Drug reference

Rabeprazole

Proton Pump Inhibitor · Antiulcer

Also known as Rabeprazole sodium, Aciphex, Pariet

START

20 mg PO once daily (most indications); 10 mg once daily for pediatric GERD

TYPICAL MAX

60 mg/dose (ZES); 120 mg/day (ZES only)

STOP IF

Severe hypersensitivity (anaphylaxis, SJS/TEN, DRESS), acute interstitial nephritis (rise in creatinine with rash/eosinophilia), C. difficile infection, magnesium <1.5 mg/dL on long-term therapy; avoid in severe hepatic impairment (Child-Pugh C)

WATCH

Magnesium levels (if on therapy >3 months), vitamin B12 (if >3 years), bone health/fracture risk (if long-term), INR if on warfarin, clopidogrel antiplatelet effect (CYP2C19 competition), signs of C. difficile

CDSCO approvedSchedule HJan AushadhiATC A02BC04

Dose laddermg/d

Renal dose adjustmenteGFR mL/min/1.73m²

KDIGO 2024 + manufacturer label

Pharmacokineticsplasma · t hours

ONSET: 1h · 1 h (antisecretory effect begins)
PEAK: 3.5h · 2-5 h (plasma Cmax); 1-2 h (acid suppression)
t½: 1.5h · 1-2 h (plasma); prolonged antisecretory effect via irreversible binding
DURATION: 1d · 24 h (once-daily dosing; irreversible pump inhibition)

EXCRETION

~90% renal as metabolites; no unchanged drug

route + CYP

INTERACTIONS

12 major

incl. contraindicated

PREGNANCY

Limited human data; no evidence of fetal harm in animal studies at clinically relevant doses. Use only if clearly needed and benefits outweigh risks. PPIs are generally considered safe in pregnancy when indicated.

FDA category + note

Top interactionssee all 12 →

RilpivirineContraindicatedDatabaseKimi deep-research + Cla
AcalabrutinibSevereDatabaseDDInter
AtazanavirSevereDatabaseKimi deep-research + Cla
ClopidogrelSevereDatabaseKimi deep-research + Cla

Available in India

2,120 branded formulations and 4,837 fixed-dose combinations. Look up specific brands in the Drugs workspace.

Jan Aushadhi — generic available at GoI pharmacies

Mechanism

Rabeprazole is a substituted benzimidazole proton pump inhibitor (PPI) that irreversibly inhibits the H+/K+-ATPase (proton pump) at the secretory surface of gastric parietal cells. This blocks the final step of acid production, producing profound and long-lasting inhibition of gastric acid secretion regardless of stimulus. It requires acid-catalyzed activation to form a sulfenamide that covalently binds the pump.

Indications

Healing of erosive or ulcerative gastroesophageal reflux disease (GERD)Maintenance of healing of erosive or ulcerative GERDTreatment of symptomatic GERDHealing of duodenal ulcersHealing of gastric ulcersHelicobacter pylori eradication (in combination with amoxicillin and clarithromycin)Treatment of pathological hypersecretory conditions including Zollinger-Ellison syndromeNSAID-associated gastric ulcers (prevention and treatment)Short-term treatment of symptomatic GERD in adolescent patients 12 years of age and older

Dosing

Adult: GERD (erosive/ulcerative): 20 mg orally once daily for 4-8 weeks. Maintenance: 10-20 mg once daily. Duodenal ulcer: 20 mg once daily for 4 weeks. Gastric ulcer: 20 mg once daily for 6-8 weeks. H. pylori eradication: 20 mg BID for 7-14 days with amoxicillin + clarithromycin. Zollinger-Ellison syndrome: 60 mg once daily; titrate up to 100 mg/day or 60 mg BID if needed. GERD (symptomatic): 10-20 mg once daily for 4 weeks.
Pediatric: GERD (1-11 years): 10 mg orally once daily for up to 12 weeks. GERD (≥12 years): 20 mg orally once daily for up to 8 weeks.
Renal adjustment: No dosage adjustment necessary for renal impairment.
Hepatic adjustment: Mild–moderate impairment (Child-Pugh A/B): no dose adjustment. Severe impairment (Child-Pugh C): AVOID — no pharmacokinetic data; FDA label advises against use.
Geriatric: No specific dosage adjustment recommended based on age alone. Monitor for potential decreased hepatic function and polypharmacy interactions (especially clopidogrel, warfarin).
Max dose: 60 mg/dose (Zollinger-Ellison); 120 mg/day (Zollinger-Ellison only, as 60 mg BID)

Pharmacokinetics

Onset

Antisecretory effect begins within 1 hour of oral administration; peak inhibition of gastric acidity within 1-2 hours.

Peak effect

2-5 hours (plasma Cmax); maximum acid suppression within 1-2 hours of first dose.

Duration

24-48 hours (due to irreversible pump binding; new pump synthesis required for acid recovery).

Half-life

1-2 hours (plasma elimination half-life of rabeprazole); 1.5 hours mean. Despite short plasma half-life, antisecretory effect persists much longer due to irreversible binding to H+/K+-ATPase.

Bioavailability

Approximately 52% (oral; increases to ~65% with repeated dosing). Absolute bioavailability is ~52% for a 20 mg oral tablet compared to IV.

Protein binding

96.3% bound to human plasma proteins (primarily albumin).

Metabolism

Extensive hepatic metabolism via two pathways: (1) non-enzymatic reduction to thioether (major), and (2) CYP2C19 (to desmethyl rabeprazole) and CYP3A4 (to rabeprazole sulfone). CYP2C19 poor metabolizers (especially Asians, 17-20%) show ~2-fold higher AUC. Thioether and sulfone metabolites are inactive.

Excretion

Approximately 90% excreted in urine (primarily as thioether carboxylic acid, glucuronide, and mercapturic acid metabolites); remainder in feces. No unchanged rabeprazole recovered in urine or feces.

Contraindications

Hypersensitivity to rabeprazole, other substituted benzimidazoles, or any component of the formulation
Patients receiving rilpivirine-containing products (reduced absorption due to increased gastric pH)
Concomitant use with products containing dasatinib, nilotinib, or pazopanib (reduced absorption due to increased gastric pH)
Hypersensitivity reactions may include anaphylaxis, anaphylactic shock, angioedema, bronchospasm, acute tubulointerstitial nephritis, and urticaria

Side effects

Common

HeadacheDiarrheaNauseaAbdominal painFlatulenceConstipationVomitingPharyngitisAstheniaInfection

Serious

Clostridioides difficile-associated diarrhea (CDAD)
Acute interstitial nephritis (AIN)
Bone fracture (osteoporosis-related: hip, wrist, spine) with long-term use
Hypomagnesemia with serious events (tetany, arrhythmias, seizures) with long-term use
Vitamin B12 deficiency with long-term use (>3 years)
Cutaneous and systemic lupus erythematosus
Severe cutaneous adverse reactions (Stevens-Johnson syndrome, toxic epidermal necrolysis, DRESS, AGEP)
Gastric fundic gland polyps (with long-term use)
Cyanocobalamin (vitamin B12) deficiency
Anaphylaxis and angioedema

Pregnancy & lactation

Pregnancy

Lactation

Excreted in rat milk; it is not known whether rabeprazole is excreted in human milk. Caution should be exercised when administering to a nursing woman. Consider the benefit of the drug to the mother versus potential risk to the infant.

Drug interactions

Rilpivirine

Contraindicated

Database

Rabeprazole increases gastric pH, which significantly reduces the solubility and absorption of rilpivirine (an HIV NNRTI that requires acidic pH for dissolution). Coadministration results in subtherapeutic rilpivirine plasma concentrations and risk of virologic failure and resistance.

CONTRAINDICATED. Do not coadminister. If PPI therapy is essential, consider alternative antiretroviral regimen (e.g., efavirenz- or dolutegravir-based).

Source: Kimi deep-research + Cla

Acalabrutinib

Severe

Database

Drug interaction classified as: absorption

Source: DDInter

Atazanavir

Severe

Database

Rabeprazole increases gastric pH, which reduces the solubility and absorption of atazanavir (a protease inhibitor that requires acidic conditions for dissolution). Results in subtherapeutic atazanavir concentrations and risk of virologic failure.

Avoid coadministration. If PPI is essential, use atazanavir 400 mg with ritonavir 100 mg once daily (but not recommended with rabeprazole >20 mg/day). Consider alternative antiretroviral or H2-blocker.

Source: Kimi deep-research + Cla

Clopidogrel

Severe

Database

Rabeprazole competitively inhibits CYP2C19, which is required to convert clopidogrel (a prodrug) to its active metabolite. This reduces antiplatelet effect and increases risk of cardiovascular events (MI, stent thrombosis).

Avoid combination if possible. If PPI is essential in a patient on dual antiplatelet therapy, consider pantoprazole (weakest CYP2C19 inhibitor among PPIs) at the lowest effective dose, or use an H2-blocker (e.g., famotidine) instead.

Source: Kimi deep-research + Cla

Dacomitinib

Severe

Database

Clinical effect not specified

Source: DDInter

Dasatinib

Severe

Database

Clinical effect not specified

Source: DDInter

Erlotinib

Severe

Database

Reduced plasma levels and potentially reduced efficacy of erlotinib.

Source: DDInter

Methotrexate

Severe

Database

PPIs may reduce renal clearance of methotrexate and/or displace it from protein binding, leading to increased methotrexate plasma concentrations and toxicity (bone marrow suppression, mucositis, renal failure).

Avoid PPIs in patients receiving high-dose methotrexate (≥15 mg/week). If unavoidable, monitor methotrexate levels closely, ensure adequate hydration, and consider leucovorin rescue. Use H2-blocker as alternative acid suppression.

Source: Kimi deep-research + Cla

Nelfinavir

Severe

Database

Significantly reduced plasma concentrations of nelfinavir, leading to loss of antiviral efficacy and potential development of drug resistance.

Concomitant use is generally not recommended. If a PPI is essential, consider alternative antiretroviral agents.

Source: DDInter

Neratinib

Severe

Database

Clinical effect not specified

Source: DDInter