Peptic ulcers may be treated with omeprazole. Infection withHelicobacter pylori can be treated by taking omeprazole,amoxicillin, andclarithromycin together for 7–14 days.[26] Amoxicillin may be replaced withmetronidazole in patients who are allergic to penicillin.[27]
Concern has been expressed regardingvitamin B12[33] andironmalabsorption,[34] but effects seem to be insignificant, especially when supplement therapy is provided.[35]
Since their introduction, proton-pump inhibitors (PPIs, especially omeprazole) have also been associated with several cases ofacute interstitial nephritis,[36] an inflammation of thekidneys that often occurs as an adverse drug reaction.
Long-term use of PPIs is strongly associated with the development of benignpolyps fromfundic glands (which is distinct fromfundic 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.[37]
There is a possible association between long-term use anddementia which requires further study to confirm.[38]
The safety of using omeprazole has not been established in pregnant or breastfeeding women.[16] Epidemiological data do not show an increased risk of major birth defects after maternal use of omeprazole duringpregnancy.[40]
Omeprazol Actavis 20 mg, bottle and pills in Sweden
Important drug interactions are rare.[41][42] However, the most significant major drug interaction concern is the decreased activation ofclopidogrel when taken together with omeprazole.[43] Although still controversial,[44] this may increase the risk of stroke or heart attack in people taking clopidogrel to prevent these events.
This interaction is possible because omeprazole is aninhibitor of the enzymesCYP2C19 andCYP3A4.[45]Clopidogrel is an inactiveprodrug 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.[46][47]
Almost allbenzodiazepines are metabolised by the CYP3A4 andCYP2D6 pathways, and inhibition of these enzymes results in a higherarea under the curve (i.e., the total effect over time of a given dose). Other examples of drugs dependent on CYP3A4 for their metabolism areescitalopram,[48]warfarin,[49]oxycodone,tramadol, andoxymorphone. The concentrations of these drugs may increase if they are used concomitantly with omeprazole.[50]
Omeprazole is also a competitive inhibitor ofp-glycoprotein, as are other PPIs.[51]
Drugs that depend on an acidic stomach environment (such asketoconazole oratazanavir) may be poorly absorbed, whereas acid-labile antibiotics (such aserythromycin 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.[50]
Omeprazole irreversibly blocks the enzyme system on parietal cells that is needed for the secretion of gastric acid. It is a specific H+/K+ATPase inhibitor. This is the enzyme needed for the final step in the secretion of gastric acid.[53]
The absorption of omeprazole takes place in the small intestine and is usually completed within three to six hours. The systemicbioavailability of omeprazole after repeated doses is about 60%.[54] Omeprazole has a volume of distribution of 0.4 L/kg. It has high plasma protein binding of 95%.[55]
Omeprazole is completely metabolized by thecytochrome P450 system, mainly in the liver, byCYP2C19 andCYP3A4isoenzymes.[16] Identified metabolites are thesulfone, thesulfide, and hydroxy-omeprazole. About 77% 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.[56] Omeprazole has a half life of 0.5 to 1 hour.[56]
As with all structurally-similar benzimidazoleproton pump inhibitors, omeprazole is aprodrug. A basic molecule, it accumulates in the acidiccanaliculi ofparietal cells in a protonated form where the S=O group becomes S-OH, which in turn is interconvertible with an achiral, reactivesulfenamide form. The sulfonamide form is able to attach onto thecysteine residue on the H+/K+-ATPase, thereby irreversibly inhibiting it.[57]
The two different chiralities of omeprazole are both metabolized into inactive products bycytochrome P450 enzymes, but each chirality is differently inactivated by specific isozymes. Compared to the (R)-enantiomer, the (S)-enantiomer is relatively more resistant to metabolism, especially metabolism byCYP2C19[58] (if it's processed by CYP2C19 at all).[59] As a result, among people with a more active version of CYP2C19 ("extensive metabolizers"), the (R) half of a dose of omeprazole is likely to perform more poorly. Conversely, among those with a less active version of CYP2C19 ("poor metabolizers"), more the (R) half is expected to survive metabolism and end up useful. The proportion of the poor metabolizerphenotype varies widely between populations, from 2.0 to 2.5% in African Americans and white Americans to >20% in Asians. Severalpharmacogenomics studies have suggested that PPI treatment should betailored according to CYP2C19 metabolism status.[60]
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 gastricparietal cells. Because this enzyme system is regarded as the acid (proton, or H+) pump within thegastric mucosa, omeprazole inhibits the final step of acid production.[53]
Omeprazole also inhibits both basal and stimulated acid secretion irrespective of the stimulus[56] as it blocks the last step in acid secretion.[56] The drug bindsnon-competitively so it has a dose-dependent effect.[55]
The inhibitory effect of omeprazole occurs within one hour after oral administration. The maximum effect occurs within two hours. The duration of inhibition is up to 72 hours. When omeprazole is stopped, baseline stomach acid secretory activity returns after three to five days. The inhibitory effect of omeprazole on acid secretion will plateau after four days of repeated daily dosing.[62]
Omeprazole is only effective on active H+/K+-ATPase pumps. These pumps are stimulated in the presence of food to aid in digestion.[63]
Omeprazole contains a tricoordinated sulfinyl sulfur in a pyramidal structure and therefore can exist as either the (S)- or (R)-enantiomers. Omeprazole is aracemate, an equal mixture of the two.[57]
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 people with acute overdose. Enantiomericchromatographic methods are available to distinguish esomeprazole from racemic omeprazole.[64]
Omeprazole was first made in 1979 by Swedish AB Hässle, part ofAstra AB. It was the first of the proton pump inhibitors (PPI).[65][66]Astra AB, now AstraZeneca, launched it as an ulcer medicine under the name Losec in Sweden. It was first sold in the United States in 1989 under the brand name Losec. In 1990, at the request of the USFood and Drug Administration, the brand name Losec was changed to Prilosec to avoid confusion with thediuretic Lasix (furosemide).[67] The new name led to confusion between omeprazole (Prilosec) andfluoxetine (Prozac), anantidepressant.[67] Prilosec is owned byProcter & Gamble in alliance with AstraZeneca[68] and the product is designed to address frequent heartburn, which can be triggered by various factors such as certain foods, stress, and smoking.
Prilosec was first introduced in 1989 as a prescription medication approved by the FDA for the treatment of severe heartburn.[69] In 2003, Prilosec OTC was launched as the first over-the-counter option for managing frequent heartburn.[70] It is known for its advertising campaign featuring Larry the Cable Guy as the spokesperson for the brand, during the 2010s, emphasizing the concept of "Zero Heartburn".[71]
When Prilosec's US patent expired in April 2001, AstraZeneca introduced esomeprazole (Nexium) as a patented replacement drug.[72] Many companies introduced generics as AstraZeneca's patents expired worldwide, which are available under many brand names.
Omeprazole was a subject of a patent litigation in the U.S.[73] The invention involved application of two different coatings to a drug in pill form to ensure that the omeprazole did not disintegrate before reaching its intended site of action in stomach. Although the solution by means of two coatings was obvious, the patent was found valid, because the source of the problem was non-obvious and was discovered by the patentee.[74]
In September 2023, AstraZeneca announced it would pay $425 million to settle product liability litigations against Prilosec in the United States.[75]
In February 2025, theCommittee for Veterinary Medicinal Products of theEuropean Medicines Agency adopted a positive opinion, recommending the granting of a marketing authorization for the veterinary medicinal product Omeprazole TriviumVet, gastro-resistant capsule, hard, intended for dogs.[76] The applicant for this veterinary medicinal product is TriviumVet DAC.[76] Omeprazole TriviumVet was authorized for veterinary use in the European Union in April 2025.[7]
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