Component

EGCG-4″-sulfate

Study-scoped entity; inspect species, exposure, model and limitations on each claim.

3 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 acts on it

  1. Human plasma EGCG-4″-sulfate Cmax was 177.9 nM versus 233.5 nM free EGCG; AUC was 715.2 versus 664.1 nM·h.

    Epigallocatechin-3-gallate (EGCG) → EGCG-4″-sulfate source_derived_draftungraded
    Experimental context and source evidence
    experimental_model
    Human liver/intestinal cytosol, enzyme assignment and a human ingestion pharmacokinetic study.
    limitations
    Formation rate and metabolite exposure do not prove identical biological effects of free and conjugated EGCG.
    nutrient_topic
    EGCG collection; comparator and shared-pathway records retain their actual intervention. · Epigallocatechin-3-gallate (EGCG)
    plain_language
    A conjugated metabolite reached exposure comparable to free EGCG.
    primary_references
    4″-Sulfation Is the Major Metabolic Pathway of Epigallocatechin-3-gallate in Humans: Characterization of Metabolites, Enzymatic Analysis, and Pharmacokinetic Profiling. · 2022 · https://pubmed.ncbi.nlm.nih.gov/35786898/ · DOI 10.1021/acs.jafc.2c02150

    EGCG: receptor signaling, metabolism, nutrient interactions and discovery questions (2026-09-18) · lines 292–298

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human liver/intestinal cytosol, enzyme assignment and a human ingestion pharmacokinetic study. · source_derived_draft · unverified_draft

    ## egcg-sulfate-exposure A conjugated metabolite reached exposure comparable to free EGCG. Human plasma EGCG-4″-sulfate Cmax was 177.9 nM versus 233.5 nM free EGCG; AUC was 715.2 versus 664.1 nM·h. Model: Human liver/intestinal cytosol, enzyme assignment and a human ingestion pharmacokinetic study. Limitations: Formation rate and metabolite exposure do not prove identical biological effects of free and conjugated EGCG. Evidence access: primary abstract. 4″-Sulfation Is the Major Metabolic Pathway of Epigallocatechin-3-gallate in Humans: Characterization of Metabolites, Enzymatic Analysis, and Pharmacokinetic Profiling. · 2022 · https://pubmed.ncbi.nlm.nih.gov/35786898/ · DOI 10.1021/acs.jafc.2c02150
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. The 2022 study assigned hepatic EGCG sulfation to SULT1A1.

    Human sulfotransferase 1A1 / SULT1A1 → Epigallocatechin-3-gallate (EGCG) source_derived_draftungraded
    Experimental context and source evidence
    experimental_model
    Human liver/intestinal cytosol, enzyme assignment and a human ingestion pharmacokinetic study.
    limitations
    Formation rate and metabolite exposure do not prove identical biological effects of free and conjugated EGCG.
    nutrient_topic
    EGCG collection; comparator and shared-pathway records retain their actual intervention. · Epigallocatechin-3-gallate (EGCG)
    plain_language
    One study identifies this enzyme as a route for processing EGCG.
    primary_references
    4″-Sulfation Is the Major Metabolic Pathway of Epigallocatechin-3-gallate in Humans: Characterization of Metabolites, Enzymatic Analysis, and Pharmacokinetic Profiling. · 2022 · https://pubmed.ncbi.nlm.nih.gov/35786898/ · DOI 10.1021/acs.jafc.2c02150

    EGCG: receptor signaling, metabolism, nutrient interactions and discovery questions (2026-09-18) · lines 276–282

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human liver/intestinal cytosol, enzyme assignment and a human ingestion pharmacokinetic study. · source_derived_draft · unverified_draft

    ## egcg-sult1a1-substrate One study identifies this enzyme as a route for processing EGCG. The 2022 study assigned hepatic EGCG sulfation to SULT1A1. Model: Human liver/intestinal cytosol, enzyme assignment and a human ingestion pharmacokinetic study. Limitations: Formation rate and metabolite exposure do not prove identical biological effects of free and conjugated EGCG. Evidence access: primary abstract. 4″-Sulfation Is the Major Metabolic Pathway of Epigallocatechin-3-gallate in Humans: Characterization of Metabolites, Enzymatic Analysis, and Pharmacokinetic Profiling. · 2022 · https://pubmed.ncbi.nlm.nih.gov/35786898/ · DOI 10.1021/acs.jafc.2c02150
    Complete structured claim and evidence

  2. The same study assigned intestinal EGCG sulfation to SULT1A3.

    Human sulfotransferase 1A3 / SULT1A3 → Epigallocatechin-3-gallate (EGCG) source_derived_draftungraded
    Experimental context and source evidence
    experimental_model
    Human liver/intestinal cytosol, enzyme assignment and a human ingestion pharmacokinetic study.
    limitations
    Formation rate and metabolite exposure do not prove identical biological effects of free and conjugated EGCG.
    nutrient_topic
    EGCG collection; comparator and shared-pathway records retain their actual intervention. · Epigallocatechin-3-gallate (EGCG)
    plain_language
    A different enzyme contributed in the intestinal preparation.
    primary_references
    4″-Sulfation Is the Major Metabolic Pathway of Epigallocatechin-3-gallate in Humans: Characterization of Metabolites, Enzymatic Analysis, and Pharmacokinetic Profiling. · 2022 · https://pubmed.ncbi.nlm.nih.gov/35786898/ · DOI 10.1021/acs.jafc.2c02150

    EGCG: receptor signaling, metabolism, nutrient interactions and discovery questions (2026-09-18) · lines 284–290

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human liver/intestinal cytosol, enzyme assignment and a human ingestion pharmacokinetic study. · source_derived_draft · unverified_draft

    ## egcg-sult1a3 A different enzyme contributed in the intestinal preparation. The same study assigned intestinal EGCG sulfation to SULT1A3. Model: Human liver/intestinal cytosol, enzyme assignment and a human ingestion pharmacokinetic study. Limitations: Formation rate and metabolite exposure do not prove identical biological effects of free and conjugated EGCG. Evidence access: primary abstract. 4″-Sulfation Is the Major Metabolic Pathway of Epigallocatechin-3-gallate in Humans: Characterization of Metabolites, Enzymatic Analysis, and Pharmacokinetic Profiling. · 2022 · https://pubmed.ncbi.nlm.nih.gov/35786898/ · DOI 10.1021/acs.jafc.2c02150
    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.

    Evidence, AI assistance and curation standards