Component

Cucurbitacin D

Context-specific entity; species, compartment and exposure are stated 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 it acts on

  1. Incubating purified human cofilin 1 with cucurbitacin D produced covalent adducts; mass shifts were compatible with about four compound molecules per cofilin under the tested excess-compound conditions.

    Cucurbitacin D → Human cofilin 1 / CFL1 source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary full text PMC3751690
    experimental_model
    Purified human cofilin 1, 5 micromolar; up to 1:100 protein:compound molar ratio, 16 hours.
    limitations
    Long, high-excess biochemical incubation; does not establish selectivity or occupancy after human ingestion.
    nutrient_topic
    Cucurbitacins collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Cucurbitacins
    plain_language
    Protein cysteines can become chemical attachment sites.
    primary_references
    Cucurbitacin covalent bonding to cysteine thiols: the filamentous-actin severing protein Cofilin1 as an exemplary target. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23945128/ · DOI 10.1186/1478-811X-11-58

    Cucurbitacins: thiol chemistry, cytoskeleton, metabolic dependencies and signaling (2026-09-20) · lines 12–18

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Purified human cofilin 1, 5 micromolar; up to 1:100 protein:compound molar ratio, 16 hours. · source_derived_draft · unverified_draft

    ## cucurbitacin-d-cofilin-adduct Protein cysteines can become chemical attachment sites. Incubating purified human cofilin 1 with cucurbitacin D produced covalent adducts; mass shifts were compatible with about four compound molecules per cofilin under the tested excess-compound conditions. Model: Purified human cofilin 1, 5 micromolar; up to 1:100 protein:compound molar ratio, 16 hours. Limitations: Long, high-excess biochemical incubation; does not establish selectivity or occupancy after human ingestion. Evidence access: Primary full text PMC3751690 Cucurbitacin covalent bonding to cysteine thiols: the filamentous-actin severing protein Cofilin1 as an exemplary target. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23945128/ · DOI 10.1186/1478-811X-11-58
    Complete structured claim and evidence

  2. Cucurbitacin D interfered with EGF–EGFR binding in a solid-phase binding assay and reduced EGFR phosphorylation in the NSCLC study.

    Cucurbitacin D → Epidermal growth factor receptor source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Binding assay and gefitinib-resistant human NSCLC cell models.
    limitations
    This does not establish a clinically effective replacement for an EGFR inhibitor.
    nutrient_topic
    Cucurbitacins collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Cucurbitacins
    plain_language
    A growth-factor interaction was tested upstream of signaling.
    primary_references
    Cucurbitacin D Overcomes Gefitinib Resistance by Blocking EGF Binding to EGFR and Inducing Cell Death in NSCLCs. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32133284/ · DOI 10.3389/fonc.2020.00062

    Cucurbitacins: thiol chemistry, cytoskeleton, metabolic dependencies and signaling (2026-09-20) · lines 332–338

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Binding assay and gefitinib-resistant human NSCLC cell models. · source_derived_draft · unverified_draft

    ## cucurbitacin-d-egf-binding A growth-factor interaction was tested upstream of signaling. Cucurbitacin D interfered with EGF–EGFR binding in a solid-phase binding assay and reduced EGFR phosphorylation in the NSCLC study. Model: Binding assay and gefitinib-resistant human NSCLC cell models. Limitations: This does not establish a clinically effective replacement for an EGFR inhibitor. Evidence access: Primary abstract Cucurbitacin D Overcomes Gefitinib Resistance by Blocking EGF Binding to EGFR and Inducing Cell Death in NSCLCs. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32133284/ · DOI 10.3389/fonc.2020.00062
    Complete structured claim and evidence

  3. Cucurbitacin D at 0.1–1 micromolar reduced glucose uptake and lactate output in human PC3 and DU145 experiments.

    Cucurbitacin D → Human prostate-cancer glucose uptake during cucurbitacin D exposure source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Human prostate-cancer cell experiments; xenografts also studied.
    limitations
    Not evidence of effective or safe diabetes treatment.
    nutrient_topic
    Cucurbitacins collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Cucurbitacins
    plain_language
    Fuel handling changed in these cancer cells.
    primary_references
    Cucurbitacin D Reprograms Glucose Metabolic Network in Prostate Cancer. · 2019 · https://pubmed.ncbi.nlm.nih.gov/30875788/ · DOI 10.3390/cancers11030364

    Cucurbitacins: thiol chemistry, cytoskeleton, metabolic dependencies and signaling (2026-09-20) · lines 308–314

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human prostate-cancer cell experiments; xenografts also studied. · source_derived_draft · unverified_draft

    ## cucurbitacin-d-glucose Fuel handling changed in these cancer cells. Cucurbitacin D at 0.1–1 micromolar reduced glucose uptake and lactate output in human PC3 and DU145 experiments. Model: Human prostate-cancer cell experiments; xenografts also studied. Limitations: Not evidence of effective or safe diabetes treatment. Evidence access: Primary abstract Cucurbitacin D Reprograms Glucose Metabolic Network in Prostate Cancer. · 2019 · https://pubmed.ncbi.nlm.nih.gov/30875788/ · DOI 10.3390/cancers11030364
    Complete structured claim and evidence

  4. Molecular docking proposed cucurbitacin D binding to GLUT1.

    Cucurbitacin D → Human glucose transporter 1 / SLC2A1 source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Computational docking within the glucose-metabolism study.
    limitations
    No transporter-binding kinetics or reconstituted transport-inhibition measurement was established by docking.
    nutrient_topic
    Cucurbitacins collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Cucurbitacins
    plain_language
    Direct transporter binding remains a prediction in this evidence record.
    primary_references
    Cucurbitacin D Reprograms Glucose Metabolic Network in Prostate Cancer. · 2019 · https://pubmed.ncbi.nlm.nih.gov/30875788/ · DOI 10.3390/cancers11030364

    Cucurbitacins: thiol chemistry, cytoskeleton, metabolic dependencies and signaling (2026-09-20) · lines 324–330

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Computational docking within the glucose-metabolism study. · source_derived_draft · unverified_draft

    ## cucurbitacin-d-glut1-docking Direct transporter binding remains a prediction in this evidence record. Molecular docking proposed cucurbitacin D binding to GLUT1. Model: Computational docking within the glucose-metabolism study. Limitations: No transporter-binding kinetics or reconstituted transport-inhibition measurement was established by docking. Evidence access: Primary abstract Cucurbitacin D Reprograms Glucose Metabolic Network in Prostate Cancer. · 2019 · https://pubmed.ncbi.nlm.nih.gov/30875788/ · DOI 10.3390/cancers11030364
    Complete structured claim and evidence

  5. Cucurbitacin D decreased GLUT1 expression in the prostate-cancer study; miR-132-associated changes were also reported.

    Cucurbitacin D → Human glucose transporter 1 / SLC2A1 source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Human PC3/DU145 cells and xenograft work.
    limitations
    Expression and correlated microRNA changes do not establish a single exclusive mechanism.
    nutrient_topic
    Cucurbitacins collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Cucurbitacins
    plain_language
    Transporter abundance offers one route to altered glucose handling.
    primary_references
    Cucurbitacin D Reprograms Glucose Metabolic Network in Prostate Cancer. · 2019 · https://pubmed.ncbi.nlm.nih.gov/30875788/ · DOI 10.3390/cancers11030364

    Cucurbitacins: thiol chemistry, cytoskeleton, metabolic dependencies and signaling (2026-09-20) · lines 316–322

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human PC3/DU145 cells and xenograft work. · source_derived_draft · unverified_draft

    ## cucurbitacin-d-glut1-expression Transporter abundance offers one route to altered glucose handling. Cucurbitacin D decreased GLUT1 expression in the prostate-cancer study; miR-132-associated changes were also reported. Model: Human PC3/DU145 cells and xenograft work. Limitations: Expression and correlated microRNA changes do not establish a single exclusive mechanism. Evidence access: Primary abstract Cucurbitacin D Reprograms Glucose Metabolic Network in Prostate Cancer. · 2019 · https://pubmed.ncbi.nlm.nih.gov/30875788/ · DOI 10.3390/cancers11030364
    Complete structured claim and evidence

  6. Cucurbitacin D enhanced LPS-associated IL-1-beta production and caspase-1-dependent inflammasome activation; the study reported NLRP3–ASC interaction and an ERK-dependent transcription component.

    Cucurbitacin D → Cucurbitacin D inflammatory response in human/mouse myeloid study panel source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Panel included human THP-1 and murine RAW264, peritoneal and bone-marrow-derived macrophages; individual assay species unresolved in accessed abstract.
    limitations
    Mixed-model process is retained explicitly; no individual molecular result is silently assigned to human cells. Different member/stimulus from CuB A549 suppression.
    nutrient_topic
    Cucurbitacins collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Cucurbitacins
    plain_language
    This member increased an inflammatory response under these conditions.
    primary_references
    Cucurbitacin D is a new inflammasome activator in macrophages. · 2013 · https://pubmed.ncbi.nlm.nih.gov/24140411/ · DOI 10.1016/j.intimp.2013.10.003

    Cucurbitacins: thiol chemistry, cytoskeleton, metabolic dependencies and signaling (2026-09-20) · lines 340–346

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Panel included human THP-1 and murine RAW264, peritoneal and bone-marrow-derived macrophages; individual assay species unresolved in accessed abstract. · source_derived_draft · unverified_draft

    ## cucurbitacin-d-inflammasome This member increased an inflammatory response under these conditions. Cucurbitacin D enhanced LPS-associated IL-1-beta production and caspase-1-dependent inflammasome activation; the study reported NLRP3–ASC interaction and an ERK-dependent transcription component. Model: Panel included human THP-1 and murine RAW264, peritoneal and bone-marrow-derived macrophages; individual assay species unresolved in accessed abstract. Limitations: Mixed-model process is retained explicitly; no individual molecular result is silently assigned to human cells. Different member/stimulus from CuB A549 suppression. Evidence access: Primary abstract Cucurbitacin D is a new inflammasome activator in macrophages. · 2013 · https://pubmed.ncbi.nlm.nih.gov/24140411/ · DOI 10.1016/j.intimp.2013.10.003
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. At equal oral formulation doses, nanosuspension increased measured peak concentration and exposure area for cucurbitacins B, D and E in rats.

    Rat oral cucurbitacin nanosuspension formulation → Cucurbitacin B source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    biomarker_context Imported condition classification; unverified.
    evidence_access
    Primary abstract
    experimental_model
    2025 rat pharmacokinetic formulation comparison; dose not specified in accessed abstract.
    limitations
    Does not establish human bioavailability or improved clinical safety.
    nutrient_topic
    Cucurbitacins collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Cucurbitacins
    plain_language
    Changing the formulation changed exposure to each member.
    primary_references
    Comparison of the pharmacokinetic profiles of three triterpenoids after oral administration of a cucurbitacin tablet and nanosuspension by UHPLC-MS/MS. · 2025 · https://pubmed.ncbi.nlm.nih.gov/41001343/ · DOI 10.3389/fphar.2025.1647015
    trigger_kind
    biomarker_context Imported condition classification; unverified.

    Cucurbitacins: thiol chemistry, cytoskeleton, metabolic dependencies and signaling (2026-09-20) · lines 388–394

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · 2025 rat pharmacokinetic formulation comparison; dose not specified in accessed abstract. · source_derived_draft · unverified_draft

    ## cucurbitacin-formulation-exposure Changing the formulation changed exposure to each member. At equal oral formulation doses, nanosuspension increased measured peak concentration and exposure area for cucurbitacins B, D and E in rats. Model: 2025 rat pharmacokinetic formulation comparison; dose not specified in accessed abstract. Limitations: Does not establish human bioavailability or improved clinical safety. Evidence access: Primary abstract Comparison of the pharmacokinetic profiles of three triterpenoids after oral administration of a cucurbitacin tablet and nanosuspension by UHPLC-MS/MS. · 2025 · https://pubmed.ncbi.nlm.nih.gov/41001343/ · DOI 10.3389/fphar.2025.1647015
    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