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Systematic (IUPAC) name
Clinical data
Trade names Prilosec (originator), many generic brands[1]
Licence data US FDA:
  • AU: B3
  • US: C (Risk not ruled out)
Legal status
Routes of
Oral, IV
Pharmacokinetic data
Bioavailability 35–76%[2][3]
Protein binding 95%
Metabolism Hepatic (CYP2C19, CYP3A4)
Biological half-life 1–1.2 hours
Excretion 80% Renal
20% Faecal
CAS Registry Number  Y
ATC code A02
PubChem CID:
DrugBank  Y
ChemSpider  Y
PDB ligand ID 1C6 (, )
Chemical data
Formula C17H19N3O3S
Molecular mass 345.4 g/mol

Omeprazole (health system.[4]


  • Medical uses 1
    • Gastroesophageal reflux disease 1.1
    • Peptic ulcers 1.2
    • Erosive esophagitis 1.3
    • Zollinger Ellison syndrome 1.4
  • Adverse effects 2
    • Interactions 2.1
    • Pregnancy and breast-feeding 2.2
  • Mechanism of action 3
  • Pharmacodynamics 4
  • Pharmacokinetics 5
    • Measurement in body fluids 5.1
  • Chemistry 6
  • History 7
  • Dosage forms 8
  • See also 9
  • References 10
  • External links 11

Medical uses

Omeprazole can be used in the treatment of gastroesophageal reflux disease (GERD), peptic ulcers, erosive esophagitis, and Zollinger-Ellison syndrome.

Gastroesophageal reflux disease

GERD is a chronic condition in which acidic stomach content leaks back into the esophagus and irritates it. It may cause heartburn, which is a painful burning feeling in the chest or throat.

Peptic ulcers

Peptic ulcers are sores that develop in the lining of either the stomach or the duodenum due to damage from stomach acid. The most common cause of a peptic ulcer is infection by Helicobacter pylori.[5] Another major cause of a peptic ulcer is long-term use of nonsteroidal anti-inflammatory drugs (NSAIDs), such as aspirin or ibuprofen.[6] Treatment of H. pylori infection can be completed by taking a triple therapy combination of omeprazole, amoxicillin, and clarithromycin for 7–14 days.[7] Amoxicillin may be replaced with metronidazole in patients who are allergic to penicillin.[8]

Erosive esophagitis

Erosive esophagitis is due to tissue damage to the lining of the esophagus, because of inflammation or irritation over time. It may be caused by acid reflux from GERD, infection by a virus or fungus, an autoimmune disorder, certain medications,[9] or alcohol abuse.

Zollinger Ellison syndrome

Zollinger Ellison syndrome is a rare disorder that occurs when a tumor of the pancreas or duodenum releases a hormone that stimulates overproduction of stomach acid. This condition may form multiple peptic ulcers.

Adverse effects

The most frequent significant adverse effects occurring in at least 1% of patients include:[10]

  • Central nervous system: headache (7%), dizziness (2%)
  • Respiratory: upper respiratory tract infection (2%), cough (1%)
  • Gastrointestinal: abdominal pain (5%), diarrhea (4%), nausea (4%), vomiting (3%), flatulence (3%), acid regurgitation (2%), constipation (2%)
  • Neuromuscular and skeletal: back pain (1%), weakness (1%)
  • Dermatologic: rash (2%)

Other significant concerns related to adverse effects are:

Concern has been expressed regarding vitamin B12[15] and iron malabsorption,[16] but effects seem to be clinically insignificant, especially when supplement therapy is provided.[17]

Since their introduction, proton pump inhibitors (PPIs, especially omeprazole) have also been associated with several cases of acute interstitial nephritis,[18] an inflammation of the kidneys that often occurs as an adverse drug reaction.

Long-term use of PPIs is strongly associated with the development of benign polyps from fundic glands (which is distinct from fundic gland polyposis); these polyps do not cause cancer and resolve when PPIs are discontinued. No association is seen between PPI use and cancer, but use of PPIs may mask gastric cancers or other serious gastric problems and physicians should be aware of this effect.[19]


Although the potential for drug interactions is high, clinically important drug interactions are rare.[20][21]

However, the most significant major drug interaction concern is the decreased activation of clopidogrel when taken together with omeprazole.[22] Although still controversial,[23] this may increase the risk of stroke or heart attack in people taking clopidogrel to prevent these events.

The mechanism by which this potential interaction occurs is because omeprazole is an inhibitor of the enzymes CYP2C19 and CYP3A4.[24] Clopidogrel is an inactive prodrug that partially depends on CYP2C19 for conversion to its active form. Inhibition of CYP2C19 may block the activation of clopidogrel, which could reduce its effects.[25][26]

Almost all benzodiazepines are metabolised by the CYP3A4 and CYP2D6 pathway, and inhibition of these enzymes results in a higher AUC (i.e. the total effect over time of a given dose). Other examples of drugs dependent on CYP3A4 for their metabolism are escitalopram,[27] warfarin,[28] oxycodone, tramadol, and oxymorphone. The concentrations of these drugs may increase if they are used concomitantly with omeprazole.[29]

Omeprazole is also a competitive inhibitor of p-glycoprotein, as are other PPIs.[30]

Drugs that depend on an acidic stomach environment (such as ketoconazole or atazanavir) may be poorly absorbed, whereas acid-labile antibiotics (such as erythromycin which is a very strong CYP3A4 inhibitor) may be absorbed to a greater extent than normal due to the more alkaline environment of the stomach.[29]

St. John's wort, a monoamine oxidase inhibitor (Hypericum perforatum), and Gingko biloba significantly reduce plasma concentrations of omeprazole through induction of CYP3A4 and CYP2C19.[31]

Proton-pump inhibitors like omeprazole have been found to increase the plasma concentrations of methotrexate.[32]

Pregnancy and breast-feeding

Epidemiological data do not show an increased risk of major birth defects after maternal use of omeprazole during pregnancy.[33]

No clinical trials have deeply evaluated the potential consequences of the use of omeprazole in breastfeeding. However, the pharmacokinetics of omeprazole molecule strongly suggest the safety of omeprazole use during breastfeeding:

  • Omeprazole has a high plasma protein binding rate (95%),[34] indicating that little amount of drug is transferred to the milk duct during breast milk formation.
  • Omeprazole needs to be administrated in an enteric-coated formulation due to its rapid degradation in the acidic conditions of the stomach. This suggests that most of the free molecules ingested by the infant are likely degraded before being absorbed.

The safety of omeprazole use in breastfeeding deduced from pharmacokinetic characteristics of the omeprazole molecule agree with a case report in which the presence of omeprazole in breast milk was analysed over 4 hours after omeprazole uptake.[35] The peak omeprazole concentration in breast milk (that occurred 3h after omeprazole ingestion) was 7% of peak serum concentration, which corresponds to less than 1% of the usual adult dose (200 to 400 ug of omeprazole/kg of body weight) for a 5-kg infant consuming 200 ml of breast milk per day.

Mechanism of action

Omeprazole is a selective and irreversible proton pump inhibitor. It suppresses stomach acid secretion by specific inhibition of the H +/K + ATPase system found at the secretory surface of gastric parietal cells. Because this enzyme system is regarded as the acid (proton, or H+) pump within the gastric mucosa, omeprazole inhibits the final step of acid production.

Omeprazole also inhibits both basal and stimulated acid secretion irrespective of the stimulus.[36]


The inhibitory effect of omeprazole occurs within 1 hour after oral administration. The maximum effect occurs within 2 hours. The duration of inhibition is up to 72 hours. When omeprazole is stopped, baseline stomach acid secretory activity returns after 3 to 5 days. The inhibitory effect of omeprazole on acid secretion will plateau after 4 days of repeated daily dosing.[37]


The absorption of omeprazole takes place in the small intestine and is usually completed within 3 to 6 hours. The systemic bioavailability of omeprazole after repeated dose is about 60%.

Omeprazole, as well as other PPIs, are only effective on active H+/K+ ATPase pumps. These pumps are stimulated in the presence of food to aid in digestion. For this reason, patients should be advised to take omeprazole with a glass of water on an empty stomach about 30–60 minutes before a meal to allow the drug to reach peak levels once food is ingested.[38][39] Additionally, most sources recommend that after taking omeprazole, at least 30 minutes should be allowed to elapse before eating[40][41] (at least 60 minutes for immediate-release omeprazole plus sodium bicarbonate products, such as Zegerid),[42] though some sources say that with delayed-release forms of omeprazole, waiting before eating after taking the medication is not necessary.[43]

Omeprazole is completely metabolized by the cytochrome P450 system, mainly in the liver. Identified metabolites are the sulfone, the sulfide, and hydroxy-omeprazole, which exert no significant effect on acid secretion. About 80% of an orally given dose is excreted as metabolites in the urine, and the remainder is found in the feces, primarily originating from bile secretion.

Measurement in body fluids

Omeprazole may be quantified in plasma or serum to monitor therapy or to confirm a diagnosis of poisoning in hospitalized patients. Plasma omeprazole concentrations are usually in a range of 0.2–1.2 mg/l in persons receiving the drug therapeutically by the oral route and 1–6 mg/l in victims of acute overdose. Enantiomeric chromatographic methods are available to distinguish esomeprazole from racemic omeprazole.[44]


(S)- and (R)-enantiomers of omeprazole, a racemate (1:1 mixture of both enantiomers)

Omeprazole contains a tricoordinated sulfinyl sulfur in a pyramidal structure and therefore can exist as either the (S)- or (R)-enantiomers. Omeprazole is a racemate, an equal mixture of the two. In the acidic conditions of the canaliculi of parietal cells, both enantiomers are converted to achiral products (sulfenic acid and sulfenamide configurations) which react with a cysteine group in H+/K+ ATPase, thereby inhibiting the ability of the parietal cells to produce gastric acid.

Omeprazol rearrangement in the body

AstraZeneca has also developed esomeprazole (Nexium) which is a eutomer, purely the (S)-enantiomer, rather than a racemate like omeprazole.

Omeprazole undergoes a chiral shift in vivo which converts the inactive (R)-enantiomer to the active (S)-enantiomer, doubling the concentration of the active form.[45] This chiral shift is accomplished by the CYP2C19 isozyme of cytochrome P450, which is not found equally in all human populations. Those who do not metabolize the drug effectively are called "poor metabolizers". The proportion of the poor metabolizer phenotype varies widely between populations, from 2.0–2.5% in African Americans and white Americans to >20% in Asians; several pharmacogenomics studies have suggested that PPI treatment should be tailored according to CYP2C19 metabolism status.[46]


Omeprazole was first marketed in the United States in 1989 by Astra AB, now AstraZeneca, under the brand name Losec. In 1990, at the request of the U.S. Food and Drug Administration, the brand name Losec was changed to Prilosec to avoid confusion with the diuretic Lasix (furosemide).[47] The new name led to confusion between omeprazole (Prilosec) and fluoxetine (Prozac), an antidepressant.[47]

When Prilosec's U.S. patent expired in April 2001, AstraZeneca introduced esomeprazole (Nexium) as a patented replacement drug.[48] Many companies introduced generics as Astrazeneca's patents expired worldwide, which are available under many brand names.[1]

Dosage forms

Package of Losec (omeprazole) 20-mg, purchased in Hong Kong
Omeprazole 10-mg, from UK

Omeprazole is available as tablets and capsules (containing omeprazole or omeprazole magnesium) in strengths of 10, 20, 40, and in some markets 80 mg; and as a powder (omeprazole sodium) for intravenous injection. Most oral omeprazole preparations are enteric-coated, due to the rapid degradation of the drug in the acidic conditions of the stomach. This is most commonly achieved by formulating enteric-coated granules within capsules, enteric-coated tablets, and the multiple-unit pellet system (MUPS).[49] An immediate release formulation was approved by the FDA in the United States,[50] which does not require enteric coating.

It is also available for use in injectable form (IV) in Europe, but not in the U.S. The injection pack is a combination pack consisting of a vial and a separate ampule of reconstituting solution. Each 10-ml clear glass vial contains a white to off-white lyophilised powder consisting of omeprazole sodium 42.6 mg, equivalent to 40 mg of omeprazole.

See also


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  2. ^ Prilosec Prescribing Information. AstraZeneca Pharmaceuticals.
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  4. ^ "WHO Model List of EssentialMedicines" (PDF). World Health Organization. October 2013. Retrieved 22 April 2014. 
  5. ^ Shiotani A, Graham DY (November 2002). "Pathogenesis and therapy of gastric and duodenal ulcer disease". Med. Clin. North Am. 86 (6): 1447–66, viii.  
  6. ^ Traversa G, Walker AM, Ippolito FM, Caffari B, Capurso L, Dezi A, Koch M, Maggini M, Alegiani SS, Raschetti R (January 1995). "Gastroduodenal toxicity of different nonsteroidal antiinflammatory drugs". Epidemiology (Cambridge, Mass.) 6 (1): 49–54.  
  7. ^ Fuccio, Lorenzo, et al. "Meta-analysis: duration of first-line proton-pump inhibitor–based triple therapy for Helicobacter pylori eradication." Annals of internal medicine 147.8 (2007): 553-562.
  8. ^ Malfertheiner P, Megraud F, O'Morain C, Bazzoli F, El-Omar E, Graham D, Hunt R, Rokkas T, Vakil N, Kuipers EJ (June 2007). infection: the Maastricht III Consensus Report"Helicobacter pylori"Current concepts in the management of . Gut 56 (6): 772–81.  
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  10. ^ McTavish D, Buckley MMT, Heel RC. Omeprazole: an updated review of its pharmacology and therapeutic use in acid-related disorders. Drugs. 1991; 42:138-70.
  11. ^ Abou Chakra CN, et al Risk factors for recurrence, complications and mortality in Clostridium difficile infection: a systematic review. PLoS One. 2014 Jun 4;9(6):e98400. PMID 24897375
  12. ^ Yang, Yu-Xiao, et al. "Long-term proton pump inhibitor therapy and risk of hip fracture." Jama 296.24 (2006): 2947-2953.
  13. ^ Yu, Elaine W., et al. "Proton pump inhibitors and risk of fractures: a meta-analysis of 11 international studies." The American journal of medicine 124.6 (2011): 519-526.
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  21. ^ Proton Pump Inhibitor: Use in Adults. CMS Medicaid Integrity Program, Aug. 2013. Web. 18 Apr. 2014.
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  27. ^ Ali Torkamani, PhD. "Selective Serotonin Reuptake Inhibitors and CYP2D6". Retrieved 14 May 2015. 
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  44. ^ Baselt RC, Disposition of Toxic Drugs and Chemicals in Man, 8th edition, Biomedical Publications, Foster City, CA, 2008, pp. 1146–7. ISBN 978-0-9626523-7-0.
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  46. ^ Furuta T, Shirai N, Sugimoto M, Nakamura A, Hishida A, Ishizaki T (Jun 2005). "Influence of CYP2C19 pharmacogenetic polymorphism on proton pump inhibitor-based therapies". Drug Metab Pharmacokinet 20 (3): 153–67.  
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  50. ^ Santarus. Santarus Receives FDA Approval for Immediate-Release Omeprazole Tablet with Dual Buffers. N.p., 4 Dec. 2009. Web. 18 Apr. 2014.

External links

  • U.S. National Library of Medicine: Drug Information Portal – Omeprazole
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