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Pantoprazole (Protonix) vs. Omeprazole (Prilosec)

Pantoprazole and Omeprazole are medications classified as proton-pump inhibitors (PPIs) and are commonly prescribed for the management of medical conditions in which stomach acid reduction is of therapeutic benefit.  Chemists at Byk Gulden, a subsidiary of Altana (a German chemical company), are credited with the synthesis of pantoprazole in 1985 – whereas Swedish chemists at the pharmaceutical company AstraZeneca (involved in a drug development project spearheaded by Ivan Östholm) are credited with the synthesis of omeprazole in 1979.

In the United States, pantoprazole received initial approval for medical use in 2000 under the brand name Protonix (following acquisition of its patent license from Altana by Wyeth) – whereas omeprazole received initial approval for medical use in 1989 under the brand name Prilosec.  That said, pantoprazole was previously approved for medical use in 1994 throughout Germany – and omeprazole was previously approved (under the brand name Losec) for medical use in 1988 throughout Europe.

Both pantoprazole and omeprazole are indicated by the U.S. FDA as (1) maintenance therapies to promote healing of erosive esophagitis and as (2) interventions for stomach acid hypersecretory conditions like Zollinger-Ellison syndrome.  Although these proton-pump inhibitors are generally used interchangeably by medical doctors, only pantoprazole is officially indicated to directly treat erosive esophagitis associated with gastroesophageal reflux disease – and only omeprazole is officially indicated to treat gastroesophageal reflux disease, ulcers (duodenal and gastric), and H. Pylori infection.

Pantoprazole vs. Omeprazole

Included below is a chart that highlights general characteristics of pantoprazole (Protonix) and omeprazole (Prilosec).  The chart should help elucidate general similarities and differences between these proton-pump inhibitors.

 PantoprazoleOmeprazole
Brand nameProtonixPrilosec
Chemical & Drug classificationBenzimidazole, Proton-Pump Inhibitor (PPI)Benzimidazole, Proton-Pump Inhibitor (PPI)
Approved medical usesErosive esophagitis associated with gastroesophageal reflux disease

Stomach acid hypersecretory conditions (e.g. Zollinger-Ellison syndrome)
Duodenal ulcer

H. pylori eradication (in combination with antibiotics).

Gastric ulcer

Gastroesophageal reflux disease (GERD)

Erosive esophagitis healing maintenance

Stomach acid hypersecretory conditions (e.g. Zollinger-Ellison syndrome)
Off-label usesDuodenal ulcer.

H. pylori eradication (in combination with antibiotics).

Gastric ulcer.

Gastroesophageal reflux disease (GERD).

Peptic ulcer disease.

Stress ulcer prophylaxis.
Erosive esophagitis associated with gastroesophageal reflux disease.

Peptic ulcer disease.

Stress ulcer prophylaxis.
Bioavailability~77% (oral)~30% to ~50% (oral)
FormatsPill. Injectable solution.Capsule. Oral suspension. Injectable solution.
DosagesPill: 20 mg, 40 mg

Vial: 40 mg
Capsule: 10 mg, 20 mg, 40 mg

Oral suspension: 20 mg, 40 mg

Vial: 40 mg
Developers & ManufacturersByk Gulden (Developer)

Wyeth (Manufacturer)
AstraZeneca (Developer & Manufacturer)
Legal statusRx (Prescription)-only (U.S.)Rx (Prescription) & Over-the-Counter (OTC) (U.S.)
Mechanism of actionProton-pump inhibitor.

Selectively and irreversibly suppresses stomach acid production by inhibiting the H+/K+-ATPase enzyme on the surface of gastric parietal cells.

Because the H+/K+ enzyme acts as an acid (proton, or H+) pump within the gastric mucosa, its inhibition interferes with the final step of stomach acid production, ultimately decreasing stomach acid concentrations in users.
Proton-pump inhibitor.

Selectively and irreversibly suppresses stomach acid production by inhibiting the H+/K+-ATPase enzyme on the surface of gastric parietal cells.

Because the H+/K+ enzyme acts as an acid (proton, or H+) pump within the gastric mucosa, its inhibition interferes with the final step of stomach acid production, ultimately decreasing stomach acid concentrations in users.
Half-Life0.9 to 1.9 hours0.5 to 2 hours
Common side effectsHeadache. Diarrhea. Nausea. Abdominal pain. Vomiting. Flatulence. Dizziness. Arthralgia.Headache. Abdominal pain. Nausea. Diarrhea. Vomiting. Flatulence.
Date approved (U.S.)20001989
Duration of effectUp to 72 hours.Up to 72 hours.
MetabolismHepatic: CYP2C19 (primary). CYP3A4 & CYP2C9 (secondary). Cytosolic sulfotransferase. (secondary).Hepatic: CYP2C19 (primary). CYP3A4 (secondary). CYP1A2 (tertiary).
Onset of actionLess than 1 hour. (Peaks within 2 hours).

(Therapeutic effect plateaus within 4 days of regular administration).
Less than 1 hour. (Peaks within 2 hours).

(Therapeutic effect plateaus within 4 days of regular administration).

Pantoprazole vs. Omeprazole: What are the general differences?

Pantoprazole and omeprazole differ in: official U.S. FDA-authorized medical indications; bioavailability; developers, date of development, and release date; formatting options; and legal status (U.S.).  Additionally, pantoprazole and omeprazole might differ slightly in elimination half-life and route of metabolism.

Of these two proton-pump inhibitors, technically only pantoprazole is approved to directly treat erosive esophagitis associated with gastroesophageal reflux disease (omeprazole is not) – and only omeprazole is approved to treat duodenal ulcer, H. Pylori infection, gastric ulcer, and gastroesophageal reflux disease (pantoprazole is not).  It also seems as though pantoprazole and omeprazole differ in bioavailability, or the percentage of each chemical that is bioactive within the body.

The oral bioavailability of pantoprazole is reportedly ~77% and does not change with repeated dosing – whereas the oral bioavailability of omeprazole reportedly ranges from 40% to 50%.  This indicates that a greater percentage (~27% to ~37%) of an ingested pantoprazole dose inhibits stomach acid secretion in comparison to an ingested omeprazole dose.

The specific developers, dates of development, and dates of pharmaceutical release also differ for pantoprazole and omeprazole.  Pantoprazole was developed by chemists at Byk Gulden (a subsidiary of the German chemical company Altana) in 1985 – and omeprazole was developed by chemists at AstraZeneca in 1979.

As of 2000, pantoprazole became the fourth proton-pump inhibitor (PPI) to receive approval for medical use in the United States – whereas in 1989 (~11 years prior to the release of pantoprazole), omeprazole became the first-ever proton-pump inhibitor (PPI) to receive approval for medical use in the United States.  Outside of the U.S., pantoprazole received approval in 1994 for medical use in Germany – whereas omeprazole received approval in 1988 (~6 years prior to pantoprazole) for medical use in Europe.

The formatting and dosing options also differ slightly between pantoprazole and omeprazole.  Pantoprazole is manufactured in delayed-release pills (pantoprazole sodium) at dosages of 20 mg and 40 mg – and in an injectable solution (pantoprazole sodium) at a dosage of 40 mg per vial.

Omeprazole is manufactured in several formats, including: standard-release capsules (omeprazole sodium) and delayed-release spansules (omeprazole magnesium) at dosages of 10 mg, 20 mg, and 40 mg; oral suspension at dosages of 20 and 40 mg; and injectable solution at a dosage of 40 mg per vial.  In addition to differences in formatting and dosing, the legal status of pantoprazole and omeprazole differ in the United States.

Specifically, pantoprazole is only available as a prescription (Rx) medication – whereas omeprazole is available as an over-the-counter (OTC) medication (but can also be attained via prescription if necessary).  Furthermore, it seems as though pantoprazole and omeprazole may differ slightly in metabolism and elimination half-life.

Though both pantoprazole and omeprazole are metabolized hepatically by CYP2C19 enzymes, and to a lesser extent by CYP3A4 enzymes, only pantoprazole is extensively conjugated by the enzyme cytosolic sulfotransferase – and only omeprazole is metabolized slightly by CYP1A2 enzymes.  The elimination half-life range estimated for pantoprazole (0.9 to 1.9 hours) is slightly narrower than the elimination half-life range estimated for omeprazole (0.5 to 2 hours).

Approved medical uses (U.S.)

If comparing the authorized medical uses associated with pantoprazole and omeprazole in the United States – there are a few technical differences.  Pantoprazole is approved by the United States FDA (Food & Drug Administration) for the: (1) treatment of erosive esophagitis associated with gastroesophageal reflux disease (GERD); (2) maintenance of healing of erosive esophagitis; and (3) treatment of pathological stomach acid hypersecretory conditions (e.g. Zollinger-Ellison syndrome).

Omeprazole is approved by the United States FDA (Food & Drug Administration) for the: (1) treatment of duodenal ulcer; (2) treatment of H. Pylori (with antibiotics); (3) treatment of gastric ulcer; (4) treatment of gastroesophageal reflux disease (GERD); (5) maintenance of healing of erosive esophagitis; and (6) treatment of stomach acid hypersecretory conditions (e.g. Zollinger-Ellison syndrome).  In total, pantoprazole has 3 official medical indications and omeprazole has 6 official medical indications within the United States.

Reflecting upon the official FDA-authorized uses for pantoprazole and omeprazole, it seems as though both medications are approved as: (1) maintenance therapies to promote healing in erosive esophagitis and (2) as treatments for stomach acid hypersecretory conditions like Zollinger-Ellison syndrome.  Technically speaking, only pantoprazole is authorized to treat erosive esophagitis as a consequence of gastroesophageal reflux disease (omeprazole is not).

Furthermore, only omeprazole is authorized to treat duodenal ulcer; H. Pylori (with antibiotics); gastric ulcer; and gastroesophageal reflux disease (pantoprazole is not).  Despite the aforementioned technical differences in respective FDA-authorized indications for pantoprazole and omeprazole, these agents generally exhibit similar efficacy in suppressing stomach acid production such that most medical doctors regard them as interchangeable treatment options.

Additionally, because there’s evidence supporting the idea that pantoprazole is effective in the treatment of duodenal ulcer; H. Pylori (with antibiotics); gastric ulcer; and gastroesophageal reflux disease – pantoprazole is frequently prescribed as an “off-label” intervention for these conditions.  Similarly, although omeprazole isn’t officially approved to treat erosive esophagitis associated with gastroesophageal reflux disease – it is regularly prescribed as an “off-label” intervention for this condition.

Conditions for which both pantoprazole and omeprazole are prescribed “off-label” include: peptic ulcer disease (treatment) and stress ulcer (prophylaxis).  According to the National Institute for Health and Care Excellence (NICE), the standard dose of pantoprazole is 40 mg per day – and the standard dose of omeprazole is 20 mg per day.

Cost: Which is more expensive?

Both pantoprazole and omeprazole retail for low prices at most pharmacies such that a majority of consumers won’t consider the cost of one medication to be significantly different than that of the other.  A total of 30 pantoprazole pills costs between $9 and $34 for the 20 mg dose – and between $8 and $24 for the 40 mg dose.

A total of 30 omeprazole pills costs between $11 and $42 for the 10 mg dose; $6 and $25 for the 20 mg dose; and $10 to $29 for the 40 mg dose.  Unlike pantoprazole, omeprazole is sold “over-the-counter” (OTC) at its 20 mg dose for ~$16 per 42-count package.  Since a subset of consumers may prefer using brand name preparations of pantoprazole (Protonix) or omeprazole (Prilosec) for various reasons, the prices of “brand name” preparations are documented below.

Pantoprazole cost

  • Pantoprazole (20 mg): $9 to $34 (30 count)
  • Pantoprazole (40 mg): $8 to $24 (30 count)
  • Protonix (20 mg): $403 to $436 (30 count)
  • Protonix (40 mg): $403 to $436 (30 count)
  • Protonix IV (40 mg): $139 (25 count)

Omeprazole cost

  • Omeprazole (10 mg): $11 to $42 (30 count)
  • Omeprazole (20 mg): $6 to $25 (30 count)
  • Omeprazole (40 mg): $10 to $29 (30 count)
  • Omeprazole OTC (20 mg): ~$16 (42 count)
  • Prilosec (10 mg): $204 to $216 (30 count)
  • Prilosec (20 mg): $226 to $241 (30 count)
  • Prilosec (40 mg): $330 to $353 (30 count)
  • Prilosec OTC (20 mg): ~$24 (42 count)
  • Prilosec (oral suspension): $213 (30 count)

Brand name Protonix (pantoprazole) costs between $403 and $436 for a 30-pill supply, and brand name Prilosec costs between $204 and $353 for a 30-pill supply – making the former (Protonix) significantly more expensive than the latter (Prilosec).  Moreover, brand name Prilosec OTC (20 mg) costs ~$24 for a 42-pill supply – making Prilosec OTC significantly less expensive than standard brand name Protonix and Prilosec prescriptions.

An injectable brand name form of pantoprazole called “Protonix IV” costs ~$139 for 25 vials of the 40 mg dose.  An oral suspension brand name form of omeprazole called “Prilosec oral suspension” costs ~$213 for a 30-count (regardless of dose).  If comparing the cost of Protonix IV ($5.56 per unit) to that of Prilosec oral suspension ($7.10 per unit), it seems as though the former (Protonix IV) is less expensive per dose than the latter (Prilosec oral suspension).

Overall, standard, generic pantoprazole and omeprazole preparations are generally regarded as inexpensive and are unlikely to significantly differ in cost; a 30-pill supply of each typically costs between $6 and $30.  However, prices of pantoprazole and omeprazole may be subject to variation depending upon the requested dosage and/or the specific retailing pharmacy – such that one agent may end up more expensive than the other.

In any regard, most omeprazole users will spend less in total costs than pantoprazole users because: (1) omeprazole is available over-the-counter (such that medical doctor appointments and their respective costs are not required to attain omeprazole – whereas pantoprazole users may end up spending hundreds in medical doctor appointment costs); and (2) the price of omeprazole tends to be relatively stable as a result of its over-the-counter availability (whereas the price of pantoprazole could fluctuate in accordance with its prescription demand).

Moreover, due to its over-the-counter availability, brand name Prilosec (omeprazole) is significantly cheaper than brand name Protonix (pantoprazole) – and nearly as cheap as generic omeprazole.  The only scenario in which pantoprazole is notably less expensive than omeprazole is if we compare the respective costs of brand name alternative formats (intravenously-injectable Protonix is less expensive per dose than oral suspension Prilosec).

Dosage & Formats

Pantoprazole is available in 2 formats: delayed-release pills (dosages: 20 mg and 40 mg) and injectable solution (dosage: 40 mg).  It should be noted that both delayed-release pantoprazole pills and injectable pantoprazole solution contain “pantoprazole sodium,” however, preparations of pantoprazole containing “pantoprazole magnesium” are available in countries outside the United States.

Omeprazole is available in 3 formats: delayed-release capsule (dosages: 10 mg, 20 mg, 40 mg); immediate-release oral suspension (dosages: 20 mg, 40 mg); and intravenously-injectable solution (dosage: 40 mg).  It should be noted that delayed-release omeprazole capsules (enterically-coated) contain “omeprazole magnesium” whereas immediate-release omeprazole (oral suspension) contains “omeprazole sodium bicarbonate.”

In general, it is most common for users of proton-pump inhibitors to receive a prescription for delayed-release pills of pantoprazole and omeprazole – rather than alternative formats such as injectable solution and oral suspension.  The use of alternative pantoprazole and omeprazole formats (injectable solution and oral suspension) is usually reserved for inpatients and medical emergencies.

Overall, there aren’t any major differences between pantoprazole and omeprazole in formatting options – both are available as delayed-release pills and injectable solution and the former (delayed-release pills) are more common than the latter (injectable solution).  Though omeprazole is available in the format of an “oral suspension” (and pantoprazole is not), an “oral suspension” of pantoprazole can be produced by blending proper quantities of pantoprazole tablets, sterile water, and sodium bicarbonate powder.

Since pantoprazole and omeprazole can be attained in delayed-release pills (with similar onsets and durations of action) – and alternative formats (if necessary) of injectable solution and oral suspension – there’s no reason to favor one medication over the other based on formatting options.  That said, because omeprazole pills are available in 3 dosing increments (10 mg, 20 mg, 40 mg) and pantoprazole pills are only available in 2 dosing increments (20 mg, 40 mg) – there may be reason to favor omeprazole over pantoprazole on the basis of its dosing options.

An additional dosage increment for omeprazole (10 mg) relative to pantoprazole could be perceived as advantageous in that it might: (1) make it easier for omeprazole users to find an optimal (safe, effective, tolerable) dose if they don’t react well to the additional dosing increments (20 mg, 40 mg) and/or (2) prove beneficial while titrating off of proton-pump inhibitors after long-term use (the lower dose might assist in stabilizing physiology prior to omeprazole discontinuation such as to reduce odds of severe discontinuation symptoms following complete cessation).

Efficacy: Which proton-pump inhibitor is more effective?

It is understood that pantoprazole and omeprazole exhibit similar mechanisms of action (as proton-pump inhibitors) to suppress stomach acid production.  Furthermore, most medical professionals consider pantoprazole and omeprazole to be equally efficacious and interchangeable interventions in the management of medical conditions associated with elevated stomach acid concentrations.

Nevertheless, many prospective and current users of proton-pump inhibitors (PPIs) are curious as to whether pantoprazole and omeprazole differ, even modestly, in therapeutic efficacy – such that one agent might reduce stomach acid more substantially than the other and/or prove therapeutically effective in a greater percentage of users (on average).  Currently, pantoprazole and omeprazole have 2 mutual FDA-authorized indications: (1) promoting healing in erosive esophagitis and (2) treating stomach acid hypersecretory conditions (e.g. Zollinger-Ellison syndrome).

If attempting to compare the respective efficacies of pantoprazole and omeprazole, it makes logical sense to perform the comparison only in medical conditions for which both agents are approved.  The medical conditions for which both pantoprazole and omeprazole are approved include: (1) erosive esophagitis (as healing promoters) and (2) stomach acid hypersecretory conditions (e.g. Zollinger-Ellison syndrome).

Erosive esophagitis

It should be stated that both pantoprazole and omeprazole have proven efficacious in double-blind, large-scale, randomized, placebo-controlled trials for the promotion of healing in patients with erosive esophagitis.  As a result, both pantoprazole and omeprazole are formally indicated by the U.S. FDA to promote healing among persons with erosive esophagitis.

Nevertheless, some individuals wonder whether one agent (pantoprazole or omeprazole) might be more effective than the other in the promotion of healing among patients with erosive esophagitis.  To determine whether one agent is more efficacious than the other for the promotion of healing among patients with erosive esophagitis, we can analyze results from studies in which the efficacies of these agents were compared.

2017: Comparative effectiveness and acceptability of the FDA-licensed proton pump inhibitors for erosive esophagitis: A PRISMA-compliant network meta-analysis.

Li et al. conducted a meta-analysis in which the efficacies of pantoprazole, omeprazole, and other proton-pump inhibitors (PPIs) were compared in the management of erosive esophagitis.  Specifically, Li et al. compared the efficacies of proton-pump inhibitors at FDA-recommended doses, including:  40 mg/day pantoprazole and 20 mg/day omeprazole (in addition to 60 mg/day dexlansoprazole; 40 mg/day esomeprazole; 20 mg/day esomeprazole; 30 mg/day lansoprazole; and 20 mg/day rabeprazole.

For the meta-analysis, researchers searched medical journal databases (PubMed, Embase, Cochrane Library) for randomized controlled trials in which efficacies of the aforementioned agents were evaluated in the management of erosive esophagitis.  A total of 25 trials with 57 study arms encompassing 25,088 patients (with erosive esophagitis verified by endoscopic exams) were included in the analysis.

The primary outcome measure was healing rate of erosive esophagitis at 4 weeks and 8 weeks – and the secondary outcome measure was heartburn relief rate.  Results of the meta-analysis indicated that esomeprazole (40 mg) was more efficacious in healing mucosal erosions associated with erosive esophagitis and in providing heartburn relief – than other treatments.

Nevertheless, pantoprazole (40 mg per day) was more efficacious than omeprazole (20 mg per day) for the promotion of healing in erosive esophagitis.  Of the 7 interventions compared, pantoprazole (40 mg/day) ranked 4th (at 4 weeks) and 3rd (at 8 weeks) in erosive esophagitis healing rate – whereas omeprazole (20 mg/day) ranked 5th (at 4 weeks) and 6th (at 8 weeks) erosive esophagitis healing rate.

Furthermore, out of 6 agents compared, pantoprazole (40 mg/day) ranked 4th and omeprazole (20 mg/day) ranked 6th in ability to alleviate heartburn.  Overall, the results of this meta-analysis support the idea that pantoprazole (40 mg/day) may be more effective than omeprazole (20 mg/day) for the promotion of healing in erosive esophagitis – and in the management of heartburn associated with erosive esophagitis.

That said, it remains unclear as to whether the superior efficacy of pantoprazole relative to omeprazole (for the promotion of healing in erosive esophagitis) may have been attributable to disparities in potency of dosing.  (Perhaps the administration of omeprazole at a dosage of 40 mg/day would’ve been more efficacious than the 20 mg/day omeprazole dose assessed in this analysis).

Other limitations associated with this meta-analysis that may have impacted its findings include: differences in the average severity of erosive esophagitis across medication trials from which data were extracted; the limited duration of these trials (4 to 8 weeks); difficulties in measuring erosive esophagitis healing; and subjective reporting of heartburn by trial participants.

2009: Comparative study of omeprazole, lansoprazole, pantoprazole and esomeprazole for symptom relief in patients with reflux esophagitis.

Zheng conducted a study in which the efficacies of various proton-pump inhibitors including omeprazole and pantoprazole were compared in the treatment of reflux esophagitis.  For the study, 274 patients with erosive reflux esophagitis were assigned at random to receive either: 20 mg/day omeprazole (68 patients); 40 mg/day pantoprazole (69 patients); 30 mg/day lansoprazole (69 patients); or 40 mg/day esomeprazole (68 patients) – for an 8-week period.

Results indicated that recipients of esomeprazole (40 mg/day) exhibited faster reductions in heartburn scores plus resolution of heartburn than recipients of other proton-pump inhibitors.  Nevertheless, there were no clinically-relevant differences observed between the 4 proton-pump inhibitors (omeprazole, pantoprazole, lansoprazole, esomeprazole) in the promotion of healing in reflux esophagitis over the 8-week study period.

Although esomeprazole (40 mg/day) facilitated faster symptom relief than other proton-pump inhibitors, healing rates of erosive reflux esophagitis in esomeprazole users did not significantly differ from users of other proton-pump inhibitors – as evidenced by high-resolution patient endoscopy.  This study supports the idea that pantoprazole (40 mg/day) and omeprazole (20 mg/day) do not significantly differ in efficacy for the promotion of healing in erosive esophagitis.

2003: Comparable efficacy of pantoprazole and omeprazole in patients with moderate to severe reflux esophagitis. Results of a multinational study.

Körner et al. conducted a randomized, double-blind, parallel group study to compare the efficacy pantoprazole to that of omeprazole MUPS (multiple-unit pellet system) in the treatment of moderate-to-severe reflux esophagitis.  For the study, a total of 669 outpatients diagnosed with moderate-to-severe gastroesophageal reflux disease (verified by endoscopy) were assigned at random to receive either: pantoprazole (40 mg/day) or omeprazole MUPS (40 mg/day).

After 4 weeks of treatment, outpatients were subject to an endoscopy to evaluate healing rate of esophagitis.  Additionally, esophagitis symptoms were evaluated with an investigator-administered questionnaire that assessed heartburn, reflux regurgitation, and swallowing-related pain – and a self-administered questionnaire that evaluated 24 additional gastrointestinal symptoms.

Of the 669 intent-to-treat participants: 337 received pantoprazole (40 mg/day) and 332 received omeprazole MUPS (40 mg/day).  A total of 552 patients (of 669) completed the study: 282 pantoprazole users (40 mg/day) and 270 omeprazole MUPS users (40 mg/day) – and of study completers, 452 patients (of 552) were “highly-compliant” (233 pantoprazole users and 219 omeprazole users).

Results of this study indicated that healing rates of moderate-to-severe esophagitis were similar among patientsregardless of whether they received pantoprazole or omeprazole MUPS.  Among the intent-to-treat sample (669 patients), healing rates of esophagitis were: 65.3% for pantoprazole users and 66.3% for omeprazole users – after a 4-week period.

In other words, there were no significant differences in the respective efficacies of pantoprazole and omeprazole for the promotion of healing in reflux esophagitis.  Additionally, pantoprazole and omeprazole appeared equally efficacious in the management of esophagitis-related symptoms such as heartburn, acid eructation, and swallowing-related pain – at 2 weeks, 4 weeks, and 8 weeks.

Researchers concluded that pantoprazole (40 mg/day) and omeprazole MUPS (40 mg/day) appear equally efficacious for the promotion of healing in moderate-to-severe (grade II or III) reflux esophagitis.  Moreover, patients with high treatment compliance appear to exhibit greater healing of esophagitis than patients with regular or low compliance – regardless of the medication.

2000: Efficacy of Pantoprazole Compared with Omeprazole in Prevention of Relapse of Reflux Esophagitis: Double Blind, Randomized, Multicenter Trial.

Lauritsen et al. organized a multinational, double-blind trial to determine whether pantoprazole and omeprazole differ in efficacy for the prophylaxis of reflux esophagitis relapse.  For the trial, 639 patients with reflux esophagitis (grades 2 through 4) were assigned at random to receive either: 20 mg/day pantoprazole (211 patients); 40 mg/day pantoprazole (218 patients); or 20 mg/day omeprazole (210 patients) – for a 12-month period.

Patients underwent symptom assessment three times per month and endoscopy at 3 months and 12 months.  Results of the trial indicated that reflux esophagitis relapse rates were: 23% among users of 20 mg/day pantoprazole; 17% among users of 40 mg/day pantoprazole; and 19% among users of 20 mg/day omeprazole.

Although the lowest reflux esophagitis relapse rate was observed among users of 40 mg/day pantoprazole (17%), this was not significantly different from the reflux esophagitis relapse rates associated with 20 mg/day pantoprazole (23%) or 20 mg/day omeprazole (19%), respectively.  Furthermore, though treatment with 40 mg/day pantoprazole yielded a marginally lower reflux esophagitis relapse rate (by ~2%) relative to 20 mg/day omeprazole, the ~2% difference may have been attributable to disparities in potency of dosing.

It’s possible that 40 mg/day pantoprazole is slightly more potent than 20 mg/day omeprazole – such that a modestly greater reduction in esophagitis relapse rate should’ve been expected for the former (pantoprazole) relative to the latter (omeprazole).  Perhaps the inclusion of a patient group receiving 40 mg/day omeprazole would’ve: (1) negated the ~2% marginal (statistically insignificant) difference in relapse rate between pantoprazole and omeprazole; or (2) demonstrated superiority of omeprazole over pantoprazole.

Nevertheless, this large-scale, long-term, randomized, double-blinded trial substantiates the idea that pantoprazole and omeprazole are equally effective in preventing reflux esophagitis relapse when administered once per day.

1999: Pantoprazole versus omeprazole in the treatment of reflux esophagitis.

Vcev et al. sought to evaluate the efficacy of pantoprazole in the treatment of reflux esophagitis by comparing it to omeprazole.  Researchers organized a single-blind, randomized, clinical trial in which a total of 120 patients with GERD (grades 1 and 2) were assigned to receive either: 40 mg/day pantoprazole (60 patients) or 20 mg/day omeprazole (60 patients) – over an 8-week period.

Among patients that followed the treatment protocol (i.e. per-protocol patients), 4-week and 8-week healing rates were: 76.3% and 94.7% among users of 40 mg/day pantoprazole versus 71.2% and 92.9% among users of 20 mg/day omeprazole.  Among the intent-to-treat participants, 4-week and 8-week healing rates were: 75% and 90% among users of 40 mg/day pantoprazole versus 70% and 86.6% among users of 20 mg/day omeprazole.

Results of this trial support the idea that pantoprazole (40 mg/day) and omeprazole (20 mg/day) exhibit similar efficacy in the short-term management of reflux esophagitis (grades 1 and 2).  That said, it seems as though pantoprazole (40 mg/day) might be marginally more effective than omeprazole (20 mg/day) – as evidenced by modestly greater healing rates among pantoprazole recipients relative to omeprazole recipients at 4 and 8 weeks.

It’s possible that the marginal (clinically insignificant) superiority of pantoprazole relative to omeprazole in this trial was attributable to disparities in potency of dosing.  Perhaps 40 mg/day pantoprazole is more potent than 20 mg/day omeprazole – thus accounting for the slightly greater healing rate of reflux esophagitis among pantoprazole users.

Verdict: Pantoprazole (40 mg) might be slightly more effective than Omeprazole (20 mg) for erosive esophagitis healing

There are data suggesting that pantoprazole (40 mg per day) may be more effective than omeprazole (20 mg per day) for the promotion of healing in erosive esophagitis.  For example, a meta-analysis performed by Li et al. (2017) including data from 25 randomized controlled trials (encompassing over 25,000 patients with erosive esophagitis) reported that pantoprazole (dosed at 40 mg per day) appears more effective than omeprazole (dosed at 20 mg per day) for the promotion of healing in erosive esophagitis.

The superior efficacy of pantoprazole over omeprazole in the meta-analysis by Li et al. (2017) was evidenced by a larger healing rate (%) among pantoprazole recipients relative to omeprazole recipients at 4 weeks and 8 weeks of treatment.  The respective probabilities of erosive esophagitis healing associated with pantoprazole and omeprazole at 4 weeks and 8 weeks [based on data included in the analysis] were: 58% and 69.4% (40 mg pantoprazole) versus 35.9% and 30.1% (20 mg omeprazole).

Furthermore, the meta-analysis by Li et al. (2017) reported a greater degree of heartburn relief for pantoprazole users (44.1%) relative to omeprazole users (30.3%).  Although there were limitations associated with the aforementioned meta-analysis (e.g. indirect comparisons, possible discrepancies in endoscopic analyses, disparities in potency of dosing, limited duration of trials), the findings support the idea that pantoprazole (40 mg/day) is superior to omeprazole (20 mg/day) for the promotion of healing in erosive esophagitis.

In trials that directly compared the efficacy of pantoprazole and omeprazole for the promotion of healing in erosive esophagitis, zero clinically-relevant differences were discovered.  For example, a trial with 274 participants by Zheng (2009) comparing pantoprazole (40 mg/day) to omeprazole (20 mg/day) discovered that these agents did not significantly differ in efficacy for the promotion of healing in erosive esophagitis over an 8-week period.

A trial by Körner et al. (2003) involving 669 patients with moderate-to-severe erosive esophagitis reported that erosive esophagitis healing rates were similar among users of pantoprazole (40 mg/day) and omeprazole MUPS (40 mg/day).  Specifically, after a 4-week treatment period, 65.3% of pantoprazole users and 66.3% of omeprazole users exhibited healing.

Additionally, a large-scale (639 patients) and long-term (12-month) trial by Lauritsen et al. (2000) reported that pantoprazole (20 mg & 40 mg) and omeprazole (20 mg) exhibit clinically-equal efficacy in the prevention of erosive esophagitis relapse.  Though this trial did not measure erosive esophagitis healing, prevention of erosive esophagitis relapse is likely relevant to efficacy in the promotion of healing.

An 8-week comparison by Vcev et al. (1999) comprised of 120 patients with gastroesophageal reflux disease (GERD) reported that pantoprazole (40 mg) and omeprazole (20 mg) were of similar efficacy in the management of reflux esophagitis.  That said, there were trends for negligibly superior healing rates (at 4 weeks and 8 weeks) with pantoprazole relative to omeprazole.

Knowing that: (1) the meta-analysis by Li et al. (2017) reported that pantoprazole (40 mg) was associated with a greater rate of esophageal healing relative to omeprazole (20 mg) after 4 weeks and 8 weeks in patients with erosive esophagitis; and (2) comparison studies have revealed trends for modestly greater esophageal healing rates with pantoprazole (40 mg) relative to omeprazole (20 mg) in patients with erosive esophagitis (but not the opposite) – it’s reasonable to surmise that pantoprazole (40 mg) is potentially superior to omeprazole (20 mg) in the healing of erosive esophagitis.

That said, the greater esophageal healing rates pantoprazole (40 mg) users with erosive esophagitis relative to omeprazole (20 mg) users with erosive esophagitis (as is documented in some studies) could be attributable to differences in potency of dosing (perhaps 40 mg pantoprazole is more potent than 20 mg omeprazole – thus accounting for disparities in healing rates at 4 and 8 weeks).  Other study limitations like: endoscopy accuracy; short-term trial duration; small sample sizes; etc. – might’ve also yielded misleading data suggesting that pantoprazole is more effective than omeprazole for esophageal healing in erosive esophagitis.

Stomach acid hypersecretory conditions (Zollinger-Ellison syndrome)

As of current (2018) there are zero large-scale, randomized, double-blind, controlled trials that’ve directly compared the efficacies of pantoprazole and omeprazole in the management of stomach acid hypersecretory conditions like Zollinger-Ellison syndrome.  For this reason, it cannot be suggested that one agent (pantoprazole or omeprazole) exhibits greater efficacy than the other in treating stomach acid hypersecretory conditions.

Nevertheless, one small-scale study by Ramdani et al. (2002) assessed the effect of pantoprazole on 24-hour intragastric pH among in 11 patients diagnosed with Zollinger-Ellison syndrome – compared to omeprazole and lansoprazole.  Below is a brief synopsis of the study with a discussion of its findings.

2002: Effect of pantoprazole versus other proton pump inhibitors on 24-hour intragastric pH and basal acid output in Zollinger-Ellison syndrome.

Ramdani et al. conducted a study to evaluate the efficacy of pantoprazole in reducing gastric acid secretion among patients with Zollinger-Ellison syndrome in comparison to other proton-pump inhibitors (including omeprazole).  The study included 11 patients who had received either omeprazole (20 mg to 100 mg per day) or lansoprazole (30 mg to 120 mg per day) – prior to treatment with pantoprazole (40 mg to 200 mg per day).

Researchers utilized 24-hour intragastric pH-metry to measure basal acid output and serum gastrin in the 11 patients.  The 24-hour intragastric pH-metry was conducted at baseline while patients received their initial therapies (omeprazole or lansoprazole) and later after 7 to 10 days of pantoprazole administration.

Results indicated that 24-hour intragastric pH among patients with Zollinger-Ellison syndrome did not differ among treatments (omeprazole, lansoprazole, and pantoprazole).  It was concluded that pantoprazole appears as potent and effective as omeprazole (and other proton-pump inhibitors) in patients with Zollinger-Ellison syndrome.

Verdict: Pantoprazole and Omeprazole equally effective as treatments for stomach acid hypersecretory conditions (e.g. Zollinger-Ellison syndrome)

Available scientific evidence suggests that flexibly-dosed pantoprazole and omeprazole are equally efficacious in the management of stomach acid hypersecretory conditions like Zollinger-Ellison syndrome.  In the standalone small-scale study by Ramdani et al. (2002) that compared the respective abilities of pantoprazole and omeprazole to reduce stomach acid secretion in patients with Zollinger-Ellison syndrome – zero clinically-relevant differences between these agents were observed in effectiveness.

Both pantoprazole (40-200 mg/day) and omeprazole (20-100 mg/day) reduced stomach acid secretion to a similar degree among patients with Zollinger-Ellison syndrome – as was evidenced by similar levels of basal acid output and serum gastrin measured by 24-hour intragastric pH-metry.  Since pantoprazole and omeprazole appear equally effective in reducing stomach acid secretion among patients with stomach acid hypersecretory conditions like Zollinger-Ellison syndrome – there’s no reason to suggest that one agent is more effective than the other for the management of stomach acid hypersecretory conditions.

Moreover, both pantoprazole and omeprazole have demonstrated efficacy in large-scale, randomized, controlled trials for the management of stomach acid hypersecretory conditions whereafter each received FDA-approval to treat these conditions.  Lastly, according to Klok et al. (2003), the efficacies of pantoprazole and omeprazole in managing medical conditions should be equal when administered at equipotent doses.

Efficacy of pantoprazole vs. omeprazole for other medical conditions…

Of pantoprazole and omeprazole, only omeprazole is officially authorized by the U.S. FDA to treat gastroesophageal reflux disease (GERD), duodenal ulcer, gastric ulcer, and H. Pylori infection.  However, it is generally suggested that, when proton-pump inhibitors are administered at equipotent doses, there’s unlikely to be clinically-significant difference in their effectiveness for any medical condition.

In other words, despite the fact that pantoprazole is not officially authorized by the U.S. FDA to treat gastroesophageal reflux disease (GERD), duodenal ulcer, gastric ulcer, and H. Pylori infection – it’s efficacy for these conditions is likely similar (on average) to omeprazole.  For this reason, most experts believe that flexibly-dosed pantoprazole is as effective as flexibly-dosed omeprazole in the treatment of gastroesophageal reflux disease (GERD), duodenal ulcer, gastric ulcer, and H. Pylori infection.

Gastroesophageal reflux disease (GERD)

The efficacy of omeprazole in the treatment of gastroesophageal reflux disease (GERD) is well-substantiated with data from well-designed clinical trials – hence its official approval from the U.S. FDA for this condition.  Although some might argue that omeprazole is a better treatment “choice” than pantoprazole for gastroesophageal reflux disease on the basis of its FDA approval (and lack thereof for pantoprazole) – this does not mean that omeprazole is more effective than pantoprazole for gastroesophageal reflux disease (GERD).

The fact that omeprazole has received FDA approval to treat gastroesophageal reflux disease (GERD) simply means that: (1) there are strong data to support its efficacy in the management of this condition and (2) the data supporting its efficacy has been independently reviewed and deemed reliable.  Despite the fact that pantoprazole is not officially approved by the FDA to treat gastroesophageal reflux disease (GERD), there preliminary data to support its efficacy in the management of this condition.

A meta-analysis conducted by Dabrowski et al. (2018) evaluated the usefulness of pantoprazole in the treatment and symptom management of gastroesophageal reflux disease (GERD) and reported that pantoprazole (40 mg/day) treatment was associated with: (1) complete relief of GERD-related symptoms in a majority of patients with ERD and NERD; (2) significant relief of GERD-related symptoms in patients without complete symptom relief; and (3) improved quality of life over 8 weeks.

The aforementioned meta-analysis was based upon data from 3 multicenter, prospective, open-label, phase IV trials encompassing 252 patients with GERD who received pantoprazole (40 mg/day) for 4 or 8 weeks.  Authors of the meta-analysis concluded that pantoprazole (40 mg/day) appears safe and effective for alleviating symptoms of gastroesophageal reflux disease (GERD).

An observational, open-label study by Remes-Troche et al. (2014) also evaluated the therapeutic potential of pantoprazole magnesium (sustained-release) in the treatment of gastroesophageal reflux disease (GERD).  The study involved observing symptoms in 4,343 patients with gastroesophageal reflux disease (GERD) who received pantoprazole magnesium (40 mg/day) for 4 weeks (~28 days).

Results of this study indicated that treatment with pantoprazole magnesium (40 mg/day) led to: (1) 73% improvement in GERD symptoms among the intent-to-treat participants (from baseline) and (2) 80% improvement in GERD symptoms among the per-protocol participants (from baseline) – as measured by a physician-administered 4-point Likert scale.  Researchers concluded that pantoprazole magnesium appears safe and effective in the treatment of gastroesophageal reflux disease (GERD).

A paper by Popadynets (2013) suggested that pantoprazole might be a better treatment choice than omeprazole among patients with gastroesophageal reflux disease (GERD) plus asthma.  In the paper, Popadynets stated that pantoprazole is associated with higher bioavailability and fewer drug interactions than omeprazole – plus a favorable safety profile.

Popadynets also reported that, pantoprazole users with GERD plus asthma exhibited significantly better indicators of lung function than omeprazole users with GERD plus asthma.  For this reason, Popadynets believes that pantoprazole might be favorable to omeprazole in the management of gastroesophageal reflux disease (GERD) among patients with GERD plus asthma.

Scholten (2007) published a paper reflecting upon the long-term use of pantoprazole in the treatment of gastroesophageal reflux disease (GERD).  In the paper, Scholten noted that oral pantoprazole appears safe, well-tolerated, and effective as an initial and maintenance therapy for non-erosive gastroesophageal reflux disease (GERD) and erosive esophagitis.

Furthermore, it Scholten stated that oral pantoprazole is: (1) more effective than H2 receptor antagonists and (2) of similar efficacy to other proton-pump inhibitors (e.g. omeprazole) as an acute therapy and maintenance therapy in gastroesophageal reflux disease (GERD).  This is yet another report supporting the use of pantoprazole (short-term or long-term) in gastroesophageal reflux disease (GERD).

Calabrese et al. (2007) published a paper discussing management strategies for gastroesophageal reflux disease (GERD) in elderly populations and noted that proton-pump inhibitors (PPIs) are presently the most effective intervention.  The paper suggested that, of available proton-pump inhibitors, pantoprazole is likely among the best selections for acute and/or long-term management of gastroesophageal reflux disease (GERD) in elderly persons due to its: (1) documented efficacy in trials and clinical reports and (2) lower propensity (than other proton-pump inhibitors) to interact with concurrently-administered medications.

A study by Janssen et al. (2005) suggests that pantoprazole is effective for the acute and longer-term treatment of mild gastroesophageal reflux disease (GERD).  In this study by Janssen et al., 558 individuals with endoscopy-confirmed, mild GERD were assigned to receive pantoprazole (20 mg) “on-demand” or “continuously” over a 24-week period.  Thereafter, the degree of GERD-related symptom control was assessed by researchers.

Results of the study indicated that pantoprazole significantly alleviated GERD-related symptoms in ~82.1% of per-protocol patients and in ~79.1% of intent-to-treat patients – over an acute period (4 weeks).  Moreover, longer-term pantoprazole administration (24 weeks) significantly controlled GERD-related in ~80% of patients receiving “continuous” treatment and in ~70% of patients receiving “on-demand” treatment.

Data presented in a review by Lehmann and Beglinger (2005) further support the idea that pantoprazole is safe and highly-effective in the treatment of gastroesophageal reflux disease (GERD) with or without esophagitis.  Lehmann and Beglinger highlighted results from a 4-week study in which pantoprazole (40 mg, daily) was significantly more effective than nizatidine (150 mg, b.i.d.) in reducing heartburn among patients with gastroesophageal reflux disease (GERD).

Authors noted that, after 7 days and 28 days, pantoprazole recipients exhibited 40% and 63% reductions in GERD-related heartburn – whereas nizatidine recipients exhibited 14% and 36% reductions in GERD-related heartburn.  Authors also referenced studies comparing pantoprazole (20 mg, daily) to ranitidine (150 mg, b.i.d.) in which GERD-related symptoms were reduced in pantoprazole users by 40%, 55%, 71%, and 77% – relative to 19%, 33%, 56%, and 59% in ranitidine users – at 4 weeks, 8 weeks, 6 months, and 1 year of treatment, respectively.

Caro et al. (2001) conducted a review to determine the efficacies of various proton-pump inhibitors for the acute and maintenance treatment of gastroesophageal reflux disease (GERD).  In this review, efficacies of proton-pump inhibitors were determined by healing and relapse rates of GERD following treatment.

Results of the review, indicated that pantoprazole exhibited similar efficacy as other proton-pump inhibitors (including omeprazole) in the acute treatment of gastroesophageal reflux disease (GERD) – as evidenced by analogous healing and relapse rates among patients with gastroesophageal reflux disease across proton-pump inhibitor treatments.  That said, researchers were unable to gather sufficient data to determine the efficacy of pantoprazole as a long-term maintenance therapy for gastroesophageal reflux disease.

Avner (2000) wrote a paper reflecting upon the usefulness of pantoprazole in the treatment of erosive esophagitis associated with gastroesophageal reflux disease (GERD) – and in the alleviation of GERD-related symptoms.  In the paper, Avner reflected upon the results of preexisting clinical studies in which pantoprazole (oral and intravenous) appeared more effective than H2 receptor antagonists in: reducing acid secretion, increasing gastric pH levels, and treating heartburn.

The paper also suggested that pantoprazole appears “at least as effective as” omeprazole in treating GERD-related symptoms such as regurgitation – and in healing GERD-related erosive esophagitis.  This is yet another paper suggesting that pantoprazole is likely effective for the direct treatment of gastroesophageal reflux disease (GERD).

Wurzer et al. (1999) organized an open-label study to evaluate the efficacy of pantoprazole in the treatment of moderate-to-severe (stage 2 or 3) gastroesophageal reflux disease (GERD).  For the study, a total of 110 individuals with endoscopy-diagnosed GERD were assigned to receive intravenous pantoprazole (40 mg/day) for 5 to 7 days – followed by oral pantoprazole tablets (40 mg/day) for up to 8 weeks.

Results of this open-label study indicated that pantoprazole treatment led to healing of GERD in: (1) 87% (85 of 98) and 95% (93 of 98) per-protocol patients after 4 and 8 weeks, respectively; and (2) 77% (85 of 110) and 85% (93 of 110) of intent-to-treat patients, respectively.  Within 2 weeks of pantoprazole treatment, GERD-related symptoms such as heartburn, acid regurgitation, and swallowing-related pain were completely resolved in nearly all per-protocol patients.

It was concluded that pantoprazole (intravenous or oral) leads to fast resolution of GERD symptoms and high healing rates.  Thought this was an open-label (uncontrolled) study, it supports the idea that pantoprazole is effective for the treatment of moderate-to-severe gastroesophageal reflux disease (GERD).

Verdict: Pantoprazole is likely as effective as Omeprazole for GERD

Although it is well-established that pantoprazole and omeprazole are efficacious in the treatment of erosive esophagitis (a condition associated with GERD), of these agents, only omeprazole is officially approved by the FDA as a direct treatment for GERD.  In fact, as of 2012, Pfizer settled a lawsuit for $55 million for illegal and/or off-label promotion of pantoprazole as a treatment for GERD (an indication for which pantoprazole lacks FDA approval).

Despite the $55 million settlement paid by Pfizer for the off-label promotion of pantoprazole to treat GERD, preliminary data suggests that pantoprazole is likely efficacious in the acute and long-term management of GERD.  As of current, all studies and reviews in which the efficacy of pantoprazole was assessed in the treatment of GERD are unanimous in suggesting that pantoprazole is effective in reducing symptoms of GERD.

Moreover, data suggests that pantoprazole is probably: (1) as effective as omeprazole (an FDA-approved intervention for GERD) and (2) more effective than H2 antagonists (that’ve received FDA-approval for the treatment of GERD) – in the treatment of GERD.  A meta-analysis by Dabrowski et al. (2018) based upon data from 3 phase IV trials (encompassing 252 patients with GERD) noted that pantoprazole (40 mg/day) is an effective treatment for GERD-related symptoms over a 4-week or 8-week span.

In the aforementioned meta-analysis, pantoprazole (40 mg/day) was effective for GERD patients (regardless of whether ERD or NERD) and led to significant improvements in quality of life.  Despite available studies suggesting that pantoprazole is effective for the treatment of GERD, most studies are of low-quality as a result of limitations such as: poor design (lack of: randomization, placebo-controlling, double-blinding); short-term duration; and/or small sample sizes.

Due to the aforementioned limitations associated with studies of pantoprazole for GERD, some might suggest that the data derived from these studies is too weak to justify the use of pantoprazole as a standalone, direct treatment for GERD.  Furthermore, because there are strong data to substantiate the usefulness of omeprazole in the treatment of GERD – some could argue that omeprazole would be a better treatment choice than pantoprazole for GERD (on the basis of its stronger evidence).

Nonetheless, because pantoprazole and omeprazole: (1) exhibit nearly identical mechanisms of action; (2) suppress stomach acid secretion to an equal extent at equipotent doses; and (3) are equally effective for the treatment of erosive esophagitis associated with GERD – there’s no reason to suspect that these agents differ in efficacy as acute therapies or long-term maintenance therapies in gastroesophageal reflux disease (GERD).

Duodenal ulcer & Gastric ulcer

Data from well-designed clinical trials supports the efficacy of omeprazole in the treatment of duodenal ulcers and gastric ulcers (two types of peptic ulcers, or sores on the inside of the stomach lining), hence its approval by the U.S. FDA for these conditions.  Because omeprazole has received official FDA-approval to treat duodenal ulcers and gastric ulcers and pantoprazole has not – some might argue that the former (omeprazole) would be a better treatment “selection” than the latter (pantoprazole) for these conditions.

That said, just because omeprazole has received FDA approval to treat duodenal ulcers and gastric ulcers does not automatically mean that it is more effective than pantoprazole (a medication lacking FDA approval) for these conditions.  Most studies that’ve evaluated the efficacy of pantoprazole in the treatment of duodenal and gastric ulcers suggest that it is an efficacious intervention.

Moreover, most experts believe that, when administered at equipotent doses, pantoprazole is as effective as omeprazole (and other proton-pump inhibitors) for the treatment of peptic ulcers (duodenal, gastric, gastroduodenal).  Included below are summaries of studies in which the efficacy of pantoprazole in the treatment of peptic ulcers was analyzed.

2017: Efficacy of proton pump inhibitors for patients with duodenal ulcers: A pairwise and network meta-analysis of randomized controlled trials.

Hu et al. conducted a meta-analysis to determine the respective efficacies of various proton-pump inhibitors (including pantoprazole and omeprazole) in the treatment of duodenal ulcers.  For the meta-analysis, Hu et al. gathered data from 24 randomized controlled trials (RCTs) encompassing 6,188 patients with duodenal ulcer – published before May 2016.

With the data collected from randomized controlled trials researchers ranked proton-pump inhibitors (PPIs) by probability of facilitating the best 4-week healing rate of duodenal ulcers.  Results indicated that, of all proton-pump inhibitor regimens compared, pantoprazole (40 mg/day) had the highest probability (36%) of facilitating the best duodenal ulcer healing rate after 4 weeks of treatment.

In comparison, omeprazole (40 mg/day) and omeprazole (20 mg/day) had respective probabilities of ~0% and ~5% of facilitating the best duodenal ulcer healing rates after 4 weeks of treatment.  The relative rankings of proton-pump inhibitor regimens for 4-week healing rates in the treatment of duodenal ulcers were: (1) pantoprazole 40 mg/day; (2) raberazole (20 mg/day); (3) lansoprazole (60 mg/day); (4) lansoprazole (30 mg/day); (5) ilaprazole (10 mg/day); (6) omeprazole (40 mg/day); (7) omeprazole (20 mg/day); (8) H2 receptor antagonists; (9) lansoprazole (15 mg/day).

Despite the fact that pantoprazole (40 mg/day) was associated with a higher probability of facilitating the best 4-week healing rate of all proton-pump inhibitor regimens, its healing rate was not significantly greater than the healing rates associated with omeprazole (40 mg/day or 20 mg/day) and other proton-pump inhibitor regimens – except lansoprazole (15 mg/day).  This meta-analysis not only supports the idea that pantoprazole is effective in the treatment of duodenal ulcers, but it suggests that pantoprazole (40 mg/day) may be [statistically] the best intervention.

2002: Are proton pump inhibitors the first choice for acute treatment of gastric ulcers? A meta-analysis of randomized clinical trials.

Salas et al. conducted a meta-analysis in which the efficacies of various proton-pump inhibitors (pantoprazole, omeprazole, rabeprazole, lansoprazole), an H2 receptor antagonist (ranitidine), and a placebo were compared for the treatment of gastric ulcers.  For the meta-analysis, Salas et al. gathered data from 16 randomized controlled trials (4 comparing a proton-pump inhibitor to a placebo, 9 comparing a proton-pump inhibitor to ranitidine, and 3 comparing a newer proton-pump inhibitor to omeprazole) – and compared healing rates associated with each intervention.

Data indicated that pantoprazole and other newer proton-pump inhibitors (rabeprazole and lansoprazole) led to greater resolution of pain (day pain and night pain) relative to omeprazole among patients with gastric ulcer.  Data further indicated that ranitidine (an H2 antagonist approved to treat duodenal ulcer) was associated with a significantly higher gastric ulcer healing rate (~52%) relative to a placebo (~39%) – and that proton-pump inhibitors (including pantoprazole and omeprazole) were associated with a significantly higher gastric ulcer healing rate (~67%) than ranitidine and the placebo.

Moreover, it was discovered that pantoprazole and lansoprazole were associated with superior 4-week gastric ulcer healing rates (by ~15%) in comparison to omeprazole.  After 2 and 4 weeks of treatment, pantoprazole (along with rabeprazole and lansoprazole) led to greater improvement in clinical symptoms of gastric ulcer – relative to omeprazole.

This meta-analysis supports the idea that pantoprazole is likely effective for the treatment of gastric ulcer.  Furthermore, most data indicate that pantoprazole is probably either “as effective” or “more effective” than omeprazole for the promotion of healing in gastric ulcer and management of symptoms resulting from gastric ulcer.

2000: Pantoprazole versus ranitidine in the treatment of duodenal ulcer: a multicenter study in Brazil.

Meneghelli et al. organized a double-blind study to compare the efficacy of pantoprazole to that of ranitidine (a medication approved by the FDA to treat gastric ulcer) – for the treatment of gastric ulcer.  For the study, a total of 222 patients with duodenal ulcers were assigned at random to receive either: 40 mg/day pantoprazole (111 patients) OR 300 mg/day ranitidine (111 patients).

Thereafter, patients underwent endoscopic assessments after 2 weeks and 4 weeks to determine gastric ulcer healing rates.  Results indicated that, among study completers: (1) 74.8% of pantoprazole users (77 of 103) and 44.7% (42 of 94) had ulcer healing after a 2-week treatment course; and (2) 22.3% (23 of 103) of pantoprazole users and 29.8% (28 of 94) of ranitidine users had ulcer healing after an additional 2-week treatment course.

In total, 97.1% (100 of 103) pantoprazole users and 74.5% (70 of 94) pantoprazole users exhibited ulcer healing throughout the entire 4-week study period.  Data indicated that pantoprazole was significantly more effective than ranitidine in the treatment of gastric ulcer after both the first treatment course (2 weeks) and second treatment course (4 weeks).

Researchers concluded that pantoprazole is more effective than ranitidine in the treatment of duodenal ulcer.  Because this was a well-designed trial (double-blinded, randomized) with a moderate-sized sample (222 participants) and demonstrated the superiority of pantoprazole over ranitidine (an FDA-approved treatment for duodenal ulcer) – it provides strong evidence to substantiate the usefulness of pantoprazole in duodenal ulcer.

2000: Efficacy of pantoprazole in the prevention of peptic ulcers, induced by non-steroidal anti-inflammatory drugs: a prospective, placebo-controlled, double-blind, parallel-group study.

Bianchi Porro et al. conducted a randomized, placebo-controlled, double-blind, parallel-group trial to evaluate the efficacy of pantoprazole in the prophylaxis of NSAID-induced peptic ulcers.  For the trial, 104 outpatients with rheumatoid arthritis who had chronically used NSAIDs for at least 8 weeks prior to trial initiation and developed NSAID-induced lesions (gastric and duodenal) – as confirmed via endoscopy – were assigned at random to receive either: 40 mg/day pantoprazole (70 patients) OR a placebo (34 patients) for a 12-week period.

Thereafter, outpatients underwent additional endoscopic assessment after 4 weeks and 12 weeks to determine the respective effects of pantoprazole and the placebo on ulceration.  Of the 95 patients who completed the trial (65 of 70 in the pantoprazole group – and 30 of 34 in the placebo group), the respective proportions of patients in remission from ulceration after 4 and 12 weeks were: 82% and 72% (pantoprazole recipients) versus 77% and 59% (placebo users).

Researchers noted that the difference in the incidence of ulceration between pantoprazole users and placebo users was even more substantial when accounting for patients with normal mucosa at baseline.  It was concluded that pantoprazole (40 mg/day) is more effective than a placebo in the prophylaxis of ulcers resulting from chronic administration of NSAIDs.

1995: Double-blind comparison of pantoprazole and omeprazole for the treatment of acute duodenal ulcer.

Beker et al. organized a double-blind, randomized trial to directly compare the effect of pantoprazole with omeprazole in the treatment of acute duodenal ulcer.  For the trial, a total of 270 patients with duodenal ulcer were assigned at random to receive either: 40 mg/day pantoprazole OR 20 mg/day omeprazole – for a 4-week duration.

Patients underwent endoscopic assessment at 2 weeks and 4 weeks to determine healing rates of duodenal ulcer in response to treatment.  Results indicated that complete ulcer healing occurred in 71% (88 of 124) pantoprazole recipients and 65% (85 of 131) omeprazole recipients – after 2 weeks of treatment.

The 4-week duodenal ulcer healing rates were: ~95% for pantoprazole recipients (118 of 124) and ~89% for omeprazole recipients (117 of 131).  There were no significant differences between pantoprazole and omeprazole in duodenal ulcer healing rates or in measures of ulcer pain at 2-weeks.

It was concluded that pantoprazole (40 mg/day) and omeprazole (20 mg/day) appear equally effective in the treatment of duodenal ulcer.  This trial provides additional data to support the usefulness of pantoprazole in the management of duodenal ulcer, a condition for which it is not officially indicated.

1995: Comparison of pantoprazole versus omeprazole in the treatment of acute duodenal ulceration–a multicentre study.

Rehner et al. sought to compare the efficacies of pantoprazole and omeprazole in the treatment of acute duodenal ulcer – and conducted a randomized, double-blind, multicenter trial.  For the trial, 276 patients with duodenal ulcer were assigned at random to receive either: 40 mg/day pantoprazole (185 patients) OR 20 mg/day omeprazole (91 patients) – for either 2 weeks or 4 weeks (depending on rate of ulcer healing).

Results of the trial indicated that 71% of pantoprazole recipients and 74% of omeprazole recipients exhibited complete duodenal ulcer healing after 2 weeks of treatment.  After 4 weeks of treatment, 96% of pantoprazole recipients and 91% of omeprazole recipients exhibited complete duodenal ulcer healing.

There were no clinically-relevant differences between pantoprazole and omeprazole in the rate of duodenal ulcer healing, nor were there clinically-relevant differences in ulcer-related pain reduction in response to treatment after 2 weeks.  It was concluded that pantoprazole appears to be equally effective to omeprazole for the treatment of duodenal ulcer.

1994: Long-term therapy with pantoprazole in patients with peptic ulceration resistant to extended high-dose ranitidine treatment.

Brunner and Harke reported that pantoprazole (40 to 80 mg, daily) led to healing of peptic ulcers within 2 to 8 weeks in 96.7% of 106 patients with treatment-resistant peptic ulceration (unresponsive to 3+ months of high-dose ranitidine).  An additional 2.3% of the 106 patients with treatment-resistant peptic ulceration exhibited healing of peptic ulcers within 12 weeks of pantoprazole treatment – and one patient required 6 months for ulceration to heal following pantoprazole treatment.

In the aftermath of ulcer healing, 98 patients received pantoprazole (40 mg/day) as a long-term therapy to prevent recurrence of peptic ulceration.  A total of 88 of 98 patients assigned to long-term pantoprazole therapy for prophylaxis of peptic ulcer recurrence had taken pantoprazole for 6 months to 3 years and achieved favorable results (peptic disease remained in remission for a majority of users).

A minority of patients (14 of 88) required higher doses of pantoprazole (80 to 120 mg, daily) for sufficient prophylaxis of gastric ulcers.  Nevertheless, this report supports the idea that pantoprazole effectively promotes healing from peptic ulcers and can be used as a long-term maintenance therapy (post-ulcer healing) as a peptic ulcer prophylactic.

1994: A review of treatment of duodenal and gastric ulcers–pantoprazole vs. omeprazole.

Schepp et al. published a report that reflected upon the efficacy of pantoprazole as an intervention for peptic (duodenal and gastric) ulcers relative to omeprazole, a medication that’s received FDA approval to treat these conditions.  In this report, it was noted that pantoprazole (40 mg/day) is effective and well-tolerated for peptic ulcers (duodenal and gastric).

The report also suggested that, based on available clinical data, pantoprazole (40 mg/day) is at least as effective as omeprazole (20 mg/day) for the treatment of duodenal and gastric ulcers.  Schepp et al. further mentioned that pantoprazole (40 mg/day) appears superior to omeprazole (20 mg/day) in the promotion of gastric ulcer healing (i.e. “healing rate”) at 4 weeks of treatment.

1992: Dose-range finding study with the proton pump inhibitor pantoprazole in acute duodenal ulcer patients.

Müller et al. (1992) organized one of the earliest trials in which the efficacy of pantoprazole was investigated in the treatment of duodenal ulcer.  The trial incorporated a randomized, double-blind design and assigned 219 patients with endoscopy-confirmed duodenal ulcer to receive one of 3 pantoprazole regimens: 20 mg/day, 40 mg/day, or 80 mg/day.

Complete ulcer healing after 2 weeks of pantoprazole treatment occurred in: 58% of the 20 mg/day users; 89% of the 40 mg/day users; and 82% of the 80 mg/day users – making the 40 mg/day dose significantly more effective (at 2 weeks) than the 20 mg/day dose.  After 4 weeks of pantoprazole treatment, complete ulcer healing occurred in: 93% of 20 mg/day users; 99% of 40 mg/day users; and 100% of 80 mg/day users.

Additionally, all pantoprazole users achieved rapid reduction in ulcer-related pain such that: 72% of 20 mg/day users; 89% of 40 mg/day users; and 84% of 80 mg/day users were pain-free after 2 weeks of treatment.  (The reduction of ulcer-related pain after 2 weeks of treatment was significantly greater among users of the 40 mg/day dose relative to users of the 20 mg/day dose).

Based on the results of this trial, researchers concluded that pantoprazole effectively promotes healing of acute duodenal ulcer and significantly reduces ulcer-related symptoms (e.g. pain).  This trial provides additional support for the idea that pantoprazole is an effective intervention for duodenal ulcer at a dose of 40 mg per day.

Verdict: Pantoprazole is at least as effective as Omeprazole for peptic ulcers (duodenal and gastric), possibly more effective

Although omeprazole is officially approved by the FDA as a treatment for peptic ulcers (duodenal and gastric) and pantoprazole is not, there’s no reason to suspect that omeprazole is more effective than pantoprazole as a treatment for peptic ulcers based on its FDA-approval (and lack thereof for pantoprazole).  Nearly all studies in which pantoprazole was evaluated as an acute or long-term treatment for peptic ulcers are unanimous in suggesting that it is an effective intervention.

In fact, some evidence from studies that indirectly or directly compared the efficacies of omeprazole and pantoprazole in the treatment of peptic ulcers indicate that pantoprazole might be more effective than omeprazole for the reversal of ulceration and/or attenuation of ulcer-related symptoms.  For example, a meta-analysis of 24 randomized controlled trials by Hu et al. (2017) ranked pantoprazole (40 mg/day) as the top intervention for duodenal ulcers over a 4-week period (based on its highest probability of having the best ulcer healing rate).

In comparison to top-ranked pantoprazole (40 mg/day), omeprazole ranked 6th (at 40 mg/day) and 7th (at 20 mg/day) of the 9 treatments compared for duodenal ulcers.  Although the meta-analysis did not suggest that pantoprazole was significantly more effective than omeprazole in the treatment of duodenal ulcers, it did indicate that pantoprazole appears to be [statistically] better than omeprazole (and other proton-pump inhibitors) for duodenal ulcer.

A meta-analysis of 16 randomized controlled trials by Salas et al. (2002) reported that pantoprazole is associated with a ~15% greater healing rate of gastric ulcers compared to omeprazole – after 4 weeks of treatment.  Pantoprazole was also associated with greater improvement in clinical symptoms of gastric ulcer (after 2 and 4 weeks of treatment) and resolution of ulcer-related pain (day and night) in comparison to omeprazole – supporting the idea that pantoprazole might be a superior intervention to omeprazole for gastric ulcer.

Additionally, the results of a double-blind, randomized trial by Beker et al. (1995) comparing pantoprazole to omeprazole for the treatment of acute duodenal ulcer in 270 patients suggested that the agents were equally effective in the promotion of ulcer healing and management of ulcer-related pain at 2 and 4 weeks.  That said, a modestly greater percentage of pantoprazole recipients exhibited ulcer healing at 2 and 4 weeks relative to omeprazole recipients.

A randomized, double-blind trial by Rehner et al. (1995) comparing pantoprazole to omeprazole in 276 patients with duodenal ulcer reported that the medications were equally effective in the promotion of duodenal ulcer healing and management of ulcer-related pain.  However, a report by Schepp et al. (1994) suggested that pantoprazole (40 mg/day): (1) is as effective as omeprazole (20 mg/day) in the treatment of duodenal and gastric ulcers and (2) appears more effective than omeprazole (20 mg/day) in the promotion of gastric ulcer healing at 4 weeks.

Other data to substantiate the efficacy of pantoprazole in the treatment of peptic ulcers can be derived from studies by Meneghelli et al. (2000), Bianchi Porro et al. (2000), Brunner and Harke (1994), and Müller et al. (1992).  In the 4-week, 222-participant, double-blind, randomized trial by Meneghelli et al. (2000), pantoprazole treatment was significantly more effective than ranitidine (a medication approved by the FDA to treat duodenal ulcer) in the treatment of gastric ulcer after 2 weeks and 4 weeks.

In the randomized, placebo-controlled, double-blind, trial by Bianchi Porro et al. (2000), pantoprazole was significantly more effective than a placebo in the treatment gastric and duodenal ulcers (resulting from chronic NSAID use) – as evidenced by ulcer healing and remission rates over 12 weeks.  Furthermore, in the study by Brunner and Harke (1994) it was noted that pantoprazole effectively reversed ranitidine-resistant peptic ulcers over 2 to 8 weeks (with a 96% heal rate) and could be used over a long-term to prevent ulcer recurrence.

The 219-patient study by Müller et al. (1992) noted that pantoprazole effectively treated duodenal ulcer at a doses of 40 mg and up.  Although omeprazole is officially indicated to treat peptic (duodenal and gastric) ulcers and pantoprazole is not – there are strong data from multiple meta-analyses and well-designed trials (randomized, double-blind, etc.) to suggest that pantoprazole is at least as effective as omeprazole for these conditions.

Moreover, there are some data to suggest that pantoprazole (40 mg/day) may be modestly or significantly more effective than omeprazole (20 mg/day or 40 mg/day) in the promotion of peptic ulcer healing and/or management of peptic ulcer-related symptoms.  Although experts and most data suggest that there are unlikely clinically-significant differences in the efficacies of pantoprazole and omeprazole in the treatment of peptic ulcers (duodenal and gastric) when administered at equipotent-doses, there are trends indicating that pantoprazole (40 mg, daily) could be modestly superior to omeprazole (20 mg, daily) for these conditions.

H. Pylori infection (with antibiotics)

There are strong data from clinical trials to support the effectiveness of omeprazole in combination with multiple antibiotics as part of a “triple therapy” for the treatment of H. Pylori infection – hence its approval by the FDA for this condition.  Since omeprazole is formally approved by the FDA to treat H. Pylori (with antibiotics) and pantoprazole is not, some could argue that omeprazole is a superior treatment “choice” over pantoprazole for this condition.

Nonetheless, although omeprazole is formally approved to treat H. Pylori infection does not mean that it is automatically more effective than pantoprazole (a similar medication devoid of FDA approval) for this condition.  In fact, nearly all studies that’ve examined the efficacy of pantoprazole in the treatment of H. Pylori infection suggest that it is highly effective.

Additionally, most medical doctors believe that, if administered at equipotent dosages, the respective efficacies of omeprazole and pantoprazole in the treatment of H. Pylori infection (in conjunction with antibiotics) are unlikely to significantly differ.  Below is a review and meta-analysis in which the effectiveness of pantoprazole in H. Pylori infection was assessed.

2004: Pantoprazole based therapies in Helicobacter pylori eradication: a systematic review and meta-analysis.

Gisbert et al. conducted a systematic review and meta-analysis to elucidate the efficacy of pantoprazole in the eradication of H. Pylori infection when administered with antibiotics.  The systematic review and meta-analysis incorporated data from 12 randomized controlled trials (RCTs) in which pantoprazole was compared to other proton-pump inhibitors (PPIs) – encompassing 534 users of pantoprazole and 603 users of other proton-pump inhibitors.

Results of the meta-analysis indicated that the average rate of H. Pylori eradication among users of pantoprazole plus clarithromycin for 14 days was 60%.  Cure rates associated with 7-day pantoprazole-based “triple therapies” were: (1) 78% for pantoprazole plus amoxicillin and clarithromycin; (2) 84% for pantoprazole plus clarithromycin and nitroimidazole; and (3) 74% for pantoprazole plus amoxicillin and nitroimidazole.

Moreover, the rate of H. Pylori eradication associated with pantoprazole plus antibiotics was 83% – whereas the rate of H. Pylori eradication associated with other proton-pump inhibitors plus antibiotics was 81%.  Gisbert et al. performed sub-analyses in which pantoprazole was directly compared to omeprazole (and other individual proton-pump inhibitors), however, no significant differences were discovered between these agents in efficacy for the treatment of H. Pylori infection.

It was concluded that pantoprazole eradicates H. Pylori infection at a similar rate to omeprazole when co-administered with antibiotics.  This review and meta-analysis provides strong data to support the use of pantoprazole (in conjunction with antibiotics) in the treatment of H. Pylori infection – and indicates that its efficacy does not differ from omeprazole (an FDA-approved agent) for this condition.

Verdict: Pantoprazole and Omeprazole are likely equally effective in H. Pylori infection

As was noted, of pantoprazole and omeprazole, only omeprazole is officially approved by the FDA for the treatment of H. Pylori infection in combination with antibiotics.  That said, a systematic review and meta-analysis conducted by Gisbert et al. (2004) suggests that pantoprazole is highly-effective in the treatment of H. Pylori infection when administered with antibiotics.

The aforementioned review and meta-analysis by Gisbert et al. (2004) incorporated data from 12 randomized controlled trials in which the efficacy of pantoprazole was tested in 534 persons with H. Pylori infection – and compared to other proton-pump inhibitors (including omeprazole) in 603 persons with H. Pylori infection.  When pantoprazole was co-administered with one antibiotic (amoxicillin) as a “double therapy,” the 14-day H. Pylori cure rate was 60%.

When pantoprazole was co-administered with 2 antibiotics as part of a “triple therapy,” 7-day cure rates were: 84% (pantoprazole with clarithromycin and nitroimidazole), 78% (pantoprazole with amoxicillin and clarithromycin), and 74% (pantoprazole with amoxicillin and nitroimidazole) – supporting the idea that pantoprazole helps eradicate H. Pylori with antibiotics.  The average rate of H. Pylori eradication associated with pantoprazole-based therapies was 83% – whereas the pooled-average rate of H. Pylori eradication associated with other proton-pump inhibitors was 81%.

Within the meta-analysis, researchers performed a sub-analysis that directly compared the respective efficacies of pantoprazole-based therapies to omeprazole-based therapies in the treatment of H. Pylori infection – and zero clinically-relevant differences were found.  Based on the data presented in this meta-analysis, it seems as though pantoprazole and omeprazole are equally effective in the treatment of H. Pylori infection.

A review by Klok et al. (2003) stated that there were no significant differences in efficacy between: (1) 40 mg/day pantoprazole vs. 40 mg/day omeprazole (2 trials, 213 participants); and (2) 80 mg/day pantoprazole vs. 40 mg/day omeprazole (2 trials, 349 participants) – in H. Pylori infection.  Both pantoprazole doses (40 mg/day and 80 mg/day) were as effective as omeprazole (40 mg/day) in the eradication of H. Pylori.

Though some researchers like Dattilo and Figura (1998) have suggested that pantoprazole exhibits a lower magnitude of “in vitro” antibacterial activity against H. Pylori compared to omeprazole [and lansoprazole] – there are zero data from controlled trials indicating that pantoprazole-based therapies are somehow ineffective or markedly less effective than omeprazole-based therapies in H. Pylori infection.  For this reason, most experts believe that, if administered at equipotent doses, pantoprazole-based therapies and omeprazole-based therapies exhibit clinically-equivalent efficacy in the eradication of H. Pylori infection.

Do pantoprazole and omeprazole differ in efficacy for any medical condition?

Most evidence suggests that pantoprazole and omeprazole exhibit clinically-equivalent efficacies when administered at equipotent doses, however, some evidence suggests that pantoprazole may be modestly more effective than omeprazole in certain medical conditions.  According to meta-analysis by Klok et al. (2003), pantoprazole and omeprazole exhibit equal efficacy in the treatment of gastroesophageal reflux disease (GERD) and H. Pylori (in combination with antibiotics).

  • Gastroesophageal reflux disease: Equal efficacy
  • Pylori infection: Equal efficacy
  • Peptic ulcers: Pantoprazole modestly superior to omeprazole
  • Healing in erosive esophagitis: Pantoprazole modestly superior to omeprazole
  • Stomach acid hypersecretory conditions: Equal efficacy

However, the meta-analysis by Klok et al. (2003) also reported that pantoprazole (40 mg/day) is modestly superior to omeprazole (20 mg/day) in the treatment of peptic ulcers (duodenal and gastric).  There are also data from a meta-analysis by Li et al. (2017) to suggest that pantoprazole (40 mg/day) might be more effective than omeprazole (20 mg/day) in the promotion of healing and management of symptoms in erosive esophagitis.

In stomach acid hypersecretory conditions like Zollinger-Ellison syndrome, there don’t appear to be any clinically-significant differences in therapeutic efficacy between flexibly-dosed pantoprazole and flexibly-dosed omeprazole.  Despite reported disparities in efficacy between pantoprazole and omeprazole for certain medical conditions (e.g. peptic ulcers and healing maintenance in erosive esophagitis), it remains unclear as to whether these disparities legitimately reflect differences in actual [real-world] response rates.

As has been mentioned, it’s possible that 40 mg pantoprazole is more potent than 20 mg omeprazole – such that superior treatment outcomes should be expected with the former (40 mg pantoprazole) relative to the latter (20 mg omeprazole) in clinical trials.  However, if controlling for differences in potency of dose (such as by administering equipotent doses), most gastroenterologists and medical doctors believe that pantoprazole and omeprazole are equally effective – regardless of the medical condition for which they’re administered.

In other words, assuming pantoprazole and omeprazole are administered at flexible or equipotent doses, these agents are unlikely to significantly differ in: (1) magnitude of stomach acid reduction; (2) degree of therapeutically-relevant symptom control; and (3) average rate of disease remission – over the short-term and/or long-term.  That said, if attempting to decide between 40 mg/day pantoprazole and 20 mg/day omeprazole, current evidence indicates that pantoprazole (40 mg/day) is a superior option to the latter (20 mg/day) in peptic ulcers and erosive esophagitis.

Mechanism of action

The primary mechanism for pantoprazole is identical to that of omeprazole: both agents function predominantly as selective and irreversible inhibitors of H+/K+-ATPase enzymes (referred to as “proton pumps”) located upon the surface of gastric parietal cells.  Specifically, pantoprazole and omeprazole are absorbed within the proximal small bowel and, post-absorption, these agents accumulate within the acidic-secreting canaliculi (small channels lined by microvilli, or tiny surface-level cellular projections, which penetrate all parts of the cytoplasm and expand in surface area during acid secretion).

After accumulating within canaliculi, pantoprazole and omeprazole are subject to acid-mediated cleavage of a chiral sulfoxide bond into active sulfenic acid and/or sulfonamide.  It is the aforementioned sulfenic acid and/or sulfonamide compounds that covalently bind to cysteine residues on H+/K+-ATPase enzymes to suppress acid secretion until replacement pumps can be synthesized, a process which can take up to 36 hours.

In other words, because H+/K+-ATPase enzymes act as acid pumps within the gastric mucosa (mucous membrane layer of the stomach), their inhibition [by pantoprazole or omeprazole] interferes with the final step of endogenous stomach acid production.  Interference with the final step of endogenous stomach acid production [predictably] leads individuals to exhibit lower concentrations of stomach acid during treatment with pantoprazole or omeprazole (relative to pre-proton-pump inhibitor administration).

Though there are subtle disparities in the respective chemical structures of pantoprazole and omeprazole (e.g. pyridine and/or benzimidazole rings), their pharmacological profiles are extremely similar.  Moreover, the magnitude of H+/K+-ATPase inhibition and corresponding degree of stomach acid reduction is generally contingent upon the potency of proton-pump inhibitor (PPI) dosing and its metabolism.

Assuming that: (1) pantoprazole and omeprazole are administered at equipotent doses and (2) there are no abnormalities in their respective metabolisms (such as might occur with genetically-mediated CYP450 polymorphisms) – the agents shouldn’t differ much in magnitude of proton-pump inhibition and therapeutic efficacy.  Research suggests that the onset of proton-pump inhibiting action associated with pantoprazole and omeprazole occurs within less than 1 hour, peaks within 2 hours, and the therapeutic effect plateaus within 4 days of administration.

In addition to the primary mechanism of action associated with both pantoprazole and omeprazole (inhibition of H+/K+-ATPase), both agents facilitate modest antibacterial effects against bacterial species like Helicobacter Pylori (H. Pylori).  As of current, it’s unclear as to whether there are any legitimate, clinically-relevant differences between pantoprazole and omeprazole in magnitude of antibacterial action.

Research by Datillo and Figura (1998) indicates that pantoprazole exhibits a lower magnitude of antibacterial action than omeprazole against H. Pylori when administered “in-vitro.”  Although it’s possible that pantoprazole facilitates a lower magnitude of antibacterial action than omeprazole against H. Pylori, additional bacteria, and/or all bacteria – no data from randomized controlled human trials support the idea that pantoprazole-based therapies are significantly less efficacious than omeprazole-based therapies in the treatment of H. Pylori.  For this reason, it’s difficult to know whether the “in-vitro” research referenced by Datillo and Figura (1998) is accurate and/or applies to whole living organisms (e.g. humans).

In summary, both pantoprazole and omeprazole function primarily via directly blocking H+/K+-ATPase (the final common pathway of acid secretion) in response to any parietal cell stimulation (e.g. gastrin, histamine, acetylcholine) – and elevate intragastric pH above 4 for a majority of the day (between 15 and 21 hours).  If controlling for potency of dosing and hepatic metabolism (e.g. genetic polymorphisms that would alter metabolism), the: (1) magnitude of proton-pump (H+/K+-ATPase) inhibition, (2) stomach acid reduction, and (3) therapeutic efficacy – shouldn’t be significantly different between pantoprazole and omeprazole.

Metabolism & Half-Life

Data from pharmacokinetic studies suggest that pantoprazole and omeprazole exhibit similar [albeit slightly different] routes of metabolism, yet different bioavailabilities and elimination half-lives.  Both pantoprazole and omeprazole are metabolized in the liver via CYP2C19 (cytochrome P450 2C19) enzymes.

Additionally, both pantoprazole and omeprazole undergo additional metabolism in the liver by CYP3A4 enzymes.  That said, there are noteworthy differences in the respective metabolisms of pantoprazole and omeprazole, including: (1) involvement of CYP2C9 in the metabolism of pantoprazole (but not omeprazole); (2) greater involvement of CYP3A4 in the metabolism of pantoprazole relative to omeprazole; (3) involvement of cytosolic sulfotransferase in the conjugation of pantoprazole (but not omeprazole); and (4) possible involvement of CYP1A2 in the metabolism of omeprazole (but not pantoprazole).

In other words, pantoprazole undergoes metabolism via CYP2C19, CYP2C9, and CYP3A4 enzymes plus conjugation via cytosolic transferase – whereas omeprazole undergoes metabolism primarily via CYP2C19 and, to a lesser extent, CYP3A4 [and possibly CYP1A2] enzymes.  The metabolism of pantoprazole leads to the formation of the biologically-inactive metabolite “hydroxypantoprazole” via CYP2C19.

The metabolism of omeprazole leads to the formation of 5-hydroxyomeprazole (OH-OPZ) via CYP2C19, omeprazole sulfone (OPZ-SFN) via CYP3A4, and hydroxyomeprazole sulfone.  In addition to differences between pantoprazole and omeprazole in metabolism specifics and metabolite formation, these agents exhibit disparities in oral bioavailability.

Research by Huber et al. (1996) indicates that the bioavailability of pantoprazole is ~77% regardless of whether administered in an acute single-dose or in multiple doses over a longer-term.  Research by Mostafavi and Tavakoli (2004) indicates that the oral bioavailability of omeprazole ranges from 40% to 50%, however, other studies suggest that the oral bioavailability of omeprazole ranges from 30% to 50%.

The elimination half-life of pantoprazole ranges from 0.9 to 1.9 hours – whereas the elimination half-life of omeprazole ranges from 0.5 to 2 hours.  This means that it’ll take between 4.95 and 10.45 hours to eliminate pantoprazole from systemic circulation and between 2.75 and 11 hours to eliminate omeprazole from systemic circulation – following cessation.

According to Meyer (1996) and Jungnickel (2000), because pantoprazole is the only proton-pump inhibitor to undergo metabolism via cytosolic sulfotransferase, pantoprazole use is associated with: (1) lower risk of pharmacokinetically-mediated interactions and (2) greater efficacy relative to other proton-pump inhibitors in populations with atypical CYP450 enzyme expression (wherein plasma concentrations of certain proton-pump inhibitors, including omeprazole, could be reduced due to reliance on CYP450 metabolism).

Since omeprazole is metabolized primarily by CYP2C19 and most affected by CYP2C19 polymorphisms of all proton-pump inhibitors, omeprazole is more likely than pantoprazole to: (1) provoke interaction effects (if administered with other substances) and/or (2) prove ineffective in certain populations with abnormal CYP2C19 expression.  In sum, the pharmacokinetics of pantoprazole should be considered superior to the pharmacokinetics of omeprazole based on bioavailability (higher for pantoprazole) and metabolism (less likely to cause problems in persons with CYP2C19 polymorphisms).

Popularity

In the U.S., pantoprazole (Protonix) was approved for medical use in 2000 – whereas omeprazole (Prilosec) was approved for medical use in 1989 as the very first proton-pump inhibitor (~11 years prior to pantoprazole).  If comparing the respective historical popularities of pantoprazole and omeprazole, the former (pantoprazole) has been substantially less popular than the latter (omeprazole).

Not only is omeprazole is the first proton-pump inhibitor synthesized to be synthesized (1979) and receive approval for medical use in the U.S., it is probably: (1) the most popular proton-pump inhibitor (PPI) medication to present date and (2) one of the most widely-utilized prescription and non-prescription (over-the-counter) medications of all time – the same cannot be said for pantoprazole.  Moreover, it seems as though pantoprazole remains significantly less popular than omeprazole as of current.

According to the most recent report from ClinCalc DrugStats Database, over 71.7 million prescriptions were filled for omeprazole in 2015 and over 24.7 million prescriptions were filled for pantoprazole in 2015 – within the United States.  Specifically, omeprazole ranked in as the 6th most-prescribed prescription medication in 2015 and pantoprazole ranked in as the 29th most-prescribed prescription medication in 2015 – within the United States.

This means that over 47 million more prescriptions were filled for omeprazole relative to pantoprazole in the U.S. throughout 2015, a discrepancy which might be surprising given that: (1) omeprazole is available over-the-counter (and number of prescriptions would likely be significantly higher if it wasn’t) and (2) both agents are available as low cost generics.  So what variables might account for the substantial difference between pantoprazole and omeprazole in popularity?

Reasons omeprazole is significantly more popular than pantoprazole might include: (1) its greater number of FDA-authorized indications (6 vs. 3); (2) its release ~11 years prior to omeprazole (possibly resulting in accumulation of a larger user-base over time); and/or (3) its availability over-the-counter (saving consumers on costs associated with doctor visits).

Reasons the popularity of pantoprazole might increase in forthcoming years might include: (1) research suggests that pantoprazole is as effective as omeprazole OR modestly more effective than omeprazole in nearly every medical condition for which the agents are compared; (2) pantoprazole is less likely than omeprazole to cause interaction effects; (3) pantoprazole is more likely to prove effective regardless of user genetics (whereas omeprazole can be ineffective with CYP2C19 polymorphisms); (4) its user-base might continue growing; and/or (5) it may eventually receive approval for over-the-counter use.

Side effects & Tolerability

According to FDA Access reports, the most common side effects for pantoprazole (Protonix), occurring in over 2% of adult users, include: headache, diarrhea, nausea, abdominal pain, vomiting, flatulence, dizziness, and arthralgia (joint pain).  According to FDA Access reports, the most common side effects for omeprazole (Prilosec), occurring in over 2% of adult users, include: headache, abdominal pain, nausea, diarrhea, vomiting, and flatulence.

Assuming data presented in FDA Access reports accurately reflect the respective “most common side effects” of pantoprazole (Protonix) and omeprazole (Prilosec), it seems as though both agents cause similar common side effects, including: headache, diarrhea, nausea, abdominal pain, diarrhea, vomiting, and flatulence.  However, according to FDA Access Data, it seems as though pantoprazole may cause 2 common side effects that omeprazole does not, including dizziness and arthralgia.

That said, it’s possible that the greater number of common side effects reported in FDA Access Data for pantoprazole relative to omeprazole do not accurately reflect significant differences in common side effects between these agents.  Furthermore, although the magnitudes and specific occurrence rates of side effects might slightly vary between pantoprazole users and omeprazole users – the differences haven’t been fully elucidated.

Based on available research, are there any significant differences between pantoprazole and omeprazole in tolerability?  A meta-analysis by Li et al. (2017) in which various proton-pump inhibitor regimens were evaluated in the treatment of erosive esophagitis over an 8-week period reported that there were no clinically-significant differences between pantoprazole (40 mg/day) and omeprazole (20 mg/day) in acceptability (i.e. “dropout rate”).

That said, the aforementioned meta-analysis indicated that pantoprazole (40 mg/day) was associated with the highest cumulative probability of acceptability (85.2%) and omeprazole (20 mg/day) was associated with the second-highest cumulative probability of acceptability (74.3%) of the 8 interventions (7 proton-pump inhibitors, 1 placebo).  Although pantoprazole (40 mg/day) was associated with a higher probability of acceptability (by ~10.9%) relative to omeprazole (20 mg/day), this difference wasn’t clinically-significant.

A different meta-analysis by Zhang et al. (2017) in which various proton-pump inhibitor regimens were assessed in the treatment of gastroesophageal reflux disease (GERD) over 4 to 8 weeks, there were no clinically-significant differences between these agents (including pantoprazole and omeprazole) in tolerability.  Tolerability rankings of pantoprazole and omeprazole regimens, in order from most to least tolerable, were as follows: omeprazole (40 mg/day); pantoprazole (40 mg/day); omeprazole (20 mg/day); pantoprazole (10-20 mg/day); omeprazole (10 mg/day).

In theory, it makes sense that pantoprazole (40 mg/day) would be modestly more tolerable (on average) than omeprazole (20 mg/day), especially among: (1) persons with genetically-mediated CYP2C19 polymorphisms that yield atypical CYP2C19 expression and/or (2) persons who use substances with their proton-pump inhibitor.  Because pantoprazole is metabolized by a variety of enzymes, this decreases odds that users will end up with atypical serum concentrations of the drug and, thereafter, experience adverse effects.

In comparison, omeprazole is metabolized mostly by CYP2C19 enzymes.  Reliance on CYP2C19 enzymes for its metabolism increases odds that select users (e.g. persons with preexisting CYP2C19 polymorphisms) will exhibit atypical serum concentrations of the medication and, as a result, experience adverse effects [some of which might impair quality-of-life and/or warrant treatment discontinuation].

Finally, based on available data, there are zero clinically-significant differences between FDA-recommended doses of pantoprazole (40 mg/day) and omeprazole (20 mg/day) in tolerability.  However, if considering the respective ways in which each agent is metabolized AND acceptability/tolerability trends [slightly] from meta-analyses, it seems as though pantoprazole (40 mg/day) might exhibit negligibly better tolerability than omeprazole (20 mg/day).

Because pantoprazole and omeprazole are both: (1) medications of the benzimidazole class; (2) exhibit identical primary mechanisms of action; and (3) facilitate similar magnitudes of stomach acid suppression (when administered at equipotent doses), these agents are unlikely to significantly differ in their respective pharmacodynamically-mediated side effects.  If there are differences between these agents in the occurrence rates and/or magnitudes of side effects – these differences might be attributable to [subtle] disparities in: (1) chemical structure; (2) metabolism; (3) secondary actions; (4) mode of administration; (5) chemical packaging (e.g. pairing with sodium bicarbonate vs. magnesium).

Withdrawal (?)

The concept of proton-pump inhibitor (PPI) “withdrawal” is relatively controversial among medical professionals, researchers, and gastroenterologists.  Some claim that physiologic reactions reported following cessation of proton-pump inhibitor therapy are merely a return of symptoms associated with preexisting medical conditions (e.g. gastroesophageal reflux disease) – whereas others suggest that these reactions (or a percentage of these reactions) are attributable to a legitimate medication-related withdrawal syndrome.

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Evidence from studies in which healthy volunteers (devoid of medical conditions like gastroesophageal reflux disease) are assigned to receive proton-pump inhibitors suggests that stomach acid hypersecretion occurs in the aftermath of treatment – such that there’s a compensatory physiologic reaction to the therapy that lingers following its discontinuation.  In the aftermath of pantoprazole or omeprazole discontinuation, the most commonly-reported withdrawal symptoms include: heartburn (45%); indigestion or dyspepsia (30%); and acid regurgitation (25%).

Additional withdrawal symptoms resulting from cessation of proton-pump inhibitors [as reported by former users] include: appetite changes; stomach aches; constipation or diarrhea; nausea and/or vomiting; and neuropsychiatric symptoms (e.g. anxiety, cognitive dysfunction, depression, insomnia, irritability, etc.).  What causes withdrawal symptoms from pantoprazole and omeprazole?

When a person uses pantoprazole or omeprazole for an extended duration (e.g. weeks, months, etc.), it’s likely that his/her physiology undergoes adaptation in response to treatment, such that: molecular signaling cascades, enzyme activation, endogenous production of gastric acid, etc. – get shifted away from homeostasis.  In the event that a moderate-term or long-term user of either pantoprazole or omeprazole discontinues treatment, his/her physiology may remain in a medication-adapted state for a period of time after treatment cessation.

Since the body remains in a proton-pump inhibitor-adapted state [following withdrawal] but is no longer receiving a proton-pump inhibitor, various treatment-related physiologic adaptations (or compensatory responses) become noticeable.  The most commonly-proposed physiologic adaptation to proton-pump inhibitor therapy that may linger post-treatment is upregulation of endogenous stomach acid production – thus explaining noticeable “rebound acid hypersecretion” in healthy volunteers following proton-pump inhibitor cessation.

Once the former proton-pump inhibitor (pantoprazole or omeprazole) user has remained medication-free for a sufficient duration, his/her physiology will have readjusted from proton-pump inhibitor-adapted – to pre-treatment homeostasis.  Once physiology has fully returned to homeostasis (from proton-pump inhibitor-adapted), withdrawal symptoms should cease.

Because pantoprazole and omeprazole do not significantly differ in (1) mechanism of action or (2) elimination half-life, these agents are unlikely to differ in withdrawal: onset; symptoms (specifics, severities, etc.); difficulty; and/or duration.  Withdrawal symptoms from pantoprazole and omeprazole will likely be most noticeable in long-term, high-dose users who refrain from using substances to control stomach acid production after proton-pump inhibitor cessation.

Similarities: Pantoprazole vs. Omeprazole (Summary)

Included below is a brief summary of general similarities between pantoprazole (Protonix) and omeprazole (Prilosec).  Ways in which pantoprazole and omeprazole are similar include: average cost; duration of effect; effectiveness (in most medical conditions); elimination half-life; mechanism of action; medical uses; onset of action; side effects; and withdrawal.

  • Average cost: Although brand name Protonix (pantoprazole) is significantly more expensive than brand name Prilosec (omeprazole), there’s no significant difference in the cost of generic pantoprazole and generic omeprazole. Generic versions of pantoprazole and omeprazole generally retail within the price range of $6 to $30 for a 30-day supply.
  • Drug classification: Both pantoprazole and omeprazole are chemically classified as “benzimidazoles.” This classification is based upon the fact that the respective chemical structures of pantoprazole and omeprazole contain a combination of benzimidazole rings and pyridine rings.
  • Duration of effect: There’s no significant difference in the respective durations of action for pantoprazole and omeprazole. Both medications require once-per-day administration, suggesting that each agent suppresses stomach acid secretion for up to ~24 hours.  Moreover, research indicates that pantoprazole and omeprazole can remain active for up to ~72 hours post-administration.
  • Efficacy: When administered at equipotent doses, most gastroenterologists and general care physicians regard pantoprazole and omeprazole as being equally efficacious interventions for medical conditions in which therapeutic effects are derived from suppressing stomach acid. Specific medical conditions for which these agents appear equally effective include: gastroesophageal reflux disease (GERD); stomach acid hypersecretory conditions (e.g. Zollinger-Ellison syndrome); and H. Pylori infection (with antibiotics).
  • Elimination half-life: The elimination half-life for pantoprazole is extremely similar to the elimination half-life for omeprazole. Pharmacokinetic research indicates that pantoprazole has an elimination half-life ranging from 9 to 1.9 hours – and omeprazole has an elimination half-life ranging from 0.5 to 2 hours.  In other words, both medications are eliminated from the body rapidly (usually less than 11 hours) after administration.
  • Formatting options: There aren’t any substantial differences in the respective formatting options for pantoprazole and omeprazole. Pantoprazole is available in delayed-release pills, injectable solution, and an oral suspension can be created if medically necessary.  Omeprazole is available in delayed-release pills, injectable solution, and oral suspension.
  • Medical uses: There are no significant differences in the respective medical uses of pantoprazole and omeprazole. Both agents are proton-pump inhibitors with similar mechanisms of action that are regarded as equally efficacious in blocking the secretion of stomach acid.  Predictably, both pantoprazole and omeprazole are utilized in the treatment of: erosive esophagitis; gastroesophageal reflux disease (GERD); stomach acid hypersecretion conditions (e.g. Zollinger-Ellison syndrome); H. Pylori infection (as part of “triple therapy”); peptic ulcers (duodenal, gastric, gastroduodenal); and stress ulcers.
  • Mechanism of action: The primary mechanisms of action exhibited by pantoprazole and omeprazole are identical. Both pantoprazole and omeprazole function as inhibitors of the H+/K+-ATPase enzyme on the surface of gastric parietal cells.  Since the H+/K+-ATPase enzyme is needed for final step of stomach acid production, H+/K+-ATPase inhibition prevents stomach acid secretion and inevitably decreases stomach acid levels.
  • Onset of action: The respective onsets of action for pantoprazole and omeprazole are nearly identical. Both medications take effect in less than 1 hour – and their effects peak within 2 hours of administration.  The respective peak onsets of therapeutic effects associated with pantoprazole and omeprazole occur within 4 days of regular administration.
  • Side effects: Evidence from clinical trials suggests that pantoprazole and omeprazole induce similar side effects and adverse reactions. According to FDA Access Data, common side effects (occurring in over 2% of adult users) shared by pantoprazole and omeprazole include: headache, diarrhea, nausea, abdominal pain, diarrhea, vomiting, and flatulence.
  • Tolerability: Data from multiple meta-analyses indicate that pantoprazole and omeprazole are among the most tolerable proton-pump inhibitors on the market. Although data indicate that pantoprazole might be modestly or negligibly more tolerable than omeprazole (on average), the difference between these agents in tolerability is not clinically-relevant.
  • Withdrawal: Research suggests that proton-pump inhibitors might cause rebound acid hypersecretion and other “withdrawal symptoms” in the aftermath of their discontinuation. Although the idea of proton-pump inhibitor withdrawal is controversial, if a withdrawal legitimately occurs, its severity and duration is unlikely to significantly differ between pantoprazole and omeprazole.

Differences: Pantoprazole vs. Omeprazole (Summary)

Included below is a brief summary of general differences between pantoprazole (Protonix) and omeprazole (Prilosec).  Ways in which pantoprazole and omeprazole differ include: bioavailability; development and release date; dosing increments; FDA-authorized uses; legal status; metabolism; over-the-counter availability; and popularity.

  • Bioavailability: There are substantial differences in the respective bioavailabilities of pantoprazole and omeprazole. Orally-administered pantoprazole exhibits a bioavailability of ~77% regardless of dosing whereas omeprazole exhibits a bioavailability that ranges from ~30% to ~50%.  This means that a greater percentage of ingested pantoprazole (27% to 47%) exerts a physiologic effect in comparison to omeprazole.
  • Development & release date: The development and release date associated with pantoprazole differs from that of omeprazole.  Pantoprazole was engineered by chemists at the pharmaceutical company Byk Gulden in Germany in 1985 – and approved for medical use within the U.S. in 2000.  Omeprazole was engineered by Swedish chemists at the pharmaceutical company AstraZeneca in 1979 – and approved for medical use within the U.S. in 1989.
  • Dosing increments: The standard (orally-administered) pill version of pantoprazole is manufactured in 2 dosing increments (20 mg and 40 mg) – whereas the standard (orally-administered) capsule version of omeprazole is manufactured in 3 dosing increments (10 mg, 20 mg, and 40 mg).
  • FDA-authorized uses: It is known that pantoprazole and omeprazole are both approved by the U.S. FDA for healing maintenance in erosive esophagitis and management of pathological stomach acid hypersecretion conditions (e.g. Zollinger-Ellison syndrome), however, additional FDA-authorized indications for these agents differ. Unlike omeprazole, pantoprazole is FDA-approved to directly treat erosive esophagitis associated with gastroesophageal reflux disease (GERD).  Unlike pantoprazole, omeprazole is FDA-approved to treat duodenal ulcer, gastric ulcer, H. Pylori infection (with antibiotics), and gastroesophageal reflux disease (GERD).
  • Ingredients: The active chemical ingredient within the “brand name” medication Protonix is “pantoprazole” – whereas the active chemical ingredient within the “brand name” medication Prilosec is “omeprazole.” Omeprazole is usually paired with magnesium (delayed-release) or sodium bicarbonate (immediate-release) and pantoprazole is usually paired with sodium (delayed-release) but is sometimes paired with magnesium.
  • Legal status (U.S.): In the United States, pantoprazole is legally classified as a “prescription-only” (Rx-only) medication – whereas omeprazole is legally classified as an “over-the-counter” (OTC) medication. This means that pantoprazole can only be legally attained from a pharmacy with a valid prescription written by a licensed medical doctor – whereas omeprazole can be attained “over-the-counter” in stores or online without a prescription.
  • Metabolism: Although pantoprazole and omeprazole are both metabolized primarily by the hepatic enzyme CYP2C19, there are disparities in secondary pathways of metabolism for these agents. Pantoprazole is hepatically metabolized by enzymes CYP2C19, CYP2C9, CYP3A4 – and conjugated by the enzyme cytosolic sulfotransferase.  Omeprazole is hepatically metabolized by enzymes CYP2C19, CYP3A4 (to a lesser extent than pantoprazole), and possibly CYP1A2.
  • Over-the-counter availability: Of pantoprazole and omeprazole – only omeprazole is approved by the FDA to be sold over-the-counter (OTC). Both omeprazole and its brand name formulation “Prilosec” are available at the 20 mg dose increment over-the-counter.  It is unknown as to whether pantoprazole will ever become available over-the-counter.
  • Popularity: Because omeprazole: (1) has been on the market for a longer-term than pantoprazole (by ~11 years); (2) is approved to treat more medical conditions than pantoprazole; (3) is available over-the-counter (pantoprazole is not) – it makes sense that omeprazole is more popular than pantoprazole. Throughout 2015, around 71.7 million prescriptions were filled for omeprazole – making it the 6th most-prescribed medication in the U.S.  Comparatively, around 24.7 million prescriptions were filled for pantoprazole in 2015 – making it the 29th most-prescribed medication in the U.S.

Which medication is “better”? (Pantoprazole vs. Omeprazole)

If attempting to decide whether pantoprazole or omeprazole might be “better” (on average) than the other – it’s necessary to compare these medications in domains that prospective users and/or medical professionals would care most about, including: (1) efficacy (in specific medical conditions) and (2) tolerability.  Other domains to consider (after efficacy and tolerability) would include: average cost; formatting and dosing options; onset and duration of action; FDA-authorized uses; and withdrawal difficulty.

Most gastroenterologists and general practitioners do not consider pantoprazole and omeprazole to differ significantly in efficacy for any medical condition – especially if we control for potency of dosing (via administration of equipotent doses) and metabolism (such that users won’t exhibit genetic polymorphisms that would impact hepatic metabolism and serum concentrations).  According to scientific research (meta-analyses and/or trials), pantoprazole and omeprazole are equally effective for: gastroesophageal reflux disease (GERD), H. Pylori infection (as adjuncts to antibiotics); and stomach acid hypersecretory conditions (e.g. Zollinger-Ellison syndrome).

However, there are data from meta-analyses to suggest that pantoprazole appears modestly superior to omeprazole in the treatment of peptic ulcers (duodenal or gastric) and erosive esophagitis.  For this reason, it might make sense for prospective proton-pump inhibitor users and/or medical professionals to favor the use of pantoprazole (over omeprazole) in the treatment of peptic ulcers and erosive esophagitis.

  • Gastroesophageal reflux disease: Equal efficacy
  • Pylori infection: Equal efficacy
  • Stomach acid hypersecretory conditions: Equal efficacy
  • Peptic ulcers: Pantoprazole modestly superior to omeprazole
  • Healing in erosive esophagitis: Pantoprazole modestly superior to omeprazole

In terms of tolerability, evidence from multiple meta-analyses of proton-pump inhibitors indicates that there’s zero significant difference between pantoprazole and omeprazole – both agents are equally tolerable when utilized at medically-recommended doses.  That said, there are trends from meta-analyses indicating that, at medically-recommended doses, pantoprazole (40 mg, daily) is negligibly more tolerable (on average) than omeprazole (20 mg, daily).

Furthermore, because pantoprazole is metabolized by a variety of enzymes such as CYP2C19, CYP2C9, CYP3A4, and cytosolic sulfotransferase – it is significantly less likely than omeprazole (which is metabolized mostly by CYP2C19) to cause interaction effects and/or pharmacokinetically-mediated adverse reactions.  Pantoprazole is also more likely than omeprazole to remain effective across persons with genetic polymorphisms that impair CYP2C19 function.

On the basis of its: (1) modestly-superior efficacy in the management of certain medical conditions; (2) potentially-superior tolerability (at medically-recommended doses) – it makes sense that some might consider pantoprazole to be “better” (on average) than omeprazole.  Comparisons of these agents in less important domains than efficacy and tolerability are made below, including: average cost; bioavailability; dosing options; and FDA-authorized uses.

The bioavailability of pantoprazole (~77%) is greater than the bioavailability of omeprazole (~30% to ~50%), indicating that a greater percentage ingested pantoprazole doses exert an acid-lowering effect – relative to ingested omeprazole doses.  The greater bioavailability for pantoprazole relative to omeprazole might explain why pantoprazole appears negligibly more tolerable than omeprazole (in meta-analyses).

The average cost of omeprazole (20 mg) may be slightly lower than the average cost of pantoprazole (40 mg) – largely due to omeprazole’s over-the-counter availability, however, both agents are relatively inexpensive ($6 to $30 for a 30-day supply).  Moreover, because pantoprazole is solely available as a prescription (which requires an appointment with a medical doctor to attain) whereas omeprazole is available over-the-counter (which does not require a doctor appointment to attain) – pantoprazole users may end up paying significantly more in annual medical expenses relative to omeprazole users (as a result of doctor appointment expenses required to attain their prescriptions).

In terms of dosing, it is known that omeprazole is available in 3 dosing increments – whereas pantoprazole is only available in 2 dosing increments. This might lead some individuals to favor the medication with 3 dosing increments (omeprazole) because the additional dosing increment may make it easier to titrate the medication during treatment (to minimize side effects) and/or during withdrawal (such as tapering to minimize withdrawal severity).

If comparing the official U.S. FDA-authorized medical uses for pantoprazole and omeprazole, respectively, there are fewer official medical uses for pantoprazole than omeprazole.  Pantoprazole is authorized by the FDA for 3 purposes: treating erosive esophagitis; promoting healing in erosive esophagitis; and treating pathological stomach acid hypersecretory conditions (e.g. Zollinger-Ellison syndrome).

Omeprazole is authorized by the FDA for 6 purposes: treating GERD; treating duodenal ulcer; treating gastric ulcer; treating H. Pylori (with antibiotics); promoting healing in erosive esophagitis; and treating stomach acid hypersecretory conditions (e.g. Zollinger-Ellison syndrome).  Some medical professionals might consider omeprazole as a better treatment option than pantoprazole in conditions such as peptic ulcers; GERD; and H. Pylori (based on the fact that pantoprazole is not officially approved to treat these conditions).

Overall, one might regard pantoprazole as “better” than omeprazole on the basis of its: (1) superior efficacy (in certain conditions); (2) potentially-superior tolerability; (3) metabolism (which reduces odds of interaction effects and adverse reactions – while increasing odds of efficacy in persons with CYP2C19 genetic polymorphisms); and/or (4) higher bioavailability (77% vs. 30-50%).

Similarly, one might regard omeprazole as “better” than pantoprazole on the basis of its: (1) lower potential cost (in terms of pills and potential savings in doctor visits); (2) over-the-counter availability (more convenient); (3) dosing increments (omeprazole is available in one more dosage increment than pantoprazole); and/or (4) FDA-authorized uses (omeprazole is approved to treat 3 more medical conditions than pantoprazole).

In conclusion, because pantoprazole (40 mg, daily) appears to be: (1) as effective as OR modestly superior to omeprazole (20 mg, daily) in efficacy for certain medical conditions (but not the opposite) and (2) potentially-superior to omeprazole in tolerability (but not the opposite), it makes logical sense to favor the use of pantoprazole ahead of omeprazole for medical conditions in which proton-pump inhibitors would prove therapeutic.

Which medication do you prefer: Pantoprazole or Omeprazole?

In the event that you’ve personally used pantoprazole and omeprazole, separately, as interventions for a specific medical condition (e.g. gastroesophageal reflux disease) – share a comment reflecting upon your respective experiences with each medication.  If you had to rate pantoprazole and omeprazole on a scale from “1” to “10” (with higher values indicating greater efficacy and tolerability), what ratings would you assign each agent in efficacy (1 to 10) and tolerability (1 to 10).

Based on your experiences with each agent (pantoprazole and omeprazole), do you consider one agent to be significantly more effective and/or tolerable than the other? Or do you regard both medications (pantoprazole and omeprazole) as being relatively equal in domains of efficacy and tolerability?

If you consider one medication (pantoprazole or omeprazole) to be more effective and/or tolerable than the other, have you considered that the differences in efficacy and/or tolerability might be attributable to disparities in: (1) dosing (using non-equipotent doses); (2) gene expression (altering the metabolism and serum concentrations of omeprazole); (3) formatting (delayed-release vs. immediate-release); (4) concurrent substance use (e.g. using a medication with pantoprazole – but not with omeprazole); and/or (5) duration of administration?

Assuming you prefer to use one medication (pantoprazole or omeprazole) over the other, what are the specific reasons for this preference?  Examples of such reasons might include: greater symptom control; fewer side effects; lower cost (in your location); easier to acquire (e.g. omeprazole over-the-counter); and/or less likely to interact with concomitant medications.

To help others accurately understand your experiences using pantoprazole and omeprazole, reflect upon things like: (1) dosages of each; (2) formats (delayed-release vs. immediate, sodium vs. magnesium formula, etc.); (3) durations of use; (4) concomitant substance use; and (5) the specific medical condition(s) for which each agent was prescribed or utilized.

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