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OM

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

PubMedGalen medical journal2026-11-08

Protective Effect of Aqueous Centella asiatica Extract on Ethanol-Induced Gastric Mucosal Injury : Short title: Centella asiatica Protects Against Ethanol-Induced Gastric Injury.

Yousif Nzar Ibrahim NI, Taha Zhala B ZB, Raouf Mohammed M Hussein M MMHM, Omer Bakhtawar Ziad BZ et al.

Gastric ulcer disease is associated with oxidative stress, inflammation, and disruption of gastric mucosal defense mechanisms. Ethanol-induced gastric injury is a widely used experimental model for evaluating gastroprotective agents. Centella asiatica is a medicinal plant rich in bioactive phytochemicals, including flavonoids, phenolic compounds, saponins, and triterpenoids, which possess antioxidant and anti-inflammatory activities.This study evaluated the gastroprotective effect of aqueous C.asiatica extract against ethanol-induced gastric mucosal injury in rats. Adult male Sprague-Dawley rats were divided into five groups (n=6): ulcer control, omeprazole-treated group (20 mg/kg), and three groups pretreated orally with aqueous C.asiatica extract at doses of 150, 300, and 600 mg/kg. Preliminary qualitative phytochemical screening of the extract was performed using standard methods. Gastric ulceration was induced using absolute ethanol (5 mL/kg). Gastric pH, mucus weight, ulcer area, and ulcer inhibition percentage were evaluated. Histopathological examination and quantitative real-time PCR analysis of Nrf2 and HO-1 expression were also performed. Phytochemical screening confirmed the presence of flavonoids, phenolic compounds, saponins, and triterpenoids in the aqueous C.asiatica extract. Pretreatment with the extract significantly reduced ethanol-induced gastric injury in a dose-dependent manner (P<0.05). Treated rats showed increased gastric pH and mucus weight with reduced ulcer area compared with the ulcer control group. The 600 mg/kg dose produced the highest ulcer inhibition (98.88%) and preserved gastric mucosal architecture with minimal epithelial disruption, edema, and inflammatory-cell infiltration. In addition, the extract significantly upregulated Nrf2 and HO-1 expression levels. Aqueous C.asiatica extract demonstrated significant gastroprotective activity against ethanol-induced gastric mucosal injury in rats, possibly through enhancement of mucosal defense mechanisms and activation of the Nrf2/HO-1 antioxidant pathway. The observed protective effects may be attributed to the phytochemical constituents present in the extract, supporting the potential therapeutic value of C.asiatica in gastric ulcer prevention.

PMID 42996818
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PubMedJournal of equine veterinary science2026-11-06

A dietary nutraceutical "Succeed Digestive Conditioning ProgramTM" is more effective than omeprazole for managing equine glandular gastric disease.

MacNicol J L JL, Korac L L, Fraser A A, Margiotta M M et al.

Equine glandular gastric disease (EGGD) responds poorly to proton pump inhibitor therapy, highlighting the need for alternative treatments. Succeed Digestive Conditioning Program (SUC) contains oat-derived ingredients, Saccharomyces cerevisiae, L-glutamine, and L-threonine that may support gastric health. To compare effects of SUC and omeprazole (OME) on squamous and glandular gastric ulcers in horses. Fifty-nine horses with squamous gastric lesions (score ≥2/4) completed a 90-day trial. Horses received either OME (4 mg/kg BW/day; n=30) or SUC (27 g/day; n=29). Forty-four horses had concurrent glandular lesions (OME, n=21; SUC, n=23). Gastroscopy was performed on Days 0, 30, 60, and 90. Squamous lesions were graded using a 0-4 scoring system. Glandular lesions were evaluated using lesion number, lesion severity, and composite ulcer index. Fecal pH was also assessed. OME reduced squamous lesion scores by Day 30 (P<0.001), and scores were lower than SUC horses on Days 30 (P=0.007), 60 (P<0.001), and 90 (P=0.02). SUC had no effect on squamous lesion scores. SUC reduced glandular lesion number scores by Day 60 (P=0.003) and Day 90 (P=0.003), and reduced glandular ulcer index scores by Day 60 (P=0.01) and Day 90 (P=0.03). OME had no effects on any glandular metrics. Neither treatment affected fecal pH. Omeprazole effective reduced squamous gastric lesions but did not improve glandular lesions. In contrast, SUC improved glandular lesion number and ulcer index without affecting squamous disease. SUC may represent a useful strategy for managing EGGD and further investigation into clinical applications are warranted.

PMID 42994740
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PubMedPloS one2026-11-06

Assessment of the appropriateness of stress ulcer prophylaxis practice among hospitalized patients across Lebanese hospitals: A multicenter prospective study.

Housary Khouloud K, Dib Carole C, Itani Rania R

Stress ulcer prophylaxis (SUP) is recommended for critically ill patients at high risk of stress-related gastrointestinal bleeding. Despite established guideline recommendations, inappropriate use of acid suppressant medications (ASMs), particularly proton pump inhibitors (PPIs), remains common worldwide and may expose patients to unnecessary adverse effects and increased healthcare costs. This study aimed to assess the appropriateness of SUP prescribing practices among hospitalized patients across Lebanese hospitals, focusing on indication, choice of pharmacologic agent, dosing regimen, route of administration, duration of therapy, discharge prescribing, and factors associated with inappropriate SUP practice. A multicenter prospective study was conducted between April 20 and May 22, 2026, across ten tertiary-care hospitals in different regions of Lebanon. Adult patients (≥18 years) admitted to Internal Medicine Unit, Intensive Care Unit (ICU), or Coronary Care Unit wards were assessed for the appropriateness of SUP, regardless of whether ASMs were prescribed. The appropriateness of SUP practice was evaluated according to the Society of Critical Care Medicine and American Society of Health-System Pharmacists (SCCM/ASHP) 2024 and ASHP 1999 guidelines. Multivariable logistic regression was performed to identify factors associated with inappropriate SUP practice. A total of 552 patients were enrolled, with a mean age of 64.3 ± 18.5 years, and 58.7% were male. According to the SCCM/ASHP 2024 and ASHP 1999 guidelines, 90.8% and 77.2% of patients, respectively, were not eligible for SUP. Omeprazole was the most frequently prescribed agent (75.4%), and PPIs were used in all SUP prescriptions. Among patients admitted to ICU, 11.2% continued receiving ASMs after the SUP indication had resolved or following ICU transfer without a persisting indication. Overall, SUP practice was inappropriate in 77.9% of patients. Multivariable analysis demonstrated that anticoagulant therapy was associated with higher odds of inappropriate SUP practice (AOR = 2.78, 95% CI = 1.35-5.74, P = 0.006). Inappropriate SUP practice is highly prevalent among hospitalized patients in Lebanon, largely due to prescribing without guideline-based indications. Inappropriate continuation after resolution of the SUP indication or ICU transfer was also observed. Strengthening adherence to evidence-based recommendations through stewardship programs, prescribing audits, standardized protocols, and updated national guidance may help optimize SUP use and improve patient care.

PMID 42993752
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PubMedExperimental physiology2026-11-05

Targeting pepsin provides superior protection to acid suppression in reflux-associated airway inflammation and lung dysfunction.

Sales Thiago Meneses Araújo Leite TMAL, da Costa Filho Humberto Barbosa HB, Gadelha Kalinne Kelly Lima KKL, Nogueira Kerolayne de Melo KM et al.

Gastro-oesophageal reflux disease is a prevalent condition associated with extra-oesophageal manifestations, such as pulmonary inflammation. Pepsin, an essential gastric enzyme, has been implicated in pulmonary complications owing to its inflammatory effects. Although acid-suppressive therapies, such as proton pump inhibitors, reduce gastric acidity, they do not prevent reflux episodes, microaspiration or the harmful effects of pepsin. This study evaluated the effects of pepsin inhibition by pepstatin on inflammation and pulmonary dysfunction in a murine model of reflux. Male Swiss mice were anaesthetized with ketamine and xylazine and subjected to a surgical procedure involving pyloric stenosis and complete stenosis of the gastric fundus to induce reflux. The mice were divided into four groups: sham, reflux, reflux + pepstatin and reflux + omeprazole. Treatments were administered daily for 28 days. The evaluated parameters included oesophageal and pulmonary wet weights, myeloperoxidase activity, cytokine levels [interleukin (IL)-6, IL-10 and keratinocyte chemoattractant], histopathological alveolitis scores, functional analyses of spirometry and tracheal contractility. The reflux group exhibited significant oesophageal and pulmonary oedema, increased myeloperoxidase activity, elevated levels of IL-6 and keratinocyte chemoattractant, reduced IL-10, severe alveolitis, impaired pulmonary function and tracheal hyper-reactivity. Pepstatin treatment significantly reduced inflammatory and functional alterations in the reflux model. In contrast, omeprazole was less effective at controlling inflammation and improving pulmonary function. These findings suggest that pepsin inhibition might reduce pulmonary inflammation and help to preserve lung function in a murine reflux model. Targeting pepsin, rather than solely suppressing gastric acidity, shows promise in mitigating reflux-related extra-oesophageal complications.

PMID 42984398
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PubMedNaunyn-Schmiedeberg's archives of pharmacology2026-11-04

Repurposing proton pump inhibitors to restore ceftriaxone activity against multidrug-resistant Klebsiella pneumoniae: phenotypic, molecular, and in silico evidence.

Hussein Eftkhar Muhammad EM, Auda Ibtesam Ghadban IG

Klebsiella pneumoniae has emerged as one of the most clinically significant multidrug-resistant (MDR) pathogens, with multidrug efflux systems playing a pivotal role in antibiotic resistance and therapeutic failure. This study investigated the contribution of the efflux-associated genes kpnE, kmrA, and kdeA to ceftriaxone resistance and evaluated proton pump inhibitors (PPIs) as efflux pump-targeting adjuvants. Fifty clinical K. pneumoniae isolates were characterized by antimicrobial susceptibility testing, MDR/XDR classification, phenotypic efflux activity assays, molecular detection of efflux-associated genes, kpnE sequencing, quantitative real-time PCR, molecular docking, and ceftriaxone minimum inhibitory concentration (MIC) determination in the presence and absence of omeprazole and lansoprazole. MDR and XDR phenotypes were identified in 70% and 18% of isolates, respectively, whereas active efflux was detected in 14% of isolates and was significantly associated with increasing resistance severity. Sequence analysis demonstrated marked conservation of kpnE, with a single D → G amino acid substitution identified in one isolate. Despite this conservation, gene expression analysis revealed substantial isolate-dependent transcriptional responses that were not directly correlated with phenotypic efflux activity, suggesting that transporter efficiency is governed by complex interactions between transcriptional regulation, structural adaptation, and protein functionality rather than gene expression alone. Molecular docking demonstrated favorable binding of both PPIs to KpnE, KmrA, and KdeA, supporting their potential to interfere with efflux-mediated drug extrusion. Consistent with these predictions, combination assays markedly potentiated ceftriaxone activity, reducing MIC values by up to 16,516-fold and restoring ceftriaxone susceptibility in all seven tested efflux-active ceftriaxone-resistant isolates, with omeprazole producing the greatest synergistic effect. Collectively, these findings provide new mechanistic insight into the role of SMR-associated efflux systems in K. pneumoniae antimicrobial resistance and identify proton pump inhibitors, particularly omeprazole, as potential antibiotic adjuvants for restoring β-lactam efficacy against MDR and XDR K. pneumoniae. Further functional and in vivo studies are warranted to determine whether these in vitro findings can be translated into clinically relevant therapeutic applications.

PMID 42980760
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PubMedCPT: pharmacometrics & systems pharmacology2026-11-04

Drug-Drug Interactions of Cenobamate With Medications: Dose-Dependent Induction/Inhibition and Clinical Implications.

Ichida Hiroyuki H, Nakao Takaharu T, Mori Takanori T, Makino Reina R et al.

Cenobamate causes dose-dependent cytochrome P450 (CYP)2B6 and CYP3A4 induction and CYP2C19 inhibition, raising concern over multi-pathway drug-drug interactions (DDIs) in patients with epilepsy treated with cardiovascular co-medications. We developed a physiologically based pharmacokinetic (PBPK) model for cenobamate and verified it using reported DDIs for cenobamate 200 mg using three probe substrates: bupropion (CYP2B6), midazolam (CYP3A4), and omeprazole (CYP2C19). The verified model predicted exposure changes (area under the curve ratio [AUCR] and maximum concentration [Cmax] ratio with/without cenobamate) for eight drugs, including anticoagulants and antiplatelets (apixaban, cilostazol, clopidogrel, and rivaroxaban), and antihypertensives (amlodipine, bisoprolol, carvedilol, and nifedipine). Regarding anticoagulants and antiplatelets, for apixaban, AUCR/Cmax ratios were 0.78/0.92 (100 mg), 0.71/0.87 (200 mg), and 0.63/0.83 (400 mg), respectively. For cilostazol, parent exposure decreased (0.67/0.85, 0.55/0.77, 0.45/0.70), while the active metabolite OPC-13015 was predicted to increase in Cmax. For clopidogrel, parent exposure was unchanged, but formation of 2-oxo-clopidogrel and clopidogrel-H4 were decreased and increased, respectively. For rivaroxaban, the AUCR/Cmax ratios were 0.78/0.90, 0.69/0.85, and 0.61/0.80. Among antihypertensives, amlodipine showed decreased AUCR/Cmax ratios (0.57/0.66, 0.45/0.55, 0.37/0.47). The exposure changes of bisoprolol were minor (AUCR 0.84-0.92, Cmax ratio 0.95-0.98); AUCR/Cmax ratios of carvedilol fell to 0.73/0.80, 0.63/0.71, and 0.55/0.64; and nifedipine decreased markedly (0.41/0.54, 0.29/0.41, 0.21/0.32). In conclusion, cenobamate induced CYP2B6 weakly and CYP3A4 moderately, and it inhibited CYP2C19 moderately to drive dose-dependent decreases in exposure for seven of eight drugs with minimal change for bisoprolol. The verified PBPK framework enables risk assessment in scenarios not yet clinically tested.

PMID 42982766
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