Component

Bortezomib

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

7 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. NMR and cell experiments characterized boronate and borate EGCG–bortezomib derivatives; adduct stability depended on structural features.

    Epigallocatechin-3-gallate (EGCG) → Bortezomib source_derived_draftungraded
    Experimental context and source evidence
    experimental_model
    Chemical characterization and cell assays.
    limitations
    A boronic-acid drug is not interchangeable with dietary boron.
    nutrient_topic
    EGCG collection; comparator and shared-pathway records retain their actual intervention. · Epigallocatechin-3-gallate (EGCG)
    plain_language
    The chemical interaction has evidence beyond a pathway diagram.
    primary_references
    Molecular characterization of the boron adducts of the proteasome inhibitor bortezomib with epigallocatechin-3-gallate and related polyphenols. · 2015 · https://pubmed.ncbi.nlm.nih.gov/25669488/ · DOI 10.1039/c4ob02512a

    EGCG: receptor signaling, metabolism, nutrient interactions and discovery questions (2026-09-18) · lines 412–418

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Chemical characterization and cell assays. · source_derived_draft · unverified_draft

    ## egcg-boronate The chemical interaction has evidence beyond a pathway diagram. NMR and cell experiments characterized boronate and borate EGCG–bortezomib derivatives; adduct stability depended on structural features. Model: Chemical characterization and cell assays. Limitations: A boronic-acid drug is not interchangeable with dietary boron. Evidence access: primary abstract. Molecular characterization of the boron adducts of the proteasome inhibitor bortezomib with epigallocatechin-3-gallate and related polyphenols. · 2015 · https://pubmed.ncbi.nlm.nih.gov/25669488/ · DOI 10.1039/c4ob02512a
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. EGCG blocked bortezomib-mediated anticancer effects in the reported models.

    Epigallocatechin-3-gallate (EGCG) → Antitumor activity of bortezomib in specified models source_derived_draftungraded
    Experimental context and source evidence
    experimental_model
    Myeloma/glioblastoma cell experiments and animal models in the 2009 Blood study.
    limitations
    Preclinical findings; no human coadministration outcome trial. Chemical form and simultaneous concentrations matter.
    nutrient_topic
    EGCG collection; comparator and shared-pathway records retain their actual intervention. · Epigallocatechin-3-gallate (EGCG)
    plain_language
    One research group found that EGCG weakened this cancer drug.
    primary_references
    Green tea polyphenols block the anticancer effects of bortezomib and other boronic acid-based proteasome inhibitors. · 2009 · https://pubmed.ncbi.nlm.nih.gov/19190249/ · DOI 10.1182/blood-2008-07-171389

    EGCG: receptor signaling, metabolism, nutrient interactions and discovery questions (2026-09-18) · lines 396–402

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Myeloma/glioblastoma cell experiments and animal models in the 2009 Blood study. · source_derived_draft · unverified_draft

    ## egcg-bortezomib-antagonism One research group found that EGCG weakened this cancer drug. EGCG blocked bortezomib-mediated anticancer effects in the reported models. Model: Myeloma/glioblastoma cell experiments and animal models in the 2009 Blood study. Limitations: Preclinical findings; no human coadministration outcome trial. Chemical form and simultaneous concentrations matter. Evidence access: primary abstract. Green tea polyphenols block the anticancer effects of bortezomib and other boronic acid-based proteasome inhibitors. · 2009 · https://pubmed.ncbi.nlm.nih.gov/19190249/ · DOI 10.1182/blood-2008-07-171389
    Complete structured claim and evidence

  2. In CWR22 xenografts, EGCG above 200 micromolar at bortezomib administration abolished measured antitumor activity.

    Epigallocatechin-3-gallate (EGCG) → Antitumor activity of bortezomib in specified models source_derived_draftungraded
    Experimental context and source evidence
    experimental_model
    Immunocompromised mice; bortezomib 0.8 mg/kg IV twice weekly.
    limitations
    Concentration-specific animal findings do not establish a human safety threshold.
    nutrient_topic
    EGCG collection; comparator and shared-pathway records retain their actual intervention. · Epigallocatechin-3-gallate (EGCG)
    plain_language
    A follow-up found antagonism at very high simultaneous exposure.
    primary_references
    Preclinical evaluation of the antitumor activity of bortezomib in combination with vitamin C or with epigallocatechin gallate, a component of green tea. · 2011 · https://pubmed.ncbi.nlm.nih.gov/21400028/ · DOI 10.1007/s00280-011-1591-2

    EGCG: receptor signaling, metabolism, nutrient interactions and discovery questions (2026-09-18) · lines 428–434

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Immunocompromised mice; bortezomib 0.8 mg/kg IV twice weekly. · source_derived_draft · unverified_draft

    ## egcg-bortezomib-high A follow-up found antagonism at very high simultaneous exposure. In CWR22 xenografts, EGCG above 200 micromolar at bortezomib administration abolished measured antitumor activity. Model: Immunocompromised mice; bortezomib 0.8 mg/kg IV twice weekly. Limitations: Concentration-specific animal findings do not establish a human safety threshold. Evidence access: primary abstract. Preclinical evaluation of the antitumor activity of bortezomib in combination with vitamin C or with epigallocatechin gallate, a component of green tea. · 2011 · https://pubmed.ncbi.nlm.nih.gov/21400028/ · DOI 10.1007/s00280-011-1591-2
    Complete structured claim and evidence

  3. At EGCG 11–16 micromolar, the same model showed no antagonism; tumor-growth inhibition was 63.5% versus 53.9–58.9% with bortezomib alone.

    Epigallocatechin-3-gallate (EGCG) → Antitumor activity of bortezomib in specified models source_derived_draftungraded
    Experimental context and source evidence
    experimental_model
    CWR22 xenograft exposure comparison.
    limitations
    Not proof of clinical synergy or unrestricted safe coadministration.
    nutrient_topic
    EGCG collection; comparator and shared-pathway records retain their actual intervention. · Epigallocatechin-3-gallate (EGCG)
    plain_language
    The drug interaction was not identical at every concentration.
    primary_references
    Preclinical evaluation of the antitumor activity of bortezomib in combination with vitamin C or with epigallocatechin gallate, a component of green tea. · 2011 · https://pubmed.ncbi.nlm.nih.gov/21400028/ · DOI 10.1007/s00280-011-1591-2

    EGCG: receptor signaling, metabolism, nutrient interactions and discovery questions (2026-09-18) · lines 436–442

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · CWR22 xenograft exposure comparison. · source_derived_draft · unverified_draft

    ## egcg-bortezomib-lower The drug interaction was not identical at every concentration. At EGCG 11–16 micromolar, the same model showed no antagonism; tumor-growth inhibition was 63.5% versus 53.9–58.9% with bortezomib alone. Model: CWR22 xenograft exposure comparison. Limitations: Not proof of clinical synergy or unrestricted safe coadministration. Evidence access: primary abstract. Preclinical evaluation of the antitumor activity of bortezomib in combination with vitamin C or with epigallocatechin gallate, a component of green tea. · 2011 · https://pubmed.ncbi.nlm.nih.gov/21400028/ · DOI 10.1007/s00280-011-1591-2
    Complete structured claim and evidence

  4. Direct EGCG–bortezomib reaction prevented proteasome inhibition and downstream stress/death responses; tested nonboronic inhibitors did not show the same antagonism.

    Epigallocatechin-3-gallate (EGCG) → Bortezomib-mediated proteasome inhibition source_derived_draftungraded
    Experimental context and source evidence
    experimental_model
    Myeloma/glioblastoma cell experiments and animal models in the 2009 Blood study.
    limitations
    Preclinical findings; no human coadministration outcome trial. Chemical form and simultaneous concentrations matter.
    nutrient_topic
    EGCG collection; comparator and shared-pathway records retain their actual intervention. · Epigallocatechin-3-gallate (EGCG)
    plain_language
    The proposed interference starts with drug chemistry.
    primary_references
    Green tea polyphenols block the anticancer effects of bortezomib and other boronic acid-based proteasome inhibitors. · 2009 · https://pubmed.ncbi.nlm.nih.gov/19190249/ · DOI 10.1182/blood-2008-07-171389

    EGCG: receptor signaling, metabolism, nutrient interactions and discovery questions (2026-09-18) · lines 404–410

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Myeloma/glioblastoma cell experiments and animal models in the 2009 Blood study. · source_derived_draft · unverified_draft

    ## egcg-bortezomib-proteasome The proposed interference starts with drug chemistry. Direct EGCG–bortezomib reaction prevented proteasome inhibition and downstream stress/death responses; tested nonboronic inhibitors did not show the same antagonism. Model: Myeloma/glioblastoma cell experiments and animal models in the 2009 Blood study. Limitations: Preclinical findings; no human coadministration outcome trial. Chemical form and simultaneous concentrations matter. Evidence access: primary abstract. Green tea polyphenols block the anticancer effects of bortezomib and other boronic acid-based proteasome inhibitors. · 2009 · https://pubmed.ncbi.nlm.nih.gov/19190249/ · DOI 10.1182/blood-2008-07-171389
    Complete structured claim and evidence

  5. A separate 2009 KM3 myeloma-cell study reported synergistic apoptosis with EGCG plus bortezomib.

    Epigallocatechin-3-gallate (EGCG) → Antitumor activity of bortezomib in specified models source_derived_draftungraded
    Experimental context and source evidence
    experimental_model
    KM3 myeloma cells; associated NF-kappaB/caspase pathway readouts.
    limitations
    Dose, timing and model were not harmonized with the antagonism study; no universal direction can be assigned.
    nutrient_topic
    EGCG collection; comparator and shared-pathway records retain their actual intervention. · Epigallocatechin-3-gallate (EGCG)
    plain_language
    Another study reported a stronger combination effect.
    primary_references
    Potentiation of (-)-epigallocatechin-3-gallate-induced apoptosis by bortezomib in multiple myeloma cells. · 2009 · https://pubmed.ncbi.nlm.nih.gov/20011976/ · DOI 10.1093/abbs/gmp094

    EGCG: receptor signaling, metabolism, nutrient interactions and discovery questions (2026-09-18) · lines 420–426

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · KM3 myeloma cells; associated NF-kappaB/caspase pathway readouts. · source_derived_draft · unverified_draft

    ## egcg-bortezomib-synergy Another study reported a stronger combination effect. A separate 2009 KM3 myeloma-cell study reported synergistic apoptosis with EGCG plus bortezomib. Model: KM3 myeloma cells; associated NF-kappaB/caspase pathway readouts. Limitations: Dose, timing and model were not harmonized with the antagonism study; no universal direction can be assigned. Evidence access: primary abstract. Potentiation of (-)-epigallocatechin-3-gallate-induced apoptosis by bortezomib in multiple myeloma cells. · 2009 · https://pubmed.ncbi.nlm.nih.gov/20011976/ · DOI 10.1093/abbs/gmp094
    Complete structured claim and evidence

  6. Oral vitamin C at 40 or 500 mg/kg did not antagonize bortezomib in the same mouse experiment.

    L-Ascorbic acid → Antitumor activity of bortezomib in specified models source_derived_draftungraded
    Experimental context and source evidence
    experimental_model
    CWR22 xenograft model.
    limitations
    Species, route and exposure matter; this comparison does not justify combining supplements with cancer treatment.
    nutrient_topic
    EGCG collection; comparator and shared-pathway records retain their actual intervention. · Epigallocatechin-3-gallate (EGCG)
    plain_language
    Another nutrient comparator did not reproduce high-EGCG antagonism.
    primary_references
    Preclinical evaluation of the antitumor activity of bortezomib in combination with vitamin C or with epigallocatechin gallate, a component of green tea. · 2011 · https://pubmed.ncbi.nlm.nih.gov/21400028/ · DOI 10.1007/s00280-011-1591-2

    EGCG: receptor signaling, metabolism, nutrient interactions and discovery questions (2026-09-18) · lines 444–450

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · CWR22 xenograft model. · source_derived_draft · unverified_draft

    ## egcg-bortezomib-vitc Another nutrient comparator did not reproduce high-EGCG antagonism. Oral vitamin C at 40 or 500 mg/kg did not antagonize bortezomib in the same mouse experiment. Model: CWR22 xenograft model. Limitations: Species, route and exposure matter; this comparison does not justify combining supplements with cancer treatment. Evidence access: primary abstract. Preclinical evaluation of the antitumor activity of bortezomib in combination with vitamin C or with epigallocatechin gallate, a component of green tea. · 2011 · https://pubmed.ncbi.nlm.nih.gov/21400028/ · DOI 10.1007/s00280-011-1591-2
    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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