Component

Vascular endothelial growth factor receptor 2 / KDR

Vascular endothelial growth factor receptor 2 / KDR. Species, exposure and limitations are retained in each linked claim.

3 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

Read recorded mechanisms Open recursive mind map

How nutrients influence it

Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.

How nutrients reach it in more than one step

Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.

Tracing routes…

What it does

Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.

Recorded relationships

What acts on it

  1. Mebendazole was determined to interfere with vascular endothelial growth factor receptor 2 kinase by competing with ATP, selectively inhibited tumour angiogenesis but not the normal brain vasculature in orthotopic medulloblastoma models, suppressed the kinase in vivo, and significantly extended survival of medulloblastoma models derived from different molecular backgrounds including a PTCH1-mutant tumour with acquired resistance to the smoothened inhibitor vismodegib.

    Mebendazole → Vascular endothelial growth factor receptor 2 / KDR source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/mebendazole-research/25253417.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "96333adbb3bce735b14f3c51317229543279992c3cd170760cc494566e49a169", "start_char": 0, "end_char": 1798, "text_sha256": "96333adbb3bce735b14f3c51317229543279992c3cd170760cc494566e49a169"}
    experimental_model
    Autophosphorylation and cell-free kinase assays with orthotopic medulloblastoma allograft and xenograft models
    exposure
    Mebendazole in PTCH1-mutant allografts, a group 3 xenograft and a vismodegib-resistant model
    limitations
    Identifies a third mechanism, kinase inhibition, with a defined competition mode. Whether this operates at achievable human concentrations is not established here.
    nutrient_topic
    Mebendazole research collection; topical membership is not evidence of a direct clinical effect, and mebendazole is recorded separately from albendazole, from the benzimidazole class and from its own crystal forms. · Mebendazole
    organism
    Mouse
    plain_language
    It also blocks the receptor that grows new tumour blood vessels, and spares the normal ones.
    primary_references
    [mbz-p25253417] Effective treatment of diverse medulloblastoma models with mebendazole and its impact on tumor angiogenesis. (2015). https://pubmed.ncbi.nlm.nih.gov/25253417/ DOI: 10.1093/neuonc/nou234
    tissue_or_cell_type
    Medulloblastoma and tumour vasculature

    Mebendazole: the tubulin it binds, why that is selective, the crystal form that decides whether any of it works, and the off-target that became an oncology programme (2026-09-22) · lines 550–561

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Autophosphorylation and cell-free kinase assays with orthotopic medulloblastoma allograft and xenograft models · source_derived_draft · unverified_draft

    ### mbz-vegfr2-atp-competition Mebendazole was determined to interfere with vascular endothelial growth factor receptor 2 kinase by competing with ATP, selectively inhibited tumour angiogenesis but not the normal brain vasculature in orthotopic medulloblastoma models, suppressed the kinase in vivo, and significantly extended survival of medulloblastoma models derived from different molecular backgrounds including a PTCH1-mutant tumour with acquired resistance to the smoothened inhibitor vismodegib. Condition category: normal nutrient_topic: Mebendazole research collection; topical membership is not evidence of a direct clinical effect, and mebendazole is recorded separately from albendazole, from the benzimidazole class and from its own crystal forms. plain_language: It also blocks the receptor that grows new tumour blood vessels, and spares the normal ones. organism: Mouse tissue_or_cell_type: Medulloblastoma and tumour vasculature experimental_model: Autophosphorylation and cell-free kinase assays with orthotopic medulloblastoma allograft and xenograft models limitations: Identifies a third mechanism, kinase inhibition, with a defined competition mode. Whether this operates at achievable human concentrations is not established here. exposure: Mebendazole in PTCH1-mutant allografts, a group 3 xenograft and a vismodegib-resistant model evidence_span: {"source_cache": "artifacts/mebendazole-research/25253417.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "96333adbb3bce735b14f3c51317229543279992c3cd170760cc494566e49a169", "start_char": 0, "end_char": 1798, "text_sha256": "96333adbb3bce735b14f3c51317229543279992c3cd170760cc494566e49a169"} [mbz-p25253417] Effective treatment of diverse medulloblastoma models with mebendazole and its impact on tumor angiogenesis. (2015). https://pubmed.ncbi.nlm.nih.gov/25253417/ DOI: 10.1093/neuonc/nou234
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Colony-forming cells rose from 16 to 26 per 100,000 monocytes plated, entirely due to the CD34-positive subpopulation, and a high proportion of progeny cells expressed receptors for vascular endothelial growth factor-2 and for stromal-derived growth factor.

    Hyperbaric oxygen therapy → Colony-forming cells from circulating monocytes source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/hbot-research/16299259.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "76c0554557a30ac9a32f25b74b27edb5f8f8a57ee0c0660dfe5619b78732c730", "start_char": 0, "end_char": 1502, "text_sha256": "76c0554557a30ac9a32f25b74b27edb5f8f8a57ee0c0660dfe5619b78732c730"}
    experimental_model
    Human volunteers, mice, and endothelial nitric oxide synthase knockout mice
    exposure
    2.0 atmospheres absolute oxygen for 2 hours, single and over 20 treatments
    limitations
    The knockout and inhibitor arms carry the causal claim. Progenitor phenotype is defined by surface markers and colony formation, not by a demonstrated contribution to a healed vessel.
    nutrient_topic
    Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. · Hyperbaric oxygen therapy
    organism
    Human and mouse
    plain_language
    The mobilised cells carry the receptors for the two signals that guide them to a wound.
    primary_references
    [hbot-p16299259] Stem cell mobilization by hyperbaric oxygen. (2006). https://pubmed.ncbi.nlm.nih.gov/16299259/ DOI: 10.1152/ajpheart.00888.2005
    tissue_or_cell_type
    Bone marrow and peripheral blood

    Hyperbaric oxygen: the exposure, its reactive species, the signals they carry, and the nutrient-dependent enzymes that handle them (2026-09-19) · lines 543–554

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human volunteers, mice, and endothelial nitric oxide synthase knockout mice · source_derived_draft · unverified_draft

    ### hbot-cfc-increase Colony-forming cells rose from 16 to 26 per 100,000 monocytes plated, entirely due to the CD34-positive subpopulation, and a high proportion of progeny cells expressed receptors for vascular endothelial growth factor-2 and for stromal-derived growth factor. Condition category: normal nutrient_topic: Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. plain_language: The mobilised cells carry the receptors for the two signals that guide them to a wound. organism: Human and mouse tissue_or_cell_type: Bone marrow and peripheral blood experimental_model: Human volunteers, mice, and endothelial nitric oxide synthase knockout mice limitations: The knockout and inhibitor arms carry the causal claim. Progenitor phenotype is defined by surface markers and colony formation, not by a demonstrated contribution to a healed vessel. exposure: 2.0 atmospheres absolute oxygen for 2 hours, single and over 20 treatments evidence_span: {"source_cache": "artifacts/hbot-research/16299259.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "76c0554557a30ac9a32f25b74b27edb5f8f8a57ee0c0660dfe5619b78732c730", "start_char": 0, "end_char": 1502, "text_sha256": "76c0554557a30ac9a32f25b74b27edb5f8f8a57ee0c0660dfe5619b78732c730"} [hbot-p16299259] Stem cell mobilization by hyperbaric oxygen. (2006). https://pubmed.ncbi.nlm.nih.gov/16299259/ DOI: 10.1152/ajpheart.00888.2005
    Complete structured claim and evidence

  2. Treatment promoted expression of HIF-1alpha, NF-kappaB, VEGFA, SDF-1, VEGFR2 and CXCR4, with SDF-1 and VEGFA rising in human skin fibroblasts and CXCR4 and VEGFR2 rising in endothelial cells.

    Hyperbaric oxygen therapy → Stromal cell-derived factor 1 / SDF-1alpha / CXCL12 source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/hbot-research/32791151.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "106ed876131af9161051c4c178d88af4afd707a20e56a91447d35aa9ed290188", "start_char": 0, "end_char": 1662, "text_sha256": "106ed876131af9161051c4c178d88af4afd707a20e56a91447d35aa9ed290188"}
    experimental_model
    Diabetic foot mouse model with human skin fibroblasts and human umbilical vein endothelial cells
    exposure
    Hyperbaric oxygen with high glucose in vitro
    limitations
    Cell and mouse work with expression endpoints. Tube formation is an angiogenesis surrogate, not a vessel in a person.
    nutrient_topic
    Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. · Hyperbaric oxygen therapy
    organism
    Mouse and human cells
    plain_language
    The signal and its receptor go up on two different cell types at once, which is what lets them find each other.
    primary_references
    [hbot-p32791151] Hyperbaric oxygen potentiates diabetic wound healing by promoting fibroblast cell proliferation and endothelial cell angiogenesis. (2020). https://pubmed.ncbi.nlm.nih.gov/32791151/ DOI: 10.1016/j.lfs.2020.118246
    tissue_or_cell_type
    Skin wound, fibroblasts and endothelium

    Hyperbaric oxygen: the exposure, its reactive species, the signals they carry, and the nutrient-dependent enzymes that handle them (2026-09-19) · lines 660–671

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Diabetic foot mouse model with human skin fibroblasts and human umbilical vein endothelial cells · source_derived_draft · unverified_draft

    ### hbot-hif-vegf-sdf-axis Treatment promoted expression of HIF-1alpha, NF-kappaB, VEGFA, SDF-1, VEGFR2 and CXCR4, with SDF-1 and VEGFA rising in human skin fibroblasts and CXCR4 and VEGFR2 rising in endothelial cells. Condition category: normal nutrient_topic: Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. plain_language: The signal and its receptor go up on two different cell types at once, which is what lets them find each other. organism: Mouse and human cells tissue_or_cell_type: Skin wound, fibroblasts and endothelium experimental_model: Diabetic foot mouse model with human skin fibroblasts and human umbilical vein endothelial cells limitations: Cell and mouse work with expression endpoints. Tube formation is an angiogenesis surrogate, not a vessel in a person. exposure: Hyperbaric oxygen with high glucose in vitro evidence_span: {"source_cache": "artifacts/hbot-research/32791151.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "106ed876131af9161051c4c178d88af4afd707a20e56a91447d35aa9ed290188", "start_char": 0, "end_char": 1662, "text_sha256": "106ed876131af9161051c4c178d88af4afd707a20e56a91447d35aa9ed290188"} [hbot-p32791151] Hyperbaric oxygen potentiates diabetic wound healing by promoting fibroblast cell proliferation and endothelial cell angiogenesis. (2020). https://pubmed.ncbi.nlm.nih.gov/32791151/ DOI: 10.1016/j.lfs.2020.118246
    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