Hubbry Logo
OmeprazoleOmeprazoleMain
Open search
Omeprazole
Community hub
Omeprazole
logo
7 pages, 0 posts
0 subscribers
Be the first to start a discussion here.
Be the first to start a discussion here.
Omeprazole
Omeprazole
Omeprazole
View on Wikipedia
from Wikipedia

Omeprazole
Clinical data
Pronunciation/oʊˈmɛprəzoʊl/ ⓘ
Trade namesLosec, Prilosec, others[1][2]
AHFS/Drugs.comMonograph
MedlinePlusa693050
License data
Pregnancy
category
Routes of
administration		By mouth, intravenous
Drug classProton-pump inhibitor
ATC code
Legal status
Legal status
Pharmacokinetic data
Bioavailability35–76%[8][9]
Protein binding95%
MetabolismLiver (CYP2C19, CYP3A4)
Elimination half-life1–1.2 hours
Excretion80% (urine)
20% (bile via feces)
Identifiers
  • 5-Methoxy-2-[(4-methoxy-3,5-dimethylpyridin-2-yl)methanesulfinyl]-1H-benzimidazole
CAS Number
PubChem CID
IUPHAR/BPS
DrugBank
ChemSpider
UNII
KEGG
ChEBI
ChEMBL
PDB ligand
CompTox Dashboard (EPA)
ECHA InfoCard100.122.967 Edit this at Wikidata
Chemical and physical data
FormulaC17H19N3O3S
Molar mass345.42 g·mol−1
3D model (JSmol)
ChiralityRacemic mixture
Density1.4±0.1[10] g/cm3
Melting point156 °C (313 °F)
  • CC1=CN=C(C(=C1OC)C)CS(=O)C2=NC3=C(N2)C=C(C=C3)OC
  • InChI=1S/C17H19N3O3S/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,(H,19,20) checkY
  • Key:SUBDBMMJDZJVOS-UHFFFAOYSA-N checkY
  (verify)

Omeprazole, sold under the brand names Prilosec and Losec among others, is a medication used in the treatment of gastroesophageal reflux disease (GERD), peptic ulcer disease, and Zollinger–Ellison syndrome.[1] It is also used to prevent upper gastrointestinal bleeding in people who are at high risk.[1] Omeprazole is a proton-pump inhibitor (PPI) and its effectiveness is similar to that of other PPIs.[11] It can be taken by mouth or by injection into a vein.[1][12] It is also available in the fixed-dose combination medication omeprazole/sodium bicarbonate as Zegerid[13][14] and as Konvomep.[15]

Common side effects include nausea, vomiting, headaches, abdominal pain, and increased intestinal gas.[1][16] Serious side effects may include Clostridioides difficile colitis, an increased risk of pneumonia, an increased risk of bone fractures, and the potential of masking stomach cancer.[1] Whether it is safe for use in pregnancy is unclear.[1] It works by blocking the release of stomach acid.[1]

Omeprazole was patented in 1978 and approved for medical use in 1988.[17][18][19] It is on the World Health Organization's List of Essential Medicines.[20] It is available as a generic medication.[1] In 2023, it was the tenth most commonly prescribed medication in the United States, with more than 45 million prescriptions.[21][22] It is also available without a prescription in the United States.[23][24]

Medical uses

[edit]
See also: Proton-pump inhibitor

Omeprazole can be used in the treatment of gastroesophageal reflux disease (GERD), heartburn, peptic ulcers, erosive esophagitis, Zollinger–Ellison syndrome, and eosinophilic esophagitis.[25][1]

Peptic ulcers

[edit]

Peptic ulcers may be treated with omeprazole. Infection with Helicobacter pylori can be treated by taking omeprazole, amoxicillin, and clarithromycin together for 7–14 days.[26] Amoxicillin may be replaced with metronidazole in patients who are allergic to penicillin.[27]

Adverse effects

[edit]

Adverse effects occurring in at least 1% of people include:[28][failed verification]

Other concerns related to adverse effects are:

Concern has been expressed regarding vitamin B12[33] and iron malabsorption,[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 of acute interstitial nephritis,[36] an inflammation of the kidneys that often occurs as an adverse drug reaction.

Long-term use

[edit]

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.[37]

There is a possible association between long-term use and dementia which requires further study to confirm.[38]

An article published in 2013 claims that the long-term use of PPIs is associated with decreased calcium absorption (causing increased risk of osteoporosis and fractures), decreased magnesium absorption (causing electrolyte disturbances), and increased risk of certain infections, such as C. difficile and community-acquired pneumonia. The authors hypothesize that this is due to decreased stomach acid production.[39]

Pregnancy and breastfeeding

[edit]

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 during pregnancy.[40]

Interactions

[edit]
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 of clopidogrel 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 an inhibitor of the enzymes CYP2C19 and CYP3A4.[45] 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.[46][47]

Almost all benzodiazepines are metabolised by the CYP3A4 and CYP2D6 pathways, and inhibition of these enzymes results in a higher area under the curve (i.e., the total effect over time of a given dose). Other examples of drugs dependent on CYP3A4 for their metabolism are escitalopram,[48] warfarin,[49] oxycodone, tramadol, and oxymorphone. The concentrations of these drugs may increase if they are used concomitantly with omeprazole.[50]

Omeprazole is also a competitive inhibitor of p-glycoprotein, as are other PPIs.[51]

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.[50]

St. John's wort (Hypericum perforatum) and Ginkgo biloba significantly reduce plasma concentrations of omeprazole through induction of CYP3A4 and CYP2C19.[52]

Pharmacology

[edit]

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]

Pharmacokinetics

[edit]

The absorption of omeprazole takes place in the small intestine and is usually completed within three to six hours. The systemic bioavailability 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 the cytochrome P450 system, mainly in the liver, by CYP2C19 and CYP3A4 isoenzymes.[16] Identified metabolites are the sulfone, the sulfide, 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]

Bioactivation

[edit]

As with all structually-similar benzimidazole proton pump inhibitors, omeprazole is a prodrug. A basic molecule, it accumulates in the acidic canaliculi of parietal cells in a protonated form where the S=O group becomes S-OH, which in turn is interconvertible with an achiral, reactive sulfenamide form. The sulfonamide form is able to attach onto the cysteine residue on the H+/K+-ATPase, thereby irreversibly inhibiting it.[57]

Omeprazol rearrangement in the body

Chirality

[edit]

The two different chiralities of omeprazole are both metabolized into inactive products by cytochrome 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 by CYP2C19[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 metabolizer phenotype varies widely between populations, from 2.0 to 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.[60]

AstraZeneca also developed esomeprazole (Nexium) which is a eutomer, purely the (S)-enantiomer, rather than a racemate like omeprazole.[61]

Mechanism of action

[edit]

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.[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 binds non-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]

PrilosecOTC Drug Facts

Chemistry

[edit]

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.[57]

Measurement in body fluids

[edit]

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. Enantiomeric chromatographic methods are available to distinguish esomeprazole from racemic omeprazole.[64]

History

[edit]
Main article: Discovery and development of proton pump inhibitors

Omeprazole was first made in 1979 by Swedish AB Hässle, part of Astra 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 US Food and Drug Administration, the brand name Losec was changed to Prilosec to avoid confusion with the diuretic Lasix (furosemide).[67] The new name led to confusion between omeprazole (Prilosec) and fluoxetine (Prozac), an antidepressant.[67] Prilosec is owned by Procter & 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]

Society and culture

[edit]

Economics

[edit]

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]

Brand names

[edit]

Brand names include Losec, Prilosec, Zegerid, Miracid, and Omez.[2][1]

Veterinary uses

[edit]

In February 2025, the Committee for Veterinary Medicinal Products of the European 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]

References

[edit]

Further reading

[edit]
Revisions and contributorsEdit on WikipediaRead on Wikipedia

Omeprazole

View on Grokipedia
from Grokipedia
Omeprazole is a (PPI) medication that reduces stomach acid production by irreversibly blocking the H+/K+ ATPase enzyme system, known as the , in the parietal cells of the . As the first commercially available PPI, discovered in 1979 and approved by the U.S. in 1989, it revolutionized the treatment of acid-related gastrointestinal conditions and remains one of the most widely prescribed drugs globally, and it is included in the World Health Organization's List of Essential Medicines (23rd list, 2023). Indications and Uses
Omeprazole is indicated for acid-related disorders of the upper gastrointestinal tract, which commonly present with symptoms such as heartburn, epigastric pain, or burning due to excess stomach acid. It is primarily indicated for the management of (GERD), (including duodenal and gastric ulcers), erosive , and pathological hypersecretory conditions such as Zollinger-Ellison syndrome. It is also used in combination with antibiotics like and amoxicillin to eradicate infections associated with ulcers, typically achieving healing within four weeks of therapy. For over-the-counter use, it treats frequent occurring at least twice weekly in adults. Off-label applications include stress ulcer prophylaxis in critically ill patients and maintenance therapy for . Pharmacology and Administration
The drug's antisecretory effects begin within one hour of administration, peak at two hours, and persist for up to 72 hours due to its covalent binding to the , allowing once-daily dosing. It is available in delayed-release oral forms, including capsules (10 mg, 20 mg, 40 mg), tablets, and powder for suspension. For optimal efficacy, omeprazole should be taken on an empty stomach 30–60 minutes (or 1 hour) before a meal; for once-daily dosing, the morning before breakfast is preferred, as this timing allows the drug to inhibit acid-producing proton pumps before they are activated by food intake, maximizing absorption and acid suppression. Some formulations (e.g., certain tablets) may be taken with food, though before a meal is generally recommended. Taking immediately after meals significantly reduces efficacy due to food affecting intestinal release and absorption; if necessary, wait at least 1-2 hours after eating, though an empty stomach remains preferable. Always follow your doctor's or package instructions. For twice-daily dosing such as 20 mg twice daily, take one dose on an empty stomach in the morning 30-60 minutes before breakfast and the second on an empty stomach in the evening before dinner; if dinner is early, before bed on an empty stomach (at least 2-3 hours after dinner) can help control nighttime acid secretion, relieving nocturnal reflux and associated nausea; capsules must be swallowed whole—do not chew or open the capsule (enteric-coated to protect from stomach acid). Dosage varies by condition—for example, 20 mg once daily for GERD maintenance or initially 60 mg once daily for hypersecretory states, which may be adjusted higher based on response—and it is suitable for adults and children over certain ages depending on the indication. Safety and Considerations
Common adverse effects include (affecting about 7% of users), (5%), (4%), and (4%), while long-term use (beyond one year) may increase risks of hypomagnesemia, Clostridium difficile-associated , bone fractures, , and fundic gland polyps. Precautions are advised for patients with , , or those taking interacting drugs like clopidogrel or rilpivirine, and monitoring for kidney function is recommended with prolonged therapy. Omeprazole's generic availability since the early has enhanced its accessibility as both prescription and over-the-counter options.

Medical Uses

Omeprazole is indicated for the treatment of acid-related gastrointestinal conditions, which frequently manifest as upper abdominal (epigastric) pain, burning sensation, heartburn, or acid indigestion. These include gastroesophageal reflux disease (GERD), erosive esophagitis, peptic ulcer disease, and hypersecretory states such as Zollinger-Ellison syndrome. It suppresses gastric acid production, with symptomatic relief often requiring several days. Omeprazole is not indicated for abdominal pain unrelated to excess gastric acid, such as lower abdominal pain from causes like appendicitis, gallstones, or infections. Patients with abdominal pain should seek medical evaluation to identify the cause, particularly if symptoms are severe, persistent, or accompanied by warning signs such as fever, vomiting, or bloody stools. Over-the-counter omeprazole is approved for short-term treatment of frequent heartburn, generally limited to 14 days without physician advice.

Gastroesophageal Reflux Disease and Erosive Esophagitis

is a characterized by the reflux of stomach contents into the , leading to symptoms such as —a burning sensation in the chest—and regurgitation of acid into the mouth or throat. , a more severe manifestation of GERD, involves and of the esophageal lining due to prolonged acid exposure, which can cause additional symptoms like difficulty and esophageal pain. Omeprazole, a , alleviates GERD symptoms and promotes healing of erosive by irreversibly inhibiting the H+/K+ in gastric parietal cells, thereby suppressing acid production and reducing esophageal acid exposure. This acid suppression mechanism allows the esophageal mucosa to recover, with effects beginning within one hour of administration and lasting up to 72 hours after a single dose. For the treatment of gastroesophageal reflux disease (GERD) without esophageal lesions, the recommended dosage is 20 mg orally once daily for up to four weeks, while for erosive , 20 mg once daily for 4-8 weeks (up to 40 mg if needed). It should be taken before a meal (preferably 30 minutes prior, in the morning), and capsules should be swallowed whole without crushing or chewing for optimal efficacy. Clinical trials demonstrate omeprazole's effectiveness, with 74% of patients achieving heartburn-free status by day 27 on 20 mg daily in a randomized, double-blind study of symptomatic GERD without . For erosive , healing rates reach 70-96% after eight weeks of treatment. Short-term focuses on symptom relief and mucosal healing, whereas long-term with the lowest effective dose, such as 20 mg daily, prevents of by sustaining acid control.

Peptic Ulcer Disease

Peptic ulcer disease (PUD) involves erosions in the mucosal lining of the stomach or duodenum, resulting from an imbalance between aggressive factors such as gastric acid and pepsin, and protective mechanisms including mucus production, bicarbonate secretion, and mucosal blood flow. Nonsteroidal anti-inflammatory drug (NSAID)-induced ulcers arise primarily from inhibition of cyclooxygenase-1 (COX-1), which reduces prostaglandin synthesis and impairs mucosal defense, making this the second most common cause of PUD after Helicobacter pylori infection. Stress-related ulcers, often superficial erosions in the gastric fundus and body, develop in critically ill patients due to conditions like shock, sepsis, or trauma, which decrease mucosal blood flow, disrupt cellular energy metabolism, and compromise epithelial barrier integrity. Omeprazole, a (PPI), promotes by profoundly suppressing secretion, thereby reducing acid-mediated damage to the mucosa and allowing epithelial regeneration. The recommended dosage for active duodenal ulcer is 20 mg once daily for 4 weeks (may extend up to 8 weeks if healing is incomplete), while for active gastric ulcer, 40 mg once daily is recommended for 4-8 weeks. Clinical trials demonstrate high healing rates, approaching 90% for duodenal ulcers at 4 weeks in responsive cases. Omeprazole should be taken before a meal, preferably 30 minutes prior in the morning, and capsules should be swallowed whole without crushing or chewing. Dosage adjustments may be needed in patients with hepatic impairment or certain populations; always consult a healthcare provider for personalized dosing. For NSAID-associated ulcers, omeprazole facilitates even when NSAIDs are continued, though discontinuation is preferred to optimize outcomes. In preventing ulcer recurrence, maintenance therapy with omeprazole 20 mg daily or intermittently (e.g., 20 mg three days per week) significantly lowers relapse rates compared to , particularly in patients with a history of frequent recurrences. Omeprazole also reduces the risk of recurrent after endoscopic in bleeding peptic ulcers, with high-dose intravenous regimens (e.g., 80 mg bolus followed by 8 mg/hour infusion for 72 hours) decreasing rebleeding by stabilizing clots through sustained pH elevation above 6. Compared to H2-receptor antagonists (H2 blockers) like or , omeprazole demonstrates superior efficacy in ulcer healing, especially for cases, with faster symptom relief and higher healing rates (e.g., 80-90% versus 60-70% at 4 weeks for duodenal ulcers). It also provides better relapse prevention during maintenance, reducing recurrence by up to 80% more effectively than H2 blockers in long-term studies. The American College of Gastroenterology (ACG) guidelines recommend omeprazole or other PPIs as first-line therapy for healing NSAID-related ulcers in high-risk patients, such as the elderly (age >60 years), those on high-dose or multiple NSAIDs, or with a history of ulcers, with co-therapy advised if NSAIDs cannot be stopped. For prevention in these groups, daily PPI use (e.g., omeprazole 20-40 mg) is indicated to mitigate risk, particularly when combined with low-dose aspirin.

Helicobacter pylori Eradication Therapy

Helicobacter pylori infection plays a central role in the pathogenesis of by inducing chronic gastric inflammation, which erodes the mucosal lining and leads to ulcer formation in the or . Additionally, H. pylori is classified as a by the , significantly elevating the risk of and mucosa-associated lymphoid tissue (MALT) lymphoma through persistent inflammation, epithelial damage, and promotion of precancerous lesions. Omeprazole, as a (PPI), is a key component in combination therapies aimed at eradicating H. pylori to resolve associated ulcers and reduce long-term cancer risk. In such eradication regimens, omeprazole may be administered at 20 mg twice daily or 40 mg once daily combined with antibiotics. The traditional first-line regimen, known as triple therapy, typically involves omeprazole 20 mg twice daily combined with amoxicillin 1 g twice daily and 500 mg twice daily, administered for 14 days. This approach leverages omeprazole's acid suppression to enhance stability and efficacy in the gastric environment. Eradication rates with this triple therapy regimen have historically achieved 80-90% success in intention-to-treat analyses, though contemporary rates often fall to 70-80% due to rising resistance. In regions with low resistance, it remains a viable option, but guidelines now conditionally recommend it only when susceptibility is confirmed. For strains resistant to , bismuth-based quadruple therapy serves as an effective alternative, incorporating omeprazole 20 mg twice daily, or subcitrate four times daily, 500 mg four times daily, and 500 mg three to four times daily for 14 days. This regimen yields eradication rates exceeding 90% in treatment-naïve patients and is now the preferred first-line therapy per the 2024 American College of Gastroenterology guidelines. Recent regional data highlight escalating H. pylori resistance patterns, with global primary resistance to at 32.6% and to at 35.3%, necessitating tailored regimens to combat treatment failures. Post-eradication monitoring is essential, typically involving a or stool antigen test performed at least four weeks after therapy completion to confirm successful elimination and guide salvage treatment if needed. Omeprazole should be taken before meals, preferably 30 minutes prior, and capsules swallowed whole without crushing or chewing. Dosage adjustments may be required in patients with hepatic impairment or in certain populations; always consult a healthcare provider for personalized dosing.

Zollinger-Ellison Syndrome

Zollinger-Ellison syndrome (ZES) is a rare condition characterized by excessive production due to gastrin-secreting tumors known as gastrinomas, typically located in the or . Clinical features include recurrent and refractory peptic ulcers that are often multiple or in atypical locations such as the distal or , as well as secretory resulting from the inactivation of pancreatic enzymes by high acid levels in the . Other common symptoms encompass , , , and , with complications like or occurring in severe cases. Diagnosis of ZES relies on demonstrating hypergastrinemia in the context of low gastric , with serum levels exceeding 1000 pg/mL and gastric below 2 considered highly suggestive. The stimulation test serves as a confirmatory diagnostic criterion: after an intravenous injection of (2-3 clinical units/kg), serum levels rise paradoxically by more than 120 pg/mL within 2-30 minutes in patients with ZES, unlike the normal suppressive response. This test is particularly useful in equivocal cases, such as those with moderate hypergastrinemia due to use, and has a sensitivity of approximately 94%. Omeprazole, a , is a cornerstone therapy for controlling the hypersecretion of in ZES by irreversibly inhibiting the H+/K+-ATPase in parietal cells, thereby reducing acid output and alleviating symptoms. The recommended initial dose is 60 mg once daily, taken before a meal, with the capsule swallowed whole without crushing or chewing. Doses are adjusted individually as needed, with daily dosages exceeding 80 mg administered in divided doses. Titration is guided by gastric pH monitoring to achieve an intragastric pH greater than 4 or basal acid output less than 10 mEq/hour measured one hour before the next dose. Dose adjustments may be necessary in patients with hepatic impairment due to increased bioavailability and prolonged plasma half-life, or in certain other populations. Patients should always consult a healthcare provider for personalized dosing. This approach effectively controls acid hypersecretion in nearly all patients, with more than 90% achieving symptom resolution or significant improvement, including healing and cessation of , as evidenced by long-term case studies and prospective trials involving dozens of patients followed for up to nine years. For long-term management, omeprazole therapy is often continued indefinitely even after successful tumor resection, as residual or recurrent gastrinomas may persist, requiring ongoing acid suppression to prevent complications. In cases of advanced or metastatic disease, analogs such as are used adjunctively to inhibit release from tumors, potentially allowing dose reduction of omeprazole while stabilizing disease progression and improving survival in responsive patients.

Adverse Effects

Common Side Effects

The most frequently reported mild adverse reactions to omeprazole during short-term use include , , , and , occurring in approximately 1-5% of patients in clinical trials. These effects are generally transient and self-limiting, with being the most common at an incidence of 6.9%, followed by (5.2%), nausea (4.0%), and (3.7%). Management typically involves symptomatic treatment, such as over-the-counter analgesics for or agents for loose stools, alongside dose adjustment to the lowest effective level to minimize discomfort while maintaining therapeutic benefit. Post-marketing surveillance data indicate that these common s often resolve upon discontinuation of the drug, with most patients experiencing improvement within days to weeks. Overall gastrointestinal incidences remain similar across the class.

Serious and Long-Term Adverse Effects

Long-term use of omeprazole, a proton pump inhibitor (PPI), has been associated with an elevated risk of certain infections due to reduced gastric acidity, which may promote bacterial overgrowth. Meta-analyses indicate an increased odds of Clostridium difficile infection (CDI) among PPI users, with one analysis reporting an odds ratio (OR) of 2.15 (95% CI 1.81–2.55) across multiple studies. Similarly, community-acquired pneumonia risk is heightened, as evidenced by a pooled relative risk (RR) of 1.49 (95% CI 1.16–1.92) in outpatient PPI users. These risks appear more pronounced with prolonged therapy, though causality remains supported primarily by observational data. Nutrient malabsorption is another concern with extended omeprazole use, particularly affecting and magnesium. Long-term PPI therapy (≥1 year) may impair absorption by inhibiting acid-dependent release from food proteins; a 2023 meta-analysis reported a slight increase in deficiency risk (OR 1.42, 95% CI 1.16–1.73), though with significant heterogeneity suggesting inconsistent evidence. Hypomagnesemia, often occurring after at least 1 year of use, can lead to severe symptoms such as arrhythmias and seizures; the FDA has noted cases requiring PPI discontinuation despite magnesium supplementation. Omeprazole has been linked to skeletal and renal complications in prolonged use. The FDA has warned of increased fracture risk for the , wrist, and spine with PPI therapy exceeding 1 year or at high doses, based on epidemiological data showing adjusted ORs of 1.44 (95% CI 1.30–1.59) for hip fractures and up to 1.60 (95% CI 1.25–2.04) for spine fractures. progression may also accelerate, with meta-analyses reporting a 20% higher risk (OR 1.20, 95% CI 1.12–1.28) and risk elevated 4.35-fold (OR 4.35, 95% CI 3.14–6.04). Recent meta-analyses (as of 2025) have associated long-term PPI use with an increased risk of gastric cancer, with pooled relative risks ranging from 1.3 to 2.9, particularly in patients with prior H. pylori eradication. This risk is based on observational studies, and further research is needed to establish causality; guidelines recommend limiting PPI duration in at-risk individuals. The interaction between omeprazole and clopidogrel, an antiplatelet agent, may attenuate clopidogrel's efficacy via CYP2C19 inhibition, potentially raising cardiovascular risks, though this remains debated. A meta-analysis of post-percutaneous coronary intervention patients found concomitant use associated with a 28% higher hazard of major adverse cardiovascular events (HR 1.28, 95% CI 1.24–1.32), including myocardial infarction (HR 1.51, 95% CI 1.40–1.62). However, some reviews conclude no definitive excess risk after adjusting for confounders. Guidelines recommend periodic monitoring of PPI users for these effects, including serum magnesium, , and renal function in at-risk patients, alongside assessment for long-term therapy. Deprescribing is advised when no ongoing indication exists, via dose tapering or abrupt cessation, with follow-up at 4–12 weeks to manage rebound symptoms; the American Gastroenterological Association emphasizes reviewing indications annually to minimize unnecessary exposure.

Use in Pregnancy and Breastfeeding

Omeprazole is classified by the U.S. (FDA) as C, meaning reproduction studies have not demonstrated a risk to the , but there are no adequate and well-controlled studies in humans, and use during should only occur when the potential benefit justifies the potential risk to the . In reproductive studies conducted in rats and rabbits, omeprazole doses up to 56 times the human dose showed no evidence of teratogenicity or impaired , though higher doses led to maternal and reduced fetal weight without direct fetal harm. Multiple cohort studies in pregnant women have provided reassuring data, with no consistent association between first-trimester exposure and adverse outcomes. Large observational studies have further supported the safety profile of omeprazole and other inhibitors (PPIs) during . For instance, a -based in involving 840,968 live births identified 5,082 first-trimester PPI exposures, including omeprazole, and found no increased risk of major congenital malformations (adjusted prevalence ratio 1.10; 95% CI, 0.91-1.34) or specific defects like cardiac anomalies or . Similarly, a Swedish registry analysis of 955 infants exposed to omeprazole reported malformation rates comparable to the general (1.0% vs. 1.6%), with no evidence of increased risk for major s. A of 18 observational studies encompassing thousands of PPI exposures during confirmed no substantial elevation in risk ( 1.13; 95% CI, 0.96-1.33). Professional guidelines, including those from the American College of Obstetricians and Gynecologists (ACOG), endorse the use of omeprazole in pregnant individuals with severe (GERD) when symptoms are refractory to lifestyle modifications and safer alternatives, provided the benefits outweigh potential risks. For mild GERD cases, antacids such as aluminum hydroxide or are preferred as first-line options due to their established safety profile and minimal systemic absorption. Regarding breastfeeding, omeprazole is excreted into human milk at very low levels, posing negligible risk to infants. Following a single 20 mg oral dose, omeprazole concentrations in breast milk were undetectable for the first 90 minutes, peaked at approximately 20 mcg/L at 3 hours, and returned to baseline by 6 hours, resulting in an estimated infant dose of less than 0.17% (range 0.07-0.34%) of the maternal weight-adjusted dose. No adverse effects have been reported in breastfed infants exposed to omeprazole, and it is considered compatible with by authoritative sources like the .

Drug Interactions and Contraindications

Drug Interactions

Omeprazole, as a potent inhibitor of the enzyme , can prolong the elimination and increase plasma concentrations of drugs metabolized primarily by this pathway, such as , , and . For instance, coadministration with omeprazole may substantially increase exposure of these agents, with studies showing up to a 60% increase in AUC in some populations and smaller effects (around 10%) for , necessitating dose adjustments or enhanced monitoring to prevent . This interaction arises from at the , which is particularly relevant for patients on long-term therapy with these narrow drugs. By elevating gastric , omeprazole can impair the absorption of certain agents that require an acidic environment for optimal , including and . Studies indicate that this leads to substantial reductions in plasma concentrations of these azoles, potentially compromising therapeutic efficacy against fungal infections. Clinicians are advised to monitor antifungal response or consider alternative agents when omeprazole is required concurrently. A clinically significant pharmacodynamic interaction occurs between omeprazole and clopidogrel, where omeprazole's inhibition of reduces the conversion of clopidogrel to its by approximately 45%, thereby decreasing the antiplatelet effect. The U.S. recommends avoiding concomitant use of omeprazole with clopidogrel due to the increased risk of cardiovascular events in at-risk patients. Alternative inhibitors with less CYP2C19 affinity, such as , may be preferable in these scenarios. In eradication regimens, omeprazole generally exhibits no significant adverse interactions with commonly used antibiotics such as amoxicillin, , or ; in fact, the elevated gastric may enhance antibiotic stability and efficacy. For drugs with narrow therapeutic indices affected by omeprazole, such as and , regular monitoring of international normalized ratio (INR), serum levels, and clinical response is recommended to guide dosing adjustments.

Contraindications and Precautions

Omeprazole is contraindicated in patients with known to substituted benzimidazoles, such as other inhibitors, or to any component of the formulation, as this may lead to severe allergic reactions including , , or urticaria. It is also contraindicated for concurrent use with rilpivirine-containing products due to reduced antiviral efficacy resulting from elevated gastric pH, and with high-dose due to potential elevation of methotrexate plasma levels leading to toxicity. In elderly patients, no specific dose adjustment is required, but they may exhibit increased sensitivity to omeprazole's effects, necessitating careful monitoring for suboptimal response or , potentially requiring . For patients with renal impairment, dose adjustment is generally not needed, though monitoring for acute tubulointerstitial is advised, with prompt discontinuation if symptoms such as decreased urination or occur. In hepatic impairment, including Child-Pugh classes A, B, or C, a reduced dose of 10 mg daily is recommended for the treatment of pathological hypersecretory conditions to avoid excessive drug exposure due to prolonged . Long-term with omeprazole, particularly for one year or more, warrants precautions due to an elevated of osteoporosis-related fractures of the , , or spine; the lowest effective dose and shortest duration should be used, with patients at high fracture monitored closely. For pediatric use, omeprazole is approved for treating and erosive in children aged 1 month and older, with dosing based on weight (typically 5-20 mg daily), though safety data beyond 12 months of use are limited, and monitoring for events like respiratory infections or is essential. Use in infants under 1 month remains off-label and should be approached cautiously. Genetic variations in the enzyme influence omeprazole's efficacy and safety, with poor metabolizers experiencing higher plasma concentrations and potentially greater acid suppression but also increased risk of adverse effects. Poor metabolizer status occurs in approximately 15-20% of Asian populations, compared to 2-5% in Caucasians, and for example, in Asian patients with pathological hypersecretory conditions, a dose of 10 mg daily is recommended.

Pharmacology

Mechanism of Action

Omeprazole acts as a that selectively accumulates in the secretory canaliculi of gastric parietal cells, where the highly acidic environment ( ≈1) facilitates its . Upon , omeprazole undergoes acid-catalyzed rearrangement to form a reactive sulfenamide intermediate, which is a thiophilic species capable of covalent bonding. This process ensures targeted delivery to the site of acid , minimizing off-target effects elsewhere in the body. The sulfenamide form of omeprazole then irreversibly binds to the luminal residues of the H+/K+-ATPase enzyme, primarily at Cys813, forming a bridge that inactivates the . This covalent inhibition disrupts the final step in production, where the enzyme exchanges intracellular H+ for extracellular K+ to generate HCl, thereby suppressing acid secretion by up to 99%. The binding is highly selective for the gastric H+/K+-ATPase compared to other ATPases, such as Na+/K+-ATPase, due to the enzyme's unique luminal exposure in the acidic canaliculi and the drug's pH-dependent activation. Inhibition by omeprazole is time-dependent, as it requires accumulation and activation during active acid secretion; maximal suppression typically occurs after 24-48 hours of dosing, with steady-state effects achieved over 2-3 days as more pumps are recruited and inhibited. Recovery of acid secretion relies on the synthesis of new enzymes, with a functional half-life of approximately 18 hours in humans, though the drug's plasma half-life is only about 1 hour. This prolonged duration of action stems from the irreversible nature of the inhibition rather than sustained drug levels.

Pharmacodynamics

Omeprazole exerts its pharmacodynamic effects primarily by potently suppressing secretion through irreversible inhibition of the H+/K+-ATPase in parietal cells, resulting in a profound and sustained elevation of intragastric pH. This leads to inhibition of both basal and meal-stimulated acid output, with the drug demonstrating near-complete suppression of acid secretion after repeated dosing. The physiological impact includes reduced volume of gastric juice and altered intragastric environment, which indirectly affects downstream processes in the . The elevation in intragastric is dose-dependent; for instance, a standard 20 mg oral dose of omeprazole increases the median 24-hour intragastric to approximately 4.2 in healthy volunteers and patients with acid-related disorders, maintaining above 4 for about 36% of the day. Higher doses, such as 40 mg, further enhance this effect, achieving median values around 4.5 and extending the time above 4 to about 62% of the 24-hour period in patients with GERD. These changes are more pronounced on daytime profiles and are sustained with once-daily dosing due to the drug's prolonged inhibitory effect on proton pumps, lasting up to 72 hours per dose. Omeprazole inhibits basal acid secretion by over 90% and meal-stimulated secretion by 70-80% at , with greater suppression of stimulated output relative to basal in some evaluations. Chronic administration of omeprazole elevates serum gastrin levels as a compensatory response to reduced acidity, with increases up to fourfold observed in patients on long-term ; this hypergastrinemia can promote enterochromaffin-like (ECL) cell hyperplasia in the gastric fundus, a reversible effect upon discontinuation. Compared to other inhibitors, omeprazole exhibits slightly lower potency in acid suppression; for example, 40 mg (the S-isomer of omeprazole) achieves a higher 24-hour (approximately 4.9) and longer duration above 4 (16.8 hours) than omeprazole 20 mg. Additionally, the reduced intragastric acidity secondarily impairs the activation of pepsinogen to active , diminishing proteolytic activity in the stomach and potentially affecting protein digestion.

Pharmacokinetics

Omeprazole is administered orally as an enteric-coated formulation to protect it from degradation, allowing absorption primarily in the . Following of 20 to 40 mg doses, it exhibits an absolute of approximately 30% to 40%, limited by extensive first-pass in the liver. Peak plasma concentrations are achieved within 0.5 to 3.5 hours, with plasma levels and area under the curve (AUC) increasing proportionally up to 40 mg, though greater-than-linear increases occur at higher doses due to saturation of presystemic . The drug is widely distributed throughout the body, with a of about 0.3 L/kg, reflecting its lipophilic nature and penetration into tissues such as gastric parietal cells. Omeprazole is highly bound to plasma proteins, approximately 95%, primarily to . occurs almost entirely in the liver via the system, predominantly through (forming 5-hydroxyomeprazole) and to a lesser extent (forming omeprazole sulfone), resulting in inactive metabolites. The rate of exhibits genetic variability based on phenotypes, with extensive metabolizers (EMs) showing 30% to 50% higher clearance compared to poor metabolizers (PMs). Elimination is rapid, with a plasma half-life of 0.5 to 1 hour in healthy individuals, extending to about 3 hours in those with hepatic impairment. Clearance is primarily hepatic, and approximately 77% of the dose is excreted in as metabolites, while the remainder undergoes biliary into , with evidence of enterohepatic recirculation contributing to a secondary plasma concentration peak in some cases. Fecal accounts for 18% to 23% of the administered dose, mainly as metabolites.

Chemistry

Chemical Structure and Properties

Omeprazole has the chemical formula C17H19N3O3S and a molecular weight of 345.42 g/mol. The molecule features a sulfinylbenzimidazole core, consisting of a benzimidazole ring substituted at the 2-position with a chiral [(4-methoxy-3,5-dimethylpyridin-2-yl)methyl]sulfinyl group. Specifically, it is named 5-methoxy-2-{[(4-methoxy-3,5-dimethylpyridin-2-yl)methyl]sulfinyl}-1H-benzimidazole, with methoxy groups at the 5-position of the benzimidazole and the 4-position of the pyridine, along with methyl substituents at the 3- and 5-positions of the pyridine ring. Omeprazole exists as a of its R- and S-enantiomers at the chiral sulfur atom in the group, with the S-enantiomer (known as ) exhibiting greater potency in inhibiting acid secretion due to more efficient bioactivation. Physically, omeprazole appears as a white to off-white crystalline powder. It is an amphoteric compound with pKa values of approximately 4.0 for the nitrogen and 0.8 for the N-H, and a logP (octanol-water partition coefficient) of 2.2, indicating moderate that aids its absorption across biological membranes. Due to its acid-labile nature, omeprazole degrades rapidly in acidic environments, such as the , which necessitates for oral formulations to protect the drug until it reaches the alkaline environment of the where it can be activated.

Synthesis and Manufacturing

Omeprazole, chemically known as 5-methoxy-2-[(4-methoxy-3,5-dimethylpyridin-2-yl)methylsulfinyl]-1H-, is synthesized through a multi-step process that couples a substituted moiety with a derivative, followed by selective oxidation. The original industrial synthesis, developed by Astra (now ), begins with the preparation of 2-chloromethyl-4-methoxy-3,5-dimethyl from 2,3,5-collidine via N-oxidation, , and subsequent functional group transformations. This chloromethyl compound is then condensed with 5-methoxy-2-mercapto in the presence of a base to form the thioether intermediate, pyrmetazole. The critical oxidation step converts the sulfide precursor to the using (mCPBA) in a non-alcoholic such as at controlled temperatures (typically 0–25°C) to minimize overoxidation to the impurity. This process yields omeprazole with high purity after purification by recrystallization from solvents like acetone or . Alternative oxidants, such as in acetic acid, have been employed in some routes for scalability, though mCPBA remains prevalent in early industrial methods due to its efficiency in achieving the desired without excessive byproducts. Following patent expiration in 2001, generic manufacturers adopted and refined these routes, introducing optimizations like one-pot reactions and enzymatic resolutions to reduce costs and impurities. For instance, processes using or peracids under phase-transfer have improved yield to over 90% while controlling stereoisomer formation, as omeprazole is a but sensitive to chiral impurities affecting stability. Challenges in synthesis include achieving for the active (S)- in related compounds like via asymmetric oxidation with catalysts and ligands, and rigorous impurity control for degradants such as the N-oxide or , which are limited to below 0.5% in pharmaceutical grades per regulatory standards. In manufacturing, purified omeprazole base is micronized and layered onto inert cores (e.g., sugar spheres) with a binder, subcoated for , and then enteric-coated with polymers like hydroxypropyl methylcellulose phthalate to enable delayed release in the intestine, protecting the acid-labile . This , often involving fluid-bed , ensures stability and , with final products encapsulated or tableted for .

Detection and Measurement in Body Fluids

The detection and measurement of omeprazole and its metabolites in body fluids, such as plasma and , primarily rely on chromatographic techniques coupled with sensitive detection systems to achieve high specificity and low limits of detection. tandem mass spectrometry (HPLC-MS/MS) serves as the gold standard for quantifying omeprazole in plasma due to its superior sensitivity and ability to distinguish the parent drug from metabolites and interferents. Typical methods involve liquid-liquid or followed by separation on reversed-phase or hydrophilic interaction columns, with in positive mode for mass detection. For instance, a validated hydrophilic interaction LC-MS/MS method achieves a limit of detection () of approximately 1 ng/mL for omeprazole in human plasma, enabling accurate measurement over a linear range of 1–1000 ng/mL with precision below 10% relative standard deviation. Spectroscopic methods, particularly (UV) detection integrated with HPLC, are commonly employed for omeprazole analysis in , where higher concentrations allow for less stringent sensitivity requirements compared to plasma. These approaches extract analytes using organic solvents like methylene chloride, followed by separation on - or reversed-phase columns and detection at wavelengths around 280–302 nm, capitalizing on omeprazole's strong UV absorbance. A established HPLC-UV method for samples reports a minimum determinable concentration of 50 nmol/L (approximately 17 ng/mL), with recoveries exceeding 95% and good linearity up to 10 μmol/L, making it suitable for pharmacokinetic profiling of omeprazole and metabolites like the and hydroxy derivatives. Therapeutic drug monitoring of omeprazole often targets plasma concentrations to assess efficacy and adherence, with post-dose levels typically ranging from 0.5 to 2 μg/mL for standard 20–40 mg oral doses, reflecting peak values achieved within 1–2 hours. These concentrations correlate with acid suppression but vary by CYP2C19 genotype, necessitating sensitive assays like HPLC-MS/MS for reliable quantification in clinical settings. Additionally, metabolite ratios, such as omeprazole to omeprazole sulfone, are used for CYP2C19 phenotyping, where ratios below 0.3 indicate poor metabolizers and higher values suggest extensive metabolism, aiding in personalized dosing. Such measurement techniques find key applications in pharmacokinetic studies, where they quantify absorption, distribution, and elimination profiles—omeprazole undergoes extensive hepatic primarily via and , as briefly referenced in broader kinetic evaluations—and in compliance checking, particularly for long-term therapy in conditions like . For example, plasma or urine assays detect subtherapeutic levels to identify non-adherence, with detection windows up to 24 hours post-dose supporting adherence verification in patient management.

History

Discovery and Development

Omeprazole, the first (PPI), was synthesized in 1979 at AB Hässle, a research division of Astra in , as compound H 168/68. The development stemmed from efforts in the late to identify novel inhibitors, building on earlier work with substituted benzimidazoles. Key contributions came from researcher Håkan Larsson, who led pharmacological evaluations demonstrating omeprazole's potent antisecretory effects. This marked a shift from reversible H2-receptor antagonists like , introduced in the 1970s, by offering irreversible inhibition of the H⁺K⁺- through covalent binding via its sulphenamide form, enabling longer-lasting acid suppression independent of secretory stimuli. Preclinical research focused on timoprazole analogs, derived from a 1974 (H 83/69) of earlier compounds, which showed promising but imperfect acid inhibition due to off-target effects like interference. Optimization efforts prioritized structural modifications, such as the 5-methoxy substitution in omeprazole, to enhance at neutral pH while retaining efficacy against the . In vitro studies using isolated guinea pig mucosa and rabbit gastric glands confirmed omeprazole's selective inhibition of H⁺K⁺-ATPase, with superior potency over timoprazole derivatives. Animal models, including anesthetized and dogs, as well as s, validated omeprazole's antisecretory profile and ulcer-healing potential. In these studies, omeprazole proved the most potent inhibitor of stimulated secretion compared to H2 blockers, with effects lasting up to 24 hours in dogs and promoting mucosal recovery in indomethacin- or stress-induced ulcer models. Initial patents protecting the compound were filed by Astra in the late 1970s, followed by an application in 1980 to support further advancement.

Regulatory Approvals and Milestones

Omeprazole's path to regulatory approval was marked by pivotal Phase III clinical trials in the 1980s that established its efficacy for peptic ulcer treatment. A multicenter, double-blind trial published in 1989 compared omeprazole (40 mg daily) to ranitidine (300 mg daily) in patients with benign gastric ulcers, demonstrating significantly higher healing rates with omeprazole (87% vs. 69% at 8 weeks) and lower relapse rates upon maintenance therapy. These trials, including endoscopically controlled studies for duodenal ulcers, confirmed omeprazole's superiority over H2-receptor antagonists like ranitidine in promoting ulcer healing and symptom relief, paving the way for regulatory submissions. The U.S. (FDA) granted initial approval for omeprazole on September 14, 1989, under the brand name Prilosec (delayed-release capsules, 10 mg and 20 mg), for short-term treatment of active duodenal ulcers and (GERD) in adults. In , national agencies approved it earlier as Losec starting in 1988 in , with subsequent harmonization across the for indications including peptic ulcers and reflux esophagitis; the (EMA) later oversaw updates to these authorizations. A significant milestone was the transition to over-the-counter (OTC) status. , the FDA approved Prilosec OTC (20 mg delayed-release tablets) on June 20, 2003, for the relief of frequent (occurring two or more days per week) in adults, marking the first available without prescription. The EMA facilitated similar OTC switches in member states, such as in 2000 for Losec MUPS 10 mg and 20 mg, allowing non-prescription access for mild acid-related symptoms under supervision. The expiration of key U.S. patents in 2001 enabled widespread generic competition, dramatically increasing accessibility and reducing costs; by 2002, generic omeprazole captured over 80% of the market previously dominated by Prilosec. During the , faced ongoing litigation over secondary patents covering omeprazole formulations, resulting in challenges from generic manufacturers like , which ultimately affirmed the availability of low-cost alternatives without biosimilar-specific hurdles, as omeprazole is a small-molecule . In recent years, a notable post-approval event was 's October 2023 settlement of approximately 11,000 lawsuits in the U.S., alleging that Prilosec and related drugs like Nexium caused ; the company agreed to pay $425 million while denying liability. No major regulatory actions, such as market withdrawals, have been imposed on omeprazole for safety concerns, reflecting its established risk-benefit profile across global approvals.

Society and Culture

Brand Names and Formulations

Omeprazole is marketed under several brand names globally, with Prilosec being the primary brand in the United States for both prescription and over-the-counter (OTC) use. In many other countries, it is sold as Losec, reflecting regional trademark preferences by the original manufacturer, . A notable combination product is Zegerid, which pairs omeprazole with to enhance rapid onset by protecting the drug from stomach acid degradation. Common formulations include delayed-release oral capsules available in 10 mg, 20 mg, and 40 mg strengths, designed to bypass initial gastric exposure for targeted release in the intestine. Delayed-release tablets are offered at 20 mg, while oral suspensions and powders for reconstitution provide options for patients unable to swallow capsules, typically in 2 mg/mL or 20 mg packet forms. For hospital settings, an intravenous (IV) formulation exists as a 40 mg powder for solution for infusion, used primarily for patients unable to take oral medications, such as those with severe peptic ulcers or post-perforation. Following the expiration of patents in the early , generic versions of omeprazole have proliferated, with over 100 manufacturers worldwide producing equivalents, including major players like and (now part of ). These generics mirror the branded formulations in dosage and delivery, ensuring broad accessibility. International variations in branding include , where it is widely available in multiple strengths, Helicid in parts of , such as and Eastern European markets, often in capsule form, and Miracid in Thailand, where it is marketed as a proton pump inhibitor. These regional names facilitate local distribution while maintaining the same and therapeutic profile.

Economics and Availability

Omeprazole achieved peak annual sales of approximately $6 billion for in the early , primarily under the brand name Prilosec, making it one of the world's top-selling pharmaceuticals at the time. Following the expiration of its patents in the early , the introduction of generic versions dramatically reduced prices, transforming it from a high-cost branded drug to an affordable essential medication. In the United States, over-the-counter (OTC) generic omeprazole for a 14-day course typically costs between $7 and $11, while prescription generics for the same duration are available for under $5 with discounts. Omeprazole ranks among the top 10 most prescribed medications in the United States, with more than 45 million prescriptions dispensed in 2023. The drug's inclusion on the World Health Organization's Model List of Essential Medicines (as of the 24th list in 2025) underscores its critical role in basic healthcare systems, promoting accessibility through generic production. Generic omeprazole is substantially cheaper than branded versions worldwide, facilitating broad access despite variations in procurement and pricing across regions. In terms of insurance coverage in the , omeprazole is widely reimbursed under and most private plans for prescription use, though many policies implement step therapy requirements that prioritize OTC versions before approving higher-cost alternatives or branded formulations. This approach helps control costs while ensuring patients first try the inexpensive generic OTC option, which is effective for many cases of frequent .

Veterinary Uses

Use in Horses

Omeprazole is widely used in to treat equine gastric ulcer syndrome (EGUS), a condition characterized by erosions and s in the gastric , particularly affecting the squamous . The prevalence of EGUS in racehorses can reach up to 90%, driven by factors such as intense training stress, frequent transportation, and diets high in concentrates with limited access, which disrupt normal gastric and . For treatment, omeprazole is administered orally at a dose of 4 mg/kg body weight once daily for 28 days, typically via the FDA-approved formulation Gastrogard paste. Endoscopic studies demonstrate that this regimen achieves complete healing in approximately 77% of affected horses, with significant improvement in 92% overall, reflecting its efficacy in reducing secretion through inhibition—a mechanism analogous to its application but requiring higher relative doses due to equine . Gastrogard received FDA approval in 1999 (NADA 141-123) specifically for the treatment and prevention of gastric ulcers in horses and foals over four weeks old. In performance horses, omeprazole is also employed for prevention, using a maintenance dose of 2 mg/kg body weight once daily to mitigate recurrence during periods of high stress or competition. This lower dose has shown 76% complete healing and 84% prevention of recurrence in controlled trials, supporting its role in maintaining mucosal integrity without the full therapeutic intensity.

Use in Dogs and Cats

Omeprazole is commonly used in dogs and cats to manage acid-related gastrointestinal disorders, including , , and (IBD). It is indicated for treating and preventing gastroduodenal ulcers and erosions (GUE), (GERD), and conditions involving excessive production, such as Helicobacter-associated . In dogs, it aids in the management of NSAID-induced gastric ulceration, while in cats, it supports treatment of chronic and mucosal lesions associated with these conditions. In April 2025, the granted approval for Omeprazole TriviumVet, the first veterinary-specific (PPI) formulation for dogs, providing a 10 mg gastro-resistant capsule for treating NSAID-induced gastric ulceration. Prior to this, omeprazole use in dogs and cats was off-label in many regions, including the , where no FDA-approved oral formulations existed, leading to widespread of the drug into flavored liquids or capsules tailored to individual animal sizes and needs. Standard dosing for dogs is 0.5–1 mg/kg orally once daily, preferably 30–60 minutes before a meal for optimal absorption, while cats receive a similar regimen of 0.5–1 mg/kg orally once daily, often compounded due to their sensitivity and dosing precision requirements. Clinical studies demonstrate omeprazole's efficacy in improving gastrointestinal symptoms, such as reduced and , in dogs and cats with acid-related disorders, particularly when used for 2–4 weeks in cases of or GUE. Veterinary journal research highlights its superiority over H2-receptor antagonists in acid suppression and healing, achieving significant elevation and mucosal protection in both species. For instance, in dogs with exercise-induced , omeprazole prevented lesion development in a majority of cases. Adverse effects in dogs and cats are rare and generally mild, mirroring those in humans but occurring at lower rates, including self-limiting , , and decreased . Long-term use beyond 3–4 weeks requires monitoring for potential intestinal or appetite loss, with tapering recommended to minimize risks; no severe effects have been widely reported in short-term veterinary applications.

Use in Other Animals

Omeprazole is used in ruminants, such as , primarily to treat abomasal ulcers by increasing abomasal luminal pH through inhibition of the . In calves, intravenous administration at 2 mg/kg effectively raises pH levels, though oral dosing at 4 mg/kg may be less consistent due to variable absorption in milk-fed animals. In adult , inhibitors like omeprazole are recommended for their acid-suppressive effects, but treatment efficacy can vary, and costs are a limiting factor. In exotic pets, including birds and reptiles, omeprazole is employed empirically for conditions involving regurgitation or gastric ulceration, where acid suppression aids in symptom management. For avian species, empirical doses of 1–10 mg/kg orally every 12–24 hours have been used for treating gastric ulcers, which may contribute to regurgitation issues. Reptiles may benefit from similar for or regurgitation, though specific dosing guidelines are limited, often starting at lower empiric ranges around 1–2 mg/kg orally to account for metabolic differences. For zoo animals, particularly , omeprazole has been applied in case reports for managing (GERD)-like conditions and associated . In rhesus monkeys, omeprazole combined with other therapies effectively treated pylori-associated , resolving histological abnormalities and reducing acid-related symptoms akin to GERD. Such applications in captive highlight its role in addressing upper gastrointestinal disorders in zoological settings, often tailored to individual cases. In research settings, omeprazole serves as a key in models to study and . In mice, omeprazole administration has been used to evaluate microbiota changes and resistance to infections like difficile, demonstrating its utility in modeling acid suppression effects without promoting pathogen overgrowth. Similarly, in rats, prolonged omeprazole dosing (20 mg/kg subcutaneously) has been employed to investigate impacts on gastric motility and long-term metabolic alterations. Species-specific variations in omeprazole necessitate dosing adjustments across animals, as the undergoes rapid absorption but differs in hepatic processing; for instance, rats favor aliphatic , while dogs and humans show distinct sulfoxidation patterns. These pharmacokinetic differences, including slower clearance in some ruminants compared to monogastrics, underscore the need for targeted studies to optimize efficacy and minimize risks in non-standard species.

References

  1. https://www.ncbi.nlm.nih.gov/books/NBK539786/
  2. https://pmc.ncbi.nlm.nih.gov/articles/PMC5427147/
  3. https://www.who.int/publications/i/item/WHO-MHP-HPS-EML-2023.02
  4. https://medlineplus.gov/druginfo/meds/a693050.html
  5. https://www.mayoclinic.org/drugs-supplements/omeprazole-oral-route/description/drg-20066836
  6. https://www.drugs.com/medical-answers/best-time-omeprazole-before-eat-after-meal-699560/
  7. https://pubmed.ncbi.nlm.nih.gov/8824658/
  8. https://www.drugs.com/dosage/omeprazole.html
  9. https://www.mayoclinic.org/drugs-supplements/omeprazole-oral-route/precautions/drg-20066836
  10. https://www.aafp.org/pubs/afp/issues/2003/1001/p1311.html
  11. https://www.accessdata.fda.gov/drugsatfda_docs/label/2012/019810s096lbl.pdf
  12. https://jamanetwork.com/journals/jamainternalmedicine/fullarticle/485364
  13. https://www.sciencedirect.com/science/article/abs/pii/001650859291790B
  14. https://pubmed.ncbi.nlm.nih.gov/9824569/
  15. https://pmc.ncbi.nlm.nih.gov/articles/PMC12173569/
  16. https://www.ncbi.nlm.nih.gov/books/NBK534792/
  17. https://pmc.ncbi.nlm.nih.gov/articles/PMC5478398/
  18. https://pubmed.ncbi.nlm.nih.gov/793064/
  19. https://emedicine.medscape.com/article/176319-overview
  20. https://pubmed.ncbi.nlm.nih.gov/9663727/
  21. https://www.accessdata.fda.gov/drugsatfda_docs/label/2008/022056s001019810s087lbl.pdf
  22. https://www.acpjournals.org/doi/10.7326/ACPJC-1991-115-3-071
  23. https://www.nejm.org/doi/full/10.1056/NEJM200008033430501
  24. https://pmc.ncbi.nlm.nih.gov/articles/PMC10538946/
  25. https://bmcgastroenterol.biomedcentral.com/articles/10.1186/1471-230X-2-17
  26. https://pubmed.ncbi.nlm.nih.gov/1983325/
  27. https://emedicine.medscape.com/article/181753-treatment
  28. https://www.ahajournals.org/doi/10.1161/circulationaha.108.191087
  29. https://www.cancer.gov/about-cancer/causes-prevention/risk/infectious-agents/h-pylori-fact-sheet
  30. https://pmc.ncbi.nlm.nih.gov/articles/PMC3449761/
  31. https://pubmed.ncbi.nlm.nih.gov/15810623/
  32. https://academic.oup.com/milmed/article/188/7-8/e2089/6985913
  33. https://gi.org/journals-publications/ebgi/schoenfeld_sep2024/
  34. https://bmcmedicine.biomedcentral.com/articles/10.1186/s12916-024-03816-y
  35. https://emedicine.medscape.com/article/2172395-overview
  36. https://www.mayoclinic.org/diseases-conditions/zollinger-ellison-syndrome/symptoms-causes/syc-20379042
  37. https://www.niddk.nih.gov/health-information/digestive-diseases/zollinger-ellison-syndrome
  38. https://www.uptodate.com/contents/zollinger-ellison-syndrome-gastrinoma-clinical-manifestations-and-diagnosis
  39. https://www.mayoclinic.org/diseases-conditions/zollinger-ellison-syndrome/diagnosis-treatment/drc-20379046
  40. https://pubmed.ncbi.nlm.nih.gov/17108779/
  41. https://pmc.ncbi.nlm.nih.gov/articles/PMC5757869/
  42. https://pubmed.ncbi.nlm.nih.gov/2979229/
  43. https://pubmed.ncbi.nlm.nih.gov/2007355/
  44. https://pubmed.ncbi.nlm.nih.gov/1426868/
  45. https://pmc.ncbi.nlm.nih.gov/articles/PMC3580316/
  46. https://pubmed.ncbi.nlm.nih.gov/8161665/
  47. https://pmc.ncbi.nlm.nih.gov/articles/PMC4320348/
  48. https://www.mayoclinic.org/drugs-supplements/omeprazole-oral-route/side-effects/drg-20066836
  49. https://www.drugs.com/sfx/omeprazole-side-effects.html
  50. https://www.aafp.org/pubs/afp/issues/2002/0715/p273.html
  51. https://pubmed.ncbi.nlm.nih.gov/37060552/
  52. https://www.fda.gov/drugs/drug-safety-and-availability/fda-drug-safety-communication-low-magnesium-levels-can-be-associated-long-term-use-proton-pump
  53. https://www.fda.gov/drugs/postmarket-drug-safety-information-patients-and-providers/fda-drug-safety-communication-possible-increased-risk-fractures-hip-wrist-and-spine-use-proton-pump
  54. https://bmjopengastro.bmj.com/content/12/1/e001719
  55. https://www.nejm.org/doi/full/10.1056/NEJMoa1002689
  56. https://www.sciencedirect.com/science/article/abs/pii/S0301211500003882
  57. https://pmc.ncbi.nlm.nih.gov/articles/PMC9856708/
  58. https://pmc.ncbi.nlm.nih.gov/articles/PMC3966174/
  59. https://pmc.ncbi.nlm.nih.gov/articles/PMC2821234/
  60. https://www.ncbi.nlm.nih.gov/books/NBK501242/
  61. https://publications.aap.org/aapbooks/book/727/chapter/11021166/Medications-and-Breastfeeding
  62. https://pubmed.ncbi.nlm.nih.gov/7628184/
  63. https://bpspubs.onlinelibrary.wiley.com/doi/pdf/10.1111/j.1365-2125.1987.tb03209.x
  64. https://pmc.ncbi.nlm.nih.gov/articles/PMC3975086/
  65. https://www.drugs.com/drug-interactions/itraconazole-with-omeprazole-1406-0-1750-0.html?professional=1
  66. https://www.accessdata.fda.gov/drugsatfda_docs/appletter/2009/020839s044ltr.pdf
  67. https://pubmed.ncbi.nlm.nih.gov/20145345/
  68. https://www.ahajournals.org/doi/10.1161/cir.0b013e3181ee08ed
  69. https://pubmed.ncbi.nlm.nih.gov/7489931/
  70. https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2820904
  71. https://www.accessdata.fda.gov/drugsatfda_docs/label/2023/022056s026lbl.pdf
  72. https://pmc.ncbi.nlm.nih.gov/articles/PMC5942154/
  73. https://pmc.ncbi.nlm.nih.gov/articles/PMC2855237/
  74. https://pmc.ncbi.nlm.nih.gov/articles/PMC3548122/
  75. https://www.sciencedirect.com/science/article/abs/pii/S1040842816302281
  76. https://jamanetwork.com/journals/jamainternalmedicine/fullarticle/484997
  77. https://pubmed.ncbi.nlm.nih.gov/12018920/
  78. https://pmc.ncbi.nlm.nih.gov/articles/PMC3959398/
  79. https://pubmed.ncbi.nlm.nih.gov/3181674/
  80. https://go.drugbank.com/drugs/DB00338
  81. https://www.nature.com/articles/s41598-022-27286-5
  82. https://www.pdr.net/drug-summary/Omeprazole-omeprazole-24360
  83. https://pubchem.ncbi.nlm.nih.gov/compound/Omeprazole
  84. https://www.chemicalbook.com/ChemicalProductProperty_EN_CB8160492.htm
  85. https://www.sciencedirect.com/topics/medicine-and-dentistry/omeprazole
  86. https://patents.google.com/patent/US4255431A/en
  87. https://www.sciencedirect.com/science/article/pii/B9780123852359000011
  88. https://patents.google.com/patent/US6166213A/en
  89. https://www.sciencedirect.com/topics/chemistry/omeprazole
  90. https://patents.google.com/patent/WO2009066309A2/en
  91. https://chemistry-europe.onlinelibrary.wiley.com/doi/abs/10.1002/slct.201700433
  92. https://www.spectrumchemical.com/media/flowchart/Flowchart_O1405.pdf
  93. https://pubmed.ncbi.nlm.nih.gov/20063355/
  94. https://pubmed.ncbi.nlm.nih.gov/6480786/
  95. https://pubmed.ncbi.nlm.nih.gov/33340169/
  96. https://www.accessdata.fda.gov/drugsatfda_docs/label/2022/022056s025lbl.pdf
  97. https://pubmed.ncbi.nlm.nih.gov/16791583/
  98. https://pubmed.ncbi.nlm.nih.gov/30033421/
  99. https://pubmed.ncbi.nlm.nih.gov/29468684/
  100. https://www.nature.com/articles/nrd1010
  101. https://pubmed.ncbi.nlm.nih.gov/6327439/
  102. https://pubmed.ncbi.nlm.nih.gov/6714055/
  103. https://www.uni-frankfurt.de/60870656/Generic_60870656.pdf
  104. https://www.nejm.org/doi/abs/10.1056/NEJM198901123200201
  105. https://www.sciencedirect.com/science/article/pii/S0140673687917260
  106. https://www.accessdata.fda.gov/drugsatfda_docs/nda/2017/209400Orig1s000CrossR.pdf
  107. https://pharmaceutical-journal.com/wp-content/uploads/2021/11/INFOGRAPHIC-The-development-and-safety-of-proton-pump-inhibitors-June-2016-1-1.pdf
  108. https://www.accessdata.fda.gov/drugsatfda_docs/nda/2003/21-229_Prilosec.cfm
  109. https://www.medsafe.govt.nz/profs/class/Agendas/agen35-Losec.pdf
  110. https://www.acs.org/molecule-of-the-week/archive/o/omeprazole.html
  111. https://www.robinskaplan.com/newsroom/insights/astrazeneca-ab-v-apotex-corp
  112. https://www.astrazeneca.com/content/astraz/media-centre/press-releases/2023/astrazeneca-settles-nexium-and-prilosec-product-liability-litigations.html
  113. https://www.drugs.com/ingredient/omeprazole.html
  114. https://publications.aap.org/pediatriccare/drug-monograph/18/5749/Omeprazole
  115. https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=cd6868b9-5824-442b-8d65-4db29ecb70a4
  116. https://www.drugs.com/pro/omeprazole.html
  117. https://www.medicines.org.uk/emc/files/pil.8756.pdf
  118. https://www.pipelinepharma.com/omeprazole-manufacturers
  119. https://www.pharmacompass.com/manufacturers-suppliers-exporters/omeprazole-4594
  120. https://www.mims.com/thailand/drug/info/miracid?type=full
  121. https://gabi-journal.net/a-case-study-of-astrazenecas-omeprazole-esomeprazole-chiral-switch-strategy.html
  122. https://www.goodrx.com/omeprazole
  123. https://www.walmart.com/ip/Prilosec-OTC-Omeprazole-20mg-Acid-Reducer-Frequent-Heartburn-Medicine-Unflavored-14-Count/10312055
  124. https://clincalc.com/drugstats/Drugs/Omeprazole
  125. https://list.essentialmeds.org/medicines/178
  126. https://www.medicalnewstoday.com/articles/does-medicare-cover-omeprazole
  127. https://www.uhcprovider.com/content/dam/provider/docs/public/resources/pharmacy/step-therapy/Step-Therapy-Proton-Pump-Inhibitors.pdf
  128. https://www.merckvetmanual.com/digestive-system/gastrointestinal-ulcers-in-large-animals/gastric-ulcers-in-horses
  129. https://pmc.ncbi.nlm.nih.gov/articles/PMC8977533/
  130. https://animaldrugsatfda.fda.gov/adafda/app/search/public/document/downloadFoi/649
  131. https://beva.onlinelibrary.wiley.com/doi/abs/10.1111/j.2042-3306.1999.tb05176.x
  132. https://thehorse.com/15848/fda-approves-anti-ulcer-medication-for-use-in-horses/
  133. https://pmc.ncbi.nlm.nih.gov/articles/PMC6271318/
  134. https://www.petplace.com/article/drug-library/drug-library/library/omeprazole-prilosec-gastrogard-for-dogs-and-cats
  135. https://avmajournals.avma.org/view/journals/javma/262/10/javma.24.07.0434.xml
  136. https://www.vmdconnect.uk/medicines-update
  137. https://www.ema.europa.eu/en/medicines/veterinary/EPAR/omeprazole-triviumvet
  138. https://vcahospitals.com/know-your-pet/omeprazole
  139. https://avmajournals.avma.org/view/journals/javma/259/4/javma.259.4.385.xml
  140. https://www.merckvetmanual.com/multimedia/table/antiulcerative-drugs
  141. https://pmc.ncbi.nlm.nih.gov/articles/PMC11047556/
  142. https://www.goodrx.com/pet-health/dog/omeprazole-for-dogs
  143. https://veterinarypartner.vin.com/default.aspx?pid=19239&catId=102894&id=4952494
  144. https://www.merckvetmanual.com/digestive-system/diseases-of-the-abomasum/abomasal-ulcers-in-cattle
  145. https://pmc.ncbi.nlm.nih.gov/articles/PMC7129257/
  146. https://pubmed.ncbi.nlm.nih.gov/9497216/
  147. https://pmc.ncbi.nlm.nih.gov/articles/PMC6887860/
  148. https://www.wjgnet.com/1007-9327/full/v26/i11/1142.htm
  149. https://pubmed.ncbi.nlm.nih.gov/3858978/
  150. https://onlinelibrary.wiley.com/doi/10.1111/jvp.13489
Add your contribution
Related Hubs
User Avatar
No comments yet.