Mitotic arrest: molecular mechanisms & dependencies

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.

Human evidence only

How nutrients reach it in more than one step

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

Tracing routes…

What it does

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

Recorded relationships

What acts on it

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

Where it participates (unsigned role)

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.
Mebendazole → Differentiation of rat embryo midbrain and limb bud cells in micromass culture source_derived_draftungraded
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

The events it takes part in

A mechanism often involves more than two components. These are the full events, with every participant and its role.

Situations it appears in

Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

Open hypotheses

Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.

This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.

Mitotic arrest