Component

PF-06835919

Investigational ketohexokinase inhibitor; the cited experiments do not establish an approved treatment or a way to offset dietary HFCS.

4 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

Read recorded mechanisms Open recursive mind map

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.

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.

Recorded relationships

What it acts on

  1. PF-06835919 reduced fructose-associated nuclear ChREBP localization in primary rat hepatocytes.

    PF-06835919 → Rat carbohydrate-responsive element-binding protein / ChREBP source_derived_draftungraded
    Experimental context and source evidence
    dose
    10 mM fructose with or without 30 micromolar PF-06835919
    duration
    Overnight
    evidence_access
    Primary full-text methods/results and metadata inspected.
    evidence_scope
    literature_reviewed; source-specific curation
    experimental_model
    Primary rat hepatocytes
    exposure_scope
    Isolated fructose / investigational drug
    limitations
    Cell-model transcriptional effect; not established human lipid or disease prevention.
    nutrient_topic
    HFCS chapter: actual formulation studies, component biochemistry and interventions are explicitly distinguished. · High-Fructose Corn Syrup / HFCS
    organism
    Primary rat hepatocytes
    plain_language
    PF-06835919 reduced fructose-associated nuclear ChREBP localization in primary rat hepatocytes.
    primary_references
    Pharmacologic inhibition of ketohexokinase prevents fructose-induced metabolic dysfunction. (2021). https://pubmed.ncbi.nlm.nih.gov/33667726/ DOI: 10.1016/j.molmet.2021.101196
    route
    In vitro exposure
    tissue
    ChREBP nuclear localization

    High-Fructose Corn Syrup: mechanism of action and metabolic impact (2026-09-20) · lines 581–591

    Original AI-assisted curation of twenty primary studies and official FDA composition information, with one reused canonical glucose-transport claim. Study-specific citations, negative findings and limitations retained. Not publisher full text. · supports · Primary rat hepatocytes · source_derived_draft · unverified_draft

    ## hfcs-pf-chrebp PF-06835919 reduced fructose-associated nuclear ChREBP localization in primary rat hepatocytes. Model/species: Primary rat hepatocytes Tissue: ChREBP nuclear localization Exposure: 10 mM fructose with or without 30 micromolar PF-06835919 Route: In vitro exposure Duration: Overnight Exposure scope: Isolated fructose / investigational drug Limits: Cell-model transcriptional effect; not established human lipid or disease prevention. Reference: Pharmacologic inhibition of ketohexokinase prevents fructose-induced metabolic dysfunction. (2021). https://pubmed.ncbi.nlm.nih.gov/33667726/ DOI: 10.1016/j.molmet.2021.101196 Access: Primary full-text methods/results and metadata inspected.
    Complete structured claim and evidence

  2. PF-06835919 inhibited labeled fructose-1-phosphate formation in primary human hepatocytes.

    PF-06835919 → Fructose-1-phosphate formation in primary human hepatocytes source_derived_draftungraded
    Experimental context and source evidence
    dose
    PF-06835919 concentration series; 10 mM labeled fructose
    duration
    30 min pretreatment; 20 min fructose reaction
    evidence_access
    Primary full-text methods/results and metadata inspected.
    evidence_scope
    literature_reviewed; source-specific curation
    experimental_model
    Primary human hepatocytes
    exposure_scope
    Isolated fructose / investigational drug
    limitations
    Functional KHK inhibition in cells; PF-06835919 is investigational. Study sponsored/conducted by industry; pharmacological target engagement is not dietary efficacy.
    nutrient_topic
    HFCS chapter: actual formulation studies, component biochemistry and interventions are explicitly distinguished. · High-Fructose Corn Syrup / HFCS
    organism
    Primary human hepatocytes
    plain_language
    PF-06835919 inhibited labeled fructose-1-phosphate formation in primary human hepatocytes.
    primary_references
    Pharmacologic inhibition of ketohexokinase prevents fructose-induced metabolic dysfunction. (2021). https://pubmed.ncbi.nlm.nih.gov/33667726/ DOI: 10.1016/j.molmet.2021.101196
    route
    In vitro inhibitor pretreatment and fructose addition
    tissue
    Labeled fructose-1-phosphate production

    High-Fructose Corn Syrup: mechanism of action and metabolic impact (2026-09-20) · lines 569–579

    Original AI-assisted curation of twenty primary studies and official FDA composition information, with one reused canonical glucose-transport claim. Study-specific citations, negative findings and limitations retained. Not publisher full text. · supports · Primary human hepatocytes · source_derived_draft · unverified_draft

    ## hfcs-pf-hepatocytes PF-06835919 inhibited labeled fructose-1-phosphate formation in primary human hepatocytes. Model/species: Primary human hepatocytes Tissue: Labeled fructose-1-phosphate production Exposure: PF-06835919 concentration series; 10 mM labeled fructose Route: In vitro inhibitor pretreatment and fructose addition Duration: 30 min pretreatment; 20 min fructose reaction Exposure scope: Isolated fructose / investigational drug Limits: Functional KHK inhibition in cells; PF-06835919 is investigational. Study sponsored/conducted by industry; pharmacological target engagement is not dietary efficacy. Reference: Pharmacologic inhibition of ketohexokinase prevents fructose-induced metabolic dysfunction. (2021). https://pubmed.ncbi.nlm.nih.gov/33667726/ DOI: 10.1016/j.molmet.2021.101196 Access: Primary full-text methods/results and metadata inspected.
    Complete structured claim and evidence

  3. PF-06835919 at 300 mg/day reduced liver fat relative to placebo by a reported 18.73% after six weeks.

    PF-06835919 → Human hepatic lipid content measured by imaging source_derived_draftungraded
    Experimental context and source evidence
    dose
    PF-06835919 75 or 300 mg once daily versus placebo
    duration
    6 weeks
    evidence_access
    Primary abstract/metadata; unrecovered methods explicitly retained.
    evidence_scope
    literature_reviewed; source-specific curation
    experimental_model
    53 randomized adults with NAFLD; 48 completed phase 2a trial
    exposure_scope
    Fructose-pathway intervention, not an HFCS challenge
    limitations
    Small Pfizer-sponsored trial; 300 mg change was relative liver fat, not 18.73 percentage points. Not evidence of an approved drug or proof that HFCS caused each participant's disease.
    nutrient_topic
    HFCS chapter: actual formulation studies, component biochemistry and interventions are explicitly distinguished. · High-Fructose Corn Syrup / HFCS
    organism
    53 randomized adults with NAFLD; 48 completed phase 2a trial
    plain_language
    PF-06835919 at 300 mg/day reduced liver fat relative to placebo by a reported 18.73% after six weeks.
    primary_references
    Inhibition of ketohexokinase in adults with NAFLD reduces liver fat and inflammatory markers: A randomized phase 2 trial. (2021). https://pubmed.ncbi.nlm.nih.gov/35590219/ DOI: 10.1016/j.medj.2021.04.007
    route
    Oral drug; no controlled HFCS exposure
    tissue
    MRI proton-density liver fat

    High-Fructose Corn Syrup: mechanism of action and metabolic impact (2026-09-20) · lines 593–603

    Original AI-assisted curation of twenty primary studies and official FDA composition information, with one reused canonical glucose-transport claim. Study-specific citations, negative findings and limitations retained. Not publisher full text. · supports · 53 randomized adults with NAFLD; 48 completed phase 2a trial · source_derived_draft · unverified_draft

    ## hfcs-pf-human-liver PF-06835919 at 300 mg/day reduced liver fat relative to placebo by a reported 18.73% after six weeks. Model/species: 53 randomized adults with NAFLD; 48 completed phase 2a trial Tissue: MRI proton-density liver fat Exposure: PF-06835919 75 or 300 mg once daily versus placebo Route: Oral drug; no controlled HFCS exposure Duration: 6 weeks Exposure scope: Fructose-pathway intervention, not an HFCS challenge Limits: Small Pfizer-sponsored trial; 300 mg change was relative liver fat, not 18.73 percentage points. Not evidence of an approved drug or proof that HFCS caused each participant's disease. Reference: Inhibition of ketohexokinase in adults with NAFLD reduces liver fat and inflammatory markers: A randomized phase 2 trial. (2021). https://pubmed.ncbi.nlm.nih.gov/35590219/ DOI: 10.1016/j.medj.2021.04.007 Access: Primary abstract/metadata; unrecovered methods explicitly retained.
    Complete structured claim and evidence

  4. The 75 mg/day PF-06835919 arm did not show a significant liver-fat reduction versus placebo.

    PF-06835919 → Human hepatic lipid content measured by imaging source_derived_draftungraded
    Experimental context and source evidence
    dose
    PF-06835919 75 or 300 mg once daily versus placebo
    duration
    6 weeks
    evidence_access
    Primary abstract/metadata; unrecovered methods explicitly retained.
    evidence_scope
    literature_reviewed; source-specific curation
    experimental_model
    53 randomized adults with NAFLD; 48 completed phase 2a trial
    exposure_scope
    Fructose-pathway intervention, not an HFCS challenge
    limitations
    Small Pfizer-sponsored trial; 300 mg change was relative liver fat, not 18.73 percentage points. Not evidence of an approved drug or proof that HFCS caused each participant's disease.
    nutrient_topic
    HFCS chapter: actual formulation studies, component biochemistry and interventions are explicitly distinguished. · High-Fructose Corn Syrup / HFCS
    organism
    53 randomized adults with NAFLD; 48 completed phase 2a trial
    plain_language
    The 75 mg/day PF-06835919 arm did not show a significant liver-fat reduction versus placebo.
    primary_references
    Inhibition of ketohexokinase in adults with NAFLD reduces liver fat and inflammatory markers: A randomized phase 2 trial. (2021). https://pubmed.ncbi.nlm.nih.gov/35590219/ DOI: 10.1016/j.medj.2021.04.007
    route
    Oral drug; no controlled HFCS exposure
    tissue
    MRI proton-density liver fat

    High-Fructose Corn Syrup: mechanism of action and metabolic impact (2026-09-20) · lines 605–615

    Original AI-assisted curation of twenty primary studies and official FDA composition information, with one reused canonical glucose-transport claim. Study-specific citations, negative findings and limitations retained. Not publisher full text. · supports · 53 randomized adults with NAFLD; 48 completed phase 2a trial · source_derived_draft · unverified_draft

    ## hfcs-pf-low-dose-null The 75 mg/day PF-06835919 arm did not show a significant liver-fat reduction versus placebo. Model/species: 53 randomized adults with NAFLD; 48 completed phase 2a trial Tissue: MRI proton-density liver fat Exposure: PF-06835919 75 or 300 mg once daily versus placebo Route: Oral drug; no controlled HFCS exposure Duration: 6 weeks Exposure scope: Fructose-pathway intervention, not an HFCS challenge Limits: Small Pfizer-sponsored trial; 300 mg change was relative liver fat, not 18.73 percentage points. Not evidence of an approved drug or proof that HFCS caused each participant's disease. Reference: Inhibition of ketohexokinase in adults with NAFLD reduces liver fat and inflammatory markers: A randomized phase 2 trial. (2021). https://pubmed.ncbi.nlm.nih.gov/35590219/ DOI: 10.1016/j.medj.2021.04.007 Access: Primary abstract/metadata; unrecovered methods explicitly retained.
    Complete structured claim and evidence

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

    This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.

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