Vonoprazan

potassium-competitive acid blocker (P-CAB)

Also sold as Voquezna, Takecab.

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Findings for this medication

Research about this medication, graded for how strongly each finding can be attributed to it. Nothing here describes your own levels.

Vonoprazan has no classical depletion machinery of its own. It is extensively metabolized by several CYP isoforms (predominantly CYP3A4/5, with CYP2C19, CYP2D6 and CYP2B6) plus sulfo- and glucuronosyl-transferases, is a weak CYP3A inhibitor, induces no enzyme, and is eliminated about 67% in urine (8% unchanged) and 31% in feces [1]. The only nutrient-relevant mechanism is the one the drug is built to produce: strong, sustained acid suppression, with a secondary rise in serum gastrin that the label says returns to normal within 4 weeks of stopping [1]. In the 5-year VISION trial, median gastrin was 625 pg/mL on vonoprazan versus 200 pg/mL on lansoprazole (read from a PubMed listing summary) [12]. Hypergastrinemia is the drug's own pharmacodynamic effect and is not filed here as a nutrient finding.

potassium-competitive acid blocker (P-CAB) · ATC A02BC08 (WHO ATC/DDD Index [3]) · also sold as Voquezna and Voquezna Dual Pak and Triple Pak (US); Takecab (Japan) · reviewed 2026-10-04. This describes research about the medication. It does not say anything about your own levels or health.

How to read the evidence grades

These colours describe how strongly a finding can be attributed to the medication in the research. They are not a severity score and they say nothing about your own health.

Grades describe how strongly a finding can be attributed to Vonoprazan in the research — not how common it is, how serious it would be, and not anything about you personally.

Red — Severe: Two or more independent Tier A sources, this drug in the cohort, the nutrient directly measured, consistent direction, clinically meaningful magnitude, a named mechanism, no substantial contradicting Tier A evidence.
Orange — Moderate: At least one Tier A source with this drug in the cohort showing a real but bounded deficit: an exposure window, a subgroup, low frequency, or a functional rather than circulating deficit.
Yellow — Low: Mechanistic plausibility only (Tier B), or class extrapolation (Tier C) with no drug-specific human status data; also used for context flags and interactions running the other direction.
Not graded — disclosed evidence gap: Nothing has been measured here, so this finding cannot be graded. That does not establish either safety or harm, and it is not the same as a White result.Source definition: Not gradeable under the rules above because nothing has been measured. Published as a documented gap, never as reassurance that there is no effect.

What the research found

Magnesium: rare postmarketing reports, mostly after months to years of continuous use

Orange — Moderate

See study details

Direction: depletion (low serum magnesium, probably by reduced intestinal absorption). Low blood magnesium has been reported with vonoprazan in the label, a pharmacovigilance analysis and several case reports, with normalization after the drug was stopped; the frequency is unknown.

Full detail and limits

What the grade means here: At least one Tier A source with this drug in the cohort showing a real but bounded deficit: an exposure window, a subgroup, low frequency, or a functional rather than circulating deficit. Orange

Limits on what this shows

Null findings: No trial reported magnesium. The 2018 review states no published reports of B12, iron, magnesium or calcium deficiency existed then [10]; the VA monograph reports no magnesium data from PHALCON-EE [11]. Both are absence of reporting, not measured nulls.
At-risk subgroups: Per the label: people on digoxin or diuretics. In the reports: older adults, diabetes, long-term continuous use (months to years; one report within 2 to 3 weeks).

Regulatory status

Label sec 5.7, as returned by the fetch tool: "Hypomagnesemia has been reported postmarketing with vonoprazan. Hypomagnesemia may lead to hypocalcemia and/or hypokalemia and may exacerbate underlying hypocalcemia in at-risk patients." Magnesium monitoring is suggested, particularly with digoxin or diuretics. Sec 6.2 lists hypomagnesemia, hypokalemia and hypocalcemia among postmarketing reactions [1]. This is Tier A, but it is a spontaneous-report listing with no case count or rate.

Population evidence

Zhong 2025 [5]: FAERS disproportionality analysis, 978 vonoprazan-related reports (Q1 2023 to Q1 2025). Hypomagnesemia: 6 cases, ROR 9.23 (95% CI 4.14 to 20.57). Blood magnesium decreased: 3 cases, ROR 7.58 (2.44 to 23.53). The authors call these hypothesis-generating signals with no exposure denominator. Aotani 2026 [6]: 78-year-old man with type 2 diabetes on vonoprazan 10 mg/day for 3 years and aspirin 100 mg/day; magnesium 0.4 mg/dL, albumin-adjusted calcium 6.1 mg/dL, potassium 4.5 mEq/L, intact PTH 45.1 pg/mL, fractional magnesium excretion 0.43%; no PPI or diuretic documented; values normalized by day 3 after stopping and did not recur after switching to an H2 blocker. Okamoto 2022 [7]: 66-year-old man with hypomagnesemia on long-term vonoprazan that improved after discontinuation (abstract only; values not retrieved). Aotani also cites three earlier cases, taken here secondhand: torsades de pointes about 2 weeks after switching from lansoprazole to vonoprazan in a carboplatin-treated patient; severe hypomagnesemia and hypocalcemia after more than 2 years; seizures 3 weeks after starting in a post-surgical lymphoma patient [6].

Mechanism

Proposed, not demonstrated for vonoprazan: pH-dependent impairment of intestinal magnesium absorption through TRPM6/TRPM7 channels, per the case authors [6]. The low fractional excretion of magnesium (0.43%) in the case points to an intestinal rather than a renal route.

Class cohort test

Not a class extrapolation: the grade rests on vonoprazan-named label text, FAERS and case reports. PPI hypomagnesemia cohorts were not borrowed.

Customer-visible string (boundary)

"Low blood magnesium has been reported rarely with vonoprazan, mostly after months to years of continuous use; how often it happens is not known."

Counter-evidence held on record

Counter-evidence and confounding Spontaneous reports have no denominator, and the label listing and the FAERS data are not independent. Confounders in the cases include type 2 diabetes (a hypomagnesemia risk by itself), carboplatin, and prior PPI exposure in the switch case. Onset times range from about 2 weeks to 3 years, which fits no single exposure window. Positive dechallenge is recorded in the cases; rechallenge is not. Framing caution This is a monitoring prompt for long-term users, not an expected effect and not a reason to take magnesium. This entry recommends no supplement. Magnesium supplements have an NIH upper limit and can accumulate in renal impairment; any decision belongs to a prescriber.

Vitamin B12: label class statement and CLASS EXTRAPOLATION; no vonoprazan measurement

Yellow — Low

See study details

Direction: depletion (reduced absorption of food-bound B12 with sustained acid suppression). The label lists B12 deficiency among postmarketing reports, but no study measured B12 in vonoprazan users.

Full detail and limits

What the grade means here: Mechanistic plausibility only (Tier B), or class extrapolation (Tier C) with no drug-specific human status data; also used for context flags and interactions running the other direction. Yellow

Limits on what this shows

Null findings: A 2018 review states no published reports addressed B12, iron, magnesium or calcium deficiency with vonoprazan, and advised continued attention [10]. This is absence of data, not a null.
At-risk subgroups: Older adults, people on metformin, vegetarians and vegans, and long-term continuous users are generic B12 risk groups, not vonoprazan findings.

Regulatory status

Label sec 5.6: "Long-term use of acid-suppressing drugs can lead to malabsorption of Vitamin B12 caused by hypo- or achlorhydria." This is a class sentence. Sec 6.2 lists vitamin B12 deficiency as a postmarketing reaction, with no counts [1].

Population evidence

CLASS EXTRAPOLATION. Lam 2013 [8]: nested case-control, Kaiser Permanente Northern California, 25,956 cases and 184,199 controls (1997 to 2011). Use for 2 or more years: PPIs OR 1.65 (95% CI 1.58 to 1.73), H2 receptor antagonists OR 1.25 (1.17 to 1.34). Individual agents were not named and vonoprazan or P-CABs are not mentioned in the retrieved text, so vonoprazan was NOT in the cohort. FAERS [5]: the extracted text gave no B12 signal values.

Mechanism

Present by the shared pathway: gastric acid releases protein-bound B12 for binding, and vonoprazan suppresses acid. Not measured with vonoprazan.

What the shared mechanism does and does not justify

It justifies a plausible direction of effect and a monitoring prompt for long-term continuous use. It does not justify the odds ratios, the 2-year threshold, or any dose-response, which were observed in other drugs. No PPI-specific or H2-blocker-specific finding is carried over.

Counter-evidence held on record

Counter-evidence and confounding Confounding by indication is presumed: reflux disease, older age, and H. pylori infection (itself linked to B12 and iron deficiency in a 2021 review abstract [13]) raise baseline deficiency, and vonoprazan is often prescribed for H. pylori eradication. Lam 2013 was observational and its effect sizes are modest. Framing caution A monitoring prompt, not a finding that vonoprazan causes B12 deficiency. Do not recommend B12 supplementation from this entry.

Calcium: secondary to low magnesium; absorption and bone not studied with vonoprazan

Yellow — Low

See study details

Direction: depletion (low serum calcium), documented only as a consequence of hypomagnesemia. Calcium absorption, bone density and fracture have not been studied with vonoprazan.

Full detail and limits

Limits on what this shows

Null findings: None retrieved with vonoprazan.

Regulatory status

Label sec 5.7 says hypomagnesemia may lead to hypocalcemia and hypokalemia; sec 6.2 lists hypocalcemia [1]. Sec 5.4 (fracture) is worded in terms of PPI observational studies and a year or longer of high-dose therapy; it does not report vonoprazan fracture data [1].

Population evidence

Aotani 2026 [6]: albumin-adjusted calcium 6.1 mg/dL with magnesium 0.4 mg/dL and an inappropriately low PTH (45.1 pg/mL), consistent with hypocalcemia from magnesium-related PTH suppression. Normalized by day 3 after stopping. No vonoprazan calcium-absorption study, bone density study or fracture analysis was retrieved.

Mechanism

For the case: low magnesium impairs PTH secretion and action. Acid-dependent absorption of poorly soluble calcium salts is a general acid-suppression idea, not demonstrated with vonoprazan.

Counter-evidence held on record

Counter-evidence The calcium drop is downstream of magnesium and is not an independent signal (see Overlap map). Fracture and low bone density are outcomes, not calcium deficiency (Hard Rule 2). Framing caution Do not present as a calcium absorption effect of vonoprazan, and do not recommend calcium supplementation from this entry.

The five body-system areas

Each finding is counted once, in a single area. Where a study is mentioned in a second area it is context only.

Mitochondrial Burden

Each finding below is counted once, in this area only.

Mitochondrial burden: cancer-cell nanocarrier data and mouse pathway data in opposite directions

Yellow — Low

See study details

One formulation study in lymphoma cells shows reduced mitochondrial membrane potential and a mouse injury study shows restored mitochondrial biogenesis signalling; neither shows a mitochondrial effect of ordinary oral vonoprazan.

Full detail and limits

Limits on what this shows

Null findings: No normal-cell data were reported in [20]. No human mitochondrial measurement exists in what was retrieved.

Regulatory status

No mitochondrial statement in the label [1].

Population evidence

None in humans. Wang 2025 [20]: macrophage-membrane-coated liposomes delivering vonoprazan to SU-DHL-8 lymphoma cells and mouse tumors (5 mg/kg intravenously every two days) lowered mitochondrial membrane potential and impaired oxidative phosphorylation; the comparisons reported are between formulations (for example 1.31 times the decline of uncoated liposomes), so the effect of free vonoprazan was not isolated, and only cancer cells were studied. The fetch tool described vonoprazan in this paper as a proton pump inhibitor, which I could not verify and do not adopt. AL-rasheedi 2026 [19]: in injured mouse liver, vonoprazan attenuated losses of phosphorylated AMPK, SIRT1 and PGC-1 alpha (mitochondrial biogenesis regulators).

Mechanism

Not established. Targeted delivery to cancer cells and an injury-model rescue are different contexts from chronic oral dosing.

Counter-evidence held on record

Counter-evidence Opposite directions in the two studies, and neither maps onto clinical use. The cancer-cell finding concerns a targeted anticancer strategy, not drug toxicity in patients. Framing caution Not a claim of mitochondrial damage. PPI mitochondrial data (other molecules) were not borrowed.

Oxidative Stress

Each finding below is counted once, in this area only.

Oxidative stress: reverse direction, protective in animal injury models

Yellow — Low

See study details

In two 2026 animal studies pretreatment with vonoprazan lowered lipid peroxidation and raised antioxidant capacity in chemically injured tissue; nothing shows a pro-oxidant or antioxidant-depleting effect in humans.

Full detail and limits

Limits on what this shows

Null findings: None in humans. The one pro-oxidant observation is in cancer cells: a vonoprazan liposome formulation raised intracellular ROS in lymphoma cells [20].

Regulatory status

No oxidative-stress statement in the label [1].

Population evidence

None in humans. AL-rasheedi 2026 [19]: 36 male mice, diethylnitrosamine 150 mg/kg injury, vonoprazan 5, 10 or 20 mg/kg orally for 7 days before injury; vonoprazan reduced hepatic malondialdehyde, raised glutathione and total antioxidant capacity and restored Nrf2 and heme oxygenase-1 (abstract page only). Alenezi 2026 [21]: 35 male Wistar rats given cisplatin with vonoprazan; vonoprazan reduced MDA and raised total antioxidant capacity in kidney, stomach and intestine (read through a summarizing fetch tool). Both are Tier B and show a reverse-direction, protective pattern against another toxin.

Mechanism

Activation of antioxidant signalling (Nrf2/HO-1) is reported in the mouse model [19]. Not shown in uninjured tissue or in people.

Counter-evidence held on record

Counter-evidence Pretreatment doses of 5 to 20 mg/kg in injury models do not map onto clinical dosing, and the findings are in injured, not healthy, tissue. Neither source measured oxidative stress in vonoprazan users. Framing caution Not an antioxidant benefit claim and not a deficiency claim. Vonoprazan should not be described as depleting antioxidants.

Copper and Iron Balance

Copper and iron are assessed separately. Nothing here is counted twice.

Iron: label pH-dependent absorption warning for iron salts; no vonoprazan iron study

Yellow — Low

See study details

Direction: depletion (reduced absorption of oral iron). The label lists iron salts among drugs whose absorption may fall with vonoprazan, but no study measured iron absorption, ferritin or iron deficiency in vonoprazan users.

Full detail and limits

Limits on what this shows

Null findings: The 2018 review found no published iron-deficiency reports for vonoprazan [10]. The FAERS extract gave no iron or anemia signal values [5]. The VA monograph reports no hemoglobin or anemia data [11]. These are absence of data, not measured nulls. Direct search for a vonoprazan iron-absorption study (see Sources access note) found none.
At-risk subgroups: Menstruating women, low dietary iron intake, GI blood loss and people already taking oral iron are generic iron-status risk groups, not vonoprazan findings.

Regulatory status

Label sec 7: vonoprazan "reduces intragastric acidity, which may decrease the absorption of drugs reducing their effectiveness," with iron salts named [1]. The statement concerns iron salts (supplements); it does not state an effect on dietary iron or iron stores. Tier A for the interaction statement, but with no magnitude.

Population evidence

CLASS EXTRAPOLATION. Lam 2017 [9]: community-based case-control, 77,046 incident iron deficiency cases and 389,314 controls (1999 to 2013). Use for 2 or more years: PPIs OR 2.49 (95% CI 2.35 to 2.64), H2 receptor antagonists OR 1.58 (1.46 to 1.71). The paper names no individual drugs and does not include vonoprazan, so vonoprazan was NOT in the cohort. A Drugs.com interaction page [22] rates the iron-vonoprazan interaction as moderate and quotes a 51% fall in serum iron AUC, but attributes that figure to PPI therapy; its references (not opened) are PPI-era studies.

Mechanism

Present by the shared pathway: acid favors solubilization and reduction of non-heme iron. Not measured with vonoprazan. Whether vonoprazan's deeper acid suppression changes the size of the effect is unstudied.

What the shared mechanism does and does not justify

It justifies a plausible reduction in absorption of oral non-heme iron. It does not justify the odds ratios, the 51% figure, or any claim of iron deficiency or anemia in vonoprazan users.

Counter-evidence held on record

Counter-evidence and confounding Iron deficiency prompts GI work-up, GI bleeding from acid disease can itself cause iron deficiency, and H. pylori infection is linked to iron deficiency [13]. Anemia is an outcome, not iron deficiency (Hard Rule 2). Framing caution An absorption interaction on oral iron salts only. Not a claim that vonoprazan causes iron deficiency. No iron dose is recommended; excess iron carries its own risks.

Copper

Not graded — disclosed evidence gap

See study details

No vonoprazan-specific or defensible class-level evidence on copper absorption, serum copper or ceruloplasmin was retrieved.

Full detail and limits

What the grade means here: Nothing has been measured here, so this finding cannot be graded. That does not establish either safety or harm, and it is not the same as a White result. Ungraded

Limits on what this shows

Why no grade: Dual condition met: no Tier B or C source was opened to support even a yellow grade, and no circulating consumer claim about vonoprazan and copper was found to rebut. This is a disclosed gap, not a finding of safety. Kept independent of Iron (Hard Rule 7). Re-check when PubMed access is restored.

What was searched

Web search "vonoprazan copper serum copper ceruloplasmin chelation": results were generic ceruloplasmin and Wilson disease pages with no vonoprazan content. The label sections retrieved [1] and the FAERS extract [5] contain no copper statement. The Sugano 2018 review [10] and the VA monograph [11] mention no copper. Pages returned for "vonoprazan nutrient depletion" searches and the GoodRx and Drugs.com pages [22][23] do not list copper.

Channel outcomes

No copper-specific PubMed listing query was completed: PubMed listing pages returned data for two queries and then HTTP 429, and the shared web-search budget was exhausted afterward, so only the one web search above was run for copper. This is tooling-limited as well as a likely genuine gap. No class extrapolation was attempted: no acid-suppression copper cohort was opened, and the acid-dependence of copper absorption was not established in anything retrieved.

Gut Microbiome Risk

Each finding below is counted once, in this area only.

Gut microbiome risk: transient shift in vonoprazan cohorts, antibiotic-confounded

Yellow — Low

See study details

Vonoprazan-named studies show a fall in gut microbial diversity within about a month that recovers, but nearly all cohorts also received antibiotics, and the single healthy-volunteer study is very small.

Full detail and limits

Limits on what this shows

Null findings: Low-dose amoxicillin with vonoprazan showed no gut microbiota change [15]. Probiotics did not prevent oral microbiota disturbance [16].
At-risk subgroups: Not defined. Adolescents with H. pylori were studied in several included cohorts but their results were not retrieved.

Regulatory status

No microbiome statement. Label sec 5.3 says vonoprazan "may be associated with an increased risk" of C. difficile-associated diarrhea [1]; that is an infection outcome and is not filed as a nutrient or microbiome measurement here.

Population evidence

Ouyang 2023 [14]: systematic review and meta-analysis of vonoprazan microbiota studies (reported as 12 studies; the table returned listed 9). Shannon index within 1 month: mean difference -0.53 (95% CI -0.76 to -0.30); at 1 to 3 months -0.28 (-0.58 to 0.02), returning toward baseline later. Firmicutes fell and Bacteroidetes rose; Bifidobacterium fell (MD -6.36, I2 96.2%). Only one study involved healthy H. pylori-negative people (Otsuka 2017, 9 volunteers, vonoprazan monotherapy for 4 weeks, significant beta diversity change); this is known only secondhand through the meta-analysis. Authors rated one article low risk, seven moderate and one serious. Hu 2022 [15]: 119 randomized, 53 analyzed with 13 controls; vonoprazan 20 mg twice daily plus amoxicillin; low-dose amoxicillin showed no microbiota change, high-dose caused temporary diversity loss recovering by week 4. Liu 2026 [17]: 110 patients (vonoprazan-amoxicillin n=50 versus esomeprazole-amoxicillin n=60) plus 22 healthy controls; both arms showed more potential pathogens and fewer short-chain-fatty-acid producers after treatment, with a more pronounced initial diversity decline in the vonoprazan arm and faster functional recovery (non-randomized). Peng 2023 [16] (oral tongue-coat microbiota, 60 patients): diversity fell after vonoprazan-amoxicillin and partly recovered; probiotics did not prevent it. Mouse study [18]: vonoprazan and rabeprazole each lowered small-intestinal Lactobacillus johnsonii and worsened indomethacin injury.

Mechanism

Plausible: higher gastric pH may let more oral and upper-GI bacteria survive transit; the meta-analysis authors link the shift to strong acid inhibition [14]. Antibiotic exposure is a competing cause in most cohorts.

Counter-evidence held on record

Counter-evidence and confounding Eradication regimens combine vonoprazan with amoxicillin (and clarithromycin), so the diversity fall cannot be attributed to vonoprazan alone; the healthy-volunteer evidence is n=9. Heterogeneity is very high. Why not orange: the vonoprazan-only evidence is too small to show a bounded real effect, and microbiome change is not a measured nutrient deficit. Framing caution This is not a claim of dysbiosis or of any nutrient deficit. PPI microbiome findings were not borrowed.

Oxygen and ATP Output

Oxygen delivery and ATP production are assessed separately. Nothing here is counted twice.

ATP production: one formulation comparison in cancer cells, mixed direction

Yellow — Low

See study details

The only vonoprazan ATP measurement is a small drop in cancer cells treated with a targeted liposome formulation; the injury-model mouse data point the other way.

Full detail and limits

Limits on what this shows

Null findings: No human ATP or energy-output data.

Regulatory status

No ATP or energy-metabolism statement in the label [1].

Population evidence

None in humans. Wang 2025 [20]: ATP content fell by about 14.16% for the macrophage-coated formulation versus uncoated liposomes in lymphoma cells; this is a formulation-to-formulation comparison, not vonoprazan versus no drug. AL-rasheedi 2026 [19]: AMPK/SIRT1/PGC-1 alpha pathway restoration in injured mouse liver, interpreted by the summarized abstract as restoration of energy metabolism; ATP itself was not reported in the extract.

Mechanism

Not established.

Counter-evidence held on record

Counter-evidence A 14% formulation difference in cancer cells is not evidence of reduced energy output in patients. The mouse pathway data suggest, if anything, preservation. Framing caution Not a "low energy" claim. Kept independent of Mitochondrial burden and Oxygen delivery/utilization (Hard Rule 7); the shared source is disclosed in the Overlap map.

Oxygen delivery/utilization

Not graded — disclosed evidence gap

See study details

No evidence was found that vonoprazan lowers hemoglobin, red-cell mass or tissue oxygen delivery by any route independent of the B12 and iron entries.

Full detail and limits

What the grade means here: Nothing has been measured here, so this finding cannot be graded. That does not establish either safety or harm, and it is not the same as a White result. Ungraded

Limits on what this shows

Why no grade: Dual condition met: no Tier B or C evidence on oxygen delivery, and no circulating claim about vonoprazan and oxygen-carrying capacity was found. Anemia, if it occurred, would be an outcome routed through the iron or B12 entries and is not counted separately (Hard Rule 2; see Overlap map). A FAERS paper speculates that malabsorption could lead to secondary anemia [5]; that is the authors' hypothesis, not a measured finding. This is a disclosed gap, not a finding of safety.

What was searched

Web search "vonoprazan anemia hemolytic OR methemoglobinemia OR thrombocytopenia case report": returned a title-only record of immune thrombocytopenia induced by vonoprazan (a platelet event, not oxygen carrying; abstract not opened because the page returned 429) and a rabeprazole methemoglobinemia case that does not concern vonoprazan. The label lists thrombocytopenia as a postmarketing reaction [1], again a platelet event. The FAERS extract gave no anemia signal values [5]. The VA monograph reports no hemoglobin or anemia data from PHALCON-EE [11]. Web search "vonoprazan oral iron absorption ... hemoglobin improvement Helicobacter pylori": no vonoprazan hemoglobin study.

Channel outcomes

PubMed listing pages were rate-limited (HTTP 429) after two queries, Europe PMC returned 429, and the web-search budget ran out, so no PubMed query on vonoprazan with hemoglobin, hemolysis or methemoglobin terms was run. Tooling-limited plus a likely thin literature.

Claims checked and not supported

These circulate online for this medication. They are listed here only so they can be answered, never as findings, and they are not graded.

A claim with no supporting evidence is not necessarily disproven. Where evidence actually argues against a claim, that is stated below.

Calcium malabsorption leading to weak bones and more fractures
Where it comes from: GoodRx side-effects page for Voquezna [23], citing a 2008 review of acid-suppressive medications and fracture in older adults (the cited review was not opened).
Why it fails: Fracture and bone loss are outcomes, not calcium deficiency (Hard Rule 2). The label's own fracture section is written from PPI observational studies [1]. No vonoprazan calcium-absorption, bone-density or fracture analysis was retrieved. The calcium signal that does exist with vonoprazan is hypocalcemia secondary to low magnesium (see Calcium entry, yellow).
"Taking Voquezna may decrease your vitamin B12 levels" stated as fact for users
Where it comes from: GoodRx page [23], citing a 2025 primary-care B12 risk-factor paper and a 2017 AFP review (neither opened).
Why it fails: The cited papers are general B12 sources, not vonoprazan studies. The label's B12 sentence is a class statement [1], and no vonoprazan B12 measurement was found [10]. Carried here as yellow class extrapolation with the confounding limits shown, not as an established effect.
Iron absorption "reduced by 51%" with vonoprazan
Where it comes from: Drugs.com interaction page [22], which quotes a 51% fall in serum iron AUC and cites PPI-era studies.
Why it fails: The page attributes the 51% figure to PPI therapy and lumps P-CABs with PPIs by mechanism. No vonoprazan iron-absorption measurement was found. The label supports only that iron salt absorption "may decrease" [1]. The figure is not carried to vonoprazan.
Magnesium: page's own citation does not support the claim
Where it comes from: GoodRx page [23] states that Voquezna "can decrease magnesium absorption," citing a Merck Manual page on hypermagnesemia.
Why it fails: The cited source concerns high, not low, magnesium. The underlying claim is supported by other evidence (label, FAERS, case reports) and is graded orange with its boundary; the page's reference does not establish it. Included so readers can see the difference.

How the body handles this medication

Metabolism and enzymes: Metabolized by multiple pathways: CYP3A4/5, CYP2C19, CYP2D6, CYP2B6, plus sulfo- and glucuronosyl-transferases. Vonoprazan is a weak CYP3A inhibitor (midazolam AUC raised 93%) and directly and time-dependently inhibits CYP2B6, CYP2C19 and CYP3A4/5. It induces no enzyme. Strong and moderate CYP3A inducers are to be avoided because vonoprazan exposure is predicted to fall 50 to 80%. That is a drug-drug interaction, not a nutrient interaction.[1] DailyMed label sec 7, 12.3 (read through a summarizing fetch tool; quotes as returned)
Elimination and half-life: About 67% of a radiolabeled dose was recovered in urine (8% as unchanged drug) and 31% in feces (1.4% unchanged). Half-life 6.8 to 7.9 hours. Steady state by day 3 to 4; accumulation index below 1.2.[1] label sec 12.3
Absorption and food: High-fat meal: Cmax up 5%, AUC up 15%, Tmax delayed 2 hours, not considered clinically significant. The named absorption transporter was not given in the label extract retrieved.[1] label sec 12.3
Renal and hepatic impairment: Severe renal impairment (eGFR below 30): AUC 2.4-fold higher; dose reduction for erosive esophagitis healing. Hepatic: Child-Pugh A 1.2-fold, B 2.4-fold, C 2.6-fold AUC; dose reduction in B and C, and H. pylori treatment is not recommended in moderate or severe hepatic or severe renal impairment.[1] label sec 8.6, 8.7, 12.3
Gastric pH and gastrin: Onset within 2 to 3 hours of a single dose. The label extract reports intragastric pH above 4 for 85.2% of the time by day 7 at 20 mg daily (the "(20 h)" qualifier in the extract was not interpretable). Fasting gastrin rises and remains elevated during treatment, with return to normal within 4 weeks of discontinuation; the label states increased gastrin causes enterochromaffin-like cell hyperplasia and raises chromogranin A.[1] label sec 12.2
Mineral and antacid interactions: Label sec 7 lists iron salts among drugs (with erlotinib, dasatinib, nilotinib, mycophenolate mofetil, azole antifungals) whose absorption may decrease because vonoprazan reduces intragastric acidity. No separation interval is given. Label warnings: B12 (5.6), hypomagnesemia and mineral metabolism (5.7), fracture (5.4, text based on PPI observational studies), C. difficile (5.3). Rilpivirine is contraindicated; atazanavir and nelfinavir are to be avoided.[1] label sec 5, 7

What the research says is worth watching

General information from the medication label and the studies above. It is not personal medical advice, and any change belongs with your prescriber.

Lab / long-term use
Serum magnesium
The label suggests considering magnesium monitoring, especially with digoxin or diuretics [1]. Worth checking with muscle cramps, tetany, arrhythmia, seizures or unexplained low calcium or potassium on continuous therapy. Reports range from weeks to 3 years of use [6]. A monitoring prompt, not a finding that every user is affected.
Lab / long-term use
Vitamin B12 status
Consider serum B12, with methylmalonic acid or homocysteine if borderline, for people on continuous therapy over many months, especially older adults and people on metformin. Basis is the label class sentence and class extrapolation, not a vonoprazan study [1][8].
Lab / symptoms
Iron indices
Ferritin and a blood count if fatigue, pallor or heavy menstrual loss, or if taking oral iron without the expected response. New iron deficiency in an adult warrants evaluation for GI blood loss rather than assumption of a drug cause.
Lab / unusual symptoms
Calcium and potassium
Check only if magnesium is low or symptoms suggest it; the documented low calcium and potassium followed low magnesium [1][6].
Drug effect, not nutrient
Gastrin and chromogranin A
Gastrin rises on vonoprazan and normalizes within 4 weeks of stopping. The label advises stopping at least 4 weeks before chromogranin A testing [1]. Liver enzyme rises above 3 times the upper limit occurred in 0.2% to 0.4% per group in PHALCON-EE [11]. These are label matters, not nutrient findings.
Timing
Supplement separation
The label gives no separation interval for iron salts or any supplement [1]. Because acid suppression lasts beyond 24 hours, spacing doses is unlikely to remove an absorption effect; that is an inference by the dossier author, not a label statement. No supplement dose is recommended or appears anywhere in this dossier, so no upper-limit comparison was needed. Any change belongs to a prescriber or pharmacist.
Special populations
Renal, hepatic, pregnancy, pediatrics
Severe renal impairment (eGFR below 30) and Child-Pugh B or C hepatic impairment raise exposure and change dosing [1]. A 2026 review states there are no adequate pregnancy studies [24]. Pediatric nutrient considerations were not assessed.

Overlap map, to prevent double counting

Magnesium
Shares evidence with: Calcium
Note: The case-report hypocalcemia [6] and the label sentence on mineral metabolism [1] are the same events, downstream of low magnesium and PTH suppression. Calcium is not an independent signal.
Magnesium (label)
Shares evidence with: Magnesium (FAERS [5])
Note: The label postmarketing listing and the FAERS analysis both derive from spontaneous reports and may include the same cases. Treated as one line of evidence, with the case reports as a second.
Vitamin B12
Shares evidence with: Iron; Calcium
Note: Same mechanism (reduced gastric acid impairing absorption), same label section family [1], and B12 and iron share the Kaiser Permanente case-control series [8][9] used as class extrapolation (vonoprazan not in either cohort). One mechanism and one data source, not independent confirmations.
Vitamin B12; Iron
Shares evidence with: Oxygen delivery/utilization (ungraded)
Note: Any anemia would be mediated through these two entries. Oxygen delivery is not counted separately.
Oxidative stress
Shares evidence with: Mitochondrial burden; ATP production
Note: AL-rasheedi 2026 [19] supplies both the Nrf2/antioxidant data (oxidative stress) and the AMPK/SIRT1/PGC-1 alpha data (mitochondrial burden, ATP). Wang 2025 [20] supplies the ROS rise (oxidative stress) and the membrane potential and ATP data (mitochondrial burden, ATP). Not independent lines of evidence.
Mitochondrial burden
Shares evidence with: ATP production
Note: Both rest on the same two papers [19][20] and the same cancer-cell formulation comparison. One body of evidence viewed twice.
Gut microbiome risk
Shares evidence with: Vitamin B12; Iron
Note: No shared source. A microbiome shift is a hypothetical modifier of absorption and is not claimed here. The H. pylori eradication cohorts [15][16][17] are also the setting of the infection-linked B12 and iron confounding noted in those entries.
Copper
Shares evidence with: Iron
Note: No shared source; both graded independently per Hard Rule 7 (copper has no evidence).

All references used above

Vonoprazan

Findings for this medication

What the research found

Magnesium: rare postmarketing reports, mostly after months to years of continuous use

Vitamin B12: label class statement and CLASS EXTRAPOLATION; no vonoprazan measurement

Calcium: secondary to low magnesium; absorption and bone not studied with vonoprazan

The five body-system areas

⚡Mitochondrial Burden

Mitochondrial burden: cancer-cell nanocarrier data and mouse pathway data in opposite directions

💥Oxidative Stress

Oxidative stress: reverse direction, protective in animal injury models

⚖️Copper and Iron Balance

Iron: label pH-dependent absorption warning for iron salts; no vonoprazan iron study

Copper

🌿Gut Microbiome Risk

Gut microbiome risk: transient shift in vonoprazan cohorts, antibiotic-confounded

💨Oxygen and ATP Output

ATP production: one formulation comparison in cancer cells, mixed direction

Oxygen delivery/utilization

Claims checked and not supported

Calcium malabsorption leading to weak bones and more fractures

"Taking Voquezna may decrease your vitamin B12 levels" stated as fact for users

Iron absorption "reduced by 51%" with vonoprazan

Magnesium: page's own citation does not support the claim

How the body handles this medication

What the research says is worth watching

Overlap map, to prevent double counting

Mitochondrial Burden

Oxidative Stress

Copper and Iron Balance

Gut Microbiome Risk

Oxygen and ATP Output