Omeprazole

Evidence Level: L3 Predicted Indications: 2

Table of Contents

  1. Omeprazole
  2. Omeprazole: From Peptic Ulcer Disease/GERD to Duodenogastric Reflux
    1. One-Sentence Summary
    2. Quick Overview
    3. Why is This Prediction Reasonable?
    4. Clinical Trial Evidence
    5. Literature Evidence
    6. India Market Information
    7. Safety Considerations
    8. Conclusion and Next Steps
    9. Disclaimer

## Pharmacist Assessment Report

Omeprazole: From Peptic Ulcer Disease/GERD to Duodenogastric Reflux

One-Sentence Summary

Omeprazole is a proton pump inhibitor (PPI) globally established for gastroesophageal reflux disease (GERD), peptic ulcer disease, and H. pylori eradication regimens. The TxGNN model predicts it may be effective for Duodenogastric Reflux, with 1 clinical trial (low direct relevance) and 20 publications currently supporting this direction, most of which are observational, cohort, or animal studies rather than dedicated treatment trials.

Quick Overview

Item Content
Original Indication Not present in the local regulatory dataset (drug is not marketed); internationally approved for GERD, peptic ulcer disease, and H. pylori eradication
Predicted New Indication Duodenogastric Reflux
TxGNN Prediction Score 99.64%
Evidence Level L3
India Market Status ✗ Not Marketed
Number of Registrations 0
Recommended Decision Hold

Why is This Prediction Reasonable?

Currently, detailed mechanism of action data is not available in the evidence pack. Based on known pharmacology, Omeprazole is a proton pump inhibitor that irreversibly inhibits the H+/K+-ATPase enzyme system in gastric parietal cells, suppressing gastric acid secretion.

Duodenogastric reflux involves backflow of duodenal contents (bile and pancreatic juice) into the stomach — these are largely non-acidic components. Omeprazole cannot directly block bile or pancreatic reflux, but by reducing gastric acid it lowers the acidic fraction of the mixed refluxate. This is why omeprazole has already been used clinically in Barrett’s esophagus patients to reduce combined acid/bile reflux exposure, even though it does not treat the underlying cause of duodenogastric reflux.

The mechanistic link is therefore partial and indirect: plausible for the acid component of the reflux picture, but not a direct treatment for the bile/pancreatic component. Notably, several animal studies in the evidence base (e.g., PMID 10389684, 33027361) suggest that acid suppression under conditions of duodenogastric reflux may actually promote gastric carcinogenesis in rat models — a caution signal that tempers the reasonableness of this prediction rather than reinforcing it.

Clinical Trial Evidence

Trial Number Phase Status Enrollment Key Findings
NCT02685150 N/A Completed 157 Evaluated endoscopic tri-modal imaging (NBI+AFI+WLI) to distinguish functional dyspepsia from reflux disease. This is a diagnostic-tool validation study, not a treatment trial of omeprazole in duodenogastric reflux — graded low relevance (C)

Literature Evidence

PMID Year Type Journal Key Findings
9824338 1998 Crossover Clinical Study Gut Omeprazole 20mg BID reduced duodenogastric and duodenogastro-oesophageal bile reflux in Barrett’s esophagus patients
10994616 2000 Cohort/Clinical Study Scand J Gastroenterol Long-term omeprazole therapy reduced antral duodenogastric reflux in Barrett’s esophagus
9841990 1998 Clinical Study J Gastrointest Surg Medical acid suppression and fundoplication both studied for bile reflux in benign/malignant Barrett’s esophagus
10389684 1999 Animal Study Dig Dis Sci Gastric acid blockade with omeprazole promoted gastric carcinogenesis in rats with induced duodenogastric reflux — safety signal
33027361 2020 Animal Study Acta Cir Bras Investigated omeprazole’s protective/harmful effect on gastric adenocarcinoma development in rats with duodenogastric reflux
21916229 2011 Cohort Eksp Klin Gastroenterol Characterized duodenogastric reflux dynamics in duodenal ulcer patients after H. pylori eradication
12836018 2003 Cohort Eur J Pediatr Described primary duodenogastric reflux presentation in children/adolescents, unresponsive to classical antacid therapy
8076761 1994 Observational Gastroenterology Related duodenogastroesophageal reflux and pH patterns to Barrett’s esophagus development
11232672 2001 Observational Am J Gastroenterol Compared acid/bile reflux burden in Barrett’s esophagus vs reflux esophagitis and effect of PPI therapy
19491829 2009 Clinical Study Am J Gastroenterol Compared degree of duodenogastroesophageal and acid reflux between once-daily PPI responders and non-responders

India Market Information

Omeprazole currently shows 0 registrations and a “Not Marketed” status in the reviewed regulatory dataset — no license records are available to summarize.

Safety Considerations

  • Drug Interactions: 673 documented interactions on file. Notable Major-level interactions include Acalabrutinib and Atazanavir (omeprazole’s acid suppression can reduce absorption/efficacy of pH-dependent drugs). Numerous Moderate-level interactions are also recorded, including Atorvastatin, Hydrochlorothiazide, Alprazolam, Amphotericin B (all formulations), Fenofibrate, Apalutamide, Armodafinil, Amikacin, and Anagrelide.

Key warnings and contraindications are not available in this dataset — please refer to the package insert for full prescribing safety information.

Conclusion and Next Steps

Decision: Hold

Rationale: Evidence for duodenogastric reflux specifically is limited to one low-relevance diagnostic imaging trial and largely observational/animal literature (L3), and the mechanistic link is only partial (omeprazole addresses acid, not bile/pancreatic reflux). More importantly, multiple animal studies raise a genuine safety signal that acid suppression may promote gastric carcinogenesis under chronic duodenogastric reflux exposure — this is a caution flag, not just an evidence gap. A Blocking data gap (missing local package-insert warnings/contraindications) also prevents entry into S1 safety review.

To proceed, the following is needed:

  • TFDA/local package insert (warnings, contraindications) to close the Blocking data gap (DG001)
  • DrugBank-confirmed mechanism of action detail (DG002)
  • Clarification of local licensing/original indication status, given the drug currently shows “Not Marketed”
  • A dedicated interventional trial evaluating omeprazole specifically for duodenogastric reflux outcomes (current data is indirect, largely from Barrett’s esophagus cohorts)
  • Follow-up on the gastric carcinogenesis signal seen in animal DGR models before advancing this candidate

    Disclaimer

This content is for research purposes only and does not constitute medical advice. Clinical validation is required before any clinical application.



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