Component

Ferrostatin-1

Independent biological entity. Read linked claims for experimental scope and context.

2 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

Where it participates (unsigned role)

  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. ATRA or ferrostatin-1 rescued differentiation under antioxidant-deprived neuronal culture conditions.

    All-trans-retinoic acid → Cortical neuronal differentiation source_derived_draftungraded
    Experimental context and source evidence
    experimental_model
    Human stem-cell neurons/organoids.
    limitations
    No dietary recommendation or evidence that vitamin A replaces vitamin E in humans.
    nutrient_topic
    Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
    organism
    Homo sapiens
    plain_language
    Suppressing ferroptosis supported this developmental model.
    primary_references
    [va-berndt2024] Suppression of ferroptosis by vitamin A or radical-trapping antioxidants is essential for neuronal development (2024). https://pubmed.ncbi.nlm.nih.gov/39218970/ DOI: 10.1038/s41467-024-51996-1
    tissue_or_cell_type
    Human neural cultures

    Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 1823–1832

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human stem-cell neurons/organoids. · source_derived_draft · unverified_draft

    ### va-atra-neuronal-ferroptosis-rescue ATRA or ferrostatin-1 rescued differentiation under antioxidant-deprived neuronal culture conditions. Condition category: normal nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: Suppressing ferroptosis supported this developmental model. organism: Homo sapiens tissue_or_cell_type: Human neural cultures experimental_model: Human stem-cell neurons/organoids. limitations: No dietary recommendation or evidence that vitamin A replaces vitamin E in humans. [va-berndt2024] Suppression of ferroptosis by vitamin A or radical-trapping antioxidants is essential for neuronal development (2024). https://pubmed.ncbi.nlm.nih.gov/39218970/ DOI: 10.1038/s41467-024-51996-1
    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