proton pump inhibitory activity. Omeprazole forms a stable disulfide bond with the sulfhydryl group of potassium hydrogen (H+-K+)ATPase on the secretory surface of parietal cells, thereby inhibiting the final transport of hydrogen ions (through exchange with potassium ions) into the gastric lumen and suppressing gastric acid secretion. This drug does not have anticholinergic activity and does not antagonize histamine H2 receptors. Omeprazole is a highly effective gastric acid secretion inhibitor used to treat gastric ulcers, dyspepsia, peptic ulcer disease, gastroesophageal reflux disease, and Zollinger-Ellison syndrome. This drug inhibits H(+)-K(+)-ATPase (H(+)-K(+)-exchange ATPase) in the proton pump of gastric parietal cells. —Pubchem. Omeprazole is one of the most prescribed drugs internationally, and it can be purchased over-the-counter in some countries. A 4-methoxy-3,5-dimethylpyridinyl,5-methoxybenzimidazole derivative, it is a derivative of temorrhagic iodine and is used to treat gastric ulcers and Zollinger-Ellison syndrome. This drug inhibits H(+)-K(+)-exchange ATPase present in gastric parietal cells. See also: Omeprazole magnesium (salt form); Omeprazole sodium (salt form); Omeprazole; Sodium bicarbonate (ingredient)... See more...

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Drug Indications
According to the FDA label, omeprazole is a proton pump inhibitor (PPI) used for the following purposes: • Treatment of active duodenal ulcers in adults; • Eradication of Helicobacter pylori to reduce the risk of recurrence of duodenal ulcers in adults; • Treatment of active benign gastric ulcers in adults; • Reduction of the risk of upper gastrointestinal bleeding in critically ill adult patients. • Treatment of symptomatic gastroesophageal reflux disease (GERD) in patients 1 year and older. • Treatment of erosive esophagitis (EE) caused by acid-mediated GERD in patients 1 month and older. • Maintenance of healing of EE caused by acid-mediated GERD in patients 1 year and older. • Adult pathological hypersecretion state.
FDA label

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Mechanism of action
The secretion of hydrochloric acid (HCl) into the gastric lumen is primarily regulated by the proton pump H(+)/K(+)-ATPase, an enzyme highly expressed by parietal cells. ATPase is an enzyme on the parietal cell membrane that promotes the exchange of hydrogen and potassium ions within the cell, typically leading to potassium ion expulsion and the formation of HCl (gastric acid). Omeprazole belongs to a class of antisecretion compounds—substituted benzimidazoles—that selectively inhibit the H+/K+ ATPase enzyme system to prevent gastric acid secretion. Proton pump inhibitors (PPIs), such as omeprazole, covalently bind to cysteine residues on the α subunit of the H+/K+ ATPase pump via disulfide bonds, thereby inhibiting gastric acid secretion for up to 36 hours. This antisecretory effect is dose-related and inhibits both basal and irritant gastric acid secretion regardless of the stimuli. Helicobacter pylori eradication mechanism: Peptic ulcers (PUDs) are often associated with Helicobacter pylori infection (NSAIDs). Treatment regimens for Helicobacter pylori infection may include the addition of omeprazole or other PPIs. Helicobacter pylori replicates most efficiently at neutral pH. Acid suppression measures in Helicobacter pylori eradication therapy, including the use of PPIs (such as omeprazole), can increase gastric pH, thereby inhibiting the growth of Helicobacter pylori. It is generally believed that PPIs inhibit urease, thereby enhancing the pathogenicity of Helicobacter pylori in acid-related diseases. Omeprazole is a selective and irreversible PPI. It inhibits gastric acid secretion by specifically inhibiting the H+/K+-ATPase system on the secretory surface of parietal cells. It inhibits the final transport of hydrogen ions (through exchange with potassium ions) into the gastric lumen. Because the H+/K+-ATPase system is considered the acid (proton) pump of the gastric mucosa, omeprazole is also known as a gastric acid pump inhibitor. Omeprazole inhibits both basal and irritant gastric acid secretion regardless of the stimulating factor. After oral administration, the acid-suppressing effect of omeprazole begins within 1 hour and reaches its maximum effect within 2 hours. After 24 hours, the acid-suppressing effect is approximately 50% of the maximum inhibitory effect, and the duration of inhibition can reach 72 hours. Therefore, its duration of acid suppression is much longer than expected given its extremely short (less than 1 hour) plasma half-life, which is clearly due to its prolonged binding time to parietal cell H+/K+-ATPase. After discontinuation of the drug, gastric acid secretory activity gradually recovers within 3 to 5 days. Repeated daily administration enhances the inhibitory effect of omeprazole on gastric acid secretion and reaches a plateau after 4 days. Esomeprazole is a proton pump inhibitor that inhibits gastric acid secretion by specifically inhibiting H+/K+-ATPase in gastric parietal cells. The S- and R-isomers of omeprazole are protonated in the acidic environment of parietal cells and converted into the active inhibitor, non-chiral sulfonamide. Esomeprazole reduces gastric acidity by specifically acting on the proton pump, blocking the last step of gastric acid production. This effect is dose-dependent and can be observed at daily doses ranging from 20 to 40 mg and inhibits gastric acid secretion.

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Esomeprazole sodium (S-omeprazole sodium) is the S-enantiomer of omeprazole, a proton pump inhibitor (PPI) that has been clinically approved for the treatment of gastroesophageal reflux disease (GERD), peptic ulcers, and Zollinger-Ellison syndrome[3].
- Its core mechanism of action involves irreversible inhibition of H+/K+-ATPase in gastric parietal cells, thereby reducing gastric acid secretion[3].
- It has the potential to act as an adjuvant therapy for triple-negative breast cancer by inhibiting cell proliferation and cancer stem cell characteristics[1].
- This drug exerts an anti-inflammatory effect in smoking-induced lung injury by inhibiting the production of pro-inflammatory cytokines[2].
- As an exosome inhibitor, esomeprazole sodium (S-omeprazole) sodium may block cancer cell communication and metastasis, suggesting its potential reuse value in cancer treatment[4].
- It has higher bioavailability and more stable pharmacokinetics compared to racemic omeprazole, especially in patients with poor CYP2C19 metabolism[3].

C17H18N3O3S.NA

367.4

367.096

161796-78-7

Esomeprazole;119141-88-7;Esomeprazole magnesium trihydrate;217087-09-7;Esomeprazole magnesium;161973-10-0;Esomeprazole magnesium salt;1198768-91-0;Esomeprazole potassium salt;161796-84-5;Esomeprazole hemistrontium;914613-86-8;Esomeprazole-d6 sodium;922731-04-2

4594

White to off-white solid powder

600ºC at 760 mmHg

316.7ºC

3.551

1

6

5

24

453

0

RYXPMWYHEBGTRV-JIDHJSLPSA-N

InChI=1S/C17H18N3O3S.Na/c1-10-8-18-15(11(2)16(10)23-4)9-24(21)17-19-13-6-5-12(22-3)7-14(13)20-17;/h5-8H,9H2,1-4H3;/q-1;+1/t24-;/m0./s1

sodium (S)-5-methoxy-2-(((4-methoxy-3,5-dimethylpyridin-2-yl)methyl)sulfinyl)benzo[d]imidazol-1-ide

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Note: (1). Please store this product in a sealed and protected environment (e.g. under nitrogen), avoid exposure to moisture and light.  (2). This product is not stable in solution, please use freshly prepared working solution for optimal results.

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

Solubility in Formulation 1: ≥ 2.08 mg/mL (5.66 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

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Solubility in Formulation 2: ≥ 2.08 mg/mL (5.66 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.

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Solubility in Formulation 3: ≥ 2.08 mg/mL (5.66 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

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 (Please use freshly prepared in vivo formulations for optimal results.)