Component
Fosmetpantotenate
Investigational phosphopantothenate-delivery prodrug studied in PKAN; distinct from dietary pantothenate.
2 recorded relationships. Experimental role, claim status and evidence remain attached to each record.
How nutrients influence it
Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
How nutrients reach it in more than one step
Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.
Tracing routes…
What it does
Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.
What it acts on
FORT found no significant difference in 24-week PKAN-ADL change between fosmetpantotenate and placebo: adjusted difference −0.09 points, 95% CI −1.69 to 1.51, P=0.9115.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- cross_nutrient
- false
- evidence_location
- Full primary BioC Methods, Results and Discussion.
- experimental_model
- FORT randomized double-blind multicenter placebo-controlled trial; 84 patients aged 6–65 with pathogenic PANK2 variants
- exposure
- 24 weeks; fosmetpantotenate 41 versus placebo 43. Adults and children at least 40 kg: 300 mg three times/day; children 20–<40 kg: 150 mg three times/day; children <20 kg: 75 mg three times/day.
- limitations
- Genetic disease, not nutritional B5 deficiency. No measure of brain target engagement was available, so a negative functional endpoint does not locate the failed biochemical step. Sponsor-funded trial; no general safety or dietary-efficacy conclusion.
- 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 prodrug did not improve the trial’s primary daily-function outcome.
- primary_references
- [b5-clin-fort2021] Fosmetpantotenate Randomized Controlled Trial in Pantothenate Kinase-Associated Neurodegeneration. (2021). https://pubmed.ncbi.nlm.nih.gov/33200489/ DOI: 10.1002/mds.28392
- tissue_or_cell_type
- Patient/surrogate functional rating and clinician-rated motor performance
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 1439–1451
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · FORT randomized double-blind multicenter placebo-controlled trial; 84 patients aged 6–65 with pathogenic PANK2 variants · source_derived_draft · unverified_draft
### b5-clin-fort-adl-null FORT found no significant difference in 24-week PKAN-ADL change between fosmetpantotenate and placebo: adjusted difference −0.09 points, 95% CI −1.69 to 1.51, P=0.9115. 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 prodrug did not improve the trial’s primary daily-function outcome. organism: Homo sapiens tissue_or_cell_type: Patient/surrogate functional rating and clinician-rated motor performance experimental_model: FORT randomized double-blind multicenter placebo-controlled trial; 84 patients aged 6–65 with pathogenic PANK2 variants limitations: Genetic disease, not nutritional B5 deficiency. No measure of brain target engagement was available, so a negative functional endpoint does not locate the failed biochemical step. Sponsor-funded trial; no general safety or dietary-efficacy conclusion. exposure: 24 weeks; fosmetpantotenate 41 versus placebo 43. Adults and children at least 40 kg: 300 mg three times/day; children 20–<40 kg: 150 mg three times/day; children <20 kg: 75 mg three times/day. cross_nutrient: false evidence_location: Full primary BioC Methods, Results and Discussion. [b5-clin-fort2021] Fosmetpantotenate Randomized Controlled Trial in Pantothenate Kinase-Associated Neurodegeneration. (2021). https://pubmed.ncbi.nlm.nih.gov/33200489/ DOI: 10.1002/mds.28392
Complete structured claim and evidenceThe secondary UPDRS III motor endpoint also showed no significant treatment difference; mean 24-week changes were +0.7 points with fosmetpantotenate and −1.0 with placebo.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- cross_nutrient
- false
- evidence_location
- Full primary BioC Methods, Results and Discussion.
- experimental_model
- FORT randomized double-blind multicenter placebo-controlled trial; 84 patients aged 6–65 with pathogenic PANK2 variants
- exposure
- 24 weeks; fosmetpantotenate 41 versus placebo 43. Adults and children at least 40 kg: 300 mg three times/day; children 20–<40 kg: 150 mg three times/day; children <20 kg: 75 mg three times/day.
- limitations
- Genetic disease, not nutritional B5 deficiency. No measure of brain target engagement was available, so a negative functional endpoint does not locate the failed biochemical step. Sponsor-funded trial; no general safety or dietary-efficacy conclusion.
- 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 clinician-rated motor outcome also failed to show benefit.
- primary_references
- [b5-clin-fort2021] Fosmetpantotenate Randomized Controlled Trial in Pantothenate Kinase-Associated Neurodegeneration. (2021). https://pubmed.ncbi.nlm.nih.gov/33200489/ DOI: 10.1002/mds.28392
- tissue_or_cell_type
- Patient/surrogate functional rating and clinician-rated motor performance
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 1453–1465
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · FORT randomized double-blind multicenter placebo-controlled trial; 84 patients aged 6–65 with pathogenic PANK2 variants · source_derived_draft · unverified_draft
### b5-clin-fort-motor-null The secondary UPDRS III motor endpoint also showed no significant treatment difference; mean 24-week changes were +0.7 points with fosmetpantotenate and −1.0 with placebo. 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 clinician-rated motor outcome also failed to show benefit. organism: Homo sapiens tissue_or_cell_type: Patient/surrogate functional rating and clinician-rated motor performance experimental_model: FORT randomized double-blind multicenter placebo-controlled trial; 84 patients aged 6–65 with pathogenic PANK2 variants limitations: Genetic disease, not nutritional B5 deficiency. No measure of brain target engagement was available, so a negative functional endpoint does not locate the failed biochemical step. Sponsor-funded trial; no general safety or dietary-efficacy conclusion. exposure: 24 weeks; fosmetpantotenate 41 versus placebo 43. Adults and children at least 40 kg: 300 mg three times/day; children 20–<40 kg: 150 mg three times/day; children <20 kg: 75 mg three times/day. cross_nutrient: false evidence_location: Full primary BioC Methods, Results and Discussion. [b5-clin-fort2021] Fosmetpantotenate Randomized Controlled Trial in Pantothenate Kinase-Associated Neurodegeneration. (2021). https://pubmed.ncbi.nlm.nih.gov/33200489/ DOI: 10.1002/mds.28392
Complete structured claim and evidence
The events it takes part in
A mechanism often involves more than two components. These are the full events, with every participant and its role.
Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
Preserved passages that mention this component, quoted exactly. Open one to read it in context.
Open hypotheses
Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.
This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.