Component

Mebendazole

Mebendazole. A benzimidazole carbamate anthelmintic introduced for human use in 1971; it is recorded as an entity distinct from albendazole, from the wider benzimidazole class and from its own crystal forms, because albendazole acts partly through a sulfoxide metabolite mebendazole does not form, because the class members differ by orders of magnitude in potency, and because polymorph A is therapeutically inert where polymorph C is active. Species, exposure and limitations are retained in each linked claim.

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

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 meningioma cell lines the half-maximal inhibitory concentration for mebendazole was 0.26 to 0.42 micromolar, mebendazole alone induced cytotoxicity but the combination with radiation gave a greater reduction in colony formation and higher levels of cleaved caspase-3, and in mice implanted intracranially with human meningioma both mebendazole alone and the combination gave a survival benefit with increased apoptosis and decreased tumour cell and vascular proliferation.

    Mebendazole → Radiotherapy source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/mebendazole-research/30414098.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "34445c01e56a2bfa33e4d1118f86c291fab041b15fa08da37592f4ec92d81400", "start_char": 0, "end_char": 1743, "text_sha256": "34445c01e56a2bfa33e4d1118f86c291fab041b15fa08da37592f4ec92d81400"}
    experimental_model
    Colony formation, proliferation and caspase assays with intracranial human meningioma implants in mice
    exposure
    Mebendazole alone and combined with radiation
    limitations
    A combination study in one meningioma line and one implanted model. The mechanism is inferred from immunohistochemistry rather than dissected.
    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
    Human cells and mouse
    plain_language
    Added to radiation it killed more tumour cells than radiation alone.
    primary_references
    [mbz-p30414098] Mebendazole and radiation in combination increase survival through anticancer mechanisms in an intracranial rodent model of malignant meningioma. (2018). https://pubmed.ncbi.nlm.nih.gov/30414098/ DOI: 10.1007/s11060-018-03009-7
    tissue_or_cell_type
    Malignant meningioma

    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 563–574

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Colony formation, proliferation and caspase assays with intracranial human meningioma implants in mice · source_derived_draft · unverified_draft

    ### mbz-adds-to-radiation In meningioma cell lines the half-maximal inhibitory concentration for mebendazole was 0.26 to 0.42 micromolar, mebendazole alone induced cytotoxicity but the combination with radiation gave a greater reduction in colony formation and higher levels of cleaved caspase-3, and in mice implanted intracranially with human meningioma both mebendazole alone and the combination gave a survival benefit with increased apoptosis and decreased tumour cell and vascular proliferation. 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: Added to radiation it killed more tumour cells than radiation alone. organism: Human cells and mouse tissue_or_cell_type: Malignant meningioma experimental_model: Colony formation, proliferation and caspase assays with intracranial human meningioma implants in mice limitations: A combination study in one meningioma line and one implanted model. The mechanism is inferred from immunohistochemistry rather than dissected. exposure: Mebendazole alone and combined with radiation evidence_span: {"source_cache": "artifacts/mebendazole-research/30414098.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "34445c01e56a2bfa33e4d1118f86c291fab041b15fa08da37592f4ec92d81400", "start_char": 0, "end_char": 1743, "text_sha256": "34445c01e56a2bfa33e4d1118f86c291fab041b15fa08da37592f4ec92d81400"} [mbz-p30414098] Mebendazole and radiation in combination increase survival through anticancer mechanisms in an intracranial rodent model of malignant meningioma. (2018). https://pubmed.ncbi.nlm.nih.gov/30414098/ DOI: 10.1007/s11060-018-03009-7
    Complete structured claim and evidence
  2. Comparing therapeutic efficacy against GL261 orthotopic tumours, mebendazole showed a significant increase in animal survival time whereas vincristine, even at a dose close to its maximum tolerated dose, failed to show any efficacy; vincristine does not penetrate well into brain tumour tissue and displays dose-limiting toxicities including peripheral neuropathy.

    Mebendazole → Vincristine source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/mebendazole-research/28386621.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "20ef610d6b4a341f8a0a3f731bbea5477badbee517062c303bbf1075f3a29865", "start_char": 0, "end_char": 1788, "text_sha256": "20ef610d6b4a341f8a0a3f731bbea5477badbee517062c303bbf1075f3a29865"}
    experimental_model
    Concentration-matched comparison of viability, microtubule polymerisation and metaphase arrest, with NCI COMPARE analysis and a head-to-head animal comparison against vincristine
    exposure
    Mebendazole against vincristine close to its maximum tolerated dose in orthotopic GL261 tumours
    limitations
    Tests whether the anticancer effect is the microtubule effect by matching concentrations across three assays, which most repurposing studies do not do.
    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
    Against brain tumours in mice it beat the microtubule drug already in clinical use, which cannot get into the brain.
    primary_references
    [mbz-p28386621] Repurposing Mebendazole as a Replacement for Vincristine for the Treatment of Brain Tumors. (2017). https://pubmed.ncbi.nlm.nih.gov/28386621/ DOI: 10.2119/molmed.2017.00011
    tissue_or_cell_type
    Glioblastoma

    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 511–522

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Concentration-matched comparison of viability, microtubule polymerisation and metaphase arrest, with NCI COMPARE analysis and a head-to-head animal comparison against vincristine · source_derived_draft · unverified_draft

    ### mbz-beats-vincristine Comparing therapeutic efficacy against GL261 orthotopic tumours, mebendazole showed a significant increase in animal survival time whereas vincristine, even at a dose close to its maximum tolerated dose, failed to show any efficacy; vincristine does not penetrate well into brain tumour tissue and displays dose-limiting toxicities including peripheral neuropathy. 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: Against brain tumours in mice it beat the microtubule drug already in clinical use, which cannot get into the brain. organism: Mouse tissue_or_cell_type: Glioblastoma experimental_model: Concentration-matched comparison of viability, microtubule polymerisation and metaphase arrest, with NCI COMPARE analysis and a head-to-head animal comparison against vincristine limitations: Tests whether the anticancer effect is the microtubule effect by matching concentrations across three assays, which most repurposing studies do not do. exposure: Mebendazole against vincristine close to its maximum tolerated dose in orthotopic GL261 tumours evidence_span: {"source_cache": "artifacts/mebendazole-research/28386621.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "20ef610d6b4a341f8a0a3f731bbea5477badbee517062c303bbf1075f3a29865", "start_char": 0, "end_char": 1788, "text_sha256": "20ef610d6b4a341f8a0a3f731bbea5477badbee517062c303bbf1075f3a29865"} [mbz-p28386621] Repurposing Mebendazole as a Replacement for Vincristine for the Treatment of Brain Tumors. (2017). https://pubmed.ncbi.nlm.nih.gov/28386621/ DOI: 10.2119/molmed.2017.00011
    Complete structured claim and evidence
  3. Inhibition of colchicine binding to Ascaris suum embryonic tubulin by mebendazole and fenbendazole appeared to be noncompetitive, whereas the same compounds appeared to be competitive inhibitors of colchicine binding to bovine brain tubulin.

    Mebendazole → The colchicine binding site on tubulin source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/mebendazole-research/7388055.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5613d7fb281b4fd39b17bfdbafaf0ea823fb63b928048a9dd112fb71bf4cd2b7", "start_char": 0, "end_char": 1209, "text_sha256": "5613d7fb281b4fd39b17bfdbafaf0ea823fb63b928048a9dd112fb71bf4cd2b7"}
    experimental_model
    Inhibition of tritiated colchicine binding to cytosolic tubulin from 8-day Ascaris suum embryos and from bovine brain
    exposure
    Mebendazole and fenbendazole compared on the two tubulins in the same assay
    limitations
    The founding selectivity result. It measures embryonic tubulin; the study in this collection that measured intestinal tubulin found a far smaller difference.
    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
    Nematode and cattle
    plain_language
    It does not even bind the two tubulins the same way: it competes with colchicine on ours and not on the worm’s.
    primary_references
    [mbz-p7388055] Interaction of anthelmintic benzimidazoles with Ascaris suum embryonic tubulin. (1980). https://pubmed.ncbi.nlm.nih.gov/7388055/ DOI: 10.1016/0304-4165(80)90431-6
    tissue_or_cell_type
    Embryonic nematode tubulin and bovine brain tubulin

    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 108–119

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Inhibition of tritiated colchicine binding to cytosolic tubulin from 8-day Ascaris suum embryos and from bovine brain · source_derived_draft · unverified_draft

    ### mbz-binding-mode-differs Inhibition of colchicine binding to Ascaris suum embryonic tubulin by mebendazole and fenbendazole appeared to be noncompetitive, whereas the same compounds appeared to be competitive inhibitors of colchicine binding to bovine brain tubulin. 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 does not even bind the two tubulins the same way: it competes with colchicine on ours and not on the worm’s. organism: Nematode and cattle tissue_or_cell_type: Embryonic nematode tubulin and bovine brain tubulin experimental_model: Inhibition of tritiated colchicine binding to cytosolic tubulin from 8-day Ascaris suum embryos and from bovine brain limitations: The founding selectivity result. It measures embryonic tubulin; the study in this collection that measured intestinal tubulin found a far smaller difference. exposure: Mebendazole and fenbendazole compared on the two tubulins in the same assay evidence_span: {"source_cache": "artifacts/mebendazole-research/7388055.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5613d7fb281b4fd39b17bfdbafaf0ea823fb63b928048a9dd112fb71bf4cd2b7", "start_char": 0, "end_char": 1209, "text_sha256": "5613d7fb281b4fd39b17bfdbafaf0ea823fb63b928048a9dd112fb71bf4cd2b7"} [mbz-p7388055] Interaction of anthelmintic benzimidazoles with Ascaris suum embryonic tubulin. (1980). https://pubmed.ncbi.nlm.nih.gov/7388055/ DOI: 10.1016/0304-4165(80)90431-6
    Complete structured claim and evidence
  4. Following intravenous administration of a 1.7 microgram tracer dose of tritiated mebendazole to a man an elimination half-life of 1.16 hours was observed with a volume of distribution of 2.03 litres per kilogram, after oral administration of the same dose the elimination half-life was 0.74 hours, and the bioavailability of mebendazole from the solution was found to be 17%.

    Mebendazole → Oral bioavailability source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/mebendazole-research/7126419.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7b69c414a01f82e177ec37b4f362337caf7327e294a13c97d299e9a7ae80a456", "start_char": 0, "end_char": 381, "text_sha256": "7b69c414a01f82e177ec37b4f362337caf7327e294a13c97d299e9a7ae80a456"}
    experimental_model
    Tracer study of tritiated mebendazole given intravenously and orally to one man
    exposure
    A 1.7 microgram tracer dose by each route
    limitations
    A single subject and a tracer dose far below any therapeutic amount, so the bioavailability figure is a lower bound on the problem rather than a population value.
    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
    Human
    plain_language
    Swallowed, roughly one sixth of the drug reaches the bloodstream.
    primary_references
    [mbz-p7126419] The pharmacokinetics and bioavailability of mebendazole in man: a pilot study using [3H]-mebendazole. (1982). https://pubmed.ncbi.nlm.nih.gov/7126419/ DOI: 10.1111/j.1365-2125.1982.tb02008.x
    tissue_or_cell_type
    Whole body

    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 407–418

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Tracer study of tritiated mebendazole given intravenously and orally to one man · source_derived_draft · unverified_draft

    ### mbz-bioavailability-17-percent Following intravenous administration of a 1.7 microgram tracer dose of tritiated mebendazole to a man an elimination half-life of 1.16 hours was observed with a volume of distribution of 2.03 litres per kilogram, after oral administration of the same dose the elimination half-life was 0.74 hours, and the bioavailability of mebendazole from the solution was found to be 17%. 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: Swallowed, roughly one sixth of the drug reaches the bloodstream. organism: Human tissue_or_cell_type: Whole body experimental_model: Tracer study of tritiated mebendazole given intravenously and orally to one man limitations: A single subject and a tracer dose far below any therapeutic amount, so the bioavailability figure is a lower bound on the problem rather than a population value. exposure: A 1.7 microgram tracer dose by each route evidence_span: {"source_cache": "artifacts/mebendazole-research/7126419.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7b69c414a01f82e177ec37b4f362337caf7327e294a13c97d299e9a7ae80a456", "start_char": 0, "end_char": 381, "text_sha256": "7b69c414a01f82e177ec37b4f362337caf7327e294a13c97d299e9a7ae80a456"} [mbz-p7126419] The pharmacokinetics and bioavailability of mebendazole in man: a pilot study using [3H]-mebendazole. (1982). https://pubmed.ncbi.nlm.nih.gov/7126419/ DOI: 10.1111/j.1365-2125.1982.tb02008.x
    Complete structured claim and evidence
  5. The relative potencies of the benzimidazole analogs in rat embryo micromass culture, nocodazole greater than mebendazole approximately equal to albendazole much greater than thiabendazole, mirrored their effectiveness in an assay for in vitro inhibition of mammalian tubulin polymerization, immunofluorescent staining with a monoclonal antibody to beta-tubulin revealed that these agents elicited mitotic arrest, and with the exception of thiabendazole these agents should be considered potential developmental toxicants since they inhibit cell growth and differentiation at nanomolar concentrations.

    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/mebendazole-research/1553749.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4c8ca680cbc4ebd8441d3d8c083a98587c81141280e9fa61388751264f1ea2ac", "start_char": 0, "end_char": 1384, "text_sha256": "4c8ca680cbc4ebd8441d3d8c083a98587c81141280e9fa61388751264f1ea2ac"}
    experimental_model
    Rat embryo midbrain and limb bud micromass cultures assessed for differentiation and cytotoxicity
    exposure
    Mebendazole, thiabendazole, nocodazole and colchicine, compared with albendazole
    limitations
    An in vitro developmental toxicity screen. It links the effect to the mammalian tubulin binding directly, by showing the potency order matches; it is not a pregnancy outcome.
    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
    Rat
    plain_language
    The very property that makes it a cancer drug candidate is the property that makes it a suspected developmental toxin.
    primary_references
    [mbz-p1553749] Effects of benzimidazole analogs on cultures of differentiating rodent embryonic cells. (1992). https://pubmed.ncbi.nlm.nih.gov/1553749/ DOI: 10.1016/0041-008x(92)90019-o
    tissue_or_cell_type
    Embryonic midbrain and limb bud cells

    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 602–613

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rat embryo midbrain and limb bud micromass cultures assessed for differentiation and cytotoxicity · source_derived_draft · unverified_draft

    ### mbz-developmental-toxicity-is-the-same-target The relative potencies of the benzimidazole analogs in rat embryo micromass culture, nocodazole greater than mebendazole approximately equal to albendazole much greater than thiabendazole, mirrored their effectiveness in an assay for in vitro inhibition of mammalian tubulin polymerization, immunofluorescent staining with a monoclonal antibody to beta-tubulin revealed that these agents elicited mitotic arrest, and with the exception of thiabendazole these agents should be considered potential developmental toxicants since they inhibit cell growth and differentiation at nanomolar concentrations. 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: The very property that makes it a cancer drug candidate is the property that makes it a suspected developmental toxin. organism: Rat tissue_or_cell_type: Embryonic midbrain and limb bud cells experimental_model: Rat embryo midbrain and limb bud micromass cultures assessed for differentiation and cytotoxicity limitations: An in vitro developmental toxicity screen. It links the effect to the mammalian tubulin binding directly, by showing the potency order matches; it is not a pregnancy outcome. exposure: Mebendazole, thiabendazole, nocodazole and colchicine, compared with albendazole evidence_span: {"source_cache": "artifacts/mebendazole-research/1553749.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4c8ca680cbc4ebd8441d3d8c083a98587c81141280e9fa61388751264f1ea2ac", "start_char": 0, "end_char": 1384, "text_sha256": "4c8ca680cbc4ebd8441d3d8c083a98587c81141280e9fa61388751264f1ea2ac"} [mbz-p1553749] Effects of benzimidazole analogs on cultures of differentiating rodent embryonic cells. (1992). https://pubmed.ncbi.nlm.nih.gov/1553749/ DOI: 10.1016/0041-008x(92)90019-o
    Complete structured claim and evidence
  6. Expressing beta-tubulin as a fusion with maltose binding protein produced a soluble protein and confirmed for the first time using a gel filtration assay that benzimidazoles indeed bind to beta-tubulin, with binding reduced by the mutation glutamate 198 to glycine which also confers resistance, while binding of phenylcarbamates was the complete opposite, reflecting their biological activity and the negative cross-resistance.

    Mebendazole → Fungal beta-tubulin source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/mebendazole-research/9736529.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "ee7cd2a364b52ba75f6f19da6935c7311ae80f514a223a50b17dbd6bbaf929d4", "start_char": 0, "end_char": 1053, "text_sha256": "ee7cd2a364b52ba75f6f19da6935c7311ae80f514a223a50b17dbd6bbaf929d4"}
    experimental_model
    Fungal beta-tubulin expressed as a maltose binding protein fusion, assayed by gel filtration
    exposure
    Benzimidazole and phenylcarbamate binding to wild-type and Glu198Gly fusion protein
    limitations
    The first direct confirmation by binding assay that benzimidazoles bind beta-tubulin itself. It is a fusion protein rather than native tubulin, which the authors address by the internal consistency of the two ligand classes.
    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
    Fungus
    plain_language
    The drug really does stick to this protein, and the mutation that resists it loosens the grip.
    primary_references
    [mbz-p9736529] Fungal beta-tubulin, expressed as a fusion protein, binds benzimidazole and phenylcarbamate fungicides. (1998). https://pubmed.ncbi.nlm.nih.gov/9736529/ DOI: 10.1128/aac.42.9.2171
    tissue_or_cell_type
    Beta-tubulin

    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 316–327

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Fungal beta-tubulin expressed as a maltose binding protein fusion, assayed by gel filtration · source_derived_draft · unverified_draft

    ### mbz-direct-binding-and-glu198 Expressing beta-tubulin as a fusion with maltose binding protein produced a soluble protein and confirmed for the first time using a gel filtration assay that benzimidazoles indeed bind to beta-tubulin, with binding reduced by the mutation glutamate 198 to glycine which also confers resistance, while binding of phenylcarbamates was the complete opposite, reflecting their biological activity and the negative cross-resistance. 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: The drug really does stick to this protein, and the mutation that resists it loosens the grip. organism: Fungus tissue_or_cell_type: Beta-tubulin experimental_model: Fungal beta-tubulin expressed as a maltose binding protein fusion, assayed by gel filtration limitations: The first direct confirmation by binding assay that benzimidazoles bind beta-tubulin itself. It is a fusion protein rather than native tubulin, which the authors address by the internal consistency of the two ligand classes. exposure: Benzimidazole and phenylcarbamate binding to wild-type and Glu198Gly fusion protein evidence_span: {"source_cache": "artifacts/mebendazole-research/9736529.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "ee7cd2a364b52ba75f6f19da6935c7311ae80f514a223a50b17dbd6bbaf929d4", "start_char": 0, "end_char": 1053, "text_sha256": "ee7cd2a364b52ba75f6f19da6935c7311ae80f514a223a50b17dbd6bbaf929d4"} [mbz-p9736529] Fungal beta-tubulin, expressed as a fusion protein, binds benzimidazole and phenylcarbamate fungicides. (1998). https://pubmed.ncbi.nlm.nih.gov/9736529/ DOI: 10.1128/aac.42.9.2171
    Complete structured claim and evidence
  7. In a 47-year-old woman with multiple hydatid cysts of the liver in whom hepatitis developed after mebendazole treatment, clinical manifestations of hypersensitivity were absent and a correlation was found between serum mebendazole concentrations and the degree of cytolysis, which is compatible with a direct hepatotoxic effect of mebendazole.

    Experimental context and source evidence
    availability_state
    biomarker_context Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/mebendazole-research/3692093.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "dd4fb3feac1314a99fa05d5d06bd35a25350bcfed9e8570a1b0c5dc702e835b1", "start_char": 0, "end_char": 379, "text_sha256": "dd4fb3feac1314a99fa05d5d06bd35a25350bcfed9e8570a1b0c5dc702e835b1"}
    experimental_model
    Case report of hepatitis after mebendazole treatment with serial serum concentrations
    exposure
    Mebendazole treatment for multiple hepatic hydatid cysts
    limitations
    A single case. The correlation between drug concentration and cytolysis within one patient is what distinguishes a direct toxic effect from hypersensitivity, and hypersensitivity features were absent.
    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
    Human
    plain_language
    The liver damage tracked the drug level rather than looking like an allergy, which points at the drug itself.
    primary_references
    [mbz-p3692093] Hepatotoxicity of mebendazole. Relationship with serum concentrations of the drug. (1987). https://pubmed.ncbi.nlm.nih.gov/3692093/
    tissue_or_cell_type
    Liver
    trigger_kind
    biomarker_context Imported condition classification; unverified.

    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 641–652

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Case report of hepatitis after mebendazole treatment with serial serum concentrations · source_derived_draft · unverified_draft

    ### mbz-dose-related-hepatotoxicity In a 47-year-old woman with multiple hydatid cysts of the liver in whom hepatitis developed after mebendazole treatment, clinical manifestations of hypersensitivity were absent and a correlation was found between serum mebendazole concentrations and the degree of cytolysis, which is compatible with a direct hepatotoxic effect of mebendazole. Condition category: biomarker_context 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: The liver damage tracked the drug level rather than looking like an allergy, which points at the drug itself. organism: Human tissue_or_cell_type: Liver experimental_model: Case report of hepatitis after mebendazole treatment with serial serum concentrations limitations: A single case. The correlation between drug concentration and cytolysis within one patient is what distinguishes a direct toxic effect from hypersensitivity, and hypersensitivity features were absent. exposure: Mebendazole treatment for multiple hepatic hydatid cysts evidence_span: {"source_cache": "artifacts/mebendazole-research/3692093.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "dd4fb3feac1314a99fa05d5d06bd35a25350bcfed9e8570a1b0c5dc702e835b1", "start_char": 0, "end_char": 379, "text_sha256": "dd4fb3feac1314a99fa05d5d06bd35a25350bcfed9e8570a1b0c5dc702e835b1"} [mbz-p3692093] Hepatotoxicity of mebendazole. Relationship with serum concentrations of the drug. (1987). https://pubmed.ncbi.nlm.nih.gov/3692093/
    Complete structured claim and evidence
  8. Benzimidazole carbamates with strong inhibitory activity against mammalian tubulin were potent inhibitors of Haemonchus contortus egg hatch while non-inhibitors failed to prevent hatching, supporting the view that the primary mode of action of these drugs on nematode eggs is inhibition of microtubule-dependent processes within the developing egg.

    Mebendazole → Hatching of nematode eggs source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/mebendazole-research/3564338.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "89495a42e9f41cac9010e20e925b802c27fde1dfac9a4a24dd2236335f4d61b1", "start_char": 0, "end_char": 818, "text_sha256": "89495a42e9f41cac9010e20e925b802c27fde1dfac9a4a24dd2236335f4d61b1"}
    experimental_model
    Correlation of Haemonchus contortus egg hatch inhibition with inhibition of mammalian tubulin polymerisation
    exposure
    Benzimidazole carbamates tested in both assays
    limitations
    A correlation rather than a demonstration of mechanism in the egg, and the hatch assay was sensitive to co-solvent concentration and incubation time.
    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
    Nematode and mammal
    plain_language
    The compounds that block tubulin are the ones that stop eggs hatching, and the ones that do not, do not.
    primary_references
    [mbz-p3564338] Comparison of inhibition of polymerisation of mammalian tubulin and helminth ovicidal activity by benzimidazole carbamates. (1987). https://pubmed.ncbi.nlm.nih.gov/3564338/ DOI: 10.1016/0304-4017(87)90029-x
    tissue_or_cell_type
    Nematode eggs and mammalian tubulin

    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 212–223

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Correlation of Haemonchus contortus egg hatch inhibition with inhibition of mammalian tubulin polymerisation · source_derived_draft · unverified_draft

    ### mbz-egg-hatch-tracks-tubulin Benzimidazole carbamates with strong inhibitory activity against mammalian tubulin were potent inhibitors of Haemonchus contortus egg hatch while non-inhibitors failed to prevent hatching, supporting the view that the primary mode of action of these drugs on nematode eggs is inhibition of microtubule-dependent processes within the developing egg. 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: The compounds that block tubulin are the ones that stop eggs hatching, and the ones that do not, do not. organism: Nematode and mammal tissue_or_cell_type: Nematode eggs and mammalian tubulin experimental_model: Correlation of Haemonchus contortus egg hatch inhibition with inhibition of mammalian tubulin polymerisation limitations: A correlation rather than a demonstration of mechanism in the egg, and the hatch assay was sensitive to co-solvent concentration and incubation time. exposure: Benzimidazole carbamates tested in both assays evidence_span: {"source_cache": "artifacts/mebendazole-research/3564338.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "89495a42e9f41cac9010e20e925b802c27fde1dfac9a4a24dd2236335f4d61b1", "start_char": 0, "end_char": 818, "text_sha256": "89495a42e9f41cac9010e20e925b802c27fde1dfac9a4a24dd2236335f4d61b1"} [mbz-p3564338] Comparison of inhibition of polymerisation of mammalian tubulin and helminth ovicidal activity by benzimidazole carbamates. (1987). https://pubmed.ncbi.nlm.nih.gov/3564338/ DOI: 10.1016/0304-4017(87)90029-x
    Complete structured claim and evidence
  9. Colchicine and a range of anthelmintic benzimidazoles inhibited in vitro polymerisation of tubulin purified from Ascaridia galli more than that purified from mammalian tissue, with oxfendazole and thiabendazole having virtually no effect on mammalian tubulin assembly while both inhibited nematode tubulin, and electron microscopy revealed no morphological differences between microtubules polymerised with or without drug although their length and number were reduced.

    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/mebendazole-research/6712717.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "dc6664076b62c0da221cce8e34690f297828b832da76857a2cc12cf9769fb282", "start_char": 0, "end_char": 949, "text_sha256": "dc6664076b62c0da221cce8e34690f297828b832da76857a2cc12cf9769fb282"}
    experimental_model
    In vitro polymerisation of tubulin purified from Ascaridia galli and from mammalian tissue, with electron microscopy
    exposure
    Colchicine and a range of anthelmintic benzimidazoles on both tubulins
    limitations
    Adds electron microscopy, which shows the drug reduces the number and length of microtubules without making abnormal ones. Purified protein rather than intact parasite.
    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
    Nematode and mammal
    plain_language
    The microtubules that do form look normal; there are simply fewer and shorter ones.
    primary_references
    [mbz-p6712717] A comparison of the interaction of anthelmintic benzimidazoles with tubulin isolated from mammalian tissue and the parasitic nematode Ascaridia galli. (1984). https://pubmed.ncbi.nlm.nih.gov/6712717/ DOI: 10.1016/0006-2952(84)90515-x
    tissue_or_cell_type
    Purified tubulin

    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 173–184

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · In vitro polymerisation of tubulin purified from Ascaridia galli and from mammalian tissue, with electron microscopy · source_derived_draft · unverified_draft

    ### mbz-fewer-not-abnormal Colchicine and a range of anthelmintic benzimidazoles inhibited in vitro polymerisation of tubulin purified from Ascaridia galli more than that purified from mammalian tissue, with oxfendazole and thiabendazole having virtually no effect on mammalian tubulin assembly while both inhibited nematode tubulin, and electron microscopy revealed no morphological differences between microtubules polymerised with or without drug although their length and number were reduced. 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: The microtubules that do form look normal; there are simply fewer and shorter ones. organism: Nematode and mammal tissue_or_cell_type: Purified tubulin experimental_model: In vitro polymerisation of tubulin purified from Ascaridia galli and from mammalian tissue, with electron microscopy limitations: Adds electron microscopy, which shows the drug reduces the number and length of microtubules without making abnormal ones. Purified protein rather than intact parasite. exposure: Colchicine and a range of anthelmintic benzimidazoles on both tubulins evidence_span: {"source_cache": "artifacts/mebendazole-research/6712717.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "dc6664076b62c0da221cce8e34690f297828b832da76857a2cc12cf9769fb282", "start_char": 0, "end_char": 949, "text_sha256": "dc6664076b62c0da221cce8e34690f297828b832da76857a2cc12cf9769fb282"} [mbz-p6712717] A comparison of the interaction of anthelmintic benzimidazoles with tubulin isolated from mammalian tissue and the parasitic nematode Ascaridia galli. (1984). https://pubmed.ncbi.nlm.nih.gov/6712717/ DOI: 10.1016/0006-2952(84)90515-x
    Complete structured claim and evidence
  10. In glioblastoma cell lines mebendazole displayed cytotoxicity with half-maximal inhibitory concentrations ranging from 0.1 to 0.3 micromolar, disrupted microtubule formation in those cells with in vitro activity correlated with reduced tubulin polymerization, and significantly extended mean survival by up to 63% in syngeneic and xenograft orthotopic mouse glioma models; the programme began with the serendipitous observation that fenbendazole, used to treat pinworm infection, inhibited brain tumour engraftment.

    Mebendazole → Viability of glioblastoma cells source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/mebendazole-research/21764822.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "31b328d5c2340f7a4e9b6a3b3d46c68a8c0265c50d483375bc6dc15bb1696ad6", "start_char": 0, "end_char": 1210, "text_sha256": "31b328d5c2340f7a4e9b6a3b3d46c68a8c0265c50d483375bc6dc15bb1696ad6"}
    experimental_model
    Cell line cytotoxicity, tubulin polymerisation and syngeneic and xenograft orthotopic mouse glioma models
    exposure
    Mebendazole compared with fenbendazole, at doses documented as safe in humans
    limitations
    The observation that started the programme was serendipitous, from pinworm treatment of laboratory animals. Mouse models, and the survival gain is a mean rather than a cure.
    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
    Human cells and mouse
    plain_language
    The worm drug killed brain tumour cells at low concentrations and let mice live substantially longer.
    primary_references
    [mbz-p21764822] Antiparasitic mebendazole shows survival benefit in 2 preclinical models of glioblastoma multiforme. (2011). https://pubmed.ncbi.nlm.nih.gov/21764822/ DOI: 10.1093/neuonc/nor077
    tissue_or_cell_type
    Glioblastoma

    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 485–496

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cell line cytotoxicity, tubulin polymerisation and syngeneic and xenograft orthotopic mouse glioma models · source_derived_draft · unverified_draft

    ### mbz-glioma-cytotoxicity In glioblastoma cell lines mebendazole displayed cytotoxicity with half-maximal inhibitory concentrations ranging from 0.1 to 0.3 micromolar, disrupted microtubule formation in those cells with in vitro activity correlated with reduced tubulin polymerization, and significantly extended mean survival by up to 63% in syngeneic and xenograft orthotopic mouse glioma models; the programme began with the serendipitous observation that fenbendazole, used to treat pinworm infection, inhibited brain tumour engraftment. 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: The worm drug killed brain tumour cells at low concentrations and let mice live substantially longer. organism: Human cells and mouse tissue_or_cell_type: Glioblastoma experimental_model: Cell line cytotoxicity, tubulin polymerisation and syngeneic and xenograft orthotopic mouse glioma models limitations: The observation that started the programme was serendipitous, from pinworm treatment of laboratory animals. Mouse models, and the survival gain is a mean rather than a cure. exposure: Mebendazole compared with fenbendazole, at doses documented as safe in humans evidence_span: {"source_cache": "artifacts/mebendazole-research/21764822.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "31b328d5c2340f7a4e9b6a3b3d46c68a8c0265c50d483375bc6dc15bb1696ad6", "start_char": 0, "end_char": 1210, "text_sha256": "31b328d5c2340f7a4e9b6a3b3d46c68a8c0265c50d483375bc6dc15bb1696ad6"} [mbz-p21764822] Antiparasitic mebendazole shows survival benefit in 2 preclinical models of glioblastoma multiforme. (2011). https://pubmed.ncbi.nlm.nih.gov/21764822/ DOI: 10.1093/neuonc/nor077
    Complete structured claim and evidence
  11. Mebendazole potently inhibited hedgehog signalling and slowed the growth of hedgehog-driven human medulloblastoma cells at clinically attainable concentrations, suppressed formation of the primary cilium, a microtubule-based organelle that functions as a signalling hub for pathway activation, and its inhibition was unaffected by mutants in the gene encoding human Smoothened that are selectively propagated in clones surviving vismodegib, with the combination of vismodegib and mebendazole giving additive inhibition.

    Mebendazole → Hedgehog signalling source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/mebendazole-research/25376612.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "fa6b6f06dfda62c5f1cc59df64f813c5d112f8d6a3bf969c6fa4432073a87ec0", "start_char": 0, "end_char": 1290, "text_sha256": "fa6b6f06dfda62c5f1cc59df64f813c5d112f8d6a3bf969c6fa4432073a87ec0"}
    experimental_model
    Hedgehog reporter and medulloblastoma cell growth assays with Smoothened mutant lines
    exposure
    Mebendazole at clinically attainable concentrations, alone and with vismodegib
    limitations
    Proposes a second mechanism which is still microtubule-based, through the primary cilium. Cell assays; the claim that the concentrations are clinically attainable is the authors’.
    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
    Human cells
    plain_language
    It blocks this growth pathway by removing the little antenna the pathway needs, so mutations that defeat the standard drug do not defeat it.
    primary_references
    [mbz-p25376612] Repurposing the antihelmintic mebendazole as a hedgehog inhibitor. (2015). https://pubmed.ncbi.nlm.nih.gov/25376612/ DOI: 10.1158/1535-7163.mct-14-0755-t
    tissue_or_cell_type
    Medulloblastoma

    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 537–548

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Hedgehog reporter and medulloblastoma cell growth assays with Smoothened mutant lines · source_derived_draft · unverified_draft

    ### mbz-hedgehog-through-the-cilium Mebendazole potently inhibited hedgehog signalling and slowed the growth of hedgehog-driven human medulloblastoma cells at clinically attainable concentrations, suppressed formation of the primary cilium, a microtubule-based organelle that functions as a signalling hub for pathway activation, and its inhibition was unaffected by mutants in the gene encoding human Smoothened that are selectively propagated in clones surviving vismodegib, with the combination of vismodegib and mebendazole giving additive inhibition. 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 blocks this growth pathway by removing the little antenna the pathway needs, so mutations that defeat the standard drug do not defeat it. organism: Human cells tissue_or_cell_type: Medulloblastoma experimental_model: Hedgehog reporter and medulloblastoma cell growth assays with Smoothened mutant lines limitations: Proposes a second mechanism which is still microtubule-based, through the primary cilium. Cell assays; the claim that the concentrations are clinically attainable is the authors’. exposure: Mebendazole at clinically attainable concentrations, alone and with vismodegib evidence_span: {"source_cache": "artifacts/mebendazole-research/25376612.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "fa6b6f06dfda62c5f1cc59df64f813c5d112f8d6a3bf969c6fa4432073a87ec0", "start_char": 0, "end_char": 1290, "text_sha256": "fa6b6f06dfda62c5f1cc59df64f813c5d112f8d6a3bf969c6fa4432073a87ec0"} [mbz-p25376612] Repurposing the antihelmintic mebendazole as a hedgehog inhibitor. (2015). https://pubmed.ncbi.nlm.nih.gov/25376612/ DOI: 10.1158/1535-7163.mct-14-0755-t
    Complete structured claim and evidence
  12. In 24 patients with newly diagnosed high-grade glioma given mebendazole with adjuvant temozolomide, four patients at 200 milligrams per kilogram per day developed elevated grade 3 alanine aminotransferase or aspartate transaminase after one month which reversed with lower dosing or discontinuation, plasma levels were variable but generally increased with dose, and mebendazole at doses up to 200 milligrams per kilogram demonstrated long-term safety and acceptable toxicity.

    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/mebendazole-research/33506200.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "ab5f2c1d14ccb7fa9f690201326bdbfcab3e07758bc78b76ff9adec2ca774ec6", "start_char": 0, "end_char": 1712, "text_sha256": "ab5f2c1d14ccb7fa9f690201326bdbfcab3e07758bc78b76ff9adec2ca774ec6"}
    experimental_model
    Single-centre dose-escalation and safety study in 24 patients with newly diagnosed high-grade glioma
    exposure
    Oral mebendazole at 25, 50, 100 and 200 milligrams per kilogram per day with adjuvant temozolomide, with trough plasma levels at 4, 8 and 16 weeks
    limitations
    The only human oncology record here. It is a single-arm dose-escalation and safety study without a control group, so the survival figures cannot be read as efficacy.
    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
    Human
    plain_language
    At the highest dose one patient in six developed liver enzyme rises that reversed on stopping.
    primary_references
    [mbz-p33506200] Mebendazole and temozolomide in patients with newly diagnosed high-grade gliomas: results of a phase 1 clinical trial. (2021). https://pubmed.ncbi.nlm.nih.gov/33506200/ DOI: 10.1093/noajnl/vdaa154
    tissue_or_cell_type
    Brain

    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 576–587

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Single-centre dose-escalation and safety study in 24 patients with newly diagnosed high-grade glioma · source_derived_draft · unverified_draft

    ### mbz-human-dose-escalation In 24 patients with newly diagnosed high-grade glioma given mebendazole with adjuvant temozolomide, four patients at 200 milligrams per kilogram per day developed elevated grade 3 alanine aminotransferase or aspartate transaminase after one month which reversed with lower dosing or discontinuation, plasma levels were variable but generally increased with dose, and mebendazole at doses up to 200 milligrams per kilogram demonstrated long-term safety and acceptable toxicity. 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: At the highest dose one patient in six developed liver enzyme rises that reversed on stopping. organism: Human tissue_or_cell_type: Brain experimental_model: Single-centre dose-escalation and safety study in 24 patients with newly diagnosed high-grade glioma limitations: The only human oncology record here. It is a single-arm dose-escalation and safety study without a control group, so the survival figures cannot be read as efficacy. exposure: Oral mebendazole at 25, 50, 100 and 200 milligrams per kilogram per day with adjuvant temozolomide, with trough plasma levels at 4, 8 and 16 weeks evidence_span: {"source_cache": "artifacts/mebendazole-research/33506200.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "ab5f2c1d14ccb7fa9f690201326bdbfcab3e07758bc78b76ff9adec2ca774ec6", "start_char": 0, "end_char": 1712, "text_sha256": "ab5f2c1d14ccb7fa9f690201326bdbfcab3e07758bc78b76ff9adec2ca774ec6"} [mbz-p33506200] Mebendazole and temozolomide in patients with newly diagnosed high-grade gliomas: results of a phase 1 clinical trial. (2021). https://pubmed.ncbi.nlm.nih.gov/33506200/ DOI: 10.1093/noajnl/vdaa154
    Complete structured claim and evidence
  13. Of four benzimidazole anthelmintics tested on purified cytoplasmic and mitochondrial malate dehydrogenase from Ascaris suum, Fasciola hepatica and Moniezia expansa, mebendazole exhibited the highest percentage inhibitions, and the authors conclude that cytoplasmic and mitochondrial malate dehydrogenase regulating glycogen synthesis are the sites of mebendazole inhibitory activity while the sites for the other anthelmintics remain unclear.

    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/mebendazole-research/3617430.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "addd86672cc2c829b72354c05387892908f94c49f81e1236e372432c68a622fe", "start_char": 0, "end_char": 589, "text_sha256": "addd86672cc2c829b72354c05387892908f94c49f81e1236e372432c68a622fe"}
    experimental_model
    Inhibition assays on purified cytoplasmic and mitochondrial malate dehydrogenase from three helminths
    exposure
    Albendazole, parbendazole, mebendazole and thiabendazole on purified enzyme extracts
    limitations
    A competing target claim. Enzyme inhibition percentages in purified extracts do not establish that this happens at therapeutic concentrations in a living parasite.
    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
    Helminth
    plain_language
    A rival account: the drug jams an enzyme of the worm’s sugar metabolism, and mebendazole does it hardest.
    primary_references
    [mbz-p3617430] Inhibition of malate dehydrogenase enzymes by benzimidazole anthelmintics. (1987). https://pubmed.ncbi.nlm.nih.gov/3617430/ DOI: 10.1016/0304-4017(87)90048-3
    tissue_or_cell_type
    Ascaris suum, Fasciola hepatica and Moniezia expansa

    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 238–249

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Inhibition assays on purified cytoplasmic and mitochondrial malate dehydrogenase from three helminths · source_derived_draft · unverified_draft

    ### mbz-inhibits-malate-dehydrogenase Of four benzimidazole anthelmintics tested on purified cytoplasmic and mitochondrial malate dehydrogenase from Ascaris suum, Fasciola hepatica and Moniezia expansa, mebendazole exhibited the highest percentage inhibitions, and the authors conclude that cytoplasmic and mitochondrial malate dehydrogenase regulating glycogen synthesis are the sites of mebendazole inhibitory activity while the sites for the other anthelmintics remain unclear. 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: A rival account: the drug jams an enzyme of the worm’s sugar metabolism, and mebendazole does it hardest. organism: Helminth tissue_or_cell_type: Ascaris suum, Fasciola hepatica and Moniezia expansa experimental_model: Inhibition assays on purified cytoplasmic and mitochondrial malate dehydrogenase from three helminths limitations: A competing target claim. Enzyme inhibition percentages in purified extracts do not establish that this happens at therapeutic concentrations in a living parasite. exposure: Albendazole, parbendazole, mebendazole and thiabendazole on purified enzyme extracts evidence_span: {"source_cache": "artifacts/mebendazole-research/3617430.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "addd86672cc2c829b72354c05387892908f94c49f81e1236e372432c68a622fe", "start_char": 0, "end_char": 589, "text_sha256": "addd86672cc2c829b72354c05387892908f94c49f81e1236e372432c68a622fe"} [mbz-p3617430] Inhibition of malate dehydrogenase enzymes by benzimidazole anthelmintics. (1987). https://pubmed.ncbi.nlm.nih.gov/3617430/ DOI: 10.1016/0304-4017(87)90048-3
    Complete structured claim and evidence
  14. Pyruvate kinase and phosphoenolpyruvate carboxykinase activities in the Echinococcus granulosus cyst wall were markedly inhibited by mebendazole and albendazole while fumarate hydratase activity showed no apparent change, with inhibition rates in the mebendazole group of 85 to 88% and 90 to 92% respectively against 55.3% and 71.6% in the albendazole group, suggesting that these two enzymes may be an important site attacked by effective anti-hydatid drugs.

    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/mebendazole-research/8010090.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "581715173f3b7176eda8a357166f1647196f646769b75ee7ca9070342a9c312b", "start_char": 0, "end_char": 933, "text_sha256": "581715173f3b7176eda8a357166f1647196f646769b75ee7ca9070342a9c312b"}
    experimental_model
    Enzyme activity assays on Echinococcus granulosus cyst wall from infected mice after 7 to 14 days of treatment
    exposure
    Mebendazole 25 to 50, albendazole 300 and praziquantel 500 milligrams per kilogram daily by gavage
    limitations
    An in vivo enzyme measurement with a head-to-head dose comparison, though the doses are not equipotent and the cyst wall is one tissue.
    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
    Cestode
    plain_language
    In a live infection mebendazole shut down two sugar-handling enzymes almost completely, and did so harder than albendazole.
    primary_references
    [mbz-p8010090] Effects of mebendazole, albendazole, and praziquantel on fumarate hydratase, pyruvate kinase, and phosphoenolpyruvate carboxykinase of Echinococcus granulosus cyst wall harbored in mice. (1994). https://pubmed.ncbi.nlm.nih.gov/8010090/
    tissue_or_cell_type
    Hydatid cyst wall

    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 251–262

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Enzyme activity assays on Echinococcus granulosus cyst wall from infected mice after 7 to 14 days of treatment · source_derived_draft · unverified_draft

    ### mbz-inhibits-pk-and-pepck Pyruvate kinase and phosphoenolpyruvate carboxykinase activities in the Echinococcus granulosus cyst wall were markedly inhibited by mebendazole and albendazole while fumarate hydratase activity showed no apparent change, with inhibition rates in the mebendazole group of 85 to 88% and 90 to 92% respectively against 55.3% and 71.6% in the albendazole group, suggesting that these two enzymes may be an important site attacked by effective anti-hydatid drugs. 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: In a live infection mebendazole shut down two sugar-handling enzymes almost completely, and did so harder than albendazole. organism: Cestode tissue_or_cell_type: Hydatid cyst wall experimental_model: Enzyme activity assays on Echinococcus granulosus cyst wall from infected mice after 7 to 14 days of treatment limitations: An in vivo enzyme measurement with a head-to-head dose comparison, though the doses are not equipotent and the cyst wall is one tissue. exposure: Mebendazole 25 to 50, albendazole 300 and praziquantel 500 milligrams per kilogram daily by gavage evidence_span: {"source_cache": "artifacts/mebendazole-research/8010090.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "581715173f3b7176eda8a357166f1647196f646769b75ee7ca9070342a9c312b", "start_char": 0, "end_char": 933, "text_sha256": "581715173f3b7176eda8a357166f1647196f646769b75ee7ca9070342a9c312b"} [mbz-p8010090] Effects of mebendazole, albendazole, and praziquantel on fumarate hydratase, pyruvate kinase, and phosphoenolpyruvate carboxykinase of Echinococcus granulosus cyst wall harbored in mice. (1994). https://pubmed.ncbi.nlm.nih.gov/8010090/
    Complete structured claim and evidence
  15. Median inhibitory concentrations for nocodazole, oxibendazole, parbendazole, mebendazole and fenbendazole against bovine brain tubulin polymerisation ranged from 1.97 x 10-6 to 6.32 x 10-6 molar, while benomyl, cambendazole and carbendazim had values from 5.83 x 10-5 to 9.01 x 10-5 molar and thiabendazole had a value of 5.49 x 10-4 molar.

    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/mebendazole-research/728472.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "544c36409218c93ebff76d932a2bc6e14ccf7fd6e217d4614c4b561281c2555a", "start_char": 0, "end_char": 1025, "text_sha256": "544c36409218c93ebff76d932a2bc6e14ccf7fd6e217d4614c4b561281c2555a"}
    experimental_model
    Turbidimetric microtubule polymerisation assay and colchicine binding assay on purified bovine brain tubulin
    exposure
    Eleven benzimidazoles compared for inhibition of the initial rate of microtubule polymerisation
    limitations
    Purified mammalian tubulin, which is the off-target rather than the parasite target. It fixes where mebendazole sits in the class by potency.
    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
    Cattle
    plain_language
    Mebendazole sits in the potent group; thiabendazole is about a hundred times weaker.
    primary_references
    [mbz-p728472] Interaction of anthelmintic benzimidazoles and benzimidazole derivatives with bovine brain tubulin. (1978). https://pubmed.ncbi.nlm.nih.gov/728472/ DOI: 10.1016/0304-4165(78)90334-3
    tissue_or_cell_type
    Brain tubulin

    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 82–93

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Turbidimetric microtubule polymerisation assay and colchicine binding assay on purified bovine brain tubulin · source_derived_draft · unverified_draft

    ### mbz-inhibits-polymerisation Median inhibitory concentrations for nocodazole, oxibendazole, parbendazole, mebendazole and fenbendazole against bovine brain tubulin polymerisation ranged from 1.97 x 10-6 to 6.32 x 10-6 molar, while benomyl, cambendazole and carbendazim had values from 5.83 x 10-5 to 9.01 x 10-5 molar and thiabendazole had a value of 5.49 x 10-4 molar. 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: Mebendazole sits in the potent group; thiabendazole is about a hundred times weaker. organism: Cattle tissue_or_cell_type: Brain tubulin experimental_model: Turbidimetric microtubule polymerisation assay and colchicine binding assay on purified bovine brain tubulin limitations: Purified mammalian tubulin, which is the off-target rather than the parasite target. It fixes where mebendazole sits in the class by potency. exposure: Eleven benzimidazoles compared for inhibition of the initial rate of microtubule polymerisation evidence_span: {"source_cache": "artifacts/mebendazole-research/728472.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "544c36409218c93ebff76d932a2bc6e14ccf7fd6e217d4614c4b561281c2555a", "start_char": 0, "end_char": 1025, "text_sha256": "544c36409218c93ebff76d932a2bc6e14ccf7fd6e217d4614c4b561281c2555a"} [mbz-p728472] Interaction of anthelmintic benzimidazoles and benzimidazole derivatives with bovine brain tubulin. (1978). https://pubmed.ncbi.nlm.nih.gov/728472/ DOI: 10.1016/0304-4165(78)90334-3
    Complete structured claim and evidence
  16. In vitro incubation of Ascaris suum with 10 micromolar mebendazole resulted in a complete loss of colchicine binding ability of extracts obtained from the parasite intestine, the colchicine binding receptor in those extracts was identified biochemically as tubulin, and that protein comprised approximately 0.8% of the soluble intestinal protein.

    Mebendazole → Nematode beta-tubulin source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/mebendazole-research/7335116.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "358adb37f881bf9fc64cf4cea24ce690792e958df702a705b2addda3295ad144", "start_char": 0, "end_char": 1621, "text_sha256": "358adb37f881bf9fc64cf4cea24ce690792e958df702a705b2addda3295ad144"}
    experimental_model
    Colchicine and tritiated mebendazole binding to partially purified tubulin from Ascaris suum intestine and porcine brain
    exposure
    In vitro incubation of Ascaris suum with 10 micromolar mebendazole, with tubulin partially purified from the intestine
    limitations
    Measures the tissue mebendazole actually damages rather than embryonic tissue, and reaches the opposite conclusion about selectivity. Solubility prevented a precise association constant for mebendazole itself.
    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
    Nematode and pig
    plain_language
    In the gut of the worm, the drug wipes out the protein it is supposed to act on.
    primary_references
    [mbz-p7335116] Intestinal tubulin as possible target for the chemotherapeutic action of mebendazole in parasitic nematodes. (1981). https://pubmed.ncbi.nlm.nih.gov/7335116/ DOI: 10.1016/0166-6851(81)90064-5
    tissue_or_cell_type
    Nematode intestinal tubulin and porcine brain tubulin

    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 121–132

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Colchicine and tritiated mebendazole binding to partially purified tubulin from Ascaris suum intestine and porcine brain · source_derived_draft · unverified_draft

    ### mbz-intestinal-tubulin-is-the-target In vitro incubation of Ascaris suum with 10 micromolar mebendazole resulted in a complete loss of colchicine binding ability of extracts obtained from the parasite intestine, the colchicine binding receptor in those extracts was identified biochemically as tubulin, and that protein comprised approximately 0.8% of the soluble intestinal protein. 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: In the gut of the worm, the drug wipes out the protein it is supposed to act on. organism: Nematode and pig tissue_or_cell_type: Nematode intestinal tubulin and porcine brain tubulin experimental_model: Colchicine and tritiated mebendazole binding to partially purified tubulin from Ascaris suum intestine and porcine brain limitations: Measures the tissue mebendazole actually damages rather than embryonic tissue, and reaches the opposite conclusion about selectivity. Solubility prevented a precise association constant for mebendazole itself. exposure: In vitro incubation of Ascaris suum with 10 micromolar mebendazole, with tubulin partially purified from the intestine evidence_span: {"source_cache": "artifacts/mebendazole-research/7335116.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "358adb37f881bf9fc64cf4cea24ce690792e958df702a705b2addda3295ad144", "start_char": 0, "end_char": 1621, "text_sha256": "358adb37f881bf9fc64cf4cea24ce690792e958df702a705b2addda3295ad144"} [mbz-p7335116] Intestinal tubulin as possible target for the chemotherapeutic action of mebendazole in parasitic nematodes. (1981). https://pubmed.ncbi.nlm.nih.gov/7335116/ DOI: 10.1016/0166-6851(81)90064-5
    Complete structured claim and evidence
  17. The plasma areas under the curve for the major metabolites of mebendazole, methyl 5-(alpha-hydroxybenzyl)-2-benzimidazole carbamate and 2-amino-5-benzoylbenzimidazole, were about five times that found for mebendazole itself in patients on chronic therapy, which the authors suggest results from enterohepatic recycling of these polar metabolites, and since mebendazole is also highly plasma protein bound caution should be observed in patients with liver disease, while concentrations in tissue and cyst material collected at surgery ranged from 59.5 to 206.6 nanograms per gram wet weight.

    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/mebendazole-research/7094986.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5948d6b41d6cf4fa0b334caac010a171c49b81afd433f1eb704b4d07cfcb86cd", "start_char": 0, "end_char": 1256, "text_sha256": "5948d6b41d6cf4fa0b334caac010a171c49b81afd433f1eb704b4d07cfcb86cd"}
    experimental_model
    Plasma monitoring of mebendazole and its metabolites in twelve patients treated for cystic hydatid disease
    exposure
    10 milligrams per kilogram, with tissue sampled at surgery in two patients
    limitations
    Twelve patients with wide between-patient variation. The enterohepatic recycling explanation is the authors’ inference from the metabolite profile.
    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
    Human
    plain_language
    What circulates is mostly the breakdown products, and they hang around five times longer than the drug.
    primary_references
    [mbz-p7094986] Clinical pharmacokinetics of high dose mebendazole in patients treated for cystic hydatid disease. (1982). https://pubmed.ncbi.nlm.nih.gov/7094986/ DOI: 10.1007/bf00542462
    tissue_or_cell_type
    Plasma, tissue and cyst material

    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 446–457

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Plasma monitoring of mebendazole and its metabolites in twelve patients treated for cystic hydatid disease · source_derived_draft · unverified_draft

    ### mbz-metabolites-outlast-the-drug The plasma areas under the curve for the major metabolites of mebendazole, methyl 5-(alpha-hydroxybenzyl)-2-benzimidazole carbamate and 2-amino-5-benzoylbenzimidazole, were about five times that found for mebendazole itself in patients on chronic therapy, which the authors suggest results from enterohepatic recycling of these polar metabolites, and since mebendazole is also highly plasma protein bound caution should be observed in patients with liver disease, while concentrations in tissue and cyst material collected at surgery ranged from 59.5 to 206.6 nanograms per gram wet weight. 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: What circulates is mostly the breakdown products, and they hang around five times longer than the drug. organism: Human tissue_or_cell_type: Plasma, tissue and cyst material experimental_model: Plasma monitoring of mebendazole and its metabolites in twelve patients treated for cystic hydatid disease limitations: Twelve patients with wide between-patient variation. The enterohepatic recycling explanation is the authors’ inference from the metabolite profile. exposure: 10 milligrams per kilogram, with tissue sampled at surgery in two patients evidence_span: {"source_cache": "artifacts/mebendazole-research/7094986.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5948d6b41d6cf4fa0b334caac010a171c49b81afd433f1eb704b4d07cfcb86cd", "start_char": 0, "end_char": 1256, "text_sha256": "5948d6b41d6cf4fa0b334caac010a171c49b81afd433f1eb704b4d07cfcb86cd"} [mbz-p7094986] Clinical pharmacokinetics of high dose mebendazole in patients treated for cystic hydatid disease. (1982). https://pubmed.ncbi.nlm.nih.gov/7094986/ DOI: 10.1007/bf00542462
    Complete structured claim and evidence
  18. Two patients on high-dose oral mebendazole for echinococcosis developed severe reversible neutropenia apparently due to marrow suppression, with platelets and red cells also reversibly suppressed in one, high blood levels of 239 nanograms per millilitre in one patient may have caused the neutropenia and several toxic side effects as well as a striking shrinkage of that patient’s pulmonary and liver cysts, neutropenia with high-dose therapy may occur in up to 5% of patients, and the white cell count should be monitored frequently during the first several weeks.

    Mebendazole → Neutropenia from marrow suppression source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    biomarker_context Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/mebendazole-research/6842806.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "bdad328a3c1865dc991e7d6825c6da6e68742c580b2f8e0d455635ab57e69031", "start_char": 0, "end_char": 755, "text_sha256": "bdad328a3c1865dc991e7d6825c6da6e68742c580b2f8e0d455635ab57e69031"}
    experimental_model
    Case reports of two patients on high-dose oral mebendazole for echinococcosis
    exposure
    High-dose oral mebendazole, with a blood level of 239 nanograms per millilitre in one patient
    limitations
    Two cases. The estimate that neutropenia may occur in up to 5% of patients is the authors’ judgement, not a measured rate from these two.
    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
    Human
    plain_language
    The patient whose cysts shrank most was the patient whose marrow was suppressed.
    primary_references
    [mbz-p6842806] Severe, reversible neutropenia during high-dose mebendazole therapy for echinococcosis. (1983). https://pubmed.ncbi.nlm.nih.gov/6842806/ DOI: 10.1001/jama.1983.03330450059026
    tissue_or_cell_type
    Bone marrow
    trigger_kind
    biomarker_context Imported condition classification; unverified.

    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 628–639

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Case reports of two patients on high-dose oral mebendazole for echinococcosis · source_derived_draft · unverified_draft

    ### mbz-neutropenia-with-the-benefit Two patients on high-dose oral mebendazole for echinococcosis developed severe reversible neutropenia apparently due to marrow suppression, with platelets and red cells also reversibly suppressed in one, high blood levels of 239 nanograms per millilitre in one patient may have caused the neutropenia and several toxic side effects as well as a striking shrinkage of that patient’s pulmonary and liver cysts, neutropenia with high-dose therapy may occur in up to 5% of patients, and the white cell count should be monitored frequently during the first several weeks. Condition category: biomarker_context 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: The patient whose cysts shrank most was the patient whose marrow was suppressed. organism: Human tissue_or_cell_type: Bone marrow experimental_model: Case reports of two patients on high-dose oral mebendazole for echinococcosis limitations: Two cases. The estimate that neutropenia may occur in up to 5% of patients is the authors’ judgement, not a measured rate from these two. exposure: High-dose oral mebendazole, with a blood level of 239 nanograms per millilitre in one patient evidence_span: {"source_cache": "artifacts/mebendazole-research/6842806.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "bdad328a3c1865dc991e7d6825c6da6e68742c580b2f8e0d455635ab57e69031", "start_char": 0, "end_char": 755, "text_sha256": "bdad328a3c1865dc991e7d6825c6da6e68742c580b2f8e0d455635ab57e69031"} [mbz-p6842806] Severe, reversible neutropenia during high-dose mebendazole therapy for echinococcosis. (1983). https://pubmed.ncbi.nlm.nih.gov/6842806/ DOI: 10.1001/jama.1983.03330450059026
    Complete structured claim and evidence
  19. Among 192 pregnancies exposed to mebendazole and followed prospectively, 71.5% with first-trimester exposure, there was no increase in the rate of major malformations against a matched control group counselled for non-teratogenic exposure, 3.3% against 1.7%, though there was a higher rate of elective termination in the exposed group at 11.5% against 1.6%, and the authors conclude that mebendazole does not represent a major teratogenic risk in humans at the doses commonly used for pinworm.

    Mebendazole → Rate of major congenital malformation source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/mebendazole-research/12548230.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "08e6e832094453e69ff88f5daeb82e145cd70180f68658be2c0c30b686fd2fad", "start_char": 0, "end_char": 1183, "text_sha256": "08e6e832094453e69ff88f5daeb82e145cd70180f68658be2c0c30b686fd2fad"}
    experimental_model
    Prospective controlled cohort of 192 pregnancies followed by the Israeli Teratogen Information Service
    exposure
    Mebendazole exposure in pregnancy, 71.5% in the first trimester, against a matched non-teratogenic control group
    limitations
    A prospective cohort of 192 pregnancies, which can exclude a large risk but not a small one, at pinworm doses rather than the high doses used for echinococcosis or oncology.
    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
    Human
    plain_language
    In nearly two hundred pregnancies there was no excess of birth defects, though many more of these pregnancies were ended by choice.
    primary_references
    [mbz-p12548230] Pregnancy outcome after gestational exposure to mebendazole: a prospective controlled cohort study. (2003). https://pubmed.ncbi.nlm.nih.gov/12548230/ DOI: 10.1067/mob.2003.79
    tissue_or_cell_type
    Pregnancy outcome

    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 615–626

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Prospective controlled cohort of 192 pregnancies followed by the Israeli Teratogen Information Service · source_derived_draft · unverified_draft

    ### mbz-no-major-teratogenic-signal Among 192 pregnancies exposed to mebendazole and followed prospectively, 71.5% with first-trimester exposure, there was no increase in the rate of major malformations against a matched control group counselled for non-teratogenic exposure, 3.3% against 1.7%, though there was a higher rate of elective termination in the exposed group at 11.5% against 1.6%, and the authors conclude that mebendazole does not represent a major teratogenic risk in humans at the doses commonly used for pinworm. 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: In nearly two hundred pregnancies there was no excess of birth defects, though many more of these pregnancies were ended by choice. organism: Human tissue_or_cell_type: Pregnancy outcome experimental_model: Prospective controlled cohort of 192 pregnancies followed by the Israeli Teratogen Information Service limitations: A prospective cohort of 192 pregnancies, which can exclude a large risk but not a small one, at pinworm doses rather than the high doses used for echinococcosis or oncology. exposure: Mebendazole exposure in pregnancy, 71.5% in the first trimester, against a matched non-teratogenic control group evidence_span: {"source_cache": "artifacts/mebendazole-research/12548230.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "08e6e832094453e69ff88f5daeb82e145cd70180f68658be2c0c30b686fd2fad", "start_char": 0, "end_char": 1183, "text_sha256": "08e6e832094453e69ff88f5daeb82e145cd70180f68658be2c0c30b686fd2fad"} [mbz-p12548230] Pregnancy outcome after gestational exposure to mebendazole: a prospective controlled cohort study. (2003). https://pubmed.ncbi.nlm.nih.gov/12548230/ DOI: 10.1067/mob.2003.79
    Complete structured claim and evidence
  20. After 6 and 9 hours of treatment the characteristic changes in Ascaris suum intestinal cells were absence of secretory granules in the terminal web, accumulation of secretory granules in the Golgi region, formation of autophagic vacuoles in the apical cell part, and loss of glycogen, and cytochemistry revealed that the accumulated granules in the Golgi area contained glycoproteins or polysaccharides.

    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/mebendazole-research/1117352.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e7cf1916636fe33e5b6ce6c22d84d2550adfd392b30b1b940f4c794b3069066f", "start_char": 0, "end_char": 1554, "text_sha256": "e7cf1916636fe33e5b6ce6c22d84d2550adfd392b30b1b940f4c794b3069066f"}
    experimental_model
    Ultrastructural and cytochemical examination of Ascaris suum intestine from pigs fed medicated food
    exposure
    Mebendazole at 30 parts per million in pig feed, with parasites collected 6, 9, 15 and 24 hours after feeding began
    limitations
    The earliest mechanistic record here and still the clearest picture of the consequence. It predates the tubulin work and describes exactly what blocking microtubule-based transport would produce.
    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
    Nematode
    plain_language
    The cargo piles up where it is made and never arrives where it is needed.
    primary_references
    [mbz-p1117352] Ultrastructural changes in Ascaris suum intestine after mebendazole treatment in vivo. (1975). https://pubmed.ncbi.nlm.nih.gov/1117352/ DOI: 10.2307/3279120
    tissue_or_cell_type
    Ascaris suum intestine

    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 186–197

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Ultrastructural and cytochemical examination of Ascaris suum intestine from pigs fed medicated food · source_derived_draft · unverified_draft

    ### mbz-secretory-transport-fails After 6 and 9 hours of treatment the characteristic changes in Ascaris suum intestinal cells were absence of secretory granules in the terminal web, accumulation of secretory granules in the Golgi region, formation of autophagic vacuoles in the apical cell part, and loss of glycogen, and cytochemistry revealed that the accumulated granules in the Golgi area contained glycoproteins or polysaccharides. 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: The cargo piles up where it is made and never arrives where it is needed. organism: Nematode tissue_or_cell_type: Ascaris suum intestine experimental_model: Ultrastructural and cytochemical examination of Ascaris suum intestine from pigs fed medicated food limitations: The earliest mechanistic record here and still the clearest picture of the consequence. It predates the tubulin work and describes exactly what blocking microtubule-based transport would produce. exposure: Mebendazole at 30 parts per million in pig feed, with parasites collected 6, 9, 15 and 24 hours after feeding began evidence_span: {"source_cache": "artifacts/mebendazole-research/1117352.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e7cf1916636fe33e5b6ce6c22d84d2550adfd392b30b1b940f4c794b3069066f", "start_char": 0, "end_char": 1554, "text_sha256": "e7cf1916636fe33e5b6ce6c22d84d2550adfd392b30b1b940f4c794b3069066f"} [mbz-p1117352] Ultrastructural changes in Ascaris suum intestine after mebendazole treatment in vivo. (1975). https://pubmed.ncbi.nlm.nih.gov/1117352/ DOI: 10.2307/3279120
    Complete structured claim and evidence
  21. The inhibition constants of mebendazole and fenbendazole for Ascaris suum embryonic tubulin were 1.9 x 10-8 and 6.5 x 10-8 molar while those for bovine brain tubulin were 7.3 x 10-6 and 1.7 x 10-5 molar, values 250 to 400 times greater, so that differential binding affinities between nematode and mammalian tubulin may explain the selective toxicity.

    Mebendazole → Nematode beta-tubulin source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/mebendazole-research/7388055.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5613d7fb281b4fd39b17bfdbafaf0ea823fb63b928048a9dd112fb71bf4cd2b7", "start_char": 0, "end_char": 1209, "text_sha256": "5613d7fb281b4fd39b17bfdbafaf0ea823fb63b928048a9dd112fb71bf4cd2b7"}
    experimental_model
    Inhibition of tritiated colchicine binding to cytosolic tubulin from 8-day Ascaris suum embryos and from bovine brain
    exposure
    Mebendazole and fenbendazole compared on the two tubulins in the same assay
    limitations
    The founding selectivity result. It measures embryonic tubulin; the study in this collection that measured intestinal tubulin found a far smaller difference.
    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
    Nematode and cattle
    plain_language
    The drug grips worm tubulin hundreds of times more tightly than ours, which is the usual explanation for why it is safe.
    primary_references
    [mbz-p7388055] Interaction of anthelmintic benzimidazoles with Ascaris suum embryonic tubulin. (1980). https://pubmed.ncbi.nlm.nih.gov/7388055/ DOI: 10.1016/0304-4165(80)90431-6
    tissue_or_cell_type
    Embryonic nematode tubulin and bovine brain tubulin

    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 95–106

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Inhibition of tritiated colchicine binding to cytosolic tubulin from 8-day Ascaris suum embryos and from bovine brain · source_derived_draft · unverified_draft

    ### mbz-selectivity-250-fold The inhibition constants of mebendazole and fenbendazole for Ascaris suum embryonic tubulin were 1.9 x 10-8 and 6.5 x 10-8 molar while those for bovine brain tubulin were 7.3 x 10-6 and 1.7 x 10-5 molar, values 250 to 400 times greater, so that differential binding affinities between nematode and mammalian tubulin may explain the selective toxicity. 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: The drug grips worm tubulin hundreds of times more tightly than ours, which is the usual explanation for why it is safe. organism: Nematode and cattle tissue_or_cell_type: Embryonic nematode tubulin and bovine brain tubulin experimental_model: Inhibition of tritiated colchicine binding to cytosolic tubulin from 8-day Ascaris suum embryos and from bovine brain limitations: The founding selectivity result. It measures embryonic tubulin; the study in this collection that measured intestinal tubulin found a far smaller difference. exposure: Mebendazole and fenbendazole compared on the two tubulins in the same assay evidence_span: {"source_cache": "artifacts/mebendazole-research/7388055.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5613d7fb281b4fd39b17bfdbafaf0ea823fb63b928048a9dd112fb71bf4cd2b7", "start_char": 0, "end_char": 1209, "text_sha256": "5613d7fb281b4fd39b17bfdbafaf0ea823fb63b928048a9dd112fb71bf4cd2b7"} [mbz-p7388055] Interaction of anthelmintic benzimidazoles with Ascaris suum embryonic tubulin. (1980). https://pubmed.ncbi.nlm.nih.gov/7388055/ DOI: 10.1016/0304-4165(80)90431-6
    Complete structured claim and evidence
  22. Mebendazole inhibited colchicine binding to partially purified Ascaris suum intestinal tubulin competitively with an inhibition constant of 4.22 x 10-6 molar and inhibited colchicine binding to porcine brain tubulin competitively with an inhibition constant of 8.0 x 10-6 molar, so that in view of the small difference in drug binding abilities it remains unclear whether the selective toxicity can be solely explained by interference with the parasite microtubular system, and the authors suggest that differential pharmacokinetic behaviour between parasite and host may be the essential basis for the difference in susceptibility.

    Mebendazole → Nematode beta-tubulin source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/mebendazole-research/7335116.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "358adb37f881bf9fc64cf4cea24ce690792e958df702a705b2addda3295ad144", "start_char": 0, "end_char": 1621, "text_sha256": "358adb37f881bf9fc64cf4cea24ce690792e958df702a705b2addda3295ad144"}
    experimental_model
    Colchicine and tritiated mebendazole binding to partially purified tubulin from Ascaris suum intestine and porcine brain
    exposure
    In vitro incubation of Ascaris suum with 10 micromolar mebendazole, with tubulin partially purified from the intestine
    limitations
    Measures the tissue mebendazole actually damages rather than embryonic tissue, and reaches the opposite conclusion about selectivity. Solubility prevented a precise association constant for mebendazole itself.
    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
    Nematode and pig
    plain_language
    Measured in the worm’s gut rather than its embryos, the drug is only about twice as selective, which is not enough to explain its safety.
    primary_references
    [mbz-p7335116] Intestinal tubulin as possible target for the chemotherapeutic action of mebendazole in parasitic nematodes. (1981). https://pubmed.ncbi.nlm.nih.gov/7335116/ DOI: 10.1016/0166-6851(81)90064-5
    tissue_or_cell_type
    Nematode intestinal tubulin and porcine brain tubulin

    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 134–145

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Colchicine and tritiated mebendazole binding to partially purified tubulin from Ascaris suum intestine and porcine brain · source_derived_draft · unverified_draft

    ### mbz-selectivity-only-twofold Mebendazole inhibited colchicine binding to partially purified Ascaris suum intestinal tubulin competitively with an inhibition constant of 4.22 x 10-6 molar and inhibited colchicine binding to porcine brain tubulin competitively with an inhibition constant of 8.0 x 10-6 molar, so that in view of the small difference in drug binding abilities it remains unclear whether the selective toxicity can be solely explained by interference with the parasite microtubular system, and the authors suggest that differential pharmacokinetic behaviour between parasite and host may be the essential basis for the difference in susceptibility. 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: Measured in the worm’s gut rather than its embryos, the drug is only about twice as selective, which is not enough to explain its safety. organism: Nematode and pig tissue_or_cell_type: Nematode intestinal tubulin and porcine brain tubulin experimental_model: Colchicine and tritiated mebendazole binding to partially purified tubulin from Ascaris suum intestine and porcine brain limitations: Measures the tissue mebendazole actually damages rather than embryonic tissue, and reaches the opposite conclusion about selectivity. Solubility prevented a precise association constant for mebendazole itself. exposure: In vitro incubation of Ascaris suum with 10 micromolar mebendazole, with tubulin partially purified from the intestine evidence_span: {"source_cache": "artifacts/mebendazole-research/7335116.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "358adb37f881bf9fc64cf4cea24ce690792e958df702a705b2addda3295ad144", "start_char": 0, "end_char": 1621, "text_sha256": "358adb37f881bf9fc64cf4cea24ce690792e958df702a705b2addda3295ad144"} [mbz-p7335116] Intestinal tubulin as possible target for the chemotherapeutic action of mebendazole in parasitic nematodes. (1981). https://pubmed.ncbi.nlm.nih.gov/7335116/ DOI: 10.1016/0166-6851(81)90064-5
    Complete structured claim and evidence
  23. Association of tritiated mebendazole to Haemonchus contortus tubulin was rapid at 2.6 x 10(5) per molar per minute but dissociation was slow at 1.58 x 10(-3) per minute, giving a kinetic affinity constant of 1.6 x 10(8) per molar against an equilibrium estimate of 5.3 x 10(6) per molar, and the slow dissociation from nematode tubulin, which contrasts with rapid dissociation from mammalian tubulin, supports the view that selective toxicity results from a difference between the affinities of mammalian and nematode tubulins.

    Mebendazole → Nematode beta-tubulin source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/mebendazole-research/1459788.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "b34533a3360a1b113dca959ed53c0c5cf9f7efe61403c2b498146c90e7085bb1", "start_char": 0, "end_char": 1160, "text_sha256": "b34533a3360a1b113dca959ed53c0c5cf9f7efe61403c2b498146c90e7085bb1"}
    experimental_model
    Kinetic and equilibrium binding of tritiated mebendazole to tubulin from third-stage Haemonchus contortus larvae
    exposure
    Association and dissociation rate constants measured in partially purified preparations and crude cytosol
    limitations
    Separates the rate of binding from the rate of release, which an equilibrium measurement cannot. The kinetic and equilibrium constants differ about thirtyfold and the authors argue for the kinetic value.
    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
    Nematode
    plain_language
    It binds worm tubulin quickly and then stays there; on ours it falls straight off again.
    primary_references
    [mbz-p1459788] The kinetics of mebendazole binding to Haemonchus contortus tubulin. (1992). https://pubmed.ncbi.nlm.nih.gov/1459788/ DOI: 10.1016/0020-7519(92)90051-l
    tissue_or_cell_type
    Larval nematode tubulin

    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 147–158

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Kinetic and equilibrium binding of tritiated mebendazole to tubulin from third-stage Haemonchus contortus larvae · source_derived_draft · unverified_draft

    ### mbz-slow-release-is-the-point Association of tritiated mebendazole to Haemonchus contortus tubulin was rapid at 2.6 x 10(5) per molar per minute but dissociation was slow at 1.58 x 10(-3) per minute, giving a kinetic affinity constant of 1.6 x 10(8) per molar against an equilibrium estimate of 5.3 x 10(6) per molar, and the slow dissociation from nematode tubulin, which contrasts with rapid dissociation from mammalian tubulin, supports the view that selective toxicity results from a difference between the affinities of mammalian and nematode tubulins. 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 binds worm tubulin quickly and then stays there; on ours it falls straight off again. organism: Nematode tissue_or_cell_type: Larval nematode tubulin experimental_model: Kinetic and equilibrium binding of tritiated mebendazole to tubulin from third-stage Haemonchus contortus larvae limitations: Separates the rate of binding from the rate of release, which an equilibrium measurement cannot. The kinetic and equilibrium constants differ about thirtyfold and the authors argue for the kinetic value. exposure: Association and dissociation rate constants measured in partially purified preparations and crude cytosol evidence_span: {"source_cache": "artifacts/mebendazole-research/1459788.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "b34533a3360a1b113dca959ed53c0c5cf9f7efe61403c2b498146c90e7085bb1", "start_char": 0, "end_char": 1160, "text_sha256": "b34533a3360a1b113dca959ed53c0c5cf9f7efe61403c2b498146c90e7085bb1"} [mbz-p1459788] The kinetics of mebendazole binding to Haemonchus contortus tubulin. (1992). https://pubmed.ncbi.nlm.nih.gov/1459788/ DOI: 10.1016/0020-7519(92)90051-l
    Complete structured claim and evidence
  24. Tritiated benzimidazole carbamate binding to mammalian brain tubulin was markedly greater at 4 degrees than at 37 degrees for all ligands, association constants and maximum binding were temperature dependent, and the first order dissociation rate constant of the mebendazole-tubulin complex was reduced by two orders of magnitude at 4 degrees compared with 37 degrees, suggesting that temperature-induced conformational changes in the tubulin dimer influence the ability to form a stable complex; this is unlike the interaction observed for parasitic nematodes where optimum binding occurs at 37 degrees and results in a pseudo-irreversible complex.

    Mebendazole → Mammalian brain tubulin source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/mebendazole-research/1554382.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "70fec1c41b747eaae6d4a47ad1075a49828ee942f7935b85eb0f51416cd57c37", "start_char": 0, "end_char": 1495, "text_sha256": "70fec1c41b747eaae6d4a47ad1075a49828ee942f7935b85eb0f51416cd57c37"}
    experimental_model
    Tritiated benzimidazole carbamate binding to mammalian brain tubulin measured at 4 and 37 degrees
    exposure
    Mebendazole, oxibendazole, oxfendazole and carbendazim binding measured across temperature
    limitations
    The temperature arm is what makes this decisive: it explains why the same drug behaves differently on host and parasite tubulin at body temperature. Binding was measured on brain tubulin, not on tubulin from a target tissue.
    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
    Mammal
    plain_language
    At body temperature the drug slides off our tubulin and locks onto the worm’s; cool ours down and it sticks to that too.
    primary_references
    [mbz-p1554382] Binding of [3H]benzimidazole carbamates to mammalian brain tubulin and the mechanism of selective toxicity of the benzimidazole anthelmintics. (1992). https://pubmed.ncbi.nlm.nih.gov/1554382/ DOI: 10.1016/0006-2952(92)90617-r
    tissue_or_cell_type
    Brain tubulin

    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 160–171

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Tritiated benzimidazole carbamate binding to mammalian brain tubulin measured at 4 and 37 degrees · source_derived_draft · unverified_draft

    ### mbz-temperature-decides Tritiated benzimidazole carbamate binding to mammalian brain tubulin was markedly greater at 4 degrees than at 37 degrees for all ligands, association constants and maximum binding were temperature dependent, and the first order dissociation rate constant of the mebendazole-tubulin complex was reduced by two orders of magnitude at 4 degrees compared with 37 degrees, suggesting that temperature-induced conformational changes in the tubulin dimer influence the ability to form a stable complex; this is unlike the interaction observed for parasitic nematodes where optimum binding occurs at 37 degrees and results in a pseudo-irreversible complex. 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: At body temperature the drug slides off our tubulin and locks onto the worm’s; cool ours down and it sticks to that too. organism: Mammal tissue_or_cell_type: Brain tubulin experimental_model: Tritiated benzimidazole carbamate binding to mammalian brain tubulin measured at 4 and 37 degrees limitations: The temperature arm is what makes this decisive: it explains why the same drug behaves differently on host and parasite tubulin at body temperature. Binding was measured on brain tubulin, not on tubulin from a target tissue. exposure: Mebendazole, oxibendazole, oxfendazole and carbendazim binding measured across temperature evidence_span: {"source_cache": "artifacts/mebendazole-research/1554382.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "70fec1c41b747eaae6d4a47ad1075a49828ee942f7935b85eb0f51416cd57c37", "start_char": 0, "end_char": 1495, "text_sha256": "70fec1c41b747eaae6d4a47ad1075a49828ee942f7935b85eb0f51416cd57c37"} [mbz-p1554382] Binding of [3H]benzimidazole carbamates to mammalian brain tubulin and the mechanism of selective toxicity of the benzimidazole anthelmintics. (1992). https://pubmed.ncbi.nlm.nih.gov/1554382/ DOI: 10.1016/0006-2952(92)90617-r
    Complete structured claim and evidence
  25. Across thirty-two methyl benzimidazol-2-yl carbamates, the size or some colinear physico-chemical characteristic of the substituent in the 5 or 6 position had a profound effect on potency against mammalian tubulin polymerisation, and branching with or without a commensurate increase in polarity adjacent to the benzimidazole ring resulted in a loss of activity.

    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/mebendazole-research/3985991.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9b881308a6051bd89e2f8323670dd08a8d5e50cf06c7705724ece611440643e5", "start_char": 0, "end_char": 680, "text_sha256": "9b881308a6051bd89e2f8323670dd08a8d5e50cf06c7705724ece611440643e5"}
    experimental_model
    Structure-activity study of thirty-two methyl benzimidazol-2-yl carbamates against mammalian tubulin polymerisation
    exposure
    Systematic variation of the 5(6)-position substituent
    limitations
    Quantitative structure-activity modelling on the off-target protein. It says which part of the molecule matters, not which target matters.
    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
    Mammal
    plain_language
    One position on the ring decides how well the whole family works.
    primary_references
    [mbz-p3985991] Structure-activity relationships of benzimidazole carbamates as inhibitors of mammalian tubulin, in vitro. (1985). https://pubmed.ncbi.nlm.nih.gov/3985991/ DOI: 10.1016/0006-2952(85)90611-2
    tissue_or_cell_type
    Tubulin

    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 225–236

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Structure-activity study of thirty-two methyl benzimidazol-2-yl carbamates against mammalian tubulin polymerisation · source_derived_draft · unverified_draft

    ### mbz-the-5-substituent-governs Across thirty-two methyl benzimidazol-2-yl carbamates, the size or some colinear physico-chemical characteristic of the substituent in the 5 or 6 position had a profound effect on potency against mammalian tubulin polymerisation, and branching with or without a commensurate increase in polarity adjacent to the benzimidazole ring resulted in a loss of activity. 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: One position on the ring decides how well the whole family works. organism: Mammal tissue_or_cell_type: Tubulin experimental_model: Structure-activity study of thirty-two methyl benzimidazol-2-yl carbamates against mammalian tubulin polymerisation limitations: Quantitative structure-activity modelling on the off-target protein. It says which part of the molecule matters, not which target matters. exposure: Systematic variation of the 5(6)-position substituent evidence_span: {"source_cache": "artifacts/mebendazole-research/3985991.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9b881308a6051bd89e2f8323670dd08a8d5e50cf06c7705724ece611440643e5", "start_char": 0, "end_char": 680, "text_sha256": "9b881308a6051bd89e2f8323670dd08a8d5e50cf06c7705724ece611440643e5"} [mbz-p3985991] Structure-activity relationships of benzimidazole carbamates as inhibitors of mammalian tubulin, in vitro. (1985). https://pubmed.ncbi.nlm.nih.gov/3985991/ DOI: 10.1016/0006-2952(85)90611-2
    Complete structured claim and evidence
  26. The effective concentrations of mebendazole to inhibit GL261 glioblastoma cell viability, microtubule polymerization and metaphase arrest were very similar, and using mebendazole as a seed for the NCI COMPARE program revealed that the top-scoring drugs were highly enriched in microtubule-targeting drugs, indicating that the cell toxicity of mebendazole is indeed caused by inhibiting microtubule formation.

    Mebendazole → Mitotic arrest source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/mebendazole-research/28386621.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "20ef610d6b4a341f8a0a3f731bbea5477badbee517062c303bbf1075f3a29865", "start_char": 0, "end_char": 1788, "text_sha256": "20ef610d6b4a341f8a0a3f731bbea5477badbee517062c303bbf1075f3a29865"}
    experimental_model
    Concentration-matched comparison of viability, microtubule polymerisation and metaphase arrest, with NCI COMPARE analysis and a head-to-head animal comparison against vincristine
    exposure
    Mebendazole against vincristine close to its maximum tolerated dose in orthotopic GL261 tumours
    limitations
    Tests whether the anticancer effect is the microtubule effect by matching concentrations across three assays, which most repurposing studies do not do.
    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
    The concentration that kills the cell is the concentration that blocks its microtubules, so it is the same mechanism.
    primary_references
    [mbz-p28386621] Repurposing Mebendazole as a Replacement for Vincristine for the Treatment of Brain Tumors. (2017). https://pubmed.ncbi.nlm.nih.gov/28386621/ DOI: 10.2119/molmed.2017.00011
    tissue_or_cell_type
    Glioblastoma

    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 498–509

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Concentration-matched comparison of viability, microtubule polymerisation and metaphase arrest, with NCI COMPARE analysis and a head-to-head animal comparison against vincristine · source_derived_draft · unverified_draft

    ### mbz-the-anticancer-effect-is-tubulin The effective concentrations of mebendazole to inhibit GL261 glioblastoma cell viability, microtubule polymerization and metaphase arrest were very similar, and using mebendazole as a seed for the NCI COMPARE program revealed that the top-scoring drugs were highly enriched in microtubule-targeting drugs, indicating that the cell toxicity of mebendazole is indeed caused by inhibiting microtubule formation. 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: The concentration that kills the cell is the concentration that blocks its microtubules, so it is the same mechanism. organism: Mouse tissue_or_cell_type: Glioblastoma experimental_model: Concentration-matched comparison of viability, microtubule polymerisation and metaphase arrest, with NCI COMPARE analysis and a head-to-head animal comparison against vincristine limitations: Tests whether the anticancer effect is the microtubule effect by matching concentrations across three assays, which most repurposing studies do not do. exposure: Mebendazole against vincristine close to its maximum tolerated dose in orthotopic GL261 tumours evidence_span: {"source_cache": "artifacts/mebendazole-research/28386621.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "20ef610d6b4a341f8a0a3f731bbea5477badbee517062c303bbf1075f3a29865", "start_char": 0, "end_char": 1788, "text_sha256": "20ef610d6b4a341f8a0a3f731bbea5477badbee517062c303bbf1075f3a29865"} [mbz-p28386621] Repurposing Mebendazole as a Replacement for Vincristine for the Treatment of Brain Tumors. (2017). https://pubmed.ncbi.nlm.nih.gov/28386621/ DOI: 10.2119/molmed.2017.00011
    Complete structured claim and evidence
  27. Degenerative changes were very pronounced after 15 and 24 hours and involved almost the entire cytoplasm, microvilli were decreased in number and appeared swollen in the majority of absorptive cells with some cells completely devoid of microvilli, and acid phosphatase activity moved from microvilli, lysosomes and Golgi apparatus into numerous autophagic vacuoles while the accumulated secretory granules remained unstained.

    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/mebendazole-research/1117352.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e7cf1916636fe33e5b6ce6c22d84d2550adfd392b30b1b940f4c794b3069066f", "start_char": 0, "end_char": 1554, "text_sha256": "e7cf1916636fe33e5b6ce6c22d84d2550adfd392b30b1b940f4c794b3069066f"}
    experimental_model
    Ultrastructural and cytochemical examination of Ascaris suum intestine from pigs fed medicated food
    exposure
    Mebendazole at 30 parts per million in pig feed, with parasites collected 6, 9, 15 and 24 hours after feeding began
    limitations
    The earliest mechanistic record here and still the clearest picture of the consequence. It predates the tubulin work and describes exactly what blocking microtubule-based transport would produce.
    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
    Nematode
    plain_language
    Within a day the absorbing surface of the worm’s gut is destroyed.
    primary_references
    [mbz-p1117352] Ultrastructural changes in Ascaris suum intestine after mebendazole treatment in vivo. (1975). https://pubmed.ncbi.nlm.nih.gov/1117352/ DOI: 10.2307/3279120
    tissue_or_cell_type
    Ascaris suum intestine

    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 199–210

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Ultrastructural and cytochemical examination of Ascaris suum intestine from pigs fed medicated food · source_derived_draft · unverified_draft

    ### mbz-the-gut-cell-dies Degenerative changes were very pronounced after 15 and 24 hours and involved almost the entire cytoplasm, microvilli were decreased in number and appeared swollen in the majority of absorptive cells with some cells completely devoid of microvilli, and acid phosphatase activity moved from microvilli, lysosomes and Golgi apparatus into numerous autophagic vacuoles while the accumulated secretory granules remained unstained. 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: Within a day the absorbing surface of the worm’s gut is destroyed. organism: Nematode tissue_or_cell_type: Ascaris suum intestine experimental_model: Ultrastructural and cytochemical examination of Ascaris suum intestine from pigs fed medicated food limitations: The earliest mechanistic record here and still the clearest picture of the consequence. It predates the tubulin work and describes exactly what blocking microtubule-based transport would produce. exposure: Mebendazole at 30 parts per million in pig feed, with parasites collected 6, 9, 15 and 24 hours after feeding began evidence_span: {"source_cache": "artifacts/mebendazole-research/1117352.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e7cf1916636fe33e5b6ce6c22d84d2550adfd392b30b1b940f4c794b3069066f", "start_char": 0, "end_char": 1554, "text_sha256": "e7cf1916636fe33e5b6ce6c22d84d2550adfd392b30b1b940f4c794b3069066f"} [mbz-p1117352] Ultrastructural changes in Ascaris suum intestine after mebendazole treatment in vivo. (1975). https://pubmed.ncbi.nlm.nih.gov/1117352/ DOI: 10.2307/3279120
    Complete structured claim and evidence
  28. Kaplan-Meier analysis showed a 21-month median overall survival with 41.7% of patients alive at 2 years and 25% at 3 and 4 years, and median progression-free survival from diagnosis was 13.1 months for 17 patients taking more than one month of mebendazole against 9.2 months for 7 patients who received less than one month, with the authors concluding that further studies are needed to determine efficacy in malignant glioma.

    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/mebendazole-research/33506200.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "ab5f2c1d14ccb7fa9f690201326bdbfcab3e07758bc78b76ff9adec2ca774ec6", "start_char": 0, "end_char": 1712, "text_sha256": "ab5f2c1d14ccb7fa9f690201326bdbfcab3e07758bc78b76ff9adec2ca774ec6"}
    experimental_model
    Single-centre dose-escalation and safety study in 24 patients with newly diagnosed high-grade glioma
    exposure
    Oral mebendazole at 25, 50, 100 and 200 milligrams per kilogram per day with adjuvant temozolomide, with trough plasma levels at 4, 8 and 16 weeks
    limitations
    The only human oncology record here. It is a single-arm dose-escalation and safety study without a control group, so the survival figures cannot be read as efficacy.
    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
    Human
    plain_language
    Patients who stayed on it longer did better, but there was no control group and staying on a drug longer is itself a sign of doing well.
    primary_references
    [mbz-p33506200] Mebendazole and temozolomide in patients with newly diagnosed high-grade gliomas: results of a phase 1 clinical trial. (2021). https://pubmed.ncbi.nlm.nih.gov/33506200/ DOI: 10.1093/noajnl/vdaa154
    tissue_or_cell_type
    Brain

    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 589–600

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Single-centre dose-escalation and safety study in 24 patients with newly diagnosed high-grade glioma · source_derived_draft · unverified_draft

    ### mbz-uncontrolled-survival-figures Kaplan-Meier analysis showed a 21-month median overall survival with 41.7% of patients alive at 2 years and 25% at 3 and 4 years, and median progression-free survival from diagnosis was 13.1 months for 17 patients taking more than one month of mebendazole against 9.2 months for 7 patients who received less than one month, with the authors concluding that further studies are needed to determine efficacy in malignant glioma. 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: Patients who stayed on it longer did better, but there was no control group and staying on a drug longer is itself a sign of doing well. organism: Human tissue_or_cell_type: Brain experimental_model: Single-centre dose-escalation and safety study in 24 patients with newly diagnosed high-grade glioma limitations: The only human oncology record here. It is a single-arm dose-escalation and safety study without a control group, so the survival figures cannot be read as efficacy. exposure: Oral mebendazole at 25, 50, 100 and 200 milligrams per kilogram per day with adjuvant temozolomide, with trough plasma levels at 4, 8 and 16 weeks evidence_span: {"source_cache": "artifacts/mebendazole-research/33506200.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "ab5f2c1d14ccb7fa9f690201326bdbfcab3e07758bc78b76ff9adec2ca774ec6", "start_char": 0, "end_char": 1712, "text_sha256": "ab5f2c1d14ccb7fa9f690201326bdbfcab3e07758bc78b76ff9adec2ca774ec6"} [mbz-p33506200] Mebendazole and temozolomide in patients with newly diagnosed high-grade gliomas: results of a phase 1 clinical trial. (2021). https://pubmed.ncbi.nlm.nih.gov/33506200/ DOI: 10.1093/noajnl/vdaa154
    Complete structured claim and evidence
  29. In twelve patients given 10 milligrams per kilogram for cystic hydatid disease the plasma concentration-time profiles differed considerably, with elimination half-lives from 2.8 to 9.0 hours, time to peak from 1.5 to 7.25 hours and peak concentrations from 17.5 to 500 nanograms per millilitre, and the mean peak after an initial dose of 69.5 nanograms per millilitre was lower than during chronic therapy at 137.4 nanograms per millilitre.

    Mebendazole → Plasma concentration of mebendazole source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/mebendazole-research/7094986.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5948d6b41d6cf4fa0b334caac010a171c49b81afd433f1eb704b4d07cfcb86cd", "start_char": 0, "end_char": 1256, "text_sha256": "5948d6b41d6cf4fa0b334caac010a171c49b81afd433f1eb704b4d07cfcb86cd"}
    experimental_model
    Plasma monitoring of mebendazole and its metabolites in twelve patients treated for cystic hydatid disease
    exposure
    10 milligrams per kilogram, with tissue sampled at surgery in two patients
    limitations
    Twelve patients with wide between-patient variation. The enterohepatic recycling explanation is the authors’ inference from the metabolite profile.
    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
    Human
    plain_language
    The same dose gives one patient thirty times the blood level of another.
    primary_references
    [mbz-p7094986] Clinical pharmacokinetics of high dose mebendazole in patients treated for cystic hydatid disease. (1982). https://pubmed.ncbi.nlm.nih.gov/7094986/ DOI: 10.1007/bf00542462
    tissue_or_cell_type
    Plasma, tissue and cyst material

    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 433–444

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Plasma monitoring of mebendazole and its metabolites in twelve patients treated for cystic hydatid disease · source_derived_draft · unverified_draft

    ### mbz-variation-is-enormous In twelve patients given 10 milligrams per kilogram for cystic hydatid disease the plasma concentration-time profiles differed considerably, with elimination half-lives from 2.8 to 9.0 hours, time to peak from 1.5 to 7.25 hours and peak concentrations from 17.5 to 500 nanograms per millilitre, and the mean peak after an initial dose of 69.5 nanograms per millilitre was lower than during chronic therapy at 137.4 nanograms per millilitre. 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: The same dose gives one patient thirty times the blood level of another. organism: Human tissue_or_cell_type: Plasma, tissue and cyst material experimental_model: Plasma monitoring of mebendazole and its metabolites in twelve patients treated for cystic hydatid disease limitations: Twelve patients with wide between-patient variation. The enterohepatic recycling explanation is the authors’ inference from the metabolite profile. exposure: 10 milligrams per kilogram, with tissue sampled at surgery in two patients evidence_span: {"source_cache": "artifacts/mebendazole-research/7094986.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5948d6b41d6cf4fa0b334caac010a171c49b81afd433f1eb704b4d07cfcb86cd", "start_char": 0, "end_char": 1256, "text_sha256": "5948d6b41d6cf4fa0b334caac010a171c49b81afd433f1eb704b4d07cfcb86cd"} [mbz-p7094986] Clinical pharmacokinetics of high dose mebendazole in patients treated for cystic hydatid disease. (1982). https://pubmed.ncbi.nlm.nih.gov/7094986/ DOI: 10.1007/bf00542462
    Complete structured claim and evidence
  30. 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.

    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. In eight patients, cimetidine lowered the one-hour specific activity in the aminopyrine breath test and increased the maximum serum concentration of mebendazole, with a significant correlation between the breath test activity and the highest mebendazole concentration both before and after cimetidine, and combined administration resulted in the complete resolution of previously unresponsive hydatid cysts.

    Cimetidine → Plasma concentration of mebendazole source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    biomarker_context Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/mebendazole-research/3663452.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9bfd138da23825906ffca0d38a5a884ac761cf028ae3e0c3ddeabcc24d1c316e", "start_char": 0, "end_char": 912, "text_sha256": "9bfd138da23825906ffca0d38a5a884ac761cf028ae3e0c3ddeabcc24d1c316e"}
    experimental_model
    Aminopyrine breath test and serum mebendazole concentrations in eight patients before and after 30 days of cimetidine
    exposure
    Mebendazole 1.5 grams three times daily, with cimetidine 400 milligrams three times daily for 30 days
    limitations
    Eight patients, five of whom had peptic ulcer rather than the target disease. The resolution of previously unresponsive cysts is reported without a control.
    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
    Human
    plain_language
    Blocking the liver enzyme that destroys it raises the blood level enough to clear cysts that had not responded.
    primary_references
    [mbz-p3663452] Cimetidine increases serum mebendazole concentrations. Implications for treatment of hepatic hydatid cysts. (1987). https://pubmed.ncbi.nlm.nih.gov/3663452/ DOI: 10.1111/j.1365-2125.1987.tb03186.x
    tissue_or_cell_type
    Liver and plasma
    trigger_kind
    biomarker_context Imported condition classification; unverified.

    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 472–483

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Aminopyrine breath test and serum mebendazole concentrations in eight patients before and after 30 days of cimetidine · source_derived_draft · unverified_draft

    ### mbz-cimetidine-raises-levels In eight patients, cimetidine lowered the one-hour specific activity in the aminopyrine breath test and increased the maximum serum concentration of mebendazole, with a significant correlation between the breath test activity and the highest mebendazole concentration both before and after cimetidine, and combined administration resulted in the complete resolution of previously unresponsive hydatid cysts. Condition category: biomarker_context 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: Blocking the liver enzyme that destroys it raises the blood level enough to clear cysts that had not responded. organism: Human tissue_or_cell_type: Liver and plasma experimental_model: Aminopyrine breath test and serum mebendazole concentrations in eight patients before and after 30 days of cimetidine limitations: Eight patients, five of whom had peptic ulcer rather than the target disease. The resolution of previously unresponsive cysts is reported without a control. exposure: Mebendazole 1.5 grams three times daily, with cimetidine 400 milligrams three times daily for 30 days evidence_span: {"source_cache": "artifacts/mebendazole-research/3663452.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9bfd138da23825906ffca0d38a5a884ac761cf028ae3e0c3ddeabcc24d1c316e", "start_char": 0, "end_char": 912, "text_sha256": "9bfd138da23825906ffca0d38a5a884ac761cf028ae3e0c3ddeabcc24d1c316e"} [mbz-p3663452] Cimetidine increases serum mebendazole concentrations. Implications for treatment of hepatic hydatid cysts. (1987). https://pubmed.ncbi.nlm.nih.gov/3663452/ DOI: 10.1111/j.1365-2125.1987.tb03186.x
    Complete structured claim and evidence
  2. Absorption of oral flubendazole in man was markedly enhanced when the drug was taken together with a meal, but a twenty times higher dose produced only an increase by a factor of 1.4 in plasma levels and area under the curve, indicating that absorption is limited by the extremely poor solubility of the drug in the contents of the gastrointestinal tract; in rats plasma levels of oral and subcutaneous mebendazole were about ten times higher than those of flubendazole.

    Flubendazole → Oral bioavailability source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/mebendazole-research/7103610.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e582dcb4657e254dfe61d437d899b2db4d2a4628aa1267fb90de6366b7b4c8f0", "start_char": 0, "end_char": 948, "text_sha256": "e582dcb4657e254dfe61d437d899b2db4d2a4628aa1267fb90de6366b7b4c8f0"}
    experimental_model
    Radioimmunoassay of mebendazole and flubendazole across rats, dogs and man
    exposure
    Oral, subcutaneous and intramuscular dosing, and a twentyfold oral dose escalation of flubendazole in man
    limitations
    The dose-escalation arm is about flubendazole rather than mebendazole, and is recorded under flubendazole; it is retained because it demonstrates the solubility limit that governs this whole class.
    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
    Rat, dog and human
    plain_language
    Twenty times the dose gave less than half again as much in the blood, because it simply will not dissolve.
    primary_references
    [mbz-p7103610] The pharmacokinetics of mebendazole and flubendazole in animals and man. (1982). https://pubmed.ncbi.nlm.nih.gov/7103610/
    tissue_or_cell_type
    Plasma

    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 459–470

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Radioimmunoassay of mebendazole and flubendazole across rats, dogs and man · source_derived_draft · unverified_draft

    ### mbz-dose-escalation-fails Absorption of oral flubendazole in man was markedly enhanced when the drug was taken together with a meal, but a twenty times higher dose produced only an increase by a factor of 1.4 in plasma levels and area under the curve, indicating that absorption is limited by the extremely poor solubility of the drug in the contents of the gastrointestinal tract; in rats plasma levels of oral and subcutaneous mebendazole were about ten times higher than those of flubendazole. 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: Twenty times the dose gave less than half again as much in the blood, because it simply will not dissolve. organism: Rat, dog and human tissue_or_cell_type: Plasma experimental_model: Radioimmunoassay of mebendazole and flubendazole across rats, dogs and man limitations: The dose-escalation arm is about flubendazole rather than mebendazole, and is recorded under flubendazole; it is retained because it demonstrates the solubility limit that governs this whole class. exposure: Oral, subcutaneous and intramuscular dosing, and a twentyfold oral dose escalation of flubendazole in man evidence_span: {"source_cache": "artifacts/mebendazole-research/7103610.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e582dcb4657e254dfe61d437d899b2db4d2a4628aa1267fb90de6366b7b4c8f0", "start_char": 0, "end_char": 948, "text_sha256": "e582dcb4657e254dfe61d437d899b2db4d2a4628aa1267fb90de6366b7b4c8f0"} [mbz-p7103610] The pharmacokinetics of mebendazole and flubendazole in animals and man. (1982). https://pubmed.ncbi.nlm.nih.gov/7103610/
    Complete structured claim and evidence
  3. When 1.5 gram doses were given to three volunteers, measurable plasma concentrations of 17 to 134 nanomoles per litre were found only if mebendazole was given together with a fatty meal, in a patient with cholestasis plasma concentrations were higher than in the three normal subjects, and in patients on long-term treatment the increase in plasma concentration after a 1 gram dose varied between 0 and 500 nanomoles per litre, so that monitoring plasma levels during long-term therapy appears advisable.

    Experimental context and source evidence
    availability_state
    biomarker_context Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/mebendazole-research/7418715.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "b3e200ec505a4a58edacfcf8a51f1073d528d8fc7718fd5cd10a6ca15cbded10", "start_char": 0, "end_char": 812, "text_sha256": "b3e200ec505a4a58edacfcf8a51f1073d528d8fc7718fd5cd10a6ca15cbded10"}
    experimental_model
    Plasma concentrations in three volunteers given 1.5 gram doses and in patients on long-term treatment
    exposure
    1.5 gram oral doses given with and without a fatty meal
    limitations
    Three volunteers. The finding that concentrations were measurable only with food is the substantive result; the cholestasis observation is a single patient.
    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
    Human
    plain_language
    Without fat in the meal the drug does not reach the blood at all, and between patients the levels vary from nothing to a great deal.
    primary_references
    [mbz-p7418715] Plasma concentrations of mebendazole during treatment of echinococcosis: preliminary results. (1980). https://pubmed.ncbi.nlm.nih.gov/7418715/ DOI: 10.1007/bf00558451
    tissue_or_cell_type
    Plasma
    trigger_kind
    biomarker_context Imported condition classification; unverified.

    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 420–431

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Plasma concentrations in three volunteers given 1.5 gram doses and in patients on long-term treatment · source_derived_draft · unverified_draft

    ### mbz-food-is-required When 1.5 gram doses were given to three volunteers, measurable plasma concentrations of 17 to 134 nanomoles per litre were found only if mebendazole was given together with a fatty meal, in a patient with cholestasis plasma concentrations were higher than in the three normal subjects, and in patients on long-term treatment the increase in plasma concentration after a 1 gram dose varied between 0 and 500 nanomoles per litre, so that monitoring plasma levels during long-term therapy appears advisable. Condition category: biomarker_context 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: Without fat in the meal the drug does not reach the blood at all, and between patients the levels vary from nothing to a great deal. organism: Human tissue_or_cell_type: Plasma experimental_model: Plasma concentrations in three volunteers given 1.5 gram doses and in patients on long-term treatment limitations: Three volunteers. The finding that concentrations were measurable only with food is the substantive result; the cholestasis observation is a single patient. exposure: 1.5 gram oral doses given with and without a fatty meal evidence_span: {"source_cache": "artifacts/mebendazole-research/7418715.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "b3e200ec505a4a58edacfcf8a51f1073d528d8fc7718fd5cd10a6ca15cbded10", "start_char": 0, "end_char": 812, "text_sha256": "b3e200ec505a4a58edacfcf8a51f1073d528d8fc7718fd5cd10a6ca15cbded10"} [mbz-p7418715] Plasma concentrations of mebendazole during treatment of echinococcosis: preliminary results. (1980). https://pubmed.ncbi.nlm.nih.gov/7418715/ DOI: 10.1007/bf00558451
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    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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