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omeprazole (Omez Insta)

✓ Approved

Dr.Reddy's Laboratories Ltd. · ATP4A · Small Molecule

What is omeprazole?

omeprazole is a small molecule developed by Dr.Reddy's Laboratories Ltd.. It is approved for therapeutic indications via oral (po).

Drug Profile

Brand NamesOmez Insta
CompanyDr.Reddy's Laboratories Ltd.
Drug ClassSmall Molecule
Molecular TargetATP4A
RouteOral (PO)
StatusApproved
Sources: ClinicalTrials.gov, Dr.Reddy's Laboratories Ltd.

Mechanism of Action

Molecular Targets

omeprazole acts on 1 molecular target:

ATP4AATPase H+/K+ transporting subunit alpha (ATP6A)
Want deeper analysis?Noah AI can explain complex mechanisms and compare to similar drugs.

Therapeutic Indications

omeprazole is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Gastrointestinal disordersGastritis✓ Approved

Related Research Articles

PubMedBMC pharmacology & toxicology2026-08-29

Pharmacokinetic and bioequivalence study of enteric-coated omeprazole capsule in healthy Chinese subjects under fasting and fed conditions.

Zhang Fucai F, Xie Jingyi J, Li Yong Y, Feng Wenlu W et al.

This study aimed to evaluate the bioequivalence of a generic enteric-coated omeprazole capsule compared with the reference product (Losec®) in healthy Chinese subjects. The fasting study was conducted using a randomized, single-centre, single-dose, two-period, two-sequence crossover design. The fed study was a randomized, single-centre, single-dose, four-period, two-sequence fully replicate crossover design. Healthy subjects were randomized and received either the test or the reference drug under fasting or fed conditions. The plasma concentration of enteric-coated omeprazole capsule at different time points was measured using high-performance liquid chromatography-tandem mass spectrometry (HPLC-MS/MS). Bioequivalence of the two formulations was evaluated through pharmacokinetic parameters and relative bioavailability. In the fasting study, the geometric mean ratios (GMRs) of Cmax, AUC0-t, and AUC0-∞ were 101.33%, 101.81%, and 101.76%, respectively, with all 90% confidence intervals (CIs) falling within the bioequivalence range of 80.00-125.00%. Under fed conditions, high intra-subject variability was observed for Cmax (CV = 46.79%) and AUC0-t (CV = 31.61%). The reference-scaled average bioequivalence (RSABE) method showed GMR point estimates of 113.31% for Cmax and 105.68% for AUC0-t (both within 80.00-125.00%), with upper 95% confidence bounds below zero. The GMR for AUC0-∞ was 108.18%, and its 90% CI (102.63-114.02%) also met the bioequivalence criteria. No serious adverse events were reported. The two enteric-coated omeprazole capsules were bioequivalent under both fasting and fed conditions and were well tolerated in healthy subjects. The trial was registered with the China Centre for Drug Testing and Registration ( http://www.chinadrugtrials.org.cn/index.html , 10/05/2022, CTR20221098 and CTR20220627).

PMID 42665804
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PubMedClinical pharmacokinetics2026-08-29

Effect of Rivoceranib 200 mg Once Daily on the Pharmacokinetics of a Cocktail Probe Substrate of Cytochrome P450 Enzymes: A Phase I Trial in Healthy Volunteers.

Nguyen David D, Wei Xiaohui Tracey XT, Meng Xianzhang X, Alexander Laura L et al.

Rivoceranib, a vascular endothelial growth factor receptor-2 tyrosine kinase inhibitor with antitumor activity, is metabolized in the liver mostly by cytochrome P450 (CYP)3A4/5. In vitro studies suggest that rivoceranib at clinically relevant concentrations may inhibit metabolism of various CYP substrates. This study evaluated the effects of rivoceranib 200 mg once daily (QD) on the pharmacokinetics of various CYP substrates using the Cooperstown 5+1 cocktail. The dosing regimen of rivoceranib used in this study is similar to the proposed rivoceranib regimen (250 mg QD) in combination with camrelizumab for the treatment of patients with hepatocellular carcinoma. This open-label, fixed-sequence, crossover, drug-drug interaction phase I study evaluated the impact of multiple oral doses of rivoceranib 200 mg QD on the single oral dose pharmacokinetics of CYP enzyme substrates administered in the modified Cooperstown 5+1 cocktail (caffeine 200 mg [CYP1A2], warfarin 10 mg [S-warfarin as CYP2C9 substrate] + vitamin K 10 mg, omeprazole 40 mg [CYP2C19], dextromethorphan 30 mg [CYP2D6], and midazolam 2 mg [CYP3A4]) in 18 healthy volunteers. After fasting, volunteers received a single dose of the Cooperstown 5+1 cocktail on day 1 and rivoceranib plus Cooperstown 5+1 cocktail on day 11. After completing a meal, volunteers received a single dose of rivoceranib on days 6-10 and 12-15. Blood samples for pharmcokinetic analyses of substrates were collected pre-dose and up to 120 h post-Cooperstown 5+1 cocktail dosing on days 1 and 11. Volunteers returned once between days 21 and 25 for safety follow-up. Rivoceranib 200 mg QD decreased the cumulative area under the plasma concentration-time curve from time 0 to infinity (AUC0-inf) for caffeine by 20% and maximum observed plasma concentration (Cmax) by 7%, increased S-warfarin AUC0-inf by 1.35-fold and Cmax by 1.05-fold, increased omeprazole AUC0-inf by 2.06-fold and Cmax by 1.64-fold, increased dextromethorphan AUC0-inf by 2.67-fold and Cmax by 1.9-fold, and increased midazolam AUC0-inf by 1.44-fold and Cmax by 1.15-fold. Rivoceranib 200 mg QD may substantially inhibit the metabolism of CYP2D6 substrates. Therefore, concomitant use of CYP2D6 substrate drugs with rivoceranib should be approached with caution, and dose adjustment of substrates of CYP2D6 may be necessary when co-administration cannot be avoided. Rivoceranib 200 mg QD may also exert weak inhibitory effects on the metabolism of CYP3A, CYP2C9, and CYP2C19 substrates. In such cases, close monitoring for substrate-related adverse reactions is recommended, particularly when toxicity is sensitive to increased exposures of these substrate drugs. ClinicalTrials.gov identifier: NCT03561298.

PMID 42667590
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PubMedThe Journal of international medical research2026-08-28

Medication-safety burden of omeprazole in psychiatric inpatients: A retrospective cross-sectional study.

Hu Wenjing W

ObjectiveOmeprazole is commonly prescribed to psychiatric inpatients with polypharmacy; however, empiric initiation, prolonged treatment, intravenous use, and screening-flagged potential drug-drug interactions or co-administration patterns may complicate medication review. This study described omeprazole prescribing patterns, appropriateness, and utilization intensity in a psychiatric specialty hospital.MethodsThis retrospective cross-sectional study used routinely collected data from hospital information systems and electronic health records of a municipal psychiatric specialty hospital in Shanghai, China. Consecutive inpatient omeprazole orders issued between 1 February 2023 and 31 December 2024 were screened. After excluding invalid, duplicate, and incomplete records, 152 eligible prescriptions of 71 inpatients were analyzed. Outcomes included guideline concordance for indication, dose, duration or review plan, route of administration, drug-drug interaction-based utilization, IV use, and screening-flagged potential drug-drug interactions or co-administration patterns. Analyses were primarily descriptive.ResultsAppropriate indication was documented in 57/152 prescriptions (37.5%), dose appropriateness in 147/152 (96.7%), and guideline-concordant duration or review plan in 36/152 (23.7%). Overall, 31/152 prescriptions (20.4%) were fully appropriate, 22/152 (14.5%) needed to be optimized, and 99/152 (65.1%) were inappropriate; thus, 121/152 prescriptions (79.6%) were not fully appropriate. Screening-flagged potential drug-drug interactions or co-administration patterns were present in 77/152 prescriptions (50.7%). Weighted exposure was 1.86 drug-drug interactions per treatment day. Intravenous therapy accounted for 13.1% of treatment days and 21.6% of total drug-drug interactions, with a median intravenous course duration of 7 days.ConclusionsOmeprazole prescribing frequently showed non-concordance with predefined appropriateness criteria, mainly involving indication documentation or selection, treatment duration, and route optimization. Screening-flagged potential drug-drug interactions and drug-drug interaction/day should be interpreted as medication-review and utilization signals rather than as confirmed adverse events or direct evidence of inappropriate prescribing.

PMID 42661495
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PubMedThe Journal of pharmacology and experimental therapeutics2026-08-28

Aryl hydrocarbon receptor as a molecular mediator in the induction of human aldehyde oxidase gene expression.

Yeap Szu Ling SL, Yap Cassandra Ching Lin CCL, Tay Shi Han SH, Zhang Linghua Harris LH et al.

Relatively little is known about receptor-mediated regulation of aldehyde oxidase (AOX). 2,3,7,8-Tetrachlorodibenzo-p-dioxin, an aryl hydrocarbon receptor (AHR) agonist, increases mouse Aox expression. However, given the species differences in ligand-dependent AHR activation and AOX regulation, it remains to be investigated whether human AHR regulates the expression of AOX1 (the human AOX isoform). Therefore, the present study was designed to determine the effect of modulating the functionality of human AHR on AOX1 gene expression in cell culture models (HepG2 and MCF-7) known to express AHR and AOX1. Treatment of HepG2 or MCF-7 cells with a noncytotoxic concentration of a classical AHR agonist (β-naphthoflavone, benzo[a]pyrene, or 3-methylcholanthrene [3-MC]), an endogenous AHR agonist (indoxyl sulfate or 6-formylindolo[3,2-b]carbazole), or a selective AHR modulator (quercetin, 3,3'-diindolylmethane, or omeprazole) increased AOX1 and AHR-regulated CYP1A1 mRNA expression. The increases in AOX1 and CYP1A1 mRNA levels were not correlated among our panel of AHR activators. The induction of AOX1 mRNA by 3-MC was time- and concentration-dependent. It was accompanied by an increase in AOX1 protein expression and AOX1-mediated enzyme activity (O6-benzylguanine 8-oxidation). An AHR antagonist (3',4'-dimethoxyflavone) completely abolished the increase in AOX1 and CYP1A1 expression by an AHR agonist (3-MC). Gene knockdown by an AHR small interfering RNA substantially decreased AHR mRNA expression and attenuated AOX1 and CYP1A1 mRNA induction by 3-MC. Overall, based on the experimental approaches involving AHR activation, AHR antagonism, and AHR gene knockdown by small interfering RNA, our novel data indicate that AHR plays a role in mediating the induction of human AOX1 gene expression. SIGNIFICANCE STATEMENT: The deployment of multiple experimental approaches involving receptor activation, receptor antagonism, and gene knockdown by small interfering RNA led to the identification of the human aryl hydrocarbon receptor as a molecular mediator of aldehyde oxidase gene induction. This novel discovery expands our limited knowledge of the identity of pharmacological receptors contributing to the functionality of human aldehyde oxidase.

PMID 42664535
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PubMedDigestive diseases (Basel, Switzerland)2026-08-24

Sucralfate/sodium alginate capsules and PPI-refractory reflux symptoms in non-erosive reflux disease and mild erosive disease: a randomized, phase 3, non-inferiority study.

Shahbazi Shaahin S, Shahbazi Erfan E, Shahbazi Mohammad-Hosein MH, Vahdat Shariatpanaahi Zahra Z

Proton pump inhibitors have failed to control symptoms in some patients with gastroesophageal reflux disease. We investigated the effect of alginate and sucralfate capsules (ALSUC) in patients who had not responded to proton pump inhibitors. From March 2024 to March 2025, 692 adult patients with mild esophagitis (Los Angeles classification grades A, B) and NERD with reflux symptoms ≥4 days/week were randomly assigned to receive ALSUC after meals and at bedtime or a double dose of omeprazole (20 mg) twice daily for 8 weeks. Patients were asked to complete a daily questionnaire. The primary endpoint was the percentage of complete heartburn-free days, analyzed for non-inferiority. The secondary endpoints were analyzed for superiority. ALSUC was noninferior to omeprazole in terms of percentage of heartburn-free days (omeprazole: 50.9%, ALSUC: 49.1%, CI: -0.003, 0.039). The percentage of regurgitation-free days was significantly higher in the ALSUC group (omeprazole: 49.8%, ALSUC: 53.5%, CI: -0.059, -0.016, p= 0.001). In the subgroup analysis, no significant differences were observed between the two groups within either the NERD or esophagitis subgroups for the evaluated outcomes. The exceptions were that omeprazole offered better heartburn control in patients with esophagitis, whereas ALSUC provided better control of regurgitation in patients with NERD. ALSUC can be a safe approach in controlling symptoms of mild esophagitis and NERD.

PMID 42636164
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PubMedMedicine2026-08-22

EBV induced Evans syndrome in a patient of SLE related MAS: A case report.

Li WeiBin W, Chen Yini Y, Chen Ya Y, Zhao Meng M et al.

Epstein-Barr virus (EBV) induced Evans syndrome in systemic lupus erythematosus (SLE) related macrophage activation syndrome (MAS) is rare with the incidence rate of 0.9% to 9% and the mortality rate of about 4% to 19%, which are misdiagnosed as hemophagocytic lymphohistiocytosis. A 15-years old female was admitted due to abdominal pain and fever. Physical examination showed butterfly-shaped erythema on her face and scattered lymph nodes of bilateral neck with a diameter of 1.5 cm × 1.0 cm. Pharyngeal mucosal congestion, bilateral tonsil swelling, and palpable 1 cm below the liver rib and no palpable spleen were observed. Medical history revealed recurrent facial erythema after puberty, which is aggravated by exposure to sunlight. Based on the results of complete blood cell count, biochemical and immunologic examination and bone marrow cytology, EBV-induced Evans syndrome of SLE-related MAS was reached. Ceftriaxone, oseltamivir, methylprednisolone, omeprazole, cyclosporine, and high-dose immunoglobulin were administrated and after 20 days the patient was discharged and regularly followed up. After 20 days of administration, the patient was significantly improved and discharged. Disease history, laboratory tests, and differential diagnosis contribute to the confirmation of EBV-induced Evans syndrome in SLE-related MAS.

PMID 42629749
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