Component

Cucurbitacin B

Context-specific entity; species, compartment and exposure are stated on each claim.

26 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. In human H358 and A549 cells, deferoxamine, ferrostatin-1 and liproxstatin-1 reversed cucurbitacin B growth inhibition, supporting a ferroptotic component.

    Cucurbitacin B → Human NSCLC ferroptotic response during cucurbitacin B exposure source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Human NSCLC cell experiments.
    limitations
    Rescue does not establish exclusive cell-death causation or clinical cancer efficacy.
    nutrient_topic
    Cucurbitacins collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Cucurbitacins
    plain_language
    Iron chelation and lipid-radical inhibitors changed the outcome.
    primary_references
    Cucurbitacin B targets STAT3 to induce ferroptosis in non-small cell lung cancer. · 2024 · https://pubmed.ncbi.nlm.nih.gov/38950838/ · DOI 10.1016/j.ejphar.2024.176805

    Cucurbitacins: thiol chemistry, cytoskeleton, metabolic dependencies and signaling (2026-09-20) · lines 252–258

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

    ## cucurbitacin-b-ferroptosis-rescue Iron chelation and lipid-radical inhibitors changed the outcome. In human H358 and A549 cells, deferoxamine, ferrostatin-1 and liproxstatin-1 reversed cucurbitacin B growth inhibition, supporting a ferroptotic component. Model: Human NSCLC cell experiments. Limitations: Rescue does not establish exclusive cell-death causation or clinical cancer efficacy. Evidence access: Primary abstract Cucurbitacin B targets STAT3 to induce ferroptosis in non-small cell lung cancer. · 2024 · https://pubmed.ncbi.nlm.nih.gov/38950838/ · DOI 10.1016/j.ejphar.2024.176805
    Complete structured claim and evidence

  2. Cucurbitacin B exposure decreased GPX4 protein expression in the human nasopharyngeal-cancer experiments.

    Cucurbitacin B → GPX4 source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Human nasopharyngeal-cancer cells; animal tumor work also reported.
    limitations
    Expression is not direct GPX4 binding or evidence of selenium depletion.
    nutrient_topic
    Cucurbitacins collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Cucurbitacins
    plain_language
    A lipid-peroxide defense protein decreased in this model.
    primary_references
    Induction of ferroptosis in human nasopharyngeal cancer cells by cucurbitacin B: molecular mechanism and therapeutic potential. · 2021 · https://pubmed.ncbi.nlm.nih.gov/33664249/ · DOI 10.1038/s41419-021-03516-y

    Cucurbitacins: thiol chemistry, cytoskeleton, metabolic dependencies and signaling (2026-09-20) · lines 244–250

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human nasopharyngeal-cancer cells; animal tumor work also reported. · source_derived_draft · unverified_draft

    ## cucurbitacin-b-gpx4-expression A lipid-peroxide defense protein decreased in this model. Cucurbitacin B exposure decreased GPX4 protein expression in the human nasopharyngeal-cancer experiments. Model: Human nasopharyngeal-cancer cells; animal tumor work also reported. Limitations: Expression is not direct GPX4 binding or evidence of selenium depletion. Evidence access: Primary abstract Induction of ferroptosis in human nasopharyngeal cancer cells by cucurbitacin B: molecular mechanism and therapeutic potential. · 2021 · https://pubmed.ncbi.nlm.nih.gov/33664249/ · DOI 10.1038/s41419-021-03516-y
    Complete structured claim and evidence

  3. UV spectroscopy and FTICR mass spectrometry detected physical interaction between cucurbitacin B and glutathione in a cell-free system.

    Cucurbitacin B → GSH source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Cell-free chemistry; exposure concentration and duration unavailable in the accessed abstract.
    limitations
    Physical interaction is not a quantified in-vivo detoxification rate or human glutathione-depletion threshold.
    nutrient_topic
    Cucurbitacins collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Cucurbitacins
    plain_language
    Glutathione can interact with the compound before a downstream signal is measured.
    primary_references
    Cucurbitacin B potently suppresses non-small-cell lung cancer growth: identification of intracellular thiols as critical targets. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23340170/ · DOI 10.1016/j.canlet.2013.01.008

    Cucurbitacins: thiol chemistry, cytoskeleton, metabolic dependencies and signaling (2026-09-20) · lines 108–114

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Cell-free chemistry; exposure concentration and duration unavailable in the accessed abstract. · source_derived_draft · unverified_draft

    ## cucurbitacin-b-gsh-interaction Glutathione can interact with the compound before a downstream signal is measured. UV spectroscopy and FTICR mass spectrometry detected physical interaction between cucurbitacin B and glutathione in a cell-free system. Model: Cell-free chemistry; exposure concentration and duration unavailable in the accessed abstract. Limitations: Physical interaction is not a quantified in-vivo detoxification rate or human glutathione-depletion threshold. Evidence access: Primary abstract Cucurbitacin B potently suppresses non-small-cell lung cancer growth: identification of intracellular thiols as critical targets. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23340170/ · DOI 10.1016/j.canlet.2013.01.008
    Complete structured claim and evidence

  4. Cucurbitacin B decreased ICAM1 expression induced by TNF-alpha or IL-1-alpha in human A549 cells.

    Cucurbitacin B → Human intercellular adhesion molecule 1 / ICAM1 source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Human lung adenocarcinoma cell model.
    limitations
    This is not a clinical anti-inflammatory outcome.
    nutrient_topic
    Cucurbitacins collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Cucurbitacins
    plain_language
    A cell-adhesion response to inflammatory signals decreased.
    primary_references
    Cucurbitacin B Down-Regulates TNF Receptor 1 Expression and Inhibits the TNF-α-Dependent Nuclear Factor κB Signaling Pathway in Human Lung Adenocarcinoma A549 Cells. · 2022 · https://pubmed.ncbi.nlm.nih.gov/35806134/ · DOI 10.3390/ijms23137130

    Cucurbitacins: thiol chemistry, cytoskeleton, metabolic dependencies and signaling (2026-09-20) · lines 212–218

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human lung adenocarcinoma cell model. · source_derived_draft · unverified_draft

    ## cucurbitacin-b-icam A cell-adhesion response to inflammatory signals decreased. Cucurbitacin B decreased ICAM1 expression induced by TNF-alpha or IL-1-alpha in human A549 cells. Model: Human lung adenocarcinoma cell model. Limitations: This is not a clinical anti-inflammatory outcome. Evidence access: Primary abstract Cucurbitacin B Down-Regulates TNF Receptor 1 Expression and Inhibits the TNF-α-Dependent Nuclear Factor κB Signaling Pathway in Human Lung Adenocarcinoma A549 Cells. · 2022 · https://pubmed.ncbi.nlm.nih.gov/35806134/ · DOI 10.3390/ijms23137130
    Complete structured claim and evidence

  5. Cucurbitacin B increased lipid ROS, malondialdehyde and measured ferrous iron while lowering glutathione in H358 and A549 experiments.

    Cucurbitacin B → Human cancer-cell lipid peroxidation during cucurbitacin B exposure source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Human NSCLC experiments; concentration and duration unavailable in accessed abstract.
    limitations
    Associated readouts do not by themselves order iron release, glutathione loss and lipid oxidation.
    nutrient_topic
    Cucurbitacins collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Cucurbitacins
    plain_language
    Iron and antioxidant balance changed together with membrane damage.
    primary_references
    Cucurbitacin B targets STAT3 to induce ferroptosis in non-small cell lung cancer. · 2024 · https://pubmed.ncbi.nlm.nih.gov/38950838/ · DOI 10.1016/j.ejphar.2024.176805

    Cucurbitacins: thiol chemistry, cytoskeleton, metabolic dependencies and signaling (2026-09-20) · lines 260–266

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human NSCLC experiments; concentration and duration unavailable in accessed abstract. · source_derived_draft · unverified_draft

    ## cucurbitacin-b-lipid-iron Iron and antioxidant balance changed together with membrane damage. Cucurbitacin B increased lipid ROS, malondialdehyde and measured ferrous iron while lowering glutathione in H358 and A549 experiments. Model: Human NSCLC experiments; concentration and duration unavailable in accessed abstract. Limitations: Associated readouts do not by themselves order iron release, glutathione loss and lipid oxidation. Evidence access: Primary abstract Cucurbitacin B targets STAT3 to induce ferroptosis in non-small cell lung cancer. · 2024 · https://pubmed.ncbi.nlm.nih.gov/38950838/ · DOI 10.1016/j.ejphar.2024.176805
    Complete structured claim and evidence

  6. UV spectroscopy and FTICR mass spectrometry detected physical interaction between cucurbitacin B and N-acetylcysteine in a cell-free system.

    Cucurbitacin B → N-Acetyl-L-cysteine source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Cell-free chemistry.
    limitations
    NAC rescue therefore does not uniquely prove ROS scavenging; it also does not rule out a role for ROS.
    nutrient_topic
    Cucurbitacins collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Cucurbitacins
    plain_language
    An antioxidant can also change the amount of available test compound.
    primary_references
    Cucurbitacin B potently suppresses non-small-cell lung cancer growth: identification of intracellular thiols as critical targets. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23340170/ · DOI 10.1016/j.canlet.2013.01.008

    Cucurbitacins: thiol chemistry, cytoskeleton, metabolic dependencies and signaling (2026-09-20) · lines 116–122

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Cell-free chemistry. · source_derived_draft · unverified_draft

    ## cucurbitacin-b-nac-interaction An antioxidant can also change the amount of available test compound. UV spectroscopy and FTICR mass spectrometry detected physical interaction between cucurbitacin B and N-acetylcysteine in a cell-free system. Model: Cell-free chemistry. Limitations: NAC rescue therefore does not uniquely prove ROS scavenging; it also does not rule out a role for ROS. Evidence access: Primary abstract Cucurbitacin B potently suppresses non-small-cell lung cancer growth: identification of intracellular thiols as critical targets. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23340170/ · DOI 10.1016/j.canlet.2013.01.008
    Complete structured claim and evidence

  7. Cucurbitacin B exposure was associated with the TLR4/mitochondrial-ROS/NLRP3 route and gasdermin D cleavage in the NSCLC pyroptosis experiments.

    Cucurbitacin B → Human NSCLC pyroptotic response during cucurbitacin B exposure source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Human NSCLC cells; mouse tumor experiments provide a separate translational level.
    limitations
    Do not merge all tumor-cell death into one obligatory linear chain.
    nutrient_topic
    Cucurbitacins collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Cucurbitacins
    plain_language
    Inflammatory membrane rupture is separate from ferroptotic lipid damage.
    primary_references
    Cucurbitacin B inhibits non-small cell lung cancer in vivo and in vitro by triggering TLR4/NLRP3/GSDMD-dependent pyroptosis. · 2021 · https://pubmed.ncbi.nlm.nih.gov/34217831/ · DOI 10.1016/j.phrs.2021.105748

    Cucurbitacins: thiol chemistry, cytoskeleton, metabolic dependencies and signaling (2026-09-20) · lines 300–306

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human NSCLC cells; mouse tumor experiments provide a separate translational level. · source_derived_draft · unverified_draft

    ## cucurbitacin-b-pyroptosis-route Inflammatory membrane rupture is separate from ferroptotic lipid damage. Cucurbitacin B exposure was associated with the TLR4/mitochondrial-ROS/NLRP3 route and gasdermin D cleavage in the NSCLC pyroptosis experiments. Model: Human NSCLC cells; mouse tumor experiments provide a separate translational level. Limitations: Do not merge all tumor-cell death into one obligatory linear chain. Evidence access: Primary abstract Cucurbitacin B inhibits non-small cell lung cancer in vivo and in vitro by triggering TLR4/NLRP3/GSDMD-dependent pyroptosis. · 2021 · https://pubmed.ncbi.nlm.nih.gov/34217831/ · DOI 10.1016/j.phrs.2021.105748
    Complete structured claim and evidence

  8. Male Wistar rats receiving oral cucurbitacin B at 2–4 mg/kg versus intravenous 0.1 mg/kg had estimated oral bioavailability of about 10%, with oral peak around 30 minutes.

    Cucurbitacin B → Rat cucurbitacin B oral bioavailability source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    biomarker_context Imported condition classification; unverified.
    evidence_access
    Primary full text PMC6609384
    experimental_model
    Rat pharmacokinetics, six animals per reported group; clear solution in 40% v/v DMSO.
    limitations
    Not a human absorption estimate or dosing recommendation.
    nutrient_topic
    Cucurbitacins collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Cucurbitacins
    plain_language
    Oral dose and systemic exposure were far from equivalent.
    primary_references
    Pharmacokinetics of cucurbitacin B from Trichosanthes cucumerina L. in rats. · 2019 · https://pubmed.ncbi.nlm.nih.gov/31272429/ · DOI 10.1186/s12906-019-2568-7
    trigger_kind
    biomarker_context Imported condition classification; unverified.

    Cucurbitacins: thiol chemistry, cytoskeleton, metabolic dependencies and signaling (2026-09-20) · lines 348–354

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Rat pharmacokinetics, six animals per reported group; clear solution in 40% v/v DMSO. · source_derived_draft · unverified_draft

    ## cucurbitacin-b-rat-absorption Oral dose and systemic exposure were far from equivalent. Male Wistar rats receiving oral cucurbitacin B at 2–4 mg/kg versus intravenous 0.1 mg/kg had estimated oral bioavailability of about 10%, with oral peak around 30 minutes. Model: Rat pharmacokinetics, six animals per reported group; clear solution in 40% v/v DMSO. Limitations: Not a human absorption estimate or dosing recommendation. Evidence access: Primary full text PMC6609384 Pharmacokinetics of cucurbitacin B from Trichosanthes cucumerina L. in rats. · 2019 · https://pubmed.ncbi.nlm.nih.gov/31272429/ · DOI 10.1186/s12906-019-2568-7
    Complete structured claim and evidence

  9. Rat cucurbitacin B metabolism profiling detected a cysteine conjugate among phase-II products; 13 metabolites were identified and seven confirmed in the overall study.

    Cucurbitacin B → Cucurbitacin B cysteine conjugate source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Rat LC-MS metabolism study.
    limitations
    Not all structures had identical confirmation strength; this record does not infer human rates.
    nutrient_topic
    Cucurbitacins collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Cucurbitacins
    plain_language
    Cysteine also appears in a measured metabolic product.
    primary_references
    Metabolic fate of the natural anticancer agent cucurbitacin B: an LC-MS/MS-enabled profiling of its major phase I and II conjugates in vivo. · 2024 · https://pubmed.ncbi.nlm.nih.gov/39441433/ · DOI 10.1007/s00216-024-05608-y

    Cucurbitacins: thiol chemistry, cytoskeleton, metabolic dependencies and signaling (2026-09-20) · lines 364–370

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Rat LC-MS metabolism study. · source_derived_draft · unverified_draft

    ## cucurbitacin-b-rat-cysteine-metabolism Cysteine also appears in a measured metabolic product. Rat cucurbitacin B metabolism profiling detected a cysteine conjugate among phase-II products; 13 metabolites were identified and seven confirmed in the overall study. Model: Rat LC-MS metabolism study. Limitations: Not all structures had identical confirmation strength; this record does not infer human rates. Evidence access: Primary abstract Metabolic fate of the natural anticancer agent cucurbitacin B: an LC-MS/MS-enabled profiling of its major phase I and II conjugates in vivo. · 2024 · https://pubmed.ncbi.nlm.nih.gov/39441433/ · DOI 10.1007/s00216-024-05608-y
    Complete structured claim and evidence

  10. The rat study estimated intravenous distribution volume near 51.65 L/kg ; lung and spleen tissue/plasma ratios were about 60 at 1 hour and about 240 at 2 hours, while liver, stomach and small intestine ratios were only 4–14 at 1 hour.

    Cucurbitacin B → Rat cucurbitacin B tissue distribution source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    biomarker_context Imported condition classification; unverified.
    evidence_access
    Primary full text PMC6609384
    experimental_model
    Male Wistar rat intravenous pharmacokinetics and tissue sampling; brain and heart amounts were below quantification.
    limitations
    Total tissue ratios do not establish free intracellular concentration or a human therapeutic window.
    nutrient_topic
    Cucurbitacins collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Cucurbitacins
    plain_language
    Measured tissue distribution differed substantially from plasma.
    primary_references
    Pharmacokinetics of cucurbitacin B from Trichosanthes cucumerina L. in rats. · 2019 · https://pubmed.ncbi.nlm.nih.gov/31272429/ · DOI 10.1186/s12906-019-2568-7
    trigger_kind
    biomarker_context Imported condition classification; unverified.

    Cucurbitacins: thiol chemistry, cytoskeleton, metabolic dependencies and signaling (2026-09-20) · lines 356–362

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Male Wistar rat intravenous pharmacokinetics and tissue sampling; brain and heart amounts were below quantification. · source_derived_draft · unverified_draft

    ## cucurbitacin-b-rat-distribution Measured tissue distribution differed substantially from plasma. The rat study estimated intravenous distribution volume near 51.65 L/kg ; lung and spleen tissue/plasma ratios were about 60 at 1 hour and about 240 at 2 hours, while liver, stomach and small intestine ratios were only 4–14 at 1 hour. Model: Male Wistar rat intravenous pharmacokinetics and tissue sampling; brain and heart amounts were below quantification. Limitations: Total tissue ratios do not establish free intracellular concentration or a human therapeutic window. Evidence access: Primary full text PMC6609384 Pharmacokinetics of cucurbitacin B from Trichosanthes cucumerina L. in rats. · 2019 · https://pubmed.ncbi.nlm.nih.gov/31272429/ · DOI 10.1186/s12906-019-2568-7
    Complete structured claim and evidence

  11. Rat cucurbitacin B metabolism profiling identified glutathione conjugation among the phase-II routes.

    Cucurbitacin B → Cucurbitacin B glutathione conjugate source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Rat LC-MS study; also hydrolysis, reduction, epoxidation, amination and other conjugation routes reported.
    limitations
    No human mass balance or obligatory single detoxification pathway was established.
    nutrient_topic
    Cucurbitacins collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Cucurbitacins
    plain_language
    The existing glutathione node connects chemical interception to metabolism.
    primary_references
    Metabolic fate of the natural anticancer agent cucurbitacin B: an LC-MS/MS-enabled profiling of its major phase I and II conjugates in vivo. · 2024 · https://pubmed.ncbi.nlm.nih.gov/39441433/ · DOI 10.1007/s00216-024-05608-y

    Cucurbitacins: thiol chemistry, cytoskeleton, metabolic dependencies and signaling (2026-09-20) · lines 372–378

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Rat LC-MS study; also hydrolysis, reduction, epoxidation, amination and other conjugation routes reported. · source_derived_draft · unverified_draft

    ## cucurbitacin-b-rat-gsh-metabolism The existing glutathione node connects chemical interception to metabolism. Rat cucurbitacin B metabolism profiling identified glutathione conjugation among the phase-II routes. Model: Rat LC-MS study; also hydrolysis, reduction, epoxidation, amination and other conjugation routes reported. Limitations: No human mass balance or obligatory single detoxification pathway was established. Evidence access: Primary abstract Metabolic fate of the natural anticancer agent cucurbitacin B: an LC-MS/MS-enabled profiling of its major phase I and II conjugates in vivo. · 2024 · https://pubmed.ncbi.nlm.nih.gov/39441433/ · DOI 10.1007/s00216-024-05608-y
    Complete structured claim and evidence

  12. Cucurbitacin B exposure lowered the GSH/GSSG ratio in the human NSCLC experiments.

    Cucurbitacin B → Human NSCLC GSH/GSSG ratio during cucurbitacin B exposure source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Human NSCLC cell study.
    limitations
    A ratio alone does not establish which synthesis, oxidation, conjugation or export flux caused the change.
    nutrient_topic
    Cucurbitacins collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Cucurbitacins
    plain_language
    The redox balance shifted alongside toxicity.
    primary_references
    Cucurbitacin B potently suppresses non-small-cell lung cancer growth: identification of intracellular thiols as critical targets. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23340170/ · DOI 10.1016/j.canlet.2013.01.008

    Cucurbitacins: thiol chemistry, cytoskeleton, metabolic dependencies and signaling (2026-09-20) · lines 132–138

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human NSCLC cell study. · source_derived_draft · unverified_draft

    ## cucurbitacin-b-redox-ratio The redox balance shifted alongside toxicity. Cucurbitacin B exposure lowered the GSH/GSSG ratio in the human NSCLC experiments. Model: Human NSCLC cell study. Limitations: A ratio alone does not establish which synthesis, oxidation, conjugation or export flux caused the change. Evidence access: Primary abstract Cucurbitacin B potently suppresses non-small-cell lung cancer growth: identification of intracellular thiols as critical targets. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23340170/ · DOI 10.1016/j.canlet.2013.01.008
    Complete structured claim and evidence

  13. Cucurbitacin B reduced TNF-alpha-induced RelA nuclear translocation and I-kappa-B-alpha phosphorylation in human A549 cells.

    Cucurbitacin B → Human NF-kappa-B subunit RelA / RELA source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Human A549 cytokine-stimulation assays.
    limitations
    Downstream readouts do not establish direct inhibition of each protein.
    nutrient_topic
    Cucurbitacins collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Cucurbitacins
    plain_language
    Less inflammatory transcription signaling reached the nucleus.
    primary_references
    Cucurbitacin B Down-Regulates TNF Receptor 1 Expression and Inhibits the TNF-α-Dependent Nuclear Factor κB Signaling Pathway in Human Lung Adenocarcinoma A549 Cells. · 2022 · https://pubmed.ncbi.nlm.nih.gov/35806134/ · DOI 10.3390/ijms23137130

    Cucurbitacins: thiol chemistry, cytoskeleton, metabolic dependencies and signaling (2026-09-20) · lines 204–210

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human A549 cytokine-stimulation assays. · source_derived_draft · unverified_draft

    ## cucurbitacin-b-rela Less inflammatory transcription signaling reached the nucleus. Cucurbitacin B reduced TNF-alpha-induced RelA nuclear translocation and I-kappa-B-alpha phosphorylation in human A549 cells. Model: Human A549 cytokine-stimulation assays. Limitations: Downstream readouts do not establish direct inhibition of each protein. Evidence access: Primary abstract Cucurbitacin B Down-Regulates TNF Receptor 1 Expression and Inhibits the TNF-α-Dependent Nuclear Factor κB Signaling Pathway in Human Lung Adenocarcinoma A549 Cells. · 2022 · https://pubmed.ncbi.nlm.nih.gov/35806134/ · DOI 10.3390/ijms23137130
    Complete structured claim and evidence

  14. Docking and cellular thermal-shift experiments supported STAT3 target engagement by cucurbitacin B, alongside reduced STAT3 phosphorylation.

    Cucurbitacin B → STAT3 source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Human NSCLC study with docking and CETSA.
    limitations
    CETSA is not purified binding kinetics or proof that STAT3 is the sole or selective target.
    nutrient_topic
    Cucurbitacins collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Cucurbitacins
    plain_language
    The paper tested target engagement as well as signaling.
    primary_references
    Cucurbitacin B targets STAT3 to induce ferroptosis in non-small cell lung cancer. · 2024 · https://pubmed.ncbi.nlm.nih.gov/38950838/ · DOI 10.1016/j.ejphar.2024.176805

    Cucurbitacins: thiol chemistry, cytoskeleton, metabolic dependencies and signaling (2026-09-20) · lines 268–274

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human NSCLC study with docking and CETSA. · source_derived_draft · unverified_draft

    ## cucurbitacin-b-stat3-engagement The paper tested target engagement as well as signaling. Docking and cellular thermal-shift experiments supported STAT3 target engagement by cucurbitacin B, alongside reduced STAT3 phosphorylation. Model: Human NSCLC study with docking and CETSA. Limitations: CETSA is not purified binding kinetics or proof that STAT3 is the sole or selective target. Evidence access: Primary abstract Cucurbitacin B targets STAT3 to induce ferroptosis in non-small cell lung cancer. · 2024 · https://pubmed.ncbi.nlm.nih.gov/38950838/ · DOI 10.1016/j.ejphar.2024.176805
    Complete structured claim and evidence

  15. Adding cucurbitacin B rapidly lowered measured protein-thiol levels in human NSCLC cells.

    Cucurbitacin B → Human NSCLC cellular protein-thiol pool source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Human H1299, A549, HCC827 and H661 study panel; exact assay allocation and dose not resolved from the abstract.
    limitations
    A cellular thiol measurement is not evidence of whole-body cysteine deficiency.
    nutrient_topic
    Cucurbitacins collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Cucurbitacins
    plain_language
    Reactive protein groups decreased after exposure.
    primary_references
    Cucurbitacin B potently suppresses non-small-cell lung cancer growth: identification of intracellular thiols as critical targets. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23340170/ · DOI 10.1016/j.canlet.2013.01.008

    Cucurbitacins: thiol chemistry, cytoskeleton, metabolic dependencies and signaling (2026-09-20) · lines 124–130

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human H1299, A549, HCC827 and H661 study panel; exact assay allocation and dose not resolved from the abstract. · source_derived_draft · unverified_draft

    ## cucurbitacin-b-thiol-loss Reactive protein groups decreased after exposure. Adding cucurbitacin B rapidly lowered measured protein-thiol levels in human NSCLC cells. Model: Human H1299, A549, HCC827 and H661 study panel; exact assay allocation and dose not resolved from the abstract. Limitations: A cellular thiol measurement is not evidence of whole-body cysteine deficiency. Evidence access: Primary abstract Cucurbitacin B potently suppresses non-small-cell lung cancer growth: identification of intracellular thiols as critical targets. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23340170/ · DOI 10.1016/j.canlet.2013.01.008
    Complete structured claim and evidence

  16. Docking and CETSA supported an interaction between cucurbitacin B and TLR4 in the NSCLC study.

    Cucurbitacin B → Human toll-like receptor 4 / TLR4 source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Human NSCLC cell experiments with animal tumor models in the same paper.
    limitations
    No purified affinity or exclusive target assignment follows from docking plus CETSA.
    nutrient_topic
    Cucurbitacins collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Cucurbitacins
    plain_language
    Another proposed target was tested in cells.
    primary_references
    Cucurbitacin B inhibits non-small cell lung cancer in vivo and in vitro by triggering TLR4/NLRP3/GSDMD-dependent pyroptosis. · 2021 · https://pubmed.ncbi.nlm.nih.gov/34217831/ · DOI 10.1016/j.phrs.2021.105748

    Cucurbitacins: thiol chemistry, cytoskeleton, metabolic dependencies and signaling (2026-09-20) · lines 284–290

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human NSCLC cell experiments with animal tumor models in the same paper. · source_derived_draft · unverified_draft

    ## cucurbitacin-b-tlr4-engagement Another proposed target was tested in cells. Docking and CETSA supported an interaction between cucurbitacin B and TLR4 in the NSCLC study. Model: Human NSCLC cell experiments with animal tumor models in the same paper. Limitations: No purified affinity or exclusive target assignment follows from docking plus CETSA. Evidence access: Primary abstract Cucurbitacin B inhibits non-small cell lung cancer in vivo and in vitro by triggering TLR4/NLRP3/GSDMD-dependent pyroptosis. · 2021 · https://pubmed.ncbi.nlm.nih.gov/34217831/ · DOI 10.1016/j.phrs.2021.105748
    Complete structured claim and evidence

  17. Cucurbitacin B lowered TNF receptor 1 expression in human A549 cells without reducing the measured TRADD, RIPK1 and TRAF2 adaptor proteins.

    Cucurbitacin B → Human TNF receptor 1 / TNFRSF1A source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    TNF-alpha-stimulated human A549 cells; dose/time not resolved in accessed abstract.
    limitations
    Protein abundance result, not demonstrated direct binding to TNFR1.
    nutrient_topic
    Cucurbitacins collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Cucurbitacins
    plain_language
    The receptor changed before treating all downstream proteins as depleted.
    primary_references
    Cucurbitacin B Down-Regulates TNF Receptor 1 Expression and Inhibits the TNF-α-Dependent Nuclear Factor κB Signaling Pathway in Human Lung Adenocarcinoma A549 Cells. · 2022 · https://pubmed.ncbi.nlm.nih.gov/35806134/ · DOI 10.3390/ijms23137130

    Cucurbitacins: thiol chemistry, cytoskeleton, metabolic dependencies and signaling (2026-09-20) · lines 188–194

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · TNF-alpha-stimulated human A549 cells; dose/time not resolved in accessed abstract. · source_derived_draft · unverified_draft

    ## cucurbitacin-b-tnfr1 The receptor changed before treating all downstream proteins as depleted. Cucurbitacin B lowered TNF receptor 1 expression in human A549 cells without reducing the measured TRADD, RIPK1 and TRAF2 adaptor proteins. Model: TNF-alpha-stimulated human A549 cells; dose/time not resolved in accessed abstract. Limitations: Protein abundance result, not demonstrated direct binding to TNFR1. Evidence access: Primary abstract Cucurbitacin B Down-Regulates TNF Receptor 1 Expression and Inhibits the TNF-α-Dependent Nuclear Factor κB Signaling Pathway in Human Lung Adenocarcinoma A549 Cells. · 2022 · https://pubmed.ncbi.nlm.nih.gov/35806134/ · DOI 10.3390/ijms23137130
    Complete structured claim and evidence

What acts on it

  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

Where it participates (unsigned role)

  1. Adding a TNF-alpha-converting-enzyme inhibitor suppressed cucurbitacin B-associated TNFR1 down-regulation in human A549 cells.

    Human ADAM metallopeptidase domain 17 / ADAM17 → Human TNF receptor 1 / TNFRSF1A source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary abstract
    experimental_model
    Human A549 pharmacological perturbation.
    limitations
    Supports involvement of ADAM17-related processing; does not prove cucurbitacin binds or directly activates ADAM17.
    nutrient_topic
    Cucurbitacins collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Cucurbitacins
    plain_language
    A receptor-processing enzyme was implicated by an inhibitor experiment.
    primary_references
    Cucurbitacin B Down-Regulates TNF Receptor 1 Expression and Inhibits the TNF-α-Dependent Nuclear Factor κB Signaling Pathway in Human Lung Adenocarcinoma A549 Cells. · 2022 · https://pubmed.ncbi.nlm.nih.gov/35806134/ · DOI 10.3390/ijms23137130
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Cucurbitacins: thiol chemistry, cytoskeleton, metabolic dependencies and signaling (2026-09-20) · lines 196–202

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human A549 pharmacological perturbation. · source_derived_draft · unverified_draft

    ## cucurbitacin-b-adam17-gate A receptor-processing enzyme was implicated by an inhibitor experiment. Adding a TNF-alpha-converting-enzyme inhibitor suppressed cucurbitacin B-associated TNFR1 down-regulation in human A549 cells. Model: Human A549 pharmacological perturbation. Limitations: Supports involvement of ADAM17-related processing; does not prove cucurbitacin binds or directly activates ADAM17. Evidence access: Primary abstract Cucurbitacin B Down-Regulates TNF Receptor 1 Expression and Inhibits the TNF-α-Dependent Nuclear Factor κB Signaling Pathway in Human Lung Adenocarcinoma A549 Cells. · 2022 · https://pubmed.ncbi.nlm.nih.gov/35806134/ · DOI 10.3390/ijms23137130
    Complete structured claim and evidence

  2. Pretreating human NSCLC cells with the glutathione-synthesis inhibitor BSO increased cucurbitacin B cytotoxicity.

    L-Buthionine-S-sulfoximine / BSO → Human NSCLC cytotoxic response to cucurbitacin B source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary abstract
    experimental_model
    Pharmacological inhibition in human cancer-cell experiments; dose/duration not in accessed abstract.
    limitations
    Experimental synthesis inhibition is not a dietary cucurbitacin deficiency or evidence that oral glutathione protects people.
    nutrient_topic
    Cucurbitacins collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Cucurbitacins
    plain_language
    Weakening glutathione production increased sensitivity in this model.
    primary_references
    Cucurbitacin B potently suppresses non-small-cell lung cancer growth: identification of intracellular thiols as critical targets. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23340170/ · DOI 10.1016/j.canlet.2013.01.008
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Cucurbitacins: thiol chemistry, cytoskeleton, metabolic dependencies and signaling (2026-09-20) · lines 140–146

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Pharmacological inhibition in human cancer-cell experiments; dose/duration not in accessed abstract. · source_derived_draft · unverified_draft

    ## cucurbitacin-b-bso-sensitivity Weakening glutathione production increased sensitivity in this model. Pretreating human NSCLC cells with the glutathione-synthesis inhibitor BSO increased cucurbitacin B cytotoxicity. Model: Pharmacological inhibition in human cancer-cell experiments; dose/duration not in accessed abstract. Limitations: Experimental synthesis inhibition is not a dietary cucurbitacin deficiency or evidence that oral glutathione protects people. Evidence access: Primary abstract Cucurbitacin B potently suppresses non-small-cell lung cancer growth: identification of intracellular thiols as critical targets. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23340170/ · DOI 10.1016/j.canlet.2013.01.008
    Complete structured claim and evidence

  3. Adding L-cysteine attenuated cucurbitacin B inhibition of TNF-alpha-induced ICAM1 expression; L-cysteine had a smaller effect than the other tested thiols.

    L-Cysteine → Human intercellular adhesion molecule 1 / ICAM1 source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Human A549 cytokine-stimulation experiment.
    limitations
    The experiment supports a chemical-reactivity dependency; it does not establish a human supplement interaction magnitude.
    nutrient_topic
    Cucurbitacins collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Cucurbitacins
    plain_language
    A separately stored thiol changed the signaling result.
    primary_references
    Cucurbitacin B Down-Regulates TNF Receptor 1 Expression and Inhibits the TNF-α-Dependent Nuclear Factor κB Signaling Pathway in Human Lung Adenocarcinoma A549 Cells. · 2022 · https://pubmed.ncbi.nlm.nih.gov/35806134/ · DOI 10.3390/ijms23137130

    Cucurbitacins: thiol chemistry, cytoskeleton, metabolic dependencies and signaling (2026-09-20) · lines 236–242

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human A549 cytokine-stimulation experiment. · source_derived_draft · unverified_draft

    ## cucurbitacin-b-cysteine-icam-rescue A separately stored thiol changed the signaling result. Adding L-cysteine attenuated cucurbitacin B inhibition of TNF-alpha-induced ICAM1 expression; L-cysteine had a smaller effect than the other tested thiols. Model: Human A549 cytokine-stimulation experiment. Limitations: The experiment supports a chemical-reactivity dependency; it does not establish a human supplement interaction magnitude. Evidence access: Primary abstract Cucurbitacin B Down-Regulates TNF Receptor 1 Expression and Inhibits the TNF-α-Dependent Nuclear Factor κB Signaling Pathway in Human Lung Adenocarcinoma A549 Cells. · 2022 · https://pubmed.ncbi.nlm.nih.gov/35806134/ · DOI 10.3390/ijms23137130
    Complete structured claim and evidence

  4. Adding glutathione attenuated cucurbitacin B inhibition of TNF-alpha-induced ICAM1 expression; L-cysteine had a smaller effect than the other tested thiols.

    GSH → Human intercellular adhesion molecule 1 / ICAM1 source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Human A549 cytokine-stimulation experiment.
    limitations
    The experiment supports a chemical-reactivity dependency; it does not establish a human supplement interaction magnitude.
    nutrient_topic
    Cucurbitacins collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Cucurbitacins
    plain_language
    A separately stored thiol changed the signaling result.
    primary_references
    Cucurbitacin B Down-Regulates TNF Receptor 1 Expression and Inhibits the TNF-α-Dependent Nuclear Factor κB Signaling Pathway in Human Lung Adenocarcinoma A549 Cells. · 2022 · https://pubmed.ncbi.nlm.nih.gov/35806134/ · DOI 10.3390/ijms23137130

    Cucurbitacins: thiol chemistry, cytoskeleton, metabolic dependencies and signaling (2026-09-20) · lines 220–226

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human A549 cytokine-stimulation experiment. · source_derived_draft · unverified_draft

    ## cucurbitacin-b-gsh-icam-rescue A separately stored thiol changed the signaling result. Adding glutathione attenuated cucurbitacin B inhibition of TNF-alpha-induced ICAM1 expression; L-cysteine had a smaller effect than the other tested thiols. Model: Human A549 cytokine-stimulation experiment. Limitations: The experiment supports a chemical-reactivity dependency; it does not establish a human supplement interaction magnitude. Evidence access: Primary abstract Cucurbitacin B Down-Regulates TNF Receptor 1 Expression and Inhibits the TNF-α-Dependent Nuclear Factor κB Signaling Pathway in Human Lung Adenocarcinoma A549 Cells. · 2022 · https://pubmed.ncbi.nlm.nih.gov/35806134/ · DOI 10.3390/ijms23137130
    Complete structured claim and evidence

  5. Adding N-acetylcysteine attenuated cucurbitacin B inhibition of TNF-alpha-induced ICAM1 expression; L-cysteine had a smaller effect than the other tested thiols.

    N-Acetyl-L-cysteine → Human intercellular adhesion molecule 1 / ICAM1 source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Human A549 cytokine-stimulation experiment.
    limitations
    The experiment supports a chemical-reactivity dependency; it does not establish a human supplement interaction magnitude.
    nutrient_topic
    Cucurbitacins collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Cucurbitacins
    plain_language
    A separately stored thiol changed the signaling result.
    primary_references
    Cucurbitacin B Down-Regulates TNF Receptor 1 Expression and Inhibits the TNF-α-Dependent Nuclear Factor κB Signaling Pathway in Human Lung Adenocarcinoma A549 Cells. · 2022 · https://pubmed.ncbi.nlm.nih.gov/35806134/ · DOI 10.3390/ijms23137130

    Cucurbitacins: thiol chemistry, cytoskeleton, metabolic dependencies and signaling (2026-09-20) · lines 228–234

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human A549 cytokine-stimulation experiment. · source_derived_draft · unverified_draft

    ## cucurbitacin-b-nac-icam-rescue A separately stored thiol changed the signaling result. Adding N-acetylcysteine attenuated cucurbitacin B inhibition of TNF-alpha-induced ICAM1 expression; L-cysteine had a smaller effect than the other tested thiols. Model: Human A549 cytokine-stimulation experiment. Limitations: The experiment supports a chemical-reactivity dependency; it does not establish a human supplement interaction magnitude. Evidence access: Primary abstract Cucurbitacin B Down-Regulates TNF Receptor 1 Expression and Inhibits the TNF-α-Dependent Nuclear Factor κB Signaling Pathway in Human Lung Adenocarcinoma A549 Cells. · 2022 · https://pubmed.ncbi.nlm.nih.gov/35806134/ · DOI 10.3390/ijms23137130
    Complete structured claim and evidence

  6. Adding N-acetylcysteine attenuated the reported cucurbitacin B cellular effects in the human NSCLC study.

    N-Acetyl-L-cysteine → Human NSCLC cytotoxic response to cucurbitacin B source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Human NSCLC experiments plus separate cell-free interaction assays.
    limitations
    Compound trapping and redox effects are not distinguished by rescue alone.
    nutrient_topic
    Cucurbitacins collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Cucurbitacins
    plain_language
    Thiol availability changed the experimental response.
    primary_references
    Cucurbitacin B potently suppresses non-small-cell lung cancer growth: identification of intracellular thiols as critical targets. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23340170/ · DOI 10.1016/j.canlet.2013.01.008

    Cucurbitacins: thiol chemistry, cytoskeleton, metabolic dependencies and signaling (2026-09-20) · lines 148–154

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human NSCLC experiments plus separate cell-free interaction assays. · source_derived_draft · unverified_draft

    ## cucurbitacin-b-nac-rescue Thiol availability changed the experimental response. Adding N-acetylcysteine attenuated the reported cucurbitacin B cellular effects in the human NSCLC study. Model: Human NSCLC experiments plus separate cell-free interaction assays. Limitations: Compound trapping and redox effects are not distinguished by rescue alone. Evidence access: Primary abstract Cucurbitacin B potently suppresses non-small-cell lung cancer growth: identification of intracellular thiols as critical targets. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23340170/ · DOI 10.1016/j.canlet.2013.01.008
    Complete structured claim and evidence

  7. STAT3 overexpression reversed tested cucurbitacin B-associated lipid ROS and iron changes, whereas STAT3 silencing enhanced them.

    STAT3 → Human cancer-cell lipid peroxidation during cucurbitacin B exposure source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary abstract
    experimental_model
    Human H358/A549 genetic perturbation experiments.
    limitations
    This establishes model-specific pathway involvement, not universal STAT3 control of ferroptosis.
    nutrient_topic
    Cucurbitacins collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Cucurbitacins
    plain_language
    Changing a signaling protein altered the iron-dependent response.
    primary_references
    Cucurbitacin B targets STAT3 to induce ferroptosis in non-small cell lung cancer. · 2024 · https://pubmed.ncbi.nlm.nih.gov/38950838/ · DOI 10.1016/j.ejphar.2024.176805
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Cucurbitacins: thiol chemistry, cytoskeleton, metabolic dependencies and signaling (2026-09-20) · lines 276–282

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human H358/A549 genetic perturbation experiments. · source_derived_draft · unverified_draft

    ## cucurbitacin-b-stat3-rescue Changing a signaling protein altered the iron-dependent response. STAT3 overexpression reversed tested cucurbitacin B-associated lipid ROS and iron changes, whereas STAT3 silencing enhanced them. Model: Human H358/A549 genetic perturbation experiments. Limitations: This establishes model-specific pathway involvement, not universal STAT3 control of ferroptosis. Evidence access: Primary abstract Cucurbitacin B targets STAT3 to induce ferroptosis in non-small cell lung cancer. · 2024 · https://pubmed.ncbi.nlm.nih.gov/38950838/ · DOI 10.1016/j.ejphar.2024.176805
    Complete structured claim and evidence

  8. TLR4 silencing reduced cucurbitacin B-induced pyroptosis and associated mitochondrial ROS and calcium signals in human NSCLC cells.

    Human toll-like receptor 4 / TLR4 → Human NSCLC pyroptotic response during cucurbitacin B exposure source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary abstract
    experimental_model
    Human NSCLC loss-of-function experiments.
    limitations
    The accessed abstract does not establish the calcium store or channel; oral calcium depletion is not implied.
    nutrient_topic
    Cucurbitacins collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Cucurbitacins
    plain_language
    Removing the receptor weakened the tested death pathway.
    primary_references
    Cucurbitacin B inhibits non-small cell lung cancer in vivo and in vitro by triggering TLR4/NLRP3/GSDMD-dependent pyroptosis. · 2021 · https://pubmed.ncbi.nlm.nih.gov/34217831/ · DOI 10.1016/j.phrs.2021.105748
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Cucurbitacins: thiol chemistry, cytoskeleton, metabolic dependencies and signaling (2026-09-20) · lines 292–298

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human NSCLC loss-of-function experiments. · source_derived_draft · unverified_draft

    ## cucurbitacin-b-tlr4-loss Removing the receptor weakened the tested death pathway. TLR4 silencing reduced cucurbitacin B-induced pyroptosis and associated mitochondrial ROS and calcium signals in human NSCLC cells. Model: Human NSCLC loss-of-function experiments. Limitations: The accessed abstract does not establish the calcium store or channel; oral calcium depletion is not implied. Evidence access: Primary abstract Cucurbitacin B inhibits non-small cell lung cancer in vivo and in vitro by triggering TLR4/NLRP3/GSDMD-dependent pyroptosis. · 2021 · https://pubmed.ncbi.nlm.nih.gov/34217831/ · DOI 10.1016/j.phrs.2021.105748
    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