Pantothenate (vitamin B5)

evidence_span

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experimental_model

Transport and inhibitor experiments in human NCM460 colonic epithelial cells

exposure

Radiolabeled biotin with sodium replacement, pantothenate and kinase modulators

limitations

Cell-line kinetics do not quantify microbiome contributions or demonstrate competition at ordinary dietary intakes.

nutrient_topic

Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin

organism

Homo sapiens

plain_language

B5 and biotin can compete for entry in this colon-cell assay.

primary_references

[b7-p9814986] Biotin uptake by human colonic epithelial NCM460 cells: a carrier-mediated process shared with pantothenic acid. (1998). https://pubmed.ncbi.nlm.nih.gov/9814986/ DOI: 10.1152/ajpcell.1998.275.5.c1365

tissue_or_cell_type

Colonic epithelium; NCM460 culture

Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 195–206

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Transport and inhibitor experiments in human NCM460 colonic epithelial cells · source_derived_draft · unverified_draft

### b7-colon-b5-competition Pantothenic acid competitively inhibited biotin uptake in NCM460 cells, with Ki 14.4 micromolar. Condition category: normal nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: B5 and biotin can compete for entry in this colon-cell assay. organism: Homo sapiens tissue_or_cell_type: Colonic epithelium; NCM460 culture experimental_model: Transport and inhibitor experiments in human NCM460 colonic epithelial cells limitations: Cell-line kinetics do not quantify microbiome contributions or demonstrate competition at ordinary dietary intakes. exposure: Radiolabeled biotin with sodium replacement, pantothenate and kinase modulators evidence_span: {"source_cache": "artifacts/biotin-research/9814986.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7cc679e31b95ae919c15fadf0d56933d2ed8074664e11cd80a96e910181857be", "start_char": 0, "end_char": 1676, "text_sha256": "7cc679e31b95ae919c15fadf0d56933d2ed8074664e11cd80a96e910181857be"} [b7-p9814986] Biotin uptake by human colonic epithelial NCM460 cells: a carrier-mediated process shared with pantothenic acid. (1998). https://pubmed.ncbi.nlm.nih.gov/9814986/ DOI: 10.1152/ajpcell.1998.275.5.c1365

availability_state

nutrient_deficiency Imported condition classification; unverified.

evidence_access

Primary full text

experimental_model

Mouse cysteine repletion with or without dietary B5; subsequent tissue GSH/CoA and weight measurements.

limitations

A direct cross-nutrient repletion experiment in mice; not an established human treatment protocol. Correction record: Author correction published 12 December 2025 (2026 issue), PMID 41388205, DOI 10.1038/s41586-025-09780-8: two incorrect day-3 muscle histology panels in Extended Data Fig. 2f,g duplicated day-7 panels and were replaced. The authors state that figure and paper conclusions were unaffected. This is a figure correction, not independent validation. https://www.nature.com/articles/s41586-025-09780-8

nutrient_topic

L-Cysteine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Cysteine

plain_language

Restoring one nutrient repaired one branch but left another branch short of its other substrate.

primary_references

Unravelling cysteine-deficiency-associated rapid weight loss. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40399674/ · DOI 10.1038/s41586-025-08996-y

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

L-Cysteine: sulfur allocation, redox supply and cross-nutrient mechanisms (2026-09-19) · lines 324–330

AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse cysteine repletion with or without dietary B5; subsequent tissue GSH/CoA and weight measurements. · source_derived_draft · unverified_draft

## l-cysteine-b5-blocks-coa-recovery Restoring one nutrient repaired one branch but left another branch short of its other substrate. After seven days of cysteine depletion, Cse-null mice repleted with cysteine but kept B5-deficient had persistently lower CoA and less weight recovery than mice receiving both nutrients, despite restored liver glutathione. Model: Mouse cysteine repletion with or without dietary B5; subsequent tissue GSH/CoA and weight measurements. Limitations: A direct cross-nutrient repletion experiment in mice; not an established human treatment protocol. Correction record: Author correction published 12 December 2025 (2026 issue), PMID 41388205, DOI 10.1038/s41586-025-09780-8: two incorrect day-3 muscle histology panels in Extended Data Fig. 2f,g duplicated day-7 panels and were replaced. The authors state that figure and paper conclusions were unaffected. This is a figure correction, not independent validation. https://www.nature.com/articles/s41586-025-09780-8 Evidence access: Primary full text Unravelling cysteine-deficiency-associated rapid weight loss. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40399674/ · DOI 10.1038/s41586-025-08996-y

availability_state

nutrient_deficiency Imported condition classification; unverified.

evidence_access

Primary full text

experimental_model

Mouse sequential nutrient-depletion/repletion experiment.

limitations

The endpoint was recovery from induced wasting, not weight gain or energy improvement in healthy people. Correction record: Author correction published 12 December 2025 (2026 issue), PMID 41388205, DOI 10.1038/s41586-025-09780-8: two incorrect day-3 muscle histology panels in Extended Data Fig. 2f,g duplicated day-7 panels and were replaced. The authors state that figure and paper conclusions were unaffected. This is a figure correction, not independent validation. https://www.nature.com/articles/s41586-025-09780-8

nutrient_topic

L-Cysteine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Cysteine

plain_language

A second missing nutrient limited recovery after the first was restored.

primary_references

Unravelling cysteine-deficiency-associated rapid weight loss. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40399674/ · DOI 10.1038/s41586-025-08996-y

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

L-Cysteine: sulfur allocation, redox supply and cross-nutrient mechanisms (2026-09-19) · lines 332–338

AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse sequential nutrient-depletion/repletion experiment. · source_derived_draft · unverified_draft

## l-cysteine-b5-restores-weight-recovery A second missing nutrient limited recovery after the first was restored. Adding B5 to drinking water after seven days on the cysteine-sufficient, B5-deficient recovery diet promptly rescued the weight-recovery difference. Model: Mouse sequential nutrient-depletion/repletion experiment. Limitations: The endpoint was recovery from induced wasting, not weight gain or energy improvement in healthy people. Correction record: Author correction published 12 December 2025 (2026 issue), PMID 41388205, DOI 10.1038/s41586-025-09780-8: two incorrect day-3 muscle histology panels in Extended Data Fig. 2f,g duplicated day-7 panels and were replaced. The authors state that figure and paper conclusions were unaffected. This is a figure correction, not independent validation. https://www.nature.com/articles/s41586-025-09780-8 Evidence access: Primary full text Unravelling cysteine-deficiency-associated rapid weight loss. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40399674/ · DOI 10.1038/s41586-025-08996-y

availability_state

nutrient_deficiency Imported condition classification; unverified.

cross_nutrient

false

evidence_location

Primary PDF pp.1643–1654; design, results and discussion.

experimental_model

Historical controlled feeding study in six adult male volunteers; two diet-only deficient, two deficient plus antagonist, two supplemented controls

exposure

Tube-fed experimental formula; controls received pantothenic acid 20 mg/day, antagonist pair 750 then 1000 mg/day omega-methyl compound; recovery included 4000 mg/day vitamin. One man per pair received 10.8 mEq/day extra potassium.

limitations

Very small historical cohort; other vitamins and formula composition were controlled imperfectly. Diet-only and antagonist groups are distinguished. Measurements do not establish a universal symptom, adrenal disease mechanism or cellular CoA threshold. This historical indirect test is not a modern diagnostic assay for adrenal insufficiency.

nutrient_topic

Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)

organism

Homo sapiens

plain_language

The altered hormone-response test did not establish adrenal failure.

primary_references

[b5-clin-hodges1958] Pantothenic acid deficiency in man. (1958). https://pubmed.ncbi.nlm.nih.gov/13587673/ DOI: 10.1172/jci103756

tissue_or_cell_type

Whole-person symptoms, serum and urine

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 1173–1185

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Historical controlled feeding study in six adult male volunteers; two diet-only deficient, two deficient plus antagonist, two supplemented controls · source_derived_draft · unverified_draft

### b5-clin-acth-not-adrenal-diagnosis The 1958 depletion study found an impaired eosinopenic response to ACTH, while urinary 17-ketosteroid excretion remained normal; the authors did not interpret this pattern as sufficient evidence of adrenal cortical hypofunction. Condition category: nutrient_deficiency nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: The altered hormone-response test did not establish adrenal failure. organism: Homo sapiens tissue_or_cell_type: Whole-person symptoms, serum and urine experimental_model: Historical controlled feeding study in six adult male volunteers; two diet-only deficient, two deficient plus antagonist, two supplemented controls limitations: Very small historical cohort; other vitamins and formula composition were controlled imperfectly. Diet-only and antagonist groups are distinguished. Measurements do not establish a universal symptom, adrenal disease mechanism or cellular CoA threshold. This historical indirect test is not a modern diagnostic assay for adrenal insufficiency. exposure: Tube-fed experimental formula; controls received pantothenic acid 20 mg/day, antagonist pair 750 then 1000 mg/day omega-methyl compound; recovery included 4000 mg/day vitamin. One man per pair received 10.8 mEq/day extra potassium. cross_nutrient: false evidence_location: Primary PDF pp.1643–1654; design, results and discussion. [b5-clin-hodges1958] Pantothenic acid deficiency in man. (1958). https://pubmed.ncbi.nlm.nih.gov/13587673/ DOI: 10.1172/jci103756

availability_state

biomarker_context Imported condition classification; unverified.

cross_nutrient

false

evidence_location

Primary indexed abstract.

experimental_model

Observational study of 63 healthy adolescents

exposure

Four-day diet records; pantothenate measured by radioimmunoassay.

limitations

Correlations and comparisons with other populations do not establish cellular adequacy, an individual requirement or a diagnostic threshold. Historical recommended-intake discussion is not used as current guidance. Below 4 mg/day was a historical descriptive cutoff, not a validated individual deficiency threshold.

nutrient_topic

Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)

organism

Homo sapiens

plain_language

A low short diet record did not reliably identify a low group-average blood value.

primary_references

[b5-clin-eissenstat1986] Pantothenic acid status of adolescents. (1986). https://pubmed.ncbi.nlm.nih.gov/3788840/ DOI: 10.1093/ajcn/44.6.931

tissue_or_cell_type

Diet records, urine, whole blood and erythrocytes

trigger_kind

biomarker_context Imported condition classification; unverified.

Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 1299–1311

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Observational study of 63 healthy adolescents · source_derived_draft · unverified_draft

### b5-clin-adolescent-intake-blood-discordance Although 49% of female and 15% of male adolescents recorded intakes below 4 mg/day, group-average blood concentrations were within the ranges reported for comparison populations. Condition category: biomarker_context nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: A low short diet record did not reliably identify a low group-average blood value. organism: Homo sapiens tissue_or_cell_type: Diet records, urine, whole blood and erythrocytes experimental_model: Observational study of 63 healthy adolescents limitations: Correlations and comparisons with other populations do not establish cellular adequacy, an individual requirement or a diagnostic threshold. Historical recommended-intake discussion is not used as current guidance. Below 4 mg/day was a historical descriptive cutoff, not a validated individual deficiency threshold. exposure: Four-day diet records; pantothenate measured by radioimmunoassay. cross_nutrient: false evidence_location: Primary indexed abstract. [b5-clin-eissenstat1986] Pantothenic acid status of adolescents. (1986). https://pubmed.ncbi.nlm.nih.gov/3788840/ DOI: 10.1093/ajcn/44.6.931

availability_state

biomarker_context Imported condition classification; unverified.

cross_nutrient

false

evidence_location

Primary indexed abstract.

experimental_model

Observational study of 63 healthy adolescents

exposure

Four-day diet records; pantothenate measured by radioimmunoassay.

limitations

Correlations and comparisons with other populations do not establish cellular adequacy, an individual requirement or a diagnostic threshold. Historical recommended-intake discussion is not used as current guidance.

nutrient_topic

Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)

organism

Homo sapiens

plain_language

Urine and red-cell measurements tracked intake in this group.

primary_references

[b5-clin-eissenstat1986] Pantothenic acid status of adolescents. (1986). https://pubmed.ncbi.nlm.nih.gov/3788840/ DOI: 10.1093/ajcn/44.6.931

tissue_or_cell_type

Diet records, urine, whole blood and erythrocytes

trigger_kind

biomarker_context Imported condition classification; unverified.

Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 1285–1297

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Observational study of 63 healthy adolescents · source_derived_draft · unverified_draft

### b5-clin-adolescent-urine-correlation In 63 adolescents, recorded pantothenate intake correlated with urinary excretion (P<0.001); erythrocyte pantothenate also correlated with intake and urinary excretion. Condition category: biomarker_context nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Urine and red-cell measurements tracked intake in this group. organism: Homo sapiens tissue_or_cell_type: Diet records, urine, whole blood and erythrocytes experimental_model: Observational study of 63 healthy adolescents limitations: Correlations and comparisons with other populations do not establish cellular adequacy, an individual requirement or a diagnostic threshold. Historical recommended-intake discussion is not used as current guidance. exposure: Four-day diet records; pantothenate measured by radioimmunoassay. cross_nutrient: false evidence_location: Primary indexed abstract. [b5-clin-eissenstat1986] Pantothenic acid status of adolescents. (1986). https://pubmed.ncbi.nlm.nih.gov/3788840/ DOI: 10.1093/ajcn/44.6.931

cross_nutrient

false

evidence_location

Primary PDF pp.1421–1425, especially Results and Summary.

experimental_model

Historical four-man controlled antagonist experiment on a balanced 3200 kcal diet

exposure

One control; three men received escalating antagonist regimens, up to 2–4 g/day in the highest-exposure subject; pantothenic acid 4 g/day was later given after antagonist withdrawal.

limitations

Pharmacological antagonist exposure with an otherwise normal diet, not dietary B5 deprivation. Very small sample and concurrent antagonist withdrawal prevent isolating a pure vitamin-rescue effect. Concurrent withdrawal prevents attributing recovery exclusively to vitamin administration.

nutrient_topic

Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)

organism

Homo sapiens

plain_language

Recovery followed both removal of the antagonist and vitamin treatment.

primary_references

[b5-clin-hodges1959] Human pantothenic acid deficiency produced by omega-methyl pantothenic acid. (1959). https://pubmed.ncbi.nlm.nih.gov/13673099/ DOI: 10.1172/jci103918

tissue_or_cell_type

Whole-person clinical symptoms and functional tests

Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 1215–1227

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Historical four-man controlled antagonist experiment on a balanced 3200 kcal diet · source_derived_draft · unverified_draft

### b5-clin-antagonist-recovery Abnormal ACTH-associated eosinopenic responses in the two more heavily exposed men recovered after the antagonist was stopped and pantothenic acid was administered. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Recovery followed both removal of the antagonist and vitamin treatment. organism: Homo sapiens tissue_or_cell_type: Whole-person clinical symptoms and functional tests experimental_model: Historical four-man controlled antagonist experiment on a balanced 3200 kcal diet limitations: Pharmacological antagonist exposure with an otherwise normal diet, not dietary B5 deprivation. Very small sample and concurrent antagonist withdrawal prevent isolating a pure vitamin-rescue effect. Concurrent withdrawal prevents attributing recovery exclusively to vitamin administration. exposure: One control; three men received escalating antagonist regimens, up to 2–4 g/day in the highest-exposure subject; pantothenic acid 4 g/day was later given after antagonist withdrawal. cross_nutrient: false evidence_location: Primary PDF pp.1421–1425, especially Results and Summary. [b5-clin-hodges1959] Human pantothenic acid deficiency produced by omega-methyl pantothenic acid. (1959). https://pubmed.ncbi.nlm.nih.gov/13673099/ DOI: 10.1172/jci103918

availability_state

biomarker_context Imported condition classification; unverified.

cross_nutrient

false

evidence_location

Primary PDF Table 1 visually checked; Tables 3–4 and Results pp.341–345.

experimental_model

Controlled 84-day feeding experiment in ten adult male inmates aged 27–33; six unsupplemented and four supplemented

exposure

Nine-week/63-day experimental diet essentially free of B5 versus 10 mg/day B5 as calcium pantothenate; both groups then received 100 mg/day for seven days.

limitations

Table 1 and the abstract distinguish unsupplemented and supplemented groups; one Methods sentence incorrectly says all received 10 mg. The table was visually checked. Historical assay and small cohort; the reported retention calculation is not direct measurement of intestinal absorption or tissue CoA.

nutrient_topic

Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)

organism

Homo sapiens

plain_language

Blood and urine measurements did not respond identically to dietary depletion.

primary_references

[b5-clin-fry1976] Metabolic response to a pantothenic acid deficient diet in humans. (1976). https://pubmed.ncbi.nlm.nih.gov/1011047/ DOI: 10.3177/jnsv.22.339

tissue_or_cell_type

Urine and whole blood; nitrogen balance

trigger_kind

biomarker_context Imported condition classification; unverified.

Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 1243–1255

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Controlled 84-day feeding experiment in ten adult male inmates aged 27–33; six unsupplemented and four supplemented · source_derived_draft · unverified_draft

### b5-clin-blood-intake-response Whole-blood pantothenate decreased in the unsupplemented group and remained broadly stable in the supplemented group, but separated intake groups less readily than urinary excretion. Condition category: biomarker_context nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Blood and urine measurements did not respond identically to dietary depletion. organism: Homo sapiens tissue_or_cell_type: Urine and whole blood; nitrogen balance experimental_model: Controlled 84-day feeding experiment in ten adult male inmates aged 27–33; six unsupplemented and four supplemented limitations: Table 1 and the abstract distinguish unsupplemented and supplemented groups; one Methods sentence incorrectly says all received 10 mg. The table was visually checked. Historical assay and small cohort; the reported retention calculation is not direct measurement of intestinal absorption or tissue CoA. exposure: Nine-week/63-day experimental diet essentially free of B5 versus 10 mg/day B5 as calcium pantothenate; both groups then received 100 mg/day for seven days. cross_nutrient: false evidence_location: Primary PDF Table 1 visually checked; Tables 3–4 and Results pp.341–345. [b5-clin-fry1976] Metabolic response to a pantothenic acid deficient diet in humans. (1976). https://pubmed.ncbi.nlm.nih.gov/1011047/ DOI: 10.3177/jnsv.22.339

availability_state

nutrient_deficiency Imported condition classification; unverified.

cross_nutrient

true

evidence_location

Publisher primary Summary at https://www.sciencedirect.com/science/article/abs/pii/S0002916523345945 ; full article not retrieved.

experimental_model

Historical two-stage combined B5/B6 depletion experiment in male volunteers

exposure

First stage: two controls, two diet-only deficient men and one receiving diet plus both antagonists. Second stage: five men received B5/B6-deficient diet plus omega-methyl pantothenic acid and desoxypyridoxine; exact doses not available in the publisher summary.

limitations

Combined nutrient restriction plus antivitamins cannot identify the separate contribution of B5 or B6, a synergistic effect, or a universal immune defect. Reimmunization also changes prior antigen exposure.

nutrient_topic

Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)

organism

Homo sapiens

plain_language

Combined depletion and antivitamins impaired some antibody responses.

primary_references

[b5-clin-hodges1962] Factors affecting human antibody response. V. Combined deficiencies of pantothenic acid and pyridoxine. (1962). https://pubmed.ncbi.nlm.nih.gov/13907960/ DOI: 10.1093/ajcn/11.3.187

tissue_or_cell_type

Immunization responses and serum proteins

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 1327–1339

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Historical two-stage combined B5/B6 depletion experiment in male volunteers · source_derived_draft · unverified_draft

### b5-clin-combined-antibody-loss The five men receiving B5/B6-deficient diet plus both antagonists failed to respond to tetanus and typhoid O immunization and had little typhoid H response. Condition category: nutrient_deficiency nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Combined depletion and antivitamins impaired some antibody responses. organism: Homo sapiens tissue_or_cell_type: Immunization responses and serum proteins experimental_model: Historical two-stage combined B5/B6 depletion experiment in male volunteers limitations: Combined nutrient restriction plus antivitamins cannot identify the separate contribution of B5 or B6, a synergistic effect, or a universal immune defect. Reimmunization also changes prior antigen exposure. exposure: First stage: two controls, two diet-only deficient men and one receiving diet plus both antagonists. Second stage: five men received B5/B6-deficient diet plus omega-methyl pantothenic acid and desoxypyridoxine; exact doses not available in the publisher summary. cross_nutrient: true evidence_location: Publisher primary Summary at https://www.sciencedirect.com/science/article/abs/pii/S0002916523345945 ; full article not retrieved. [b5-clin-hodges1962] Factors affecting human antibody response. V. Combined deficiencies of pantothenic acid and pyridoxine. (1962). https://pubmed.ncbi.nlm.nih.gov/13907960/ DOI: 10.1093/ajcn/11.3.187

availability_state

nutrient_deficiency Imported condition classification; unverified.

cross_nutrient

true

evidence_location

Publisher primary Summary at https://www.sciencedirect.com/science/article/abs/pii/S0002916523345945 ; full article not retrieved.

experimental_model

Historical two-stage combined B5/B6 depletion experiment in male volunteers

exposure

First stage: two controls, two diet-only deficient men and one receiving diet plus both antagonists. Second stage: five men received B5/B6-deficient diet plus omega-methyl pantothenic acid and desoxypyridoxine; exact doses not available in the publisher summary.

limitations

Combined nutrient restriction plus antivitamins cannot identify the separate contribution of B5 or B6, a synergistic effect, or a universal immune defect. Reimmunization also changes prior antigen exposure. This is not a blinded comparison of B5 alone, B6 alone or their interaction.

nutrient_topic

Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)

organism

Homo sapiens

plain_language

Responses recovered after combined vitamin restoration and another immunization.

primary_references

[b5-clin-hodges1962] Factors affecting human antibody response. V. Combined deficiencies of pantothenic acid and pyridoxine. (1962). https://pubmed.ncbi.nlm.nih.gov/13907960/ DOI: 10.1093/ajcn/11.3.187

tissue_or_cell_type

Immunization responses and serum proteins

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 1355–1367

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Historical two-stage combined B5/B6 depletion experiment in male volunteers · source_derived_draft · unverified_draft

### b5-clin-combined-immune-recovery After vitamins were restored and the five subjects were reimmunized, tetanus and typhoid antibody responses were reported as normal. Condition category: nutrient_deficiency nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Responses recovered after combined vitamin restoration and another immunization. organism: Homo sapiens tissue_or_cell_type: Immunization responses and serum proteins experimental_model: Historical two-stage combined B5/B6 depletion experiment in male volunteers limitations: Combined nutrient restriction plus antivitamins cannot identify the separate contribution of B5 or B6, a synergistic effect, or a universal immune defect. Reimmunization also changes prior antigen exposure. This is not a blinded comparison of B5 alone, B6 alone or their interaction. exposure: First stage: two controls, two diet-only deficient men and one receiving diet plus both antagonists. Second stage: five men received B5/B6-deficient diet plus omega-methyl pantothenic acid and desoxypyridoxine; exact doses not available in the publisher summary. cross_nutrient: true evidence_location: Publisher primary Summary at https://www.sciencedirect.com/science/article/abs/pii/S0002916523345945 ; full article not retrieved. [b5-clin-hodges1962] Factors affecting human antibody response. V. Combined deficiencies of pantothenic acid and pyridoxine. (1962). https://pubmed.ncbi.nlm.nih.gov/13907960/ DOI: 10.1093/ajcn/11.3.187

availability_state

nutrient_deficiency Imported condition classification; unverified.

cross_nutrient

true

evidence_location

Publisher primary Summary at https://www.sciencedirect.com/science/article/abs/pii/S0002916523345945 ; full article not retrieved.

experimental_model

Historical two-stage combined B5/B6 depletion experiment in male volunteers

exposure

First stage: two controls, two diet-only deficient men and one receiving diet plus both antagonists. Second stage: five men received B5/B6-deficient diet plus omega-methyl pantothenic acid and desoxypyridoxine; exact doses not available in the publisher summary.

limitations

Combined nutrient restriction plus antivitamins cannot identify the separate contribution of B5 or B6, a synergistic effect, or a universal immune defect. Reimmunization also changes prior antigen exposure.

nutrient_topic

Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)

organism

Homo sapiens

plain_language

The immune impairment did not affect every tested antigen equally.

primary_references

[b5-clin-hodges1962] Factors affecting human antibody response. V. Combined deficiencies of pantothenic acid and pyridoxine. (1962). https://pubmed.ncbi.nlm.nih.gov/13907960/ DOI: 10.1093/ajcn/11.3.187

tissue_or_cell_type

Immunization responses and serum proteins

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 1341–1353

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Historical two-stage combined B5/B6 depletion experiment in male volunteers · source_derived_draft · unverified_draft

### b5-clin-combined-polio-preserved The same five men retained strong antibody responses to polio immunization despite their impaired tetanus and typhoid responses. Condition category: nutrient_deficiency nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: The immune impairment did not affect every tested antigen equally. organism: Homo sapiens tissue_or_cell_type: Immunization responses and serum proteins experimental_model: Historical two-stage combined B5/B6 depletion experiment in male volunteers limitations: Combined nutrient restriction plus antivitamins cannot identify the separate contribution of B5 or B6, a synergistic effect, or a universal immune defect. Reimmunization also changes prior antigen exposure. exposure: First stage: two controls, two diet-only deficient men and one receiving diet plus both antagonists. Second stage: five men received B5/B6-deficient diet plus omega-methyl pantothenic acid and desoxypyridoxine; exact doses not available in the publisher summary. cross_nutrient: true evidence_location: Publisher primary Summary at https://www.sciencedirect.com/science/article/abs/pii/S0002916523345945 ; full article not retrieved. [b5-clin-hodges1962] Factors affecting human antibody response. V. Combined deficiencies of pantothenic acid and pyridoxine. (1962). https://pubmed.ncbi.nlm.nih.gov/13907960/ DOI: 10.1093/ajcn/11.3.187

availability_state

nutrient_deficiency Imported condition classification; unverified.

cross_nutrient

true

evidence_location

Publisher primary Summary at https://www.sciencedirect.com/science/article/abs/pii/S0002916523345945 ; full article not retrieved.

experimental_model

Historical two-stage combined B5/B6 depletion experiment in male volunteers

exposure

First stage: two controls, two diet-only deficient men and one receiving diet plus both antagonists. Second stage: five men received B5/B6-deficient diet plus omega-methyl pantothenic acid and desoxypyridoxine; exact doses not available in the publisher summary.

limitations

Combined nutrient restriction plus antivitamins cannot identify the separate contribution of B5 or B6, a synergistic effect, or a universal immune defect. Reimmunization also changes prior antigen exposure. Only two subjects; not proof that prolonged isolated dietary deficiency cannot impair immunity.

nutrient_topic

Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)

organism

Homo sapiens

plain_language

Diet-only restriction gave a different result from the later antivitamin regimen.

primary_references

[b5-clin-hodges1962] Factors affecting human antibody response. V. Combined deficiencies of pantothenic acid and pyridoxine. (1962). https://pubmed.ncbi.nlm.nih.gov/13907960/ DOI: 10.1093/ajcn/11.3.187

tissue_or_cell_type

Immunization responses and serum proteins

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 1369–1381

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Historical two-stage combined B5/B6 depletion experiment in male volunteers · source_derived_draft · unverified_draft

### b5-clin-diet-only-immune-result The two men receiving the B5/B6-deficient diet without antagonists in the first stage showed minor abnormalities but no impairment of antibody production in that stage. Condition category: nutrient_deficiency nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Diet-only restriction gave a different result from the later antivitamin regimen. organism: Homo sapiens tissue_or_cell_type: Immunization responses and serum proteins experimental_model: Historical two-stage combined B5/B6 depletion experiment in male volunteers limitations: Combined nutrient restriction plus antivitamins cannot identify the separate contribution of B5 or B6, a synergistic effect, or a universal immune defect. Reimmunization also changes prior antigen exposure. Only two subjects; not proof that prolonged isolated dietary deficiency cannot impair immunity. exposure: First stage: two controls, two diet-only deficient men and one receiving diet plus both antagonists. Second stage: five men received B5/B6-deficient diet plus omega-methyl pantothenic acid and desoxypyridoxine; exact doses not available in the publisher summary. cross_nutrient: true evidence_location: Publisher primary Summary at https://www.sciencedirect.com/science/article/abs/pii/S0002916523345945 ; full article not retrieved. [b5-clin-hodges1962] Factors affecting human antibody response. V. Combined deficiencies of pantothenic acid and pyridoxine. (1962). https://pubmed.ncbi.nlm.nih.gov/13907960/ DOI: 10.1093/ajcn/11.3.187

availability_state

nutrient_deficiency Imported condition classification; unverified.

cross_nutrient

false

evidence_location

Primary PDF pp.1643–1654; design, results and discussion.

experimental_model

Historical controlled feeding study in six adult male volunteers; two diet-only deficient, two deficient plus antagonist, two supplemented controls

exposure

Tube-fed experimental formula; controls received pantothenic acid 20 mg/day, antagonist pair 750 then 1000 mg/day omega-methyl compound; recovery included 4000 mg/day vitamin. One man per pair received 10.8 mEq/day extra potassium.

limitations

Very small historical cohort; other vitamins and formula composition were controlled imperfectly. Diet-only and antagonist groups are distinguished. Measurements do not establish a universal symptom, adrenal disease mechanism or cellular CoA threshold.

nutrient_topic

Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)

organism

Homo sapiens

plain_language

Prolonged dietary depletion produced symptoms in this small controlled study, with earlier changes when an antagonist was also given.

primary_references

[b5-clin-hodges1958] Pantothenic acid deficiency in man. (1958). https://pubmed.ncbi.nlm.nih.gov/13587673/ DOI: 10.1172/jci103756

tissue_or_cell_type

Whole-person symptoms, serum and urine

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 1145–1157

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Historical controlled feeding study in six adult male volunteers; two diet-only deficient, two deficient plus antagonist, two supplemented controls · source_derived_draft · unverified_draft

### b5-clin-diet-symptoms In the 1958 six-man study, the two men on the B5-devoid diet developed fatigue, behavioral and gastrointestinal complaints and impaired coordination after the antagonist-treated pair; the supplemented controls remained well. Condition category: nutrient_deficiency nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Prolonged dietary depletion produced symptoms in this small controlled study, with earlier changes when an antagonist was also given. organism: Homo sapiens tissue_or_cell_type: Whole-person symptoms, serum and urine experimental_model: Historical controlled feeding study in six adult male volunteers; two diet-only deficient, two deficient plus antagonist, two supplemented controls limitations: Very small historical cohort; other vitamins and formula composition were controlled imperfectly. Diet-only and antagonist groups are distinguished. Measurements do not establish a universal symptom, adrenal disease mechanism or cellular CoA threshold. exposure: Tube-fed experimental formula; controls received pantothenic acid 20 mg/day, antagonist pair 750 then 1000 mg/day omega-methyl compound; recovery included 4000 mg/day vitamin. One man per pair received 10.8 mEq/day extra potassium. cross_nutrient: false evidence_location: Primary PDF pp.1643–1654; design, results and discussion. [b5-clin-hodges1958] Pantothenic acid deficiency in man. (1958). https://pubmed.ncbi.nlm.nih.gov/13587673/ DOI: 10.1172/jci103756

availability_state

nutrient_deficiency Imported condition classification; unverified.

cross_nutrient

false

evidence_location

Primary PDF pp.1643–1654; design, results and discussion.

experimental_model

Historical controlled feeding study in six adult male volunteers; two diet-only deficient, two deficient plus antagonist, two supplemented controls

exposure

Tube-fed experimental formula; controls received pantothenic acid 20 mg/day, antagonist pair 750 then 1000 mg/day omega-methyl compound; recovery included 4000 mg/day vitamin. One man per pair received 10.8 mEq/day extra potassium.

limitations

Very small historical cohort; other vitamins and formula composition were controlled imperfectly. Diet-only and antagonist groups are distinguished. Measurements do not establish a universal symptom, adrenal disease mechanism or cellular CoA threshold.

nutrient_topic

Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)

organism

Homo sapiens

plain_language

Urinary B5 fell substantially during sustained dietary depletion.

primary_references

[b5-clin-hodges1958] Pantothenic acid deficiency in man. (1958). https://pubmed.ncbi.nlm.nih.gov/13587673/ DOI: 10.1172/jci103756

tissue_or_cell_type

Whole-person symptoms, serum and urine

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 1159–1171

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Historical controlled feeding study in six adult male volunteers; two diet-only deficient, two deficient plus antagonist, two supplemented controls · source_derived_draft · unverified_draft

### b5-clin-diet-urine Urinary pantothenic acid approached zero after the eleventh week of the deficient diet in the 1958 experiment. Condition category: nutrient_deficiency nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Urinary B5 fell substantially during sustained dietary depletion. organism: Homo sapiens tissue_or_cell_type: Whole-person symptoms, serum and urine experimental_model: Historical controlled feeding study in six adult male volunteers; two diet-only deficient, two deficient plus antagonist, two supplemented controls limitations: Very small historical cohort; other vitamins and formula composition were controlled imperfectly. Diet-only and antagonist groups are distinguished. Measurements do not establish a universal symptom, adrenal disease mechanism or cellular CoA threshold. exposure: Tube-fed experimental formula; controls received pantothenic acid 20 mg/day, antagonist pair 750 then 1000 mg/day omega-methyl compound; recovery included 4000 mg/day vitamin. One man per pair received 10.8 mEq/day extra potassium. cross_nutrient: false evidence_location: Primary PDF pp.1643–1654; design, results and discussion. [b5-clin-hodges1958] Pantothenic acid deficiency in man. (1958). https://pubmed.ncbi.nlm.nih.gov/13587673/ DOI: 10.1172/jci103756

availability_state

nutrient_deficiency Imported condition classification; unverified.

cross_nutrient

false

evidence_location

Primary PDF Table 1 visually checked; Tables 3–4 and Results pp.341–345.

experimental_model

Controlled 84-day feeding experiment in ten adult male inmates aged 27–33; six unsupplemented and four supplemented

exposure

Nine-week/63-day experimental diet essentially free of B5 versus 10 mg/day B5 as calcium pantothenate; both groups then received 100 mg/day for seven days.

limitations

Table 1 and the abstract distinguish unsupplemented and supplemented groups; one Methods sentence incorrectly says all received 10 mg. The table was visually checked. Historical assay and small cohort; the reported retention calculation is not direct measurement of intestinal absorption or tissue CoA. The authors reported no defined clinical deficiency syndrome over nine weeks, although listlessness and fatigue were noted near the end.

nutrient_topic

Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)

organism

Homo sapiens

plain_language

Urinary excretion responded strongly to whether B5 was supplied.

primary_references

[b5-clin-fry1976] Metabolic response to a pantothenic acid deficient diet in humans. (1976). https://pubmed.ncbi.nlm.nih.gov/1011047/ DOI: 10.3177/jnsv.22.339

tissue_or_cell_type

Urine and whole blood; nitrogen balance

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 1229–1241

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Controlled 84-day feeding experiment in ten adult male inmates aged 27–33; six unsupplemented and four supplemented · source_derived_draft · unverified_draft

### b5-clin-urine-intake-response After 63 days, mean urinary pantothenate fell from 3.05 to 0.79 mg/day in the unsupplemented men; it rose from 3.95 to 5.84 mg/day with 10 mg/day supplementation. Condition category: nutrient_deficiency nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Urinary excretion responded strongly to whether B5 was supplied. organism: Homo sapiens tissue_or_cell_type: Urine and whole blood; nitrogen balance experimental_model: Controlled 84-day feeding experiment in ten adult male inmates aged 27–33; six unsupplemented and four supplemented limitations: Table 1 and the abstract distinguish unsupplemented and supplemented groups; one Methods sentence incorrectly says all received 10 mg. The table was visually checked. Historical assay and small cohort; the reported retention calculation is not direct measurement of intestinal absorption or tissue CoA. The authors reported no defined clinical deficiency syndrome over nine weeks, although listlessness and fatigue were noted near the end. exposure: Nine-week/63-day experimental diet essentially free of B5 versus 10 mg/day B5 as calcium pantothenate; both groups then received 100 mg/day for seven days. cross_nutrient: false evidence_location: Primary PDF Table 1 visually checked; Tables 3–4 and Results pp.341–345. [b5-clin-fry1976] Metabolic response to a pantothenic acid deficient diet in humans. (1976). https://pubmed.ncbi.nlm.nih.gov/1011047/ DOI: 10.3177/jnsv.22.339

availability_state

nutrient_deficiency Imported condition classification; unverified.

cross_nutrient

true

evidence_location

Full text lines 107, 123–125; Fig. 4F–G; Extended Data Fig. 5G–H

experimental_model

Matched PA-free/control diets in NOD/Scid mice bearing orthotopic human HCI002 breast-cancer xenografts with carbon-13 glucose tracing

exposure

Diets introduced at 6 weeks of age, progressively over 4 days; typically 5 weeks on the assigned diet before implantation and continued until collection. PA absence verified by LC-MS; control was composition-matched with PA added. Control n=7, PA-free n=8 tumors from independent mice. Carbon-13 glucose tracing followed by LC-MS.

limitations

The same paper found no significant fall in the corresponding CoA/acetyl-CoA pools in WMmix tumors. Tumor concentration and tracer labeling do not establish universal CoA depletion or a human anticancer diet; cellular composition and pool size can affect the measured label. This experiment does not establish a dietary pantothenate threshold or benefit from B5 supplementation.

nutrient_topic

Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)

organism

Human HCI002 grafts in Mus musculus hosts

plain_language

B5 restriction also reduced the measured labeled acetyl-CoA formed from glucose in these tumors.

primary_references

[b5-met-myc2024] Vitamin B&lt;sub&gt;5&lt;/sub&gt; supports MYC oncogenic metabolism and tumor progression in breast cancer. (2023). https://pubmed.ncbi.nlm.nih.gov/37946084/ DOI: 10.1038/s42255-023-00915-7

tissue_or_cell_type

Orthotopic HCI002 tumor tissue

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 1117–1129

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Matched PA-free/control diets in NOD/Scid mice bearing orthotopic human HCI002 breast-cancer xenografts with carbon-13 glucose tracing · source_derived_draft · unverified_draft

### b5-met-diet-hci002-acetylcoa Pantothenate deprivation reduced the amount of glucose-derived carbon-13-labeled acetyl-CoA in HCI002 xenografts. Condition category: nutrient_deficiency nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: B5 restriction also reduced the measured labeled acetyl-CoA formed from glucose in these tumors. organism: Human HCI002 grafts in Mus musculus hosts tissue_or_cell_type: Orthotopic HCI002 tumor tissue experimental_model: Matched PA-free/control diets in NOD/Scid mice bearing orthotopic human HCI002 breast-cancer xenografts with carbon-13 glucose tracing limitations: The same paper found no significant fall in the corresponding CoA/acetyl-CoA pools in WMmix tumors. Tumor concentration and tracer labeling do not establish universal CoA depletion or a human anticancer diet; cellular composition and pool size can affect the measured label. This experiment does not establish a dietary pantothenate threshold or benefit from B5 supplementation. exposure: Diets introduced at 6 weeks of age, progressively over 4 days; typically 5 weeks on the assigned diet before implantation and continued until collection. PA absence verified by LC-MS; control was composition-matched with PA added. Control n=7, PA-free n=8 tumors from independent mice. Carbon-13 glucose tracing followed by LC-MS. cross_nutrient: true evidence_location: Full text lines 107, 123–125; Fig. 4F–G; Extended Data Fig. 5G–H [b5-met-myc2024] Vitamin B&lt;sub&gt;5&lt;/sub&gt; supports MYC oncogenic metabolism and tumor progression in breast cancer. (2023). https://pubmed.ncbi.nlm.nih.gov/37946084/ DOI: 10.1038/s42255-023-00915-7

availability_state

nutrient_deficiency Imported condition classification; unverified.

cross_nutrient

false

evidence_location

Full text lines 123–125, 173, 229; Fig. 4F; Extended Data Fig. 5G–H

experimental_model

Matched PA-free/control diets in NOD/Scid mice bearing orthotopic human HCI002 breast-cancer xenografts

exposure

Diets introduced at 6 weeks of age, progressively over 4 days; typically 5 weeks on the assigned diet before implantation and continued until collection. PA absence verified by LC-MS; control was composition-matched with PA added. Control n=7, PA-free n=8 tumors from independent mice.

limitations

The same paper found no significant fall in the corresponding CoA/acetyl-CoA pools in WMmix tumors. Tumor concentration and tracer labeling do not establish universal CoA depletion or a human anticancer diet; cellular composition and pool size can affect the measured label. This experiment does not establish a dietary pantothenate threshold or benefit from B5 supplementation.

nutrient_topic

Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)

organism

Human HCI002 grafts in Mus musculus hosts

plain_language

Direct B5 restriction lowered the tumor CoA pool in this particular graft model.

primary_references

[b5-met-myc2024] Vitamin B&lt;sub&gt;5&lt;/sub&gt; supports MYC oncogenic metabolism and tumor progression in breast cancer. (2023). https://pubmed.ncbi.nlm.nih.gov/37946084/ DOI: 10.1038/s42255-023-00915-7

tissue_or_cell_type

Orthotopic HCI002 tumor tissue

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 1103–1115

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Matched PA-free/control diets in NOD/Scid mice bearing orthotopic human HCI002 breast-cancer xenografts · source_derived_draft · unverified_draft

### b5-met-diet-hci002-coa A pantothenate-free diet reduced free CoA measured in human HCI002 breast-cancer xenografts grown in mice. Condition category: nutrient_deficiency nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Direct B5 restriction lowered the tumor CoA pool in this particular graft model. organism: Human HCI002 grafts in Mus musculus hosts tissue_or_cell_type: Orthotopic HCI002 tumor tissue experimental_model: Matched PA-free/control diets in NOD/Scid mice bearing orthotopic human HCI002 breast-cancer xenografts limitations: The same paper found no significant fall in the corresponding CoA/acetyl-CoA pools in WMmix tumors. Tumor concentration and tracer labeling do not establish universal CoA depletion or a human anticancer diet; cellular composition and pool size can affect the measured label. This experiment does not establish a dietary pantothenate threshold or benefit from B5 supplementation. exposure: Diets introduced at 6 weeks of age, progressively over 4 days; typically 5 weeks on the assigned diet before implantation and continued until collection. PA absence verified by LC-MS; control was composition-matched with PA added. Control n=7, PA-free n=8 tumors from independent mice. cross_nutrient: false evidence_location: Full text lines 123–125, 173, 229; Fig. 4F; Extended Data Fig. 5G–H [b5-met-myc2024] Vitamin B&lt;sub&gt;5&lt;/sub&gt; supports MYC oncogenic metabolism and tumor progression in breast cancer. (2023). https://pubmed.ncbi.nlm.nih.gov/37946084/ DOI: 10.1038/s42255-023-00915-7

availability_state

nutrient_deficiency Imported condition classification; unverified.

cross_nutrient

false

evidence_location

Primary abstract, first four sentences

experimental_model

Rat pantothenate-deficient versus regular-diet feeding experiment

exposure

Pantothenic-acid-deficient diet; concentration and feeding duration unavailable in the abstract.

limitations

Whole-tissue CoA measurement does not establish unchanged subcellular pools or flux. Growth was impaired, so maintained CoA did not show nutritional adequacy. Different tissues/models from the tumor study do not constitute a same-context contradiction. This experiment does not establish a dietary pantothenate threshold or benefit from B5 supplementation.

nutrient_topic

Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)

organism

Rattus norvegicus

plain_language

Large drops in tissue B5 did not necessarily deplete the measured CoA pool in this rat experiment.

primary_references

[b5-met-rat1982] Coenzyme A metabolism in pantothenic acid-deficient rats. (1982). https://pubmed.ncbi.nlm.nih.gov/7086543/ DOI: 10.1093/jn/112.6.1144

tissue_or_cell_type

Heart, kidney, gastrocnemius, testes and liver

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 1131–1143

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rat pantothenate-deficient versus regular-diet feeding experiment · source_derived_draft · unverified_draft

### b5-met-rat-diet-coa-preserved Rats fed the pantothenate-deficient diet retained control-level tissue CoA despite more than 90% lower pantothenate in heart, kidney, gastrocnemius and testes and about 70% lower liver pantothenate. Condition category: nutrient_deficiency nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Large drops in tissue B5 did not necessarily deplete the measured CoA pool in this rat experiment. organism: Rattus norvegicus tissue_or_cell_type: Heart, kidney, gastrocnemius, testes and liver experimental_model: Rat pantothenate-deficient versus regular-diet feeding experiment limitations: Whole-tissue CoA measurement does not establish unchanged subcellular pools or flux. Growth was impaired, so maintained CoA did not show nutritional adequacy. Different tissues/models from the tumor study do not constitute a same-context contradiction. This experiment does not establish a dietary pantothenate threshold or benefit from B5 supplementation. exposure: Pantothenic-acid-deficient diet; concentration and feeding duration unavailable in the abstract. cross_nutrient: false evidence_location: Primary abstract, first four sentences [b5-met-rat1982] Coenzyme A metabolism in pantothenic acid-deficient rats. (1982). https://pubmed.ncbi.nlm.nih.gov/7086543/ DOI: 10.1093/jn/112.6.1144

availability_state

nutrient_deficiency Imported condition classification; unverified.

cross_nutrient

false

experimental_model

Mice fed pantothenic-acid-deficient, normal or high-pantothenic-acid diets; intestinal uptake assays

exposure

High, normal and deficient pantothenate diets; uptake assayed at 5 micromolar. An antibiotic was needed to elicit severe deficiency; exact diet amounts and antibiotic are not reported in the abstract.

limitations

The abstract also describes a small late-deficiency increase in Vmax. A null result at 5 micromolar does not rule out all transport adaptation. Antibiotic use complicates attribution and does not quantify the human microbiome contribution.

nutrient_topic

Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)

organism

Mus musculus

plain_language

Low dietary B5 did not cause a clear increase in intestinal B5 uptake at the tested concentration.

primary_references

[b5-trans-diet1989] Do dietary levels of pantothenic acid regulate its intestinal uptake in mice? (1989). https://pubmed.ncbi.nlm.nih.gov/2621490/ DOI: 10.1093/jn/119.12.1973

tissue_or_cell_type

Small intestine

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 262–273

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mice fed pantothenic-acid-deficient, normal or high-pantothenic-acid diets; intestinal uptake assays · source_derived_draft · unverified_draft

### b5-trans-dietary-deficiency-uptake Dietary pantothenate level did not change mouse intestinal pantothenate uptake assayed at 5 micromolar, including comparisons involving pantothenate-deficient diets. Condition category: nutrient_deficiency nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Low dietary B5 did not cause a clear increase in intestinal B5 uptake at the tested concentration. organism: Mus musculus tissue_or_cell_type: Small intestine experimental_model: Mice fed pantothenic-acid-deficient, normal or high-pantothenic-acid diets; intestinal uptake assays limitations: The abstract also describes a small late-deficiency increase in Vmax. A null result at 5 micromolar does not rule out all transport adaptation. Antibiotic use complicates attribution and does not quantify the human microbiome contribution. exposure: High, normal and deficient pantothenate diets; uptake assayed at 5 micromolar. An antibiotic was needed to elicit severe deficiency; exact diet amounts and antibiotic are not reported in the abstract. cross_nutrient: false [b5-trans-diet1989] Do dietary levels of pantothenic acid regulate its intestinal uptake in mice? (1989). https://pubmed.ncbi.nlm.nih.gov/2621490/ DOI: 10.1093/jn/119.12.1973

cross_nutrient

true

experimental_model

Human SMVT cloned from JAR cells, expressed in human retinal pigment epithelial cells and Xenopus laevis oocytes

exposure

Electrophysiology after human SMVT expression; pantothenate and extracellular sodium varied.

limitations

Heterologous human-protein experiments establish transport properties; they do not quantify whole-body absorption or nutrient deficiency from supplement competition.

nutrient_topic

Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)

organism

Homo sapiens (protein); Xenopus laevis (expression host)

plain_language

Pantothenate transport through human SMVT moves net positive charge inward.

primary_references

[b5-trans-wang1999] Human placental Na+-dependent multivitamin transporter. Cloning, functional expression, gene structure, and chromosomal localization. (1999). https://pubmed.ncbi.nlm.nih.gov/10329687/ DOI: 10.1074/jbc.274.21.14875

tissue_or_cell_type

Oocyte plasma membrane

Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 210–221

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human SMVT cloned from JAR cells, expressed in human retinal pigment epithelial cells and Xenopus laevis oocytes · source_derived_draft · unverified_draft

### b5-trans-pantothenate-current Pantothenate evoked sodium-, concentration- and potential-dependent inward currents in Xenopus oocytes expressing human SLC5A6. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Pantothenate transport through human SMVT moves net positive charge inward. organism: Homo sapiens (protein); Xenopus laevis (expression host) tissue_or_cell_type: Oocyte plasma membrane experimental_model: Human SMVT cloned from JAR cells, expressed in human retinal pigment epithelial cells and Xenopus laevis oocytes limitations: Heterologous human-protein experiments establish transport properties; they do not quantify whole-body absorption or nutrient deficiency from supplement competition. exposure: Electrophysiology after human SMVT expression; pantothenate and extracellular sodium varied. cross_nutrient: true [b5-trans-wang1999] Human placental Na+-dependent multivitamin transporter. Cloning, functional expression, gene structure, and chromosomal localization. (1999). https://pubmed.ncbi.nlm.nih.gov/10329687/ DOI: 10.1074/jbc.274.21.14875

cross_nutrient

true

experimental_model

Cryo-EM of engineered human SMVT with nanobody-assisted alignment; functional uptake assays in HEK293T cells

exposure

Biotin uptake assay: 5 micromolar unlabeled biotin plus [3H]biotin at a 300:1 molar ratio; 30 degrees C for ten minutes; inhibitor concentration varied.

limitations

In-vitro IC50 depends on tracer/substrate concentration and expression conditions; it is not a human supplement dose, affinity constant, or threshold for biotin deficiency.

nutrient_topic

Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)

organism

Homo sapiens

plain_language

D-pantothenic acid competed with biotin uptake in the SMVT cell assay.

primary_references

[b5-trans-structure2026] Structural basis for multivitamin recognition and transport by human SMVT. (2026). https://pubmed.ncbi.nlm.nih.gov/42364996/ DOI: 10.1038/s41467-026-74948-3

tissue_or_cell_type

HEK293T cells expressing human SMVT

Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 431–442

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cryo-EM of engineered human SMVT with nanobody-assisted alignment; functional uptake assays in HEK293T cells · source_derived_draft · unverified_draft

### b5-trans-pantothenate-inhibits-biotin D-pantothenic acid inhibited human SMVT-mediated radiolabeled biotin uptake with an IC50 of 89.7 micromolar in the 2026 HEK293T assay. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: D-pantothenic acid competed with biotin uptake in the SMVT cell assay. organism: Homo sapiens tissue_or_cell_type: HEK293T cells expressing human SMVT experimental_model: Cryo-EM of engineered human SMVT with nanobody-assisted alignment; functional uptake assays in HEK293T cells limitations: In-vitro IC50 depends on tracer/substrate concentration and expression conditions; it is not a human supplement dose, affinity constant, or threshold for biotin deficiency. exposure: Biotin uptake assay: 5 micromolar unlabeled biotin plus [3H]biotin at a 300:1 molar ratio; 30 degrees C for ten minutes; inhibitor concentration varied. cross_nutrient: true [b5-trans-structure2026] Structural basis for multivitamin recognition and transport by human SMVT. (2026). https://pubmed.ncbi.nlm.nih.gov/42364996/ DOI: 10.1038/s41467-026-74948-3

cross_nutrient

true

experimental_model

Isolated human peripheral blood mononuclear cells; radiolabeled biotin uptake and efflux assays

exposure

[3H]biotin-loaded PBMC challenged with extracellular pantothenate; efflux-specific concentration not supplied in the abstract.

limitations

P greater than 0.05 is a null result in this assay, not proof of no effect under every condition. The experiment does not identify a general B5 export transporter or SMVT-mediated exchange mechanism.

nutrient_topic

Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)

organism

Homo sapiens

plain_language

Adding B5 outside these blood cells did not drive biotin back out.

primary_references

[b5-trans-pbmc1999] Human peripheral blood mononuclear cells: ; Inhibition of biotin transport by reversible competition with pantothenic acid is quantitatively minor. (1999). https://pubmed.ncbi.nlm.nih.gov/15539319/ DOI: 10.1016/s0955-2863(99)00024-8

tissue_or_cell_type

Isolated peripheral blood mononuclear cells

Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 470–481

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Isolated human peripheral blood mononuclear cells; radiolabeled biotin uptake and efflux assays · source_derived_draft · unverified_draft

### b5-trans-pbmc-efflux-null Extracellular pantothenate did not significantly change biotin efflux from radiolabeled-biotin-loaded human peripheral blood mononuclear cells. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Adding B5 outside these blood cells did not drive biotin back out. organism: Homo sapiens tissue_or_cell_type: Isolated peripheral blood mononuclear cells experimental_model: Isolated human peripheral blood mononuclear cells; radiolabeled biotin uptake and efflux assays limitations: P greater than 0.05 is a null result in this assay, not proof of no effect under every condition. The experiment does not identify a general B5 export transporter or SMVT-mediated exchange mechanism. exposure: [3H]biotin-loaded PBMC challenged with extracellular pantothenate; efflux-specific concentration not supplied in the abstract. cross_nutrient: true [b5-trans-pbmc1999] Human peripheral blood mononuclear cells: ; Inhibition of biotin transport by reversible competition with pantothenic acid is quantitatively minor. (1999). https://pubmed.ncbi.nlm.nih.gov/15539319/ DOI: 10.1016/s0955-2863(99)00024-8

cross_nutrient

true

experimental_model

Isolated human peripheral blood mononuclear cells; radiolabeled biotin uptake and efflux assays

exposure

10–1000 nmol/L pantothenic acid with 475 pmol/L [3H]biotin.

limitations

Cell-type-specific assay; the transporter was not molecularly identified as SLC5A6. This does not negate shared SMVT competition in other models and does not test high-dose supplementation.

nutrient_topic

Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)

organism

Homo sapiens

plain_language

At the tested physiological concentrations, B5 only slightly reduced biotin entry into these blood cells.

primary_references

[b5-trans-pbmc1999] Human peripheral blood mononuclear cells: ; Inhibition of biotin transport by reversible competition with pantothenic acid is quantitatively minor. (1999). https://pubmed.ncbi.nlm.nih.gov/15539319/ DOI: 10.1016/s0955-2863(99)00024-8

tissue_or_cell_type

Isolated peripheral blood mononuclear cells

Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 457–468

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Isolated human peripheral blood mononuclear cells; radiolabeled biotin uptake and efflux assays · source_derived_draft · unverified_draft

### b5-trans-pbmc-small-competition Pantothenate at 10–1000 nmol/L reduced uptake of 475 pmol/L biotin by less than 12% in isolated human peripheral blood mononuclear cells. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: At the tested physiological concentrations, B5 only slightly reduced biotin entry into these blood cells. organism: Homo sapiens tissue_or_cell_type: Isolated peripheral blood mononuclear cells experimental_model: Isolated human peripheral blood mononuclear cells; radiolabeled biotin uptake and efflux assays limitations: Cell-type-specific assay; the transporter was not molecularly identified as SLC5A6. This does not negate shared SMVT competition in other models and does not test high-dose supplementation. exposure: 10–1000 nmol/L pantothenic acid with 475 pmol/L [3H]biotin. cross_nutrient: true [b5-trans-pbmc1999] Human peripheral blood mononuclear cells: ; Inhibition of biotin transport by reversible competition with pantothenic acid is quantitatively minor. (1999). https://pubmed.ncbi.nlm.nih.gov/15539319/ DOI: 10.1016/s0955-2863(99)00024-8

cross_nutrient

true

experimental_model

Purified recombinant human PANK3, crystallography and biochemical ligand-binding/heterodimer experiments

exposure

In-vitro biochemical exposure; concentrations not extracted.

limitations

Abstract-level structural and biochemical findings; no diet or Mg-repletion experiment. Substrate concentrations not established here.

nutrient_topic

Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)

organism

Homo sapiens

plain_language

PANK3 starts vitamin B5 activation by adding phosphate.

primary_references

[b5-bio-pank3allosteric] Allosteric Regulation of Mammalian Pantothenate Kinase. (2016). https://pubmed.ncbi.nlm.nih.gov/27555321/ DOI: 10.1074/jbc.m116.748061

tissue_or_cell_type

Purified recombinant protein; no intact tissue

Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 483–494

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Purified recombinant human PANK3, crystallography and biochemical ligand-binding/heterodimer experiments · source_derived_draft · unverified_draft

### b5-bio-pank3-phosphorylation Human PANK3 catalyzes ATP-dependent conversion of pantothenate to 4′-phosphopantothenate. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: PANK3 starts vitamin B5 activation by adding phosphate. organism: Homo sapiens tissue_or_cell_type: Purified recombinant protein; no intact tissue experimental_model: Purified recombinant human PANK3, crystallography and biochemical ligand-binding/heterodimer experiments limitations: Abstract-level structural and biochemical findings; no diet or Mg-repletion experiment. Substrate concentrations not established here. exposure: In-vitro biochemical exposure; concentrations not extracted. cross_nutrient: true [b5-bio-pank3allosteric] Allosteric Regulation of Mammalian Pantothenate Kinase. (2016). https://pubmed.ncbi.nlm.nih.gov/27555321/ DOI: 10.1074/jbc.m116.748061

cross_nutrient

false

experimental_model

Recombinant human PANK4 biochemistry with evolutionary sequence and mutagenesis comparisons

exposure

Recombinant enzyme and catalytic-residue mutagenesis comparison; assay concentrations not extracted.

limitations

This is evidence about an enzyme paralogue, not loss of all cellular pantothenate phosphorylation. Other species PANK4 enzymes differ.

nutrient_topic

Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)

organism

Homo sapiens

plain_language

The protein named PANK4 is not another working B5 kinase in humans.

primary_references

[b5-bio-pank4pseudo] Human pantothenate kinase 4 is a pseudo-pantothenate kinase. (2019). https://pubmed.ncbi.nlm.nih.gov/30927326/ DOI: 10.1002/pro.3611

tissue_or_cell_type

Purified recombinant protein; no intact tissue

Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 652–663

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant human PANK4 biochemistry with evolutionary sequence and mutagenesis comparisons · source_derived_draft · unverified_draft

### b5-bio-pank4-pseudokinase Biochemical testing found that human PANK4 lacks pantothenate kinase activity, unlike active PANK1–3 enzymes. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: The protein named PANK4 is not another working B5 kinase in humans. organism: Homo sapiens tissue_or_cell_type: Purified recombinant protein; no intact tissue experimental_model: Recombinant human PANK4 biochemistry with evolutionary sequence and mutagenesis comparisons limitations: This is evidence about an enzyme paralogue, not loss of all cellular pantothenate phosphorylation. Other species PANK4 enzymes differ. exposure: Recombinant enzyme and catalytic-residue mutagenesis comparison; assay concentrations not extracted. cross_nutrient: false [b5-bio-pank4pseudo] Human pantothenate kinase 4 is a pseudo-pantothenate kinase. (2019). https://pubmed.ncbi.nlm.nih.gov/30927326/ DOI: 10.1002/pro.3611

cross_nutrient

false

evidence_location

Primary indexed abstract.

experimental_model

Pharmacokinetic/metabolic study in four children with nephropathic cystinosis

exposure

Historical oral D-pantethine exposures 70–1000 mg/kg/day.

limitations

Very high drug-like exposures in a rare disease; not nutritional dosing, ordinary healthy-person pharmacokinetics or proof of the mechanism behind lipid-trial effects. Rat intestinal-enzyme kinetic data in the same paper are not assigned to humans. The primary authors described rapid hydrolysis. This human observation does not by itself specify the reductive/disulfide steps or a human vanin isoform.

nutrient_topic

Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)

organism

Homo sapiens

plain_language

The administered derivative was rapidly converted; the blood exposure was not simply unchanged pantethine.

primary_references

[b5-clin-wittwer1985] Metabolism of pantethine in cystinosis. (1985). https://pubmed.ncbi.nlm.nih.gov/4056044/ DOI: 10.1172/jci112152

tissue_or_cell_type

Plasma after oral D-pantethine

Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 1467–1479

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Pharmacokinetic/metabolic study in four children with nephropathic cystinosis · source_derived_draft · unverified_draft

### b5-clin-pantethine-human-products After oral D-pantethine in the four cystinotic children, pantothenic acid and cysteamine appeared as products, while intact pantethine was not detected in plasma. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: The administered derivative was rapidly converted; the blood exposure was not simply unchanged pantethine. organism: Homo sapiens tissue_or_cell_type: Plasma after oral D-pantethine experimental_model: Pharmacokinetic/metabolic study in four children with nephropathic cystinosis limitations: Very high drug-like exposures in a rare disease; not nutritional dosing, ordinary healthy-person pharmacokinetics or proof of the mechanism behind lipid-trial effects. Rat intestinal-enzyme kinetic data in the same paper are not assigned to humans. The primary authors described rapid hydrolysis. This human observation does not by itself specify the reductive/disulfide steps or a human vanin isoform. exposure: Historical oral D-pantethine exposures 70–1000 mg/kg/day. cross_nutrient: false evidence_location: Primary indexed abstract. [b5-clin-wittwer1985] Metabolism of pantethine in cystinosis. (1985). https://pubmed.ncbi.nlm.nih.gov/4056044/ DOI: 10.1172/jci112152

availability_state

biomarker_context Imported condition classification; unverified.

cross_nutrient

false

evidence_location

Primary indexed abstract.

experimental_model

Observational study of 91 adults aged at least 65, including institutionalized and community participants

exposure

Microbiological and radioimmunoassay analyses of free and derivative pantothenate fractions.

limitations

Assay-specific findings; urinary free pantothenate is distinct from intracellular CoA and its acyl derivatives.

nutrient_topic

Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)

organism

Homo sapiens

plain_language

The urinary assay mostly described free vitamin, not the cell’s activated CoA pool.

primary_references

[b5-clin-tarr1981] Pantothenic acid nutritional status in the elderly--institutionalized and noninstitutionalized. (1981). https://pubmed.ncbi.nlm.nih.gov/7025609/ DOI: 10.1093/ajcn/34.9.1736

tissue_or_cell_type

Fasting blood, 24-hour urine and seven-day diet records

trigger_kind

biomarker_context Imported condition classification; unverified.

Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 1313–1325

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Observational study of 91 adults aged at least 65, including institutionalized and community participants · source_derived_draft · unverified_draft

### b5-clin-urinary-species In the elderly cohort, free pantothenic acid was detected in urine, whereas the measured phosphoderivative fraction was not; microbiological and radioimmunoassay estimates correlated at r=0.91. Condition category: biomarker_context nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: The urinary assay mostly described free vitamin, not the cell’s activated CoA pool. organism: Homo sapiens tissue_or_cell_type: Fasting blood, 24-hour urine and seven-day diet records experimental_model: Observational study of 91 adults aged at least 65, including institutionalized and community participants limitations: Assay-specific findings; urinary free pantothenate is distinct from intracellular CoA and its acyl derivatives. exposure: Microbiological and radioimmunoassay analyses of free and derivative pantothenate fractions. cross_nutrient: false evidence_location: Primary indexed abstract. [b5-clin-tarr1981] Pantothenic acid nutritional status in the elderly--institutionalized and noninstitutionalized. (1981). https://pubmed.ncbi.nlm.nih.gov/7025609/ DOI: 10.1093/ajcn/34.9.1736

cross_nutrient

true

experimental_model

Cryo-EM of engineered human SMVT with nanobody-assisted alignment; functional uptake assays in HEK293T cells

exposure

3.7-angstrom cryo-EM pantothenate complex; molecular-dynamics support for the binding model.

limitations

Engineered, purified transporter structure supports a binding mechanism; it does not establish nutritional competition severity in vivo. The structural construct has altered biotin transport kinetics relative to wild type. Atom-level interactions are structural-model interpretations; no specific dietary threshold follows.

nutrient_topic

Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)

organism

Homo sapiens

plain_language

SMVT anchors the charged end of B5 through specific contacts in its binding pocket.

primary_references

[b5-trans-structure2026] Structural basis for multivitamin recognition and transport by human SMVT. (2026). https://pubmed.ncbi.nlm.nih.gov/42364996/ DOI: 10.1038/s41467-026-74948-3

tissue_or_cell_type

Purified human SMVT ligand-binding pocket

Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 418–429

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cryo-EM of engineered human SMVT with nanobody-assisted alignment; functional uptake assays in HEK293T cells · source_derived_draft · unverified_draft

### b5-trans-pantothenate-carboxyl-recognition In the human SMVT–pantothenate structural model, the substrate carboxyl group interacts with backbone amino groups of Ser81/Ala84 and hydrogen-bonds to Tyr156. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: SMVT anchors the charged end of B5 through specific contacts in its binding pocket. organism: Homo sapiens tissue_or_cell_type: Purified human SMVT ligand-binding pocket experimental_model: Cryo-EM of engineered human SMVT with nanobody-assisted alignment; functional uptake assays in HEK293T cells limitations: Engineered, purified transporter structure supports a binding mechanism; it does not establish nutritional competition severity in vivo. The structural construct has altered biotin transport kinetics relative to wild type. Atom-level interactions are structural-model interpretations; no specific dietary threshold follows. exposure: 3.7-angstrom cryo-EM pantothenate complex; molecular-dynamics support for the binding model. cross_nutrient: true [b5-trans-structure2026] Structural basis for multivitamin recognition and transport by human SMVT. (2026). https://pubmed.ncbi.nlm.nih.gov/42364996/ DOI: 10.1038/s41467-026-74948-3

cross_nutrient

true

experimental_model

Cryo-EM of engineered human SMVT with nanobody-assisted alignment; functional uptake assays in HEK293T cells

exposure

SMVTEM/NbALFA complexes incubated with 2 mM D-pantothenic acid, 4 mM biotin or 22 mM oxidized alpha-lipoic acid for separate structures.

limitations

Engineered, purified transporter structure supports a binding mechanism; it does not establish nutritional competition severity in vivo. The structural construct has altered biotin transport kinetics relative to wild type. These are separate ligand-bound complexes, not simultaneous occupancy.

nutrient_topic

Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)

organism

Homo sapiens

plain_language

B5, biotin and free lipoate use the same binding pocket in SMVT.

primary_references

[b5-trans-structure2026] Structural basis for multivitamin recognition and transport by human SMVT. (2026). https://pubmed.ncbi.nlm.nih.gov/42364996/ DOI: 10.1038/s41467-026-74948-3

tissue_or_cell_type

Purified human SMVT; HEK293-derived expression system

Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 405–416

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cryo-EM of engineered human SMVT with nanobody-assisted alignment; functional uptake assays in HEK293T cells · source_derived_draft · unverified_draft

### b5-trans-shared-substrate-site Human SMVT cryo-EM complexes placed pantothenate, biotin and oxidized lipoate in substantially overlapping positions within one central substrate-binding pocket. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: B5, biotin and free lipoate use the same binding pocket in SMVT. organism: Homo sapiens tissue_or_cell_type: Purified human SMVT; HEK293-derived expression system experimental_model: Cryo-EM of engineered human SMVT with nanobody-assisted alignment; functional uptake assays in HEK293T cells limitations: Engineered, purified transporter structure supports a binding mechanism; it does not establish nutritional competition severity in vivo. The structural construct has altered biotin transport kinetics relative to wild type. These are separate ligand-bound complexes, not simultaneous occupancy. exposure: SMVTEM/NbALFA complexes incubated with 2 mM D-pantothenic acid, 4 mM biotin or 22 mM oxidized alpha-lipoic acid for separate structures. cross_nutrient: true [b5-trans-structure2026] Structural basis for multivitamin recognition and transport by human SMVT. (2026). https://pubmed.ncbi.nlm.nih.gov/42364996/ DOI: 10.1038/s41467-026-74948-3

cross_nutrient

true

experimental_model

Human SMVT cloned from JAR cells, expressed in human retinal pigment epithelial cells and Xenopus laevis oocytes

exposure

Sodium concentration-response of cloned human SMVT-mediated vitamin uptake.

limitations

Heterologous human-protein experiments establish transport properties; they do not quantify whole-body absorption or nutrient deficiency from supplement competition. The ratio is inferred from transport kinetics, rather than direct counting of individual cotransport events.

nutrient_topic

Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)

organism

Homo sapiens

plain_language

Two sodium ions accompany each pantothenate molecule in the reported SMVT transport model.

primary_references

[b5-trans-wang1999] Human placental Na+-dependent multivitamin transporter. Cloning, functional expression, gene structure, and chromosomal localization. (1999). https://pubmed.ncbi.nlm.nih.gov/10329687/ DOI: 10.1074/jbc.274.21.14875

tissue_or_cell_type

HRPE cell plasma membrane

Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 197–208

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human SMVT cloned from JAR cells, expressed in human retinal pigment epithelial cells and Xenopus laevis oocytes · source_derived_draft · unverified_draft

### b5-trans-two-sodium-pantothenate Sodium-dependence kinetics of human SLC5A6-mediated pantothenate uptake supported a 2:1 sodium:pantothenate coupling ratio. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Two sodium ions accompany each pantothenate molecule in the reported SMVT transport model. organism: Homo sapiens tissue_or_cell_type: HRPE cell plasma membrane experimental_model: Human SMVT cloned from JAR cells, expressed in human retinal pigment epithelial cells and Xenopus laevis oocytes limitations: Heterologous human-protein experiments establish transport properties; they do not quantify whole-body absorption or nutrient deficiency from supplement competition. The ratio is inferred from transport kinetics, rather than direct counting of individual cotransport events. exposure: Sodium concentration-response of cloned human SMVT-mediated vitamin uptake. cross_nutrient: true [b5-trans-wang1999] Human placental Na+-dependent multivitamin transporter. Cloning, functional expression, gene structure, and chromosomal localization. (1999). https://pubmed.ncbi.nlm.nih.gov/10329687/ DOI: 10.1074/jbc.274.21.14875

availability_state

machinery_impairment Imported condition classification; unverified.

evidence_span

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experimental_model

Chronic ethanol exposure in rodents and human Caco-2 cells

exposure

Chronic ethanol feeding or culture exposure

limitations

Animal feeding and human cell experiments are separate; no human dietary depletion threshold was established.

nutrient_topic

Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin

organism

Homo sapiens

plain_language

Alcohol exposure reduced the cell signals that produce the shared vitamin transporter.

primary_references

[b7-p21148397] Inhibition of intestinal biotin absorption by chronic alcohol feeding: cellular and molecular mechanisms. (2011). https://pubmed.ncbi.nlm.nih.gov/21148397/ DOI: 10.1152/ajpgi.00465.2010

tissue_or_cell_type

Caco-2 intestinal epithelial cells

trigger_kind

machinery_impairment Imported condition classification; unverified.

Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 221–232

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Chronic ethanol exposure in rodents and human Caco-2 cells · source_derived_draft · unverified_draft

### b7-alcohol-promoters Chronic ethanol exposure reduced activity of both SLC5A6 promoters P1 and P2 in human Caco-2 cells. Condition category: machinery_impairment nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Alcohol exposure reduced the cell signals that produce the shared vitamin transporter. organism: Homo sapiens tissue_or_cell_type: Caco-2 intestinal epithelial cells experimental_model: Chronic ethanol exposure in rodents and human Caco-2 cells limitations: Animal feeding and human cell experiments are separate; no human dietary depletion threshold was established. exposure: Chronic ethanol feeding or culture exposure evidence_span: {"source_cache": "artifacts/biotin-research/21148397.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2398f4926e678d4650eba6488cab945c2d651a7c8e6c2f8fd00794c0ea891d4d", "start_char": 0, "end_char": 1829, "text_sha256": "2398f4926e678d4650eba6488cab945c2d651a7c8e6c2f8fd00794c0ea891d4d"} [b7-p21148397] Inhibition of intestinal biotin absorption by chronic alcohol feeding: cellular and molecular mechanisms. (2011). https://pubmed.ncbi.nlm.nih.gov/21148397/ DOI: 10.1152/ajpgi.00465.2010

cross_nutrient

Provides the B5-derived CoA partner required by PDH, OGDH, BCKDH and OADH; simultaneous B1/B5 depletion was not tested.

evidence

[{"paper_key": "daugherty-2002-coa", "source_bundle": "artifacts/thiamine_metabolism_sources.json", "passage_ids": ["abstract"], "locator": "Primary publication abstract", "preservation": "Exact text retained in the source bundle; full source document retained when openly retrievable."}]

experimental_model

Reconstituted human enzyme pathway.

limitations

Cross-pathway connection is biochemical integration, not a tested clinical supplementation interaction.

nutrient

Thiamine (vitamin B1) · Thiamine (vitamin B1)

nutrient_topic

Thiamine research collection; topical membership is not evidence of a direct dietary effect. · Thiamine (vitamin B1)

organism

Homo sapiens

plain_language

Vitamin B5 supplies a separate carrier used after B1-dependent decarboxylation. The experiment starts with phosphorylated B5, so it does not test absorption or the first phosphorylation step.

primary_references

[daugherty-2002-coa] Complete reconstitution of the human coenzyme A biosynthetic pathway via comparative genomics (2002). https://pubmed.ncbi.nlm.nih.gov/11923312/ DOI: 10.1074/jbc.m201708200

tissue_or_cell_type

Purified recombinant enzymes

Thiamine: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 731–743

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Reconstituted human enzyme pathway. · source_derived_draft · unverified_draft

### b1-coa-b5-downstream-biosynthesis Purified human PPCS, PPCDC and bifunctional CoA synthase reconstituted CoA synthesis from phosphopantothenate in vitro. Condition category: normal nutrient_topic: Thiamine research collection; topical membership is not evidence of a direct dietary effect. plain_language: Vitamin B5 supplies a separate carrier used after B1-dependent decarboxylation. The experiment starts with phosphorylated B5, so it does not test absorption or the first phosphorylation step. organism: Homo sapiens tissue_or_cell_type: Purified recombinant enzymes experimental_model: Reconstituted human enzyme pathway. limitations: Cross-pathway connection is biochemical integration, not a tested clinical supplementation interaction. evidence: [{"paper_key": "daugherty-2002-coa", "source_bundle": "artifacts/thiamine_metabolism_sources.json", "passage_ids": ["abstract"], "locator": "Primary publication abstract", "preservation": "Exact text retained in the source bundle; full source document retained when openly retrievable."}] cross_nutrient: Provides the B5-derived CoA partner required by PDH, OGDH, BCKDH and OADH; simultaneous B1/B5 depletion was not tested. nutrient: Thiamine (vitamin B1) [daugherty-2002-coa] Complete reconstitution of the human coenzyme A biosynthetic pathway via comparative genomics (2002). https://pubmed.ncbi.nlm.nih.gov/11923312/ DOI: 10.1074/jbc.m201708200

cross_nutrient

B1-dependent E1 and B5-derived CoA participate in different sequential steps.

evidence

[{"paper_key": "jiang-2018-pdh-core", "source_bundle": "artifacts/thiamine_metabolism_sources.json", "passage_ids": ["p-32"], "locator": "acetyl-accepting CoA", "preservation": "Exact text retained in the source bundle; full source document retained when openly retrievable."}]

experimental_model

Human DLAT cryo-EM; bacterial ligand poses used for modeling.

limitations

Ligand positions were modeled, not directly resolved in a human substrate-bound structure; no intake experiment.

nutrient

Thiamine (vitamin B1) · Thiamine (vitamin B1)

nutrient_topic

Thiamine research collection; topical membership is not evidence of a direct dietary effect. · Thiamine (vitamin B1)

organism

Homo sapiens

plain_language

After B1 acts at E1, the E2 protein transfers the acetyl group onto CoA, a vitamin B5-derived carrier.

primary_references

[jiang-2018-pdh-core] Atomic Structure of the E2 Inner Core of Human Pyruvate Dehydrogenase Complex (2018). https://pubmed.ncbi.nlm.nih.gov/29608861/ DOI: 10.1021/acs.biochem.8b00357

tissue_or_cell_type

Purified catalytic core

Thiamine: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 690–702

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human DLAT cryo-EM; bacterial ligand poses used for modeling. · source_derived_draft · unverified_draft

### b1-pdh-dlat-coa-acetylation The human DLAT catalytic core contains a channel for the acetylated lipoyl group and CoA; substrate modeling positions CoA for acetyl-CoA formation. Condition category: normal nutrient_topic: Thiamine research collection; topical membership is not evidence of a direct dietary effect. plain_language: After B1 acts at E1, the E2 protein transfers the acetyl group onto CoA, a vitamin B5-derived carrier. organism: Homo sapiens tissue_or_cell_type: Purified catalytic core experimental_model: Human DLAT cryo-EM; bacterial ligand poses used for modeling. limitations: Ligand positions were modeled, not directly resolved in a human substrate-bound structure; no intake experiment. evidence: [{"paper_key": "jiang-2018-pdh-core", "source_bundle": "artifacts/thiamine_metabolism_sources.json", "passage_ids": ["p-32"], "locator": "acetyl-accepting CoA", "preservation": "Exact text retained in the source bundle; full source document retained when openly retrievable."}] cross_nutrient: B1-dependent E1 and B5-derived CoA participate in different sequential steps. nutrient: Thiamine (vitamin B1) [jiang-2018-pdh-core] Atomic Structure of the E2 Inner Core of Human Pyruvate Dehydrogenase Complex (2018). https://pubmed.ncbi.nlm.nih.gov/29608861/ DOI: 10.1021/acs.biochem.8b00357

availability_state

nutrient_deficiency Imported condition classification; unverified.

evidence_access

Primary full text

experimental_model

Mouse genetic/dietary depletion; tissue CoA measurements at days 2 and 7.

limitations

CoA depletion accompanies several changes; do not assign all weight loss to one metabolite. Correction record: Author correction published 12 December 2025 (2026 issue), PMID 41388205, DOI 10.1038/s41586-025-09780-8: two incorrect day-3 muscle histology panels in Extended Data Fig. 2f,g duplicated day-7 panels and were replaced. The authors state that figure and paper conclusions were unaffected. This is a figure correction, not independent validation. https://www.nature.com/articles/s41586-025-09780-8

nutrient_topic

L-Cysteine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Cysteine

plain_language

A cysteine shortage reduced an energy-metabolism cofactor as well as an antioxidant.

primary_references

Unravelling cysteine-deficiency-associated rapid weight loss. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40399674/ · DOI 10.1038/s41586-025-08996-y

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

L-Cysteine: sulfur allocation, redox supply and cross-nutrient mechanisms (2026-09-19) · lines 308–314

AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse genetic/dietary depletion; tissue CoA measurements at days 2 and 7. · source_derived_draft · unverified_draft

## l-cysteine-depletion-coa A cysteine shortage reduced an energy-metabolism cofactor as well as an antioxidant. Combined Cse loss and cysteine-free feeding reduced liver and muscle CoA, alongside glutathione depletion and major metabolic changes. Model: Mouse genetic/dietary depletion; tissue CoA measurements at days 2 and 7. Limitations: CoA depletion accompanies several changes; do not assign all weight loss to one metabolite. Correction record: Author correction published 12 December 2025 (2026 issue), PMID 41388205, DOI 10.1038/s41586-025-09780-8: two incorrect day-3 muscle histology panels in Extended Data Fig. 2f,g duplicated day-7 panels and were replaced. The authors state that figure and paper conclusions were unaffected. This is a figure correction, not independent validation. https://www.nature.com/articles/s41586-025-09780-8 Evidence access: Primary full text Unravelling cysteine-deficiency-associated rapid weight loss. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40399674/ · DOI 10.1038/s41586-025-08996-y

evidence_access

Primary full text

experimental_model

Human PDAC stable-isotope tracing.

limitations

No labeling of taurine, lactate, citrate or glutamate was detected in these assays; that does not abolish those routes in other tissues.

nutrient_topic

L-Cysteine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Cysteine

plain_language

Cysteine-derived material entered more than one protective metabolic pool.

primary_references

Cysteine depletion induces pancreatic tumor ferroptosis in mice. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32241947/ · DOI 10.1126/science.aaw9872

L-Cysteine: sulfur allocation, redox supply and cross-nutrient mechanisms (2026-09-19) · lines 188–194

AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human PDAC stable-isotope tracing. · source_derived_draft · unverified_draft

## l-cysteine-pdac-carbon-tracing Cysteine-derived material entered more than one protective metabolic pool. Carbon-13 cystine tracing showed labeling of glutathione and CoA over the experiment, including CoA labeling over 24 hours. Model: Human PDAC stable-isotope tracing. Limitations: No labeling of taurine, lactate, citrate or glutamate was detected in these assays; that does not abolish those routes in other tissues. Evidence access: Primary full text Cysteine depletion induces pancreatic tumor ferroptosis in mice. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32241947/ · DOI 10.1126/science.aaw9872

availability_state

machinery_impairment Imported condition classification; unverified.

evidence_access

Primary full text

experimental_model

Human PDAC cultures with cystine-import inhibition and metabolomics.

limitations

Pantothenate accumulation is not proof of B5 toxicity or a clinical biomarker threshold.

nutrient_topic

L-Cysteine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Cysteine

plain_language

Vitamin B5 could accumulate while its downstream product fell because another substrate was missing.

primary_references

Cysteine depletion induces pancreatic tumor ferroptosis in mice. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32241947/ · DOI 10.1126/science.aaw9872

trigger_kind

machinery_impairment Imported condition classification; unverified.

L-Cysteine: sulfur allocation, redox supply and cross-nutrient mechanisms (2026-09-19) · lines 196–202

AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human PDAC cultures with cystine-import inhibition and metabolomics. · source_derived_draft · unverified_draft

## l-cysteine-pdac-coa-branch Vitamin B5 could accumulate while its downstream product fell because another substrate was missing. System xc− inhibition lowered CoA and increased upstream pantothenate in the tested pancreatic cancer cells. Model: Human PDAC cultures with cystine-import inhibition and metabolomics. Limitations: Pantothenate accumulation is not proof of B5 toxicity or a clinical biomarker threshold. Evidence access: Primary full text Cysteine depletion induces pancreatic tumor ferroptosis in mice. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32241947/ · DOI 10.1126/science.aaw9872

availability_state

machinery_impairment Imported condition classification; unverified.

evidence_access

Primary full text

experimental_model

Human PDAC culture; pharmacological PANKi/BSO combination.

limitations

This is a demonstrated drug-combination interaction in this assay, not evidence for oral B5/cysteine supplement synergy.

nutrient_topic

L-Cysteine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Cysteine

plain_language

Two protective branches were experimentally blocked together.

primary_references

Cysteine depletion induces pancreatic tumor ferroptosis in mice. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32241947/ · DOI 10.1126/science.aaw9872

trigger_kind

machinery_impairment Imported condition classification; unverified.

L-Cysteine: sulfur allocation, redox supply and cross-nutrient mechanisms (2026-09-19) · lines 212–218

AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human PDAC culture; pharmacological PANKi/BSO combination. · source_derived_draft · unverified_draft

## l-cysteine-pdac-dual-block Two protective branches were experimentally blocked together. Pantothenate-kinase inhibition combined with BSO synergistically induced ferroptosis in the reported PDAC assays. Model: Human PDAC culture; pharmacological PANKi/BSO combination. Limitations: This is a demonstrated drug-combination interaction in this assay, not evidence for oral B5/cysteine supplement synergy. Evidence access: Primary full text Cysteine depletion induces pancreatic tumor ferroptosis in mice. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32241947/ · DOI 10.1126/science.aaw9872

cross_nutrient

B5-derived CoA supplies phosphopantetheine; direct CoA handoff tested, dietary B5 link upstream.

experimental_model

Reconstitution and site-directed mutagenesis

exposure

Assay conditions described in the linked primary study.

limitations

Does not establish dietary B5 deficiency or repletion effects.

nutrient_topic

Folate and folic acid research collection; topical membership is not evidence of a direct dietary effect. · Folate (vitamin B9)

organism

Homo sapiens

plain_language

A CoA-derived arm prepares the folate enzyme for catalysis.

primary_references

[strickland-2011] Enzymatic properties of ALDH1L2, a mitochondrial 10-formyltetrahydrofolate dehydrogenase (2011). https://pubmed.ncbi.nlm.nih.gov/21238436/ DOI: 10.1016/j.cbi.2011.01.008

tissue_or_cell_type

Cell-free

Folate and folic acid: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1046–1057

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Reconstitution and site-directed mutagenesis · source_derived_draft · unverified_draft

### aldh1l2-coa-arm Human phosphopantetheinyl transferase transfers a CoA-derived prosthetic group to ALDH1L2 Ser375. Condition category: normal nutrient_topic: Folate and folic acid research collection; topical membership is not evidence of a direct dietary effect. plain_language: A CoA-derived arm prepares the folate enzyme for catalysis. organism: Homo sapiens tissue_or_cell_type: Cell-free experimental_model: Reconstitution and site-directed mutagenesis limitations: Does not establish dietary B5 deficiency or repletion effects. exposure: Assay conditions described in the linked primary study. cross_nutrient: B5-derived CoA supplies phosphopantetheine; direct CoA handoff tested, dietary B5 link upstream. [strickland-2011] Enzymatic properties of ALDH1L2, a mitochondrial 10-formyltetrahydrofolate dehydrogenase (2011). https://pubmed.ncbi.nlm.nih.gov/21238436/ DOI: 10.1016/j.cbi.2011.01.008

cross_nutrient

false

experimental_model

Human cultured-cell metabolomics and isotope tracing, PANK4 editing/re-expression and immunopurified human PANK4 phosphatase assays

exposure

PI3K–AKT signalling and PANK4 phosphorylation manipulations; no nutrient dosing trial.

limitations

Primary abstract with supporting cellular assays; mechanism is not a rationale for treating insulin signalling or increasing B5 intake.

nutrient_topic

Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)

organism

Homo sapiens

plain_language

Growth-factor signalling can ease the PANK4 brake on CoA production.

primary_references

[b5-bio-dibble2022] PI3K drives the de novo synthesis of coenzyme A from vitamin B5. (2022). https://pubmed.ncbi.nlm.nih.gov/35896750/ DOI: 10.1038/s41586-022-04984-8

tissue_or_cell_type

Human cultured-cell models

Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 691–702

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human cultured-cell metabolomics and isotope tracing, PANK4 editing/re-expression and immunopurified human PANK4 phosphatase assays · source_derived_draft · unverified_draft

### b5-bio-akt-pank4-regulation AKT phosphorylation of PANK4 relieved its suppression of de novo CoA synthesis in the study models. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Growth-factor signalling can ease the PANK4 brake on CoA production. organism: Homo sapiens tissue_or_cell_type: Human cultured-cell models experimental_model: Human cultured-cell metabolomics and isotope tracing, PANK4 editing/re-expression and immunopurified human PANK4 phosphatase assays limitations: Primary abstract with supporting cellular assays; mechanism is not a rationale for treating insulin signalling or increasing B5 intake. exposure: PI3K–AKT signalling and PANK4 phosphorylation manipulations; no nutrient dosing trial. cross_nutrient: false [b5-bio-dibble2022] PI3K drives the de novo synthesis of coenzyme A from vitamin B5. (2022). https://pubmed.ncbi.nlm.nih.gov/35896750/ DOI: 10.1038/s41586-022-04984-8

cross_nutrient

false

experimental_model

Human PANK2 in 293T-cell lysates and purified enzyme assays

exposure

293T-cell-lysate inhibition IC50 was 0.3 micromolar acetyl-CoA; purified-enzyme assays established ATP competition.

limitations

The lysate IC50 is preparation-specific and is not a intracellular or dietary adequacy threshold. Purified-enzyme competition and lysate potency are separately identified.

nutrient_topic

Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)

organism

Homo sapiens

plain_language

An existing CoA derivative feeds back to restrain PANK2.

primary_references

[b5-bio-pank2reg] Activation of human mitochondrial pantothenate kinase 2 by palmitoylcarnitine. (2007). https://pubmed.ncbi.nlm.nih.gov/17242360/ DOI: 10.1073/pnas.0607621104

tissue_or_cell_type

Purified recombinant protein; no intact tissue

Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 600–611

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human PANK2 in 293T-cell lysates and purified enzyme assays · source_derived_draft · unverified_draft

### b5-bio-pank2-acetyl-inhibition Acetyl-CoA inhibited purified human PANK2 competitively with ATP; PANK2 inhibition was submicromolar in the reported preparations. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: An existing CoA derivative feeds back to restrain PANK2. organism: Homo sapiens tissue_or_cell_type: Purified recombinant protein; no intact tissue experimental_model: Human PANK2 in 293T-cell lysates and purified enzyme assays limitations: The lysate IC50 is preparation-specific and is not a intracellular or dietary adequacy threshold. Purified-enzyme competition and lysate potency are separately identified. exposure: 293T-cell-lysate inhibition IC50 was 0.3 micromolar acetyl-CoA; purified-enzyme assays established ATP competition. cross_nutrient: false [b5-bio-pank2reg] Activation of human mitochondrial pantothenate kinase 2 by palmitoylcarnitine. (2007). https://pubmed.ncbi.nlm.nih.gov/17242360/ DOI: 10.1073/pnas.0607621104

cross_nutrient

true

experimental_model

Human PANK2 in 293T-cell lysates and purified enzyme assays

exposure

Human PANK2 in 293T lysates and purified-enzyme assays; indexed Fig. 1 used 0.2 micromolar acetyl-CoA.

limitations

Acylcarnitine is a specific molecule; this does not show that free-carnitine supplements activate PANK2 in people. Intact-organism fatty-acid-demand interpretation was proposed.

nutrient_topic

Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)

organism

Homo sapiens

plain_language

A long-chain acylcarnitine can release the brake on PANK2.

primary_references

[b5-bio-pank2reg] Activation of human mitochondrial pantothenate kinase 2 by palmitoylcarnitine. (2007). https://pubmed.ncbi.nlm.nih.gov/17242360/ DOI: 10.1073/pnas.0607621104

tissue_or_cell_type

Purified recombinant protein; no intact tissue

Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 613–624

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human PANK2 in 293T-cell lysates and purified enzyme assays · source_derived_draft · unverified_draft

### b5-bio-pank2-palmitoylcarnitine Palmitoylcarnitine antagonized acetyl-CoA inhibition of human PANK2, providing a positive regulatory input in biochemical assays. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: A long-chain acylcarnitine can release the brake on PANK2. organism: Homo sapiens tissue_or_cell_type: Purified recombinant protein; no intact tissue experimental_model: Human PANK2 in 293T-cell lysates and purified enzyme assays limitations: Acylcarnitine is a specific molecule; this does not show that free-carnitine supplements activate PANK2 in people. Intact-organism fatty-acid-demand interpretation was proposed. exposure: Human PANK2 in 293T lysates and purified-enzyme assays; indexed Fig. 1 used 0.2 micromolar acetyl-CoA. cross_nutrient: true [b5-bio-pank2reg] Activation of human mitochondrial pantothenate kinase 2 by palmitoylcarnitine. (2007). https://pubmed.ncbi.nlm.nih.gov/17242360/ DOI: 10.1073/pnas.0607621104

cross_nutrient

false

experimental_model

Purified recombinant human PANK3, crystallography and biochemical ligand-binding/heterodimer experiments

exposure

In-vitro biochemical exposure; concentrations not extracted.

limitations

Abstract-level structural and biochemical findings; no diet or Mg-repletion experiment. Substrate concentrations not established here.

nutrient_topic

Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)

organism

Homo sapiens

plain_language

Accumulated acyl-CoA can slow the first step of new CoA production.

primary_references

[b5-bio-pank3allosteric] Allosteric Regulation of Mammalian Pantothenate Kinase. (2016). https://pubmed.ncbi.nlm.nih.gov/27555321/ DOI: 10.1074/jbc.m116.748061

tissue_or_cell_type

Purified recombinant protein; no intact tissue

Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 509–520

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Purified recombinant human PANK3, crystallography and biochemical ligand-binding/heterodimer experiments · source_derived_draft · unverified_draft

### b5-bio-pank3-feedback Acetyl-CoA stabilizes an inactive human PANK3 dimer conformation, whereas ATP–Mg favors the active state; biochemical analyses showed coordinated switching of its two active sites. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Accumulated acyl-CoA can slow the first step of new CoA production. organism: Homo sapiens tissue_or_cell_type: Purified recombinant protein; no intact tissue experimental_model: Purified recombinant human PANK3, crystallography and biochemical ligand-binding/heterodimer experiments limitations: Abstract-level structural and biochemical findings; no diet or Mg-repletion experiment. Substrate concentrations not established here. exposure: In-vitro biochemical exposure; concentrations not extracted. cross_nutrient: false [b5-bio-pank3allosteric] Allosteric Regulation of Mammalian Pantothenate Kinase. (2016). https://pubmed.ncbi.nlm.nih.gov/27555321/ DOI: 10.1074/jbc.m116.748061

cross_nutrient

true

experimental_model

Purified recombinant human PANK3, crystallography and biochemical ligand-binding/heterodimer experiments

exposure

In-vitro biochemical exposure; concentrations not extracted.

limitations

Structures used AMPPNP, ADP and related nucleotide complexes; ATP–Mg binding was assessed biochemically. This demonstrates catalytic-complex participation, not a dietary magnesium threshold or supplementation requirement.

nutrient_topic

Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)

organism

Homo sapiens

plain_language

Magnesium is part of the nucleotide complex used by PANK3.

primary_references

[b5-bio-pank3allosteric] Allosteric Regulation of Mammalian Pantothenate Kinase. (2016). https://pubmed.ncbi.nlm.nih.gov/27555321/ DOI: 10.1074/jbc.m116.748061

tissue_or_cell_type

Purified recombinant protein; no intact tissue

Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 496–507

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Purified recombinant human PANK3, crystallography and biochemical ligand-binding/heterodimer experiments · source_derived_draft · unverified_draft

### b5-bio-pank3-magnesium Human PANK3 structures resolved Mg2+ in nucleotide-bound substrate and product complexes, directly connecting magnesium to the B5-phosphorylation machinery. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Magnesium is part of the nucleotide complex used by PANK3. organism: Homo sapiens tissue_or_cell_type: Purified recombinant protein; no intact tissue experimental_model: Purified recombinant human PANK3, crystallography and biochemical ligand-binding/heterodimer experiments limitations: Structures used AMPPNP, ADP and related nucleotide complexes; ATP–Mg binding was assessed biochemically. This demonstrates catalytic-complex participation, not a dietary magnesium threshold or supplementation requirement. exposure: In-vitro biochemical exposure; concentrations not extracted. cross_nutrient: true [b5-bio-pank3allosteric] Allosteric Regulation of Mammalian Pantothenate Kinase. (2016). https://pubmed.ncbi.nlm.nih.gov/27555321/ DOI: 10.1074/jbc.m116.748061

cross_nutrient

false

experimental_model

Human cultured-cell metabolomics and isotope tracing, PANK4 editing/re-expression and immunopurified human PANK4 phosphatase assays

exposure

Wild-type versus D623A or D659A PANK4 re-expression; 3-hour carbon-13/nitrogen-15 vitamin-B5 labelling with growth factors.

limitations

Engineered cellular PI3K–AKT context; isotope concentration not verified. No claim that PANK4 controls every tissue or that dietary B5 produces the same response.

nutrient_topic

Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)

organism

Homo sapiens

plain_language

PANK4 phosphatase activity can reduce new CoA production in cultured cells.

primary_references

[b5-bio-dibble2022] PI3K drives the de novo synthesis of coenzyme A from vitamin B5. (2022). https://pubmed.ncbi.nlm.nih.gov/35896750/ DOI: 10.1038/s41586-022-04984-8

tissue_or_cell_type

Human MCF10A mammary epithelial cells

Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 678–689

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human cultured-cell metabolomics and isotope tracing, PANK4 editing/re-expression and immunopurified human PANK4 phosphatase assays · source_derived_draft · unverified_draft

### b5-bio-pank4-flux-suppression Re-expression of active PANK4 in PANK4-knockout AKT p.E17K/+ MCF10A cells suppressed newly synthesized CoA, whereas phosphatase-inactive mutants did not reproduce the suppression. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: PANK4 phosphatase activity can reduce new CoA production in cultured cells. organism: Homo sapiens tissue_or_cell_type: Human MCF10A mammary epithelial cells experimental_model: Human cultured-cell metabolomics and isotope tracing, PANK4 editing/re-expression and immunopurified human PANK4 phosphatase assays limitations: Engineered cellular PI3K–AKT context; isotope concentration not verified. No claim that PANK4 controls every tissue or that dietary B5 produces the same response. exposure: Wild-type versus D623A or D659A PANK4 re-expression; 3-hour carbon-13/nitrogen-15 vitamin-B5 labelling with growth factors. cross_nutrient: false [b5-bio-dibble2022] PI3K drives the de novo synthesis of coenzyme A from vitamin B5. (2022). https://pubmed.ncbi.nlm.nih.gov/35896750/ DOI: 10.1038/s41586-022-04984-8

cross_nutrient

false

evidence_location

Primary PDF pp.1421–1425, especially Results and Summary.

experimental_model

Historical four-man controlled antagonist experiment on a balanced 3200 kcal diet

exposure

One control; three men received escalating antagonist regimens, up to 2–4 g/day in the highest-exposure subject; pantothenic acid 4 g/day was later given after antagonist withdrawal.

limitations

Pharmacological antagonist exposure with an otherwise normal diet, not dietary B5 deprivation. Very small sample and concurrent antagonist withdrawal prevent isolating a pure vitamin-rescue effect. The interindividual pattern is not a monotonic dose-response or a direct assay of a specific PANK isoform.

nutrient_topic

Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)

organism

Homo sapiens

plain_language

Blocking vitamin use experimentally produced variable illness despite a normal diet.

primary_references

[b5-clin-hodges1959] Human pantothenic acid deficiency produced by omega-methyl pantothenic acid. (1959). https://pubmed.ncbi.nlm.nih.gov/13673099/ DOI: 10.1172/jci103918

tissue_or_cell_type

Whole-person clinical symptoms and functional tests

Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 1201–1213

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Historical four-man controlled antagonist experiment on a balanced 3200 kcal diet · source_derived_draft · unverified_draft

### b5-clin-antagonist-variable-symptoms In the four-man normal-diet experiment, the intermediate-antagonist subject developed gastrointestinal and neurological symptoms, while the highest-exposure subject had mainly a transient tremor; the control and lowest-exposure subject remained relatively well. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Blocking vitamin use experimentally produced variable illness despite a normal diet. organism: Homo sapiens tissue_or_cell_type: Whole-person clinical symptoms and functional tests experimental_model: Historical four-man controlled antagonist experiment on a balanced 3200 kcal diet limitations: Pharmacological antagonist exposure with an otherwise normal diet, not dietary B5 deprivation. Very small sample and concurrent antagonist withdrawal prevent isolating a pure vitamin-rescue effect. The interindividual pattern is not a monotonic dose-response or a direct assay of a specific PANK isoform. exposure: One control; three men received escalating antagonist regimens, up to 2–4 g/day in the highest-exposure subject; pantothenic acid 4 g/day was later given after antagonist withdrawal. cross_nutrient: false evidence_location: Primary PDF pp.1421–1425, especially Results and Summary. [b5-clin-hodges1959] Human pantothenic acid deficiency produced by omega-methyl pantothenic acid. (1959). https://pubmed.ncbi.nlm.nih.gov/13673099/ DOI: 10.1172/jci103918

cross_nutrient

false

evidence_location

Primary PDF Table 1 visually checked; Tables 3–4 and Results pp.341–345.

experimental_model

Controlled 84-day feeding experiment in ten adult male inmates aged 27–33; six unsupplemented and four supplemented

exposure

Nine-week/63-day experimental diet essentially free of B5 versus 10 mg/day B5 as calcium pantothenate; both groups then received 100 mg/day for seven days.

limitations

Table 1 and the abstract distinguish unsupplemented and supplemented groups; one Methods sentence incorrectly says all received 10 mg. The table was visually checked. Historical assay and small cohort; the reported retention calculation is not direct measurement of intestinal absorption or tissue CoA. The paper called the unexcreted fractions 63% and 48% retained on day one. These calculations do not directly measure absorption, tissue storage or CoA synthesis.

nutrient_topic

Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)

organism

Homo sapiens

plain_language

Prior intake changed urinary recovery of a loading dose, and the groups became more similar over a week.

primary_references

[b5-clin-fry1976] Metabolic response to a pantothenic acid deficient diet in humans. (1976). https://pubmed.ncbi.nlm.nih.gov/1011047/ DOI: 10.3177/jnsv.22.339

tissue_or_cell_type

Urine and whole blood; nitrogen balance

Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 1257–1269

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Controlled 84-day feeding experiment in ten adult male inmates aged 27–33; six unsupplemented and four supplemented · source_derived_draft · unverified_draft

### b5-clin-loading-urinary-recovery On the first 100 mg B5 loading day, prior unsupplemented subjects excreted about 37 mg and supplemented subjects about 52 mg in urine; by day seven the means were about 59 and 62 mg. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Prior intake changed urinary recovery of a loading dose, and the groups became more similar over a week. organism: Homo sapiens tissue_or_cell_type: Urine and whole blood; nitrogen balance experimental_model: Controlled 84-day feeding experiment in ten adult male inmates aged 27–33; six unsupplemented and four supplemented limitations: Table 1 and the abstract distinguish unsupplemented and supplemented groups; one Methods sentence incorrectly says all received 10 mg. The table was visually checked. Historical assay and small cohort; the reported retention calculation is not direct measurement of intestinal absorption or tissue CoA. The paper called the unexcreted fractions 63% and 48% retained on day one. These calculations do not directly measure absorption, tissue storage or CoA synthesis. exposure: Nine-week/63-day experimental diet essentially free of B5 versus 10 mg/day B5 as calcium pantothenate; both groups then received 100 mg/day for seven days. cross_nutrient: false evidence_location: Primary PDF Table 1 visually checked; Tables 3–4 and Results pp.341–345. [b5-clin-fry1976] Metabolic response to a pantothenic acid deficient diet in humans. (1976). https://pubmed.ncbi.nlm.nih.gov/1011047/ DOI: 10.3177/jnsv.22.339

cross_nutrient

false

evidence_location

Primary indexed abstract.

experimental_model

Pharmacokinetic/metabolic study in four children with nephropathic cystinosis

exposure

Historical oral D-pantethine exposures 70–1000 mg/kg/day.

limitations

Very high drug-like exposures in a rare disease; not nutritional dosing, ordinary healthy-person pharmacokinetics or proof of the mechanism behind lipid-trial effects. Rat intestinal-enzyme kinetic data in the same paper are not assigned to humans. Model-specific estimate at high exposures in four children; not a normal dietary half-life.

nutrient_topic

Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)

organism

Homo sapiens

plain_language

Vitamin exposure persisted after the parent derivative was administered.

primary_references

[b5-clin-wittwer1985] Metabolism of pantethine in cystinosis. (1985). https://pubmed.ncbi.nlm.nih.gov/4056044/ DOI: 10.1172/jci112152

tissue_or_cell_type

Plasma after oral D-pantethine

Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 1481–1493

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Pharmacokinetic/metabolic study in four children with nephropathic cystinosis · source_derived_draft · unverified_draft

### b5-clin-pantethine-pantothenate-kinetics Pantothenate after oral pantethine peaked at about 2.5 hours and fitted a two-compartment model with an estimated elimination half-life of 28 hours in the reported cystinosis study. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Vitamin exposure persisted after the parent derivative was administered. organism: Homo sapiens tissue_or_cell_type: Plasma after oral D-pantethine experimental_model: Pharmacokinetic/metabolic study in four children with nephropathic cystinosis limitations: Very high drug-like exposures in a rare disease; not nutritional dosing, ordinary healthy-person pharmacokinetics or proof of the mechanism behind lipid-trial effects. Rat intestinal-enzyme kinetic data in the same paper are not assigned to humans. Model-specific estimate at high exposures in four children; not a normal dietary half-life. exposure: Historical oral D-pantethine exposures 70–1000 mg/kg/day. cross_nutrient: false evidence_location: Primary indexed abstract. [b5-clin-wittwer1985] Metabolism of pantethine in cystinosis. (1985). https://pubmed.ncbi.nlm.nih.gov/4056044/ DOI: 10.1172/jci112152

cross_nutrient

true

evidence_location

Primary PDF pp.1643–1654; design, results and discussion.

experimental_model

Historical controlled feeding study in six adult male volunteers; two diet-only deficient, two deficient plus antagonist, two supplemented controls

exposure

Tube-fed experimental formula; controls received pantothenic acid 20 mg/day, antagonist pair 750 then 1000 mg/day omega-methyl compound; recovery included 4000 mg/day vitamin. One man per pair received 10.8 mEq/day extra potassium.

limitations

Very small historical cohort; other vitamins and formula composition were controlled imperfectly. Diet-only and antagonist groups are distinguished. Measurements do not establish a universal symptom, adrenal disease mechanism or cellular CoA threshold. No full potassium balance study was done; the record does not establish B5-dependent renal potassium wasting or refractory potassium repletion.

nutrient_topic

Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)

organism

Homo sapiens

plain_language

Potassium supply affected the blood result independently of how the B5 groups were assigned.

primary_references

[b5-clin-hodges1958] Pantothenic acid deficiency in man. (1958). https://pubmed.ncbi.nlm.nih.gov/13587673/ DOI: 10.1172/jci103756

tissue_or_cell_type

Whole-person symptoms, serum and urine

Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 1187–1199

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Historical controlled feeding study in six adult male volunteers; two diet-only deficient, two deficient plus antagonist, two supplemented controls · source_derived_draft · unverified_draft

### b5-clin-potassium-context On the experimental formula, men receiving 20.5 mEq/day potassium had serum potassium near the lower normal limit, while an extra 10.8 mEq/day maintained somewhat higher values across the paired B5 regimens. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Potassium supply affected the blood result independently of how the B5 groups were assigned. organism: Homo sapiens tissue_or_cell_type: Whole-person symptoms, serum and urine experimental_model: Historical controlled feeding study in six adult male volunteers; two diet-only deficient, two deficient plus antagonist, two supplemented controls limitations: Very small historical cohort; other vitamins and formula composition were controlled imperfectly. Diet-only and antagonist groups are distinguished. Measurements do not establish a universal symptom, adrenal disease mechanism or cellular CoA threshold. No full potassium balance study was done; the record does not establish B5-dependent renal potassium wasting or refractory potassium repletion. exposure: Tube-fed experimental formula; controls received pantothenic acid 20 mg/day, antagonist pair 750 then 1000 mg/day omega-methyl compound; recovery included 4000 mg/day vitamin. One man per pair received 10.8 mEq/day extra potassium. cross_nutrient: true evidence_location: Primary PDF pp.1643–1654; design, results and discussion. [b5-clin-hodges1958] Pantothenic acid deficiency in man. (1958). https://pubmed.ncbi.nlm.nih.gov/13587673/ DOI: 10.1172/jci103756

availability_state

nutrient_deficiency Imported condition classification; unverified.

cross_nutrient

true

experimental_model

Human JAr choriocarcinoma cells cultured for three weeks with deficient, physiological or pharmacological biotin

exposure

Three weeks at 25 pmol/L deficient, 250 pmol/L physiological, or 10000 pmol/L pharmacological biotin.

limitations

Tumor-derived placental cell model. The paper also measured biotin uptake and promoter activity, but a resulting change in pantothenate uptake or whole-placenta fetal delivery is not demonstrated by this abstract.

nutrient_topic

Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)

organism

Homo sapiens

plain_language

Cells exposed to less biotin made more of the transporter also used by B5.

primary_references

[b5-trans-biotin-supply2004] Biotin supply affects rates of cell proliferation, biotinylation of carboxylases and histones, and expression of the gene encoding the sodium-dependent multivitamin transporter in JAr choriocarcinoma cells. (2004). https://pubmed.ncbi.nlm.nih.gov/14991266/ DOI: 10.1007/s00394-004-0435-9

tissue_or_cell_type

JAr placental choriocarcinoma cells

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 327–338

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human JAr choriocarcinoma cells cultured for three weeks with deficient, physiological or pharmacological biotin · source_derived_draft · unverified_draft

### b5-trans-biotin-supply-smvt Across 25, 250 and 10000 pmol/L biotin culture conditions for three weeks, biotin availability correlated negatively with SMVT protein abundance in human JAr cells. Condition category: nutrient_deficiency nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Cells exposed to less biotin made more of the transporter also used by B5. organism: Homo sapiens tissue_or_cell_type: JAr placental choriocarcinoma cells experimental_model: Human JAr choriocarcinoma cells cultured for three weeks with deficient, physiological or pharmacological biotin limitations: Tumor-derived placental cell model. The paper also measured biotin uptake and promoter activity, but a resulting change in pantothenate uptake or whole-placenta fetal delivery is not demonstrated by this abstract. exposure: Three weeks at 25 pmol/L deficient, 250 pmol/L physiological, or 10000 pmol/L pharmacological biotin. cross_nutrient: true [b5-trans-biotin-supply2004] Biotin supply affects rates of cell proliferation, biotinylation of carboxylases and histones, and expression of the gene encoding the sodium-dependent multivitamin transporter in JAr choriocarcinoma cells. (2004). https://pubmed.ncbi.nlm.nih.gov/14991266/ DOI: 10.1007/s00394-004-0435-9

cross_nutrient

true

experimental_model

Human and monkey brain microvessel analyses; SLC5A6-siRNA experiments in human hCMEC/D3 endothelial cells

exposure

Antibody-free membrane-localization method, with human/monkey microvessel proteomics and human expression analyses.

limitations

Abstract does not resolve which species supplied every localization preparation. The result addresses blood-facing localization, not the unidentified abluminal export step.

nutrient_topic

Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)

organism

Homo sapiens and monkey microvessel preparations; localization sample allocation not detailed in abstract

plain_language

Brain capillary SMVT is concentrated on the side facing the blood.

primary_references

[b5-trans-brain2015] Major involvement of Na(+) -dependent multivitamin transporter (SLC5A6/SMVT) in uptake of biotin and pantothenic acid by human brain capillary endothelial cells. (2015). https://pubmed.ncbi.nlm.nih.gov/25809983/ DOI: 10.1111/jnc.13092

tissue_or_cell_type

Brain capillary endothelium

Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 301–312

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human and monkey brain microvessel analyses; SLC5A6-siRNA experiments in human hCMEC/D3 endothelial cells · source_derived_draft · unverified_draft

### b5-trans-brain-luminal-localization The brain-microvessel study localized SLC5A6 preferentially to the luminal membrane of brain capillary endothelium. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Brain capillary SMVT is concentrated on the side facing the blood. organism: Homo sapiens and monkey microvessel preparations; localization sample allocation not detailed in abstract tissue_or_cell_type: Brain capillary endothelium experimental_model: Human and monkey brain microvessel analyses; SLC5A6-siRNA experiments in human hCMEC/D3 endothelial cells limitations: Abstract does not resolve which species supplied every localization preparation. The result addresses blood-facing localization, not the unidentified abluminal export step. exposure: Antibody-free membrane-localization method, with human/monkey microvessel proteomics and human expression analyses. cross_nutrient: true [b5-trans-brain2015] Major involvement of Na(+) -dependent multivitamin transporter (SLC5A6/SMVT) in uptake of biotin and pantothenic acid by human brain capillary endothelial cells. (2015). https://pubmed.ncbi.nlm.nih.gov/25809983/ DOI: 10.1111/jnc.13092

availability_state

machinery_impairment Imported condition classification; unverified.

cross_nutrient

true

experimental_model

Human and monkey brain microvessel analyses; SLC5A6-siRNA experiments in human hCMEC/D3 endothelial cells

exposure

SLC5A6-specific siRNA and radiolabeled substrate uptake; tracer concentration not specified in the abstract.

limitations

Cellular luminal uptake is not itself a measurement of complete transendothelial delivery into brain tissue. Reported percentages apply to hCMEC/D3 under these assay conditions, not every human tissue.

nutrient_topic

Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)

organism

Homo sapiens

plain_language

SMVT supplied most measured pantothenate uptake in the human brain endothelial cell model.

primary_references

[b5-trans-brain2015] Major involvement of Na(+) -dependent multivitamin transporter (SLC5A6/SMVT) in uptake of biotin and pantothenic acid by human brain capillary endothelial cells. (2015). https://pubmed.ncbi.nlm.nih.gov/25809983/ DOI: 10.1111/jnc.13092

tissue_or_cell_type

hCMEC/D3 cerebral microvascular endothelial cells

trigger_kind

machinery_impairment Imported condition classification; unverified.

Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 275–286

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human and monkey brain microvessel analyses; SLC5A6-siRNA experiments in human hCMEC/D3 endothelial cells · source_derived_draft · unverified_draft

### b5-trans-brain-pantothenate SLC5A6 knockdown analysis attributed 98.6% of total radiolabeled pantothenate uptake to SLC5A6 in human hCMEC/D3 brain endothelial cells. Condition category: machinery_impairment nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: SMVT supplied most measured pantothenate uptake in the human brain endothelial cell model. organism: Homo sapiens tissue_or_cell_type: hCMEC/D3 cerebral microvascular endothelial cells experimental_model: Human and monkey brain microvessel analyses; SLC5A6-siRNA experiments in human hCMEC/D3 endothelial cells limitations: Cellular luminal uptake is not itself a measurement of complete transendothelial delivery into brain tissue. Reported percentages apply to hCMEC/D3 under these assay conditions, not every human tissue. exposure: SLC5A6-specific siRNA and radiolabeled substrate uptake; tracer concentration not specified in the abstract. cross_nutrient: true [b5-trans-brain2015] Major involvement of Na(+) -dependent multivitamin transporter (SLC5A6/SMVT) in uptake of biotin and pantothenic acid by human brain capillary endothelial cells. (2015). https://pubmed.ncbi.nlm.nih.gov/25809983/ DOI: 10.1111/jnc.13092

cross_nutrient

true

experimental_model

Functional human SMVT-GFP expression and imaging in polarized renal and intestinal epithelial cell lines

exposure

Full-length human SMVT-GFP expression and polarized membrane imaging.

limitations

Abstract-only; fluorescent fusion-protein localization in cell lines is not a measurement of net intestinal pantothenate absorption. The abstract does not name the intestinal cell line.

nutrient_topic

Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)

organism

Homo sapiens (transporter); expression-host species not specified in the retrieved abstract

plain_language

In the intestinal cell models, SMVT sits on the surface facing the intestinal contents.

primary_references

[b5-trans-targeting2009] Membrane targeting and intracellular trafficking of the human sodium-dependent multivitamin transporter in polarized epithelial cells. (2009). https://pubmed.ncbi.nlm.nih.gov/19211916/ DOI: 10.1152/ajpcell.00396.2008

tissue_or_cell_type

Polarized intestinal epithelial cell model

Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 223–234

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Functional human SMVT-GFP expression and imaging in polarized renal and intestinal epithelial cell lines · source_derived_draft · unverified_draft

### b5-trans-epithelial-apical-targeting Functional full-length human SMVT-GFP localized to the apical membrane in the studied polarized intestinal epithelial cell lines. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: In the intestinal cell models, SMVT sits on the surface facing the intestinal contents. organism: Homo sapiens (transporter); expression-host species not specified in the retrieved abstract tissue_or_cell_type: Polarized intestinal epithelial cell model experimental_model: Functional human SMVT-GFP expression and imaging in polarized renal and intestinal epithelial cell lines limitations: Abstract-only; fluorescent fusion-protein localization in cell lines is not a measurement of net intestinal pantothenate absorption. The abstract does not name the intestinal cell line. exposure: Full-length human SMVT-GFP expression and polarized membrane imaging. cross_nutrient: true [b5-trans-targeting2009] Membrane targeting and intracellular trafficking of the human sodium-dependent multivitamin transporter in polarized epithelial cells. (2009). https://pubmed.ncbi.nlm.nih.gov/19211916/ DOI: 10.1152/ajpcell.00396.2008

availability_state

machinery_impairment Imported condition classification; unverified.

cross_nutrient

true

experimental_model

Intestine-specific Slc5a6 conditional knockout mice compared with sex-matched littermates; in vivo and in vitro uptake

exposure

Cre/lox-mediated intestinal Slc5a6 deletion; in vivo and in vitro biotin transport assays.

limitations

This is shared transporter machinery impairment, not a dietary B5 depletion experiment. The abstract directly reports biotin uptake; no numerical pantothenate or lipoate absorption deficit is inferred. Passive uptake outside the measured carrier component is not excluded.

nutrient_topic

Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)

organism

Mus musculus

plain_language

Removing the shared vitamin transporter eliminated active intestinal biotin uptake in these mice.

primary_references

[b5-trans-intestinal-knockout2013] Conditional knockout of the Slc5a6 gene in mouse intestine impairs biotin absorption. (2013). https://pubmed.ncbi.nlm.nih.gov/23104561/ DOI: 10.1152/ajpgi.00379.2012

tissue_or_cell_type

Intestinal epithelium

trigger_kind

machinery_impairment Imported condition classification; unverified.

Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 314–325

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Intestine-specific Slc5a6 conditional knockout mice compared with sex-matched littermates; in vivo and in vitro uptake · source_derived_draft · unverified_draft

### b5-trans-intestinal-knockout-biotin Intestine-specific Slc5a6 deletion completely inhibited the measured carrier-mediated intestinal biotin uptake component relative to littermate controls. Condition category: machinery_impairment nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Removing the shared vitamin transporter eliminated active intestinal biotin uptake in these mice. organism: Mus musculus tissue_or_cell_type: Intestinal epithelium experimental_model: Intestine-specific Slc5a6 conditional knockout mice compared with sex-matched littermates; in vivo and in vitro uptake limitations: This is shared transporter machinery impairment, not a dietary B5 depletion experiment. The abstract directly reports biotin uptake; no numerical pantothenate or lipoate absorption deficit is inferred. Passive uptake outside the measured carrier component is not excluded. exposure: Cre/lox-mediated intestinal Slc5a6 deletion; in vivo and in vitro biotin transport assays. cross_nutrient: true [b5-trans-intestinal-knockout2013] Conditional knockout of the Slc5a6 gene in mouse intestine impairs biotin absorption. (2013). https://pubmed.ncbi.nlm.nih.gov/23104561/ DOI: 10.1152/ajpgi.00379.2012

cross_nutrient

true

experimental_model

Cryo-EM of engineered human SMVT with nanobody-assisted alignment; functional uptake assays in HEK293T cells

exposure

Biotin uptake assay: 5 micromolar unlabeled biotin plus [3H]biotin at a 300:1 molar ratio; 30 degrees C for ten minutes; inhibitor concentration varied.

limitations

In-vitro IC50 depends on tracer/substrate concentration and expression conditions; it is not a human supplement dose, affinity constant, or threshold for biotin deficiency.

nutrient_topic

Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)

organism

Homo sapiens

plain_language

Oxidized alpha-lipoic acid competed with biotin uptake in the SMVT cell assay.

primary_references

[b5-trans-structure2026] Structural basis for multivitamin recognition and transport by human SMVT. (2026). https://pubmed.ncbi.nlm.nih.gov/42364996/ DOI: 10.1038/s41467-026-74948-3

tissue_or_cell_type

HEK293T cells expressing human SMVT

Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 444–455

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cryo-EM of engineered human SMVT with nanobody-assisted alignment; functional uptake assays in HEK293T cells · source_derived_draft · unverified_draft

### b5-trans-lipoate-inhibits-biotin Oxidized alpha-lipoic acid inhibited human SMVT-mediated radiolabeled biotin uptake with an IC50 of 9.1 micromolar in the 2026 HEK293T assay. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Oxidized alpha-lipoic acid competed with biotin uptake in the SMVT cell assay. organism: Homo sapiens tissue_or_cell_type: HEK293T cells expressing human SMVT experimental_model: Cryo-EM of engineered human SMVT with nanobody-assisted alignment; functional uptake assays in HEK293T cells limitations: In-vitro IC50 depends on tracer/substrate concentration and expression conditions; it is not a human supplement dose, affinity constant, or threshold for biotin deficiency. exposure: Biotin uptake assay: 5 micromolar unlabeled biotin plus [3H]biotin at a 300:1 molar ratio; 30 degrees C for ten minutes; inhibitor concentration varied. cross_nutrient: true [b5-trans-structure2026] Structural basis for multivitamin recognition and transport by human SMVT. (2026). https://pubmed.ncbi.nlm.nih.gov/42364996/ DOI: 10.1038/s41467-026-74948-3

availability_state

machinery_impairment Imported condition classification; unverified.

cross_nutrient

true

experimental_model

Patient-derived fibroblasts in a human SLC5A6 family study; molecular and radiolabeled biotin uptake analysis

exposure

The p.Ser429Gly allele supplied canonically spliced transcripts in the compound-heterozygous proband; uptake compared with control fibroblasts.

limitations

Abstract-only transport extraction. This is one proband genotype, not an isolated p.Ser429Gly dose-response study; neither pantothenate uptake nor the relative contribution of individual supplements is quantified.

nutrient_topic

Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)

organism

Homo sapiens

plain_language

A patient with two SLC5A6 variants had a large defect in cellular biotin entry.

primary_references

[b5-trans-neuropathy2024] Genome sequencing enables diagnosis and treatment of SLC5A6 neuropathy. (2024). https://pubmed.ncbi.nlm.nih.gov/38816490/ DOI: 10.1038/s41431-024-01641-8

tissue_or_cell_type

Patient-derived fibroblasts

trigger_kind

machinery_impairment Imported condition classification; unverified.

Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 392–403

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Patient-derived fibroblasts in a human SLC5A6 family study; molecular and radiolabeled biotin uptake analysis · source_derived_draft · unverified_draft

### b5-trans-patient-fibroblast-biotin Fibroblasts from the proband with SLC5A6 c.393+2T>C and p.Ser429Gly variants showed approximately 90% lower biotin uptake than controls. Condition category: machinery_impairment nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: A patient with two SLC5A6 variants had a large defect in cellular biotin entry. organism: Homo sapiens tissue_or_cell_type: Patient-derived fibroblasts experimental_model: Patient-derived fibroblasts in a human SLC5A6 family study; molecular and radiolabeled biotin uptake analysis limitations: Abstract-only transport extraction. This is one proband genotype, not an isolated p.Ser429Gly dose-response study; neither pantothenate uptake nor the relative contribution of individual supplements is quantified. exposure: The p.Ser429Gly allele supplied canonically spliced transcripts in the compound-heterozygous proband; uptake compared with control fibroblasts. cross_nutrient: true [b5-trans-neuropathy2024] Genome sequencing enables diagnosis and treatment of SLC5A6 neuropathy. (2024). https://pubmed.ncbi.nlm.nih.gov/38816490/ DOI: 10.1038/s41431-024-01641-8

availability_state

machinery_impairment Imported condition classification; unverified.

cross_nutrient

true

experimental_model

Human intestinal HuTu-80 and brain-derived U87 cell transfection and live-cell imaging of patient-derived SLC5A6 variants

exposure

Forty-eight hours after transfection; 5 nM [3H]biotin, pH 7.4, 37 degrees C, five-minute uptake.

limitations

Human transformed cell models expressing GFP-tagged constructs. Biotin is the measured substrate; impaired B5/lipoate transport is plausible through shared machinery but is not directly quantified here. Genetic dysfunction is not dietary B5 deficiency.

nutrient_topic

Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)

organism

Homo sapiens

plain_language

The R123L SMVT variant lost the uptake activity seen with the normal transporter.

primary_references

[b5-trans-slc5a6-variants2017] Mutations in SLC5A6 associated with brain, immune, bone, and intestinal dysfunction in a young child. (2017). https://pubmed.ncbi.nlm.nih.gov/27904971/ DOI: 10.1007/s00439-016-1751-x

tissue_or_cell_type

HuTu-80 duodenal-derived epithelial and U87 brain-derived glioma cells

trigger_kind

machinery_impairment Imported condition classification; unverified.

Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 353–364

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human intestinal HuTu-80 and brain-derived U87 cell transfection and live-cell imaging of patient-derived SLC5A6 variants · source_derived_draft · unverified_draft

### b5-trans-r123l-biotin Expression of human SLC5A6 R123L failed to induce biotin uptake above control in HuTu-80 and U87 cells, whereas wild-type SLC5A6 increased uptake. Condition category: machinery_impairment nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: The R123L SMVT variant lost the uptake activity seen with the normal transporter. organism: Homo sapiens tissue_or_cell_type: HuTu-80 duodenal-derived epithelial and U87 brain-derived glioma cells experimental_model: Human intestinal HuTu-80 and brain-derived U87 cell transfection and live-cell imaging of patient-derived SLC5A6 variants limitations: Human transformed cell models expressing GFP-tagged constructs. Biotin is the measured substrate; impaired B5/lipoate transport is plausible through shared machinery but is not directly quantified here. Genetic dysfunction is not dietary B5 deficiency. exposure: Forty-eight hours after transfection; 5 nM [3H]biotin, pH 7.4, 37 degrees C, five-minute uptake. cross_nutrient: true [b5-trans-slc5a6-variants2017] Mutations in SLC5A6 associated with brain, immune, bone, and intestinal dysfunction in a young child. (2017). https://pubmed.ncbi.nlm.nih.gov/27904971/ DOI: 10.1007/s00439-016-1751-x

availability_state

machinery_impairment Imported condition classification; unverified.

cross_nutrient

true

experimental_model

Human intestinal HuTu-80 and brain-derived U87 cell transfection and live-cell imaging of patient-derived SLC5A6 variants

exposure

Forty-eight hours after transfection; 5 nM [3H]biotin, pH 7.4, 37 degrees C, five-minute uptake.

limitations

Human transformed cell models expressing GFP-tagged constructs. Biotin is the measured substrate; impaired B5/lipoate transport is plausible through shared machinery but is not directly quantified here. Genetic dysfunction is not dietary B5 deficiency.

nutrient_topic

Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)

organism

Homo sapiens

plain_language

The R94X SMVT variant lost the uptake activity seen with the normal transporter.

primary_references

[b5-trans-slc5a6-variants2017] Mutations in SLC5A6 associated with brain, immune, bone, and intestinal dysfunction in a young child. (2017). https://pubmed.ncbi.nlm.nih.gov/27904971/ DOI: 10.1007/s00439-016-1751-x

tissue_or_cell_type

HuTu-80 duodenal-derived epithelial and U87 brain-derived glioma cells

trigger_kind

machinery_impairment Imported condition classification; unverified.

Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 340–351

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human intestinal HuTu-80 and brain-derived U87 cell transfection and live-cell imaging of patient-derived SLC5A6 variants · source_derived_draft · unverified_draft

### b5-trans-r94x-biotin Expression of human SLC5A6 R94X failed to induce biotin uptake above control in HuTu-80 and U87 cells, whereas wild-type SLC5A6 increased uptake. Condition category: machinery_impairment nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: The R94X SMVT variant lost the uptake activity seen with the normal transporter. organism: Homo sapiens tissue_or_cell_type: HuTu-80 duodenal-derived epithelial and U87 brain-derived glioma cells experimental_model: Human intestinal HuTu-80 and brain-derived U87 cell transfection and live-cell imaging of patient-derived SLC5A6 variants limitations: Human transformed cell models expressing GFP-tagged constructs. Biotin is the measured substrate; impaired B5/lipoate transport is plausible through shared machinery but is not directly quantified here. Genetic dysfunction is not dietary B5 deficiency. exposure: Forty-eight hours after transfection; 5 nM [3H]biotin, pH 7.4, 37 degrees C, five-minute uptake. cross_nutrient: true [b5-trans-slc5a6-variants2017] Mutations in SLC5A6 associated with brain, immune, bone, and intestinal dysfunction in a young child. (2017). https://pubmed.ncbi.nlm.nih.gov/27904971/ DOI: 10.1007/s00439-016-1751-x

cross_nutrient

true

experimental_model

Isolated rabbit renal brush-border membrane vesicles with controlled ion gradients and membrane potentials

exposure

Inside-negative membrane potential imposed with sodium present but no transmembrane sodium gradient.

limitations

Rabbit isolated-membrane experiment; this predates molecular identification of SMVT and does not independently assign the effect to human SLC5A6 or establish a human renal clearance threshold.

nutrient_topic

Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)

organism

Oryctolagus cuniculus

plain_language

Electrical potential also helps power renal pantothenate uptake.

primary_references

[b5-trans-renal1986] Pantothenate-sodium cotransport in renal brush-border membranes. (1986). https://pubmed.ncbi.nlm.nih.gov/3771539/ DOI: 10.1016/s0021-9258(18)66891-7

tissue_or_cell_type

Renal brush-border membrane vesicles

Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 249–260

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Isolated rabbit renal brush-border membrane vesicles with controlled ion gradients and membrane potentials · source_derived_draft · unverified_draft

### b5-trans-renal-membrane-potential An inside-negative membrane potential drove uphill pantothenate accumulation in rabbit renal brush-border vesicles when sodium was present even without a sodium concentration gradient. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Electrical potential also helps power renal pantothenate uptake. organism: Oryctolagus cuniculus tissue_or_cell_type: Renal brush-border membrane vesicles experimental_model: Isolated rabbit renal brush-border membrane vesicles with controlled ion gradients and membrane potentials limitations: Rabbit isolated-membrane experiment; this predates molecular identification of SMVT and does not independently assign the effect to human SLC5A6 or establish a human renal clearance threshold. exposure: Inside-negative membrane potential imposed with sodium present but no transmembrane sodium gradient. cross_nutrient: true [b5-trans-renal1986] Pantothenate-sodium cotransport in renal brush-border membranes. (1986). https://pubmed.ncbi.nlm.nih.gov/3771539/ DOI: 10.1016/s0021-9258(18)66891-7

cross_nutrient

true

experimental_model

Isolated rabbit renal brush-border membrane vesicles with controlled ion gradients and membrane potentials

exposure

Inward NaCl gradient under voltage clamp; potassium, rubidium, lithium, ammonium and choline could not substitute for sodium.

limitations

Rabbit isolated-membrane experiment; this predates molecular identification of SMVT and does not independently assign the effect to human SLC5A6 or establish a human renal clearance threshold.

nutrient_topic

Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)

organism

Oryctolagus cuniculus

plain_language

Sodium provides energy for pantothenate uptake at the rabbit kidney brush border.

primary_references

[b5-trans-renal1986] Pantothenate-sodium cotransport in renal brush-border membranes. (1986). https://pubmed.ncbi.nlm.nih.gov/3771539/ DOI: 10.1016/s0021-9258(18)66891-7

tissue_or_cell_type

Renal brush-border membrane vesicles

Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 236–247

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Isolated rabbit renal brush-border membrane vesicles with controlled ion gradients and membrane potentials · source_derived_draft · unverified_draft

### b5-trans-renal-sodium-gradient An inward sodium gradient drove transient pantothenate accumulation against its concentration gradient in voltage-clamped rabbit renal brush-border vesicles. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Sodium provides energy for pantothenate uptake at the rabbit kidney brush border. organism: Oryctolagus cuniculus tissue_or_cell_type: Renal brush-border membrane vesicles experimental_model: Isolated rabbit renal brush-border membrane vesicles with controlled ion gradients and membrane potentials limitations: Rabbit isolated-membrane experiment; this predates molecular identification of SMVT and does not independently assign the effect to human SLC5A6 or establish a human renal clearance threshold. exposure: Inward NaCl gradient under voltage clamp; potassium, rubidium, lithium, ammonium and choline could not substitute for sodium. cross_nutrient: true [b5-trans-renal1986] Pantothenate-sodium cotransport in renal brush-border membranes. (1986). https://pubmed.ncbi.nlm.nih.gov/3771539/ DOI: 10.1016/s0021-9258(18)66891-7

cross_nutrient

true

experimental_model

Human SMVT cloned from JAR cells, expressed in human retinal pigment epithelial cells and Xenopus laevis oocytes

exposure

Human SMVT cDNA expression; substrate concentrations not specified in the abstract.

limitations

Heterologous human-protein experiments establish transport properties; they do not quantify whole-body absorption or nutrient deficiency from supplement competition.

nutrient_topic

Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)

organism

Homo sapiens (protein and HRPE expression cells)

plain_language

SMVT carries pantothenate into cells using sodium-dependent transport.

primary_references

[b5-trans-wang1999] Human placental Na+-dependent multivitamin transporter. Cloning, functional expression, gene structure, and chromosomal localization. (1999). https://pubmed.ncbi.nlm.nih.gov/10329687/ DOI: 10.1074/jbc.274.21.14875

tissue_or_cell_type

HRPE cell plasma membrane

Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 158–169

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human SMVT cloned from JAR cells, expressed in human retinal pigment epithelial cells and Xenopus laevis oocytes · source_derived_draft · unverified_draft

### b5-trans-smvt-pantothenate Expression of cloned human SLC5A6 in HRPE cells conferred sodium-dependent uptake of pantothenate. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: SMVT carries pantothenate into cells using sodium-dependent transport. organism: Homo sapiens (protein and HRPE expression cells) tissue_or_cell_type: HRPE cell plasma membrane experimental_model: Human SMVT cloned from JAR cells, expressed in human retinal pigment epithelial cells and Xenopus laevis oocytes limitations: Heterologous human-protein experiments establish transport properties; they do not quantify whole-body absorption or nutrient deficiency from supplement competition. exposure: Human SMVT cDNA expression; substrate concentrations not specified in the abstract. cross_nutrient: true [b5-trans-wang1999] Human placental Na+-dependent multivitamin transporter. Cloning, functional expression, gene structure, and chromosomal localization. (1999). https://pubmed.ncbi.nlm.nih.gov/10329687/ DOI: 10.1074/jbc.274.21.14875