Dexrabeprazole
| 證據等級: L5 | 預測適應症: 6 個 |
目錄
Dexrabeprazole: From Acid Peptic Disorders to Active Peptic Ulcer Disease
One-Sentence Summary
Dexrabeprazole is the R(+) enantiomer of Rabeprazole, a proton pump inhibitor developed for the treatment of acid peptic disorders — commercially available in India since at least 2009 based on published surveillance data, though currently absent from the CDSCO registration database. The TxGNN model predicts it may be effective for Active Peptic Ulcer Disease, with 0 registered clinical trials and 19 publications currently supporting this direction — including one large-scale direct observational study of Dexrabeprazole itself (4,931 patients in India) and multiple Phase 3 RCTs for its parent compound Rabeprazole.
Quick Overview
| Item | Content |
|---|---|
| Original Indication | Acid peptic disorders (based on published evidence; no formal CDSCO registration data available) |
| Predicted New Indication | Active Peptic Ulcer Disease |
| TxGNN Prediction Score | 99.90% |
| Evidence Level | L3 |
| India Market Status | Not registered (CDSCO) |
| Number of Registrations | 0 |
| Recommended Decision | Proceed with Guardrails |
Why is This Prediction Reasonable?
Dexrabeprazole is the R(+) enantiomer — the pharmacologically active optical isomer — of Rabeprazole, a second-generation proton pump inhibitor. While formal DrugBank MOA documentation is unavailable for Dexrabeprazole as a standalone entity, published literature establishes that it shares the same mechanism as its parent compound: irreversible inhibition of the H+/K+-ATPase enzyme (the gastric “proton pump”) at the secretory surface of parietal cells, leading to potent and sustained suppression of both basal and stimulated gastric acid secretion. A key pharmacokinetic advantage over racemic Rabeprazole is that Dexrabeprazole achieves equivalent or superior acid suppression at half the dose — because the S(−) enantiomer contributes negligible therapeutic activity while adding to systemic exposure and hepatic metabolic burden.
Active peptic ulcer disease is directly driven by an imbalance between acid-mediated mucosal injury (compounded by H. pylori infection or NSAID use) and the stomach’s protective mechanisms. Because acid suppression is the mechanistic cornerstone of peptic ulcer treatment, the applicability of a potent, enantioselective PPI like Dexrabeprazole to this indication is conceptually direct rather than speculative — this is a “mechanism-first” prediction with a high prior probability of success.
Empirically, the parent compound Rabeprazole has multiple Phase 3 RCTs demonstrating efficacy in active duodenal ulcer, gastric ulcer, and H. pylori eradication (PMIDs 9590413, 12694089, 10763941). More directly, a large-scale Indian postmarketing surveillance study (PMID 19585824, n=4,931) specifically evaluated Dexrabeprazole in acid peptic disorders and confirmed safety, faster healing kinetics, and superior pharmacokinetics relative to racemic Rabeprazole — making this one of the rare TxGNN drug repurposing predictions backed by direct compound-level evidence in the target market.
Clinical Trial Evidence
Currently no related clinical trials are registered for Dexrabeprazole in active peptic ulcer disease (ClinicalTrials.gov and ICTRP queried on 2026-03-26, 0 results).
Literature Evidence
| PMID | Year | Type | Journal | Key Findings |
|---|---|---|---|---|
| 19585824 | 2009 | Postmarketing Surveillance | Journal of the Indian Medical Association | Direct Dexrabeprazole study: 4,931 patients with acid peptic disorders in India; confirmed superior pharmacokinetics, faster and greater healing activity vs. Rabeprazole at half the dose; safety reconfirmed |
| 9590413 | 1998 | RCT (Placebo-controlled) | Digestive Diseases and Sciences | Three placebo-controlled trials of Rabeprazole in duodenal ulcer, gastric ulcer, and GERD; Rabeprazole 20 mg and 40 mg both significantly superior to placebo for ulcer healing |
| 12694089 | 2003 | RCT | Alimentary Pharmacology & Therapeutics | Double-blind RCT: Rabeprazole-based vs. omeprazole-based 7-day triple therapy for H. pylori eradication in documented peptic ulcer disease; regimens therapeutically equivalent |
| 22526273 | 2012 | RCT | Journal of Gastroenterology | Rabeprazole significantly reduces recurrence of peptic ulcers in cardiovascular/cerebrovascular patients on low-dose aspirin; prospective randomized active-controlled trial |
| 10763941 | 2000 | RCT | The American Journal of Gastroenterology | Rabeprazole superior to ranitidine for healing active duodenal ulcer disease in a double-blind North American study |
| 16911680 | 2006 | RCT | Journal of Gastroenterology and Hepatology | Low-dose Rabeprazole 10 mg shown equivalent to Omeprazole 20 mg for active peptic ulcer healing rapidity; CYP2C19 genotype effects on healing also investigated |
| 38345252 | 2024 | Systematic Review & Network Meta-analysis | The American Journal of Gastroenterology | P-CAB vs. PPI comparison for severe esophagitis; establishes current context for acid suppressant class comparisons relevant to Dexrabeprazole positioning |
| 10491723 | 1999 | Review | Alimentary Pharmacology & Therapeutics | Pharmacology review of Rabeprazole: more potent H+/K+-ATPase inhibitor than omeprazole; faster activation in parietal cell canaliculus; once-daily dosing adequate |
| 41809210 | 2026 | Expert Consensus | World Journal of Gastrointestinal Pharmacology and Therapeutics | Indian expert consensus on comprehensive management of acid peptic disorders; addresses PPI role and risks of unsupervised acid suppressant use in Indian population |
| 9506245 | 1998 | Review | Drugs | Foundational review of Rabeprazole pharmacology: 2–10× greater antisecretory activity than omeprazole in vitro; clinically superior to placebo and famotidine across acid-peptic conditions |
India Market Information
No CDSCO-registered products were found for Dexrabeprazole. The current regulatory database shows zero active licenses (queried 2026-04-04).
Important note: Published Indian literature (PMID 19585824, 2009) documents that Dexrabeprazole was commercially launched in India for acid peptic diseases, with a postmarketing surveillance program enrolling 4,931 patients across multiple centers. The absence from the current CDSCO database likely reflects a data gap in the evidence pack rather than true non-availability. A direct search of the CDSCO online drug database and review of historical approval records is strongly recommended before drawing regulatory conclusions.
Safety Considerations
Please refer to the package insert for safety information. No key warnings, contraindications, or drug interaction data are currently available for Dexrabeprazole in this evidence pack.
Conclusion and Next Steps
Decision: Proceed with Guardrails
Rationale: Dexrabeprazole’s prediction for active peptic ulcer disease is mechanistically direct (proton pump inhibition is the established treatment pathway), supported by a large Indian postmarketing observational study specifically for this compound (n=4,931; PMID 19585824), and further anchored by robust Phase 3 RCT evidence for the parent compound Rabeprazole. The L3 evidence level reflects the lack of Dexrabeprazole-specific RCTs — a gap that is addressable rather than a fundamental scientific uncertainty.
To proceed, the following is needed:
- Regulatory verification: Confirm current CDSCO registration status through a direct database search; retrieve historical approval records and the Indian package insert to clarify the drug’s formal regulatory standing
- Safety dossier: Extract and document contraindications, boxed warnings, and drug interactions from the Indian prescribing information or the parent compound’s regulatory filings
- Pharmacogenomics plan: Develop a CYP2C19 genotyping strategy, as PPI-class drugs show clinically significant metabolic variability — though Dexrabeprazole’s enantiomeric purity may reduce (but not eliminate) this variability
- Dose-ranging evidence: Formalize the therapeutic dose for the Indian indication; published evidence suggests half the racemic Rabeprazole dose, but a prospective dose-confirmation study would be required for regulatory submission
- Enantiomer-specific RCT: To upgrade from L3 to L2/L1, at least one Phase 2/3 RCT specifically comparing Dexrabeprazole against standard-of-care PPI therapy in active peptic ulcer disease is needed — this would also close the gap between postmarketing surveillance data and regulatory-grade evidence
Disclaimer
This content is for research purposes only and does not constitute medical advice. Clinical validation is required before any clinical application.