Nutrient chapter

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.

44 recorded mechanisms · 6 availability situations · 1 preserved sources. Draft and verified records are labeled separately.

Read recorded mechanisms Open recursive mind map

The mechanisms

What the sources say this nutrient does, one relationship at a time. Plain wording comes first; the technical statement follows.

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.
Mebendazole → Polymerisation of tubulin into microtubules source_derived_draftungraded
Experimental context and source evidence
evidence_span
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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
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
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
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
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
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
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
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.
Mebendazole → Polymerisation of tubulin into microtubules source_derived_draftungraded
Experimental context and source evidence
evidence_span
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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
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.
Mebendazole → Transport of secretory granules to the terminal web source_derived_draftungraded
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
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.
Mebendazole → Integrity and number of intestinal microvilli source_derived_draftungraded
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
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
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.
Mebendazole → Polymerisation of tubulin into microtubules source_derived_draftungraded
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
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.
Mebendazole → Cytoplasmic and mitochondrial malate dehydrogenase of helminths source_derived_draftungraded
Experimental context and source evidence
evidence_span
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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
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.
Mebendazole → Pyruvate kinase of the Echinococcus cyst wall source_derived_draftungraded
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
All Haemonchus contortus tub-1 constructs encoding phenylalanine at position 200 conferred susceptibility to thiabendazole in benzimidazole-resistant Caenorhabditis elegans ben-1 mutants, whereas constructs carrying tyrosine at position 200 did not alter the resistant phenotype, leading to the conclusion that the single phenylalanine to tyrosine mutation at position 200 in beta-tubulin isotype 1 is the cause of benzimidazole resistance in Haemonchus contortus.
Beta-tubulin carrying tyrosine at position 200 → Resistance to benzimidazole anthelmintics source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/mebendazole-research/7877171.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "091ba3ac445b68112bac29dec56d0d1a48e0d258714ebdbe090b5e7728e6ceaa", "start_char": 0, "end_char": 1532, "text_sha256": "091ba3ac445b68112bac29dec56d0d1a48e0d258714ebdbe090b5e7728e6ceaa"}
experimental_model
Heterologous expression of Haemonchus contortus beta-tubulin alleles in Caenorhabditis elegans ben-1 mutants
exposure
Parasite benzimidazole-sensitive and resistant alleles and in vitro mutagenised constructs, assayed with benomyl and thiabendazole
limitations
A functional test rather than an association: the alleles were put into a resistant host and the phenotype followed the codon. The assay drugs were benomyl and thiabendazole rather than mebendazole.
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
Swapping one amino acid back made resistant worms susceptible again, which makes it the cause and not a coincidence.
primary_references
[mbz-p7877171] Beta-tubulin genes from the parasitic nematode Haemonchus contortus modulate drug resistance in Caenorhabditis elegans. (1995). https://pubmed.ncbi.nlm.nih.gov/7877171/ DOI: 10.1006/jmbi.1994.0102
tissue_or_cell_type
Beta-tubulin isotype 1
trigger_kind
machinery_impairment 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 264–275
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Heterologous expression of Haemonchus contortus beta-tubulin alleles in Caenorhabditis elegans ben-1 mutants · source_derived_draft · unverified_draft
### mbz-phe200-causes-resistance All Haemonchus contortus tub-1 constructs encoding phenylalanine at position 200 conferred susceptibility to thiabendazole in benzimidazole-resistant Caenorhabditis elegans ben-1 mutants, whereas constructs carrying tyrosine at position 200 did not alter the resistant phenotype, leading to the conclusion that the single phenylalanine to tyrosine mutation at position 200 in beta-tubulin isotype 1 is the cause of benzimidazole resistance in Haemonchus contortus. Condition category: machinery_impairment 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: Swapping one amino acid back made resistant worms susceptible again, which makes it the cause and not a coincidence. organism: Nematode tissue_or_cell_type: Beta-tubulin isotype 1 experimental_model: Heterologous expression of Haemonchus contortus beta-tubulin alleles in Caenorhabditis elegans ben-1 mutants limitations: A functional test rather than an association: the alleles were put into a resistant host and the phenotype followed the codon. The assay drugs were benomyl and thiabendazole rather than mebendazole. exposure: Parasite benzimidazole-sensitive and resistant alleles and in vitro mutagenised constructs, assayed with benomyl and thiabendazole evidence_span: {"source_cache": "artifacts/mebendazole-research/7877171.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "091ba3ac445b68112bac29dec56d0d1a48e0d258714ebdbe090b5e7728e6ceaa", "start_char": 0, "end_char": 1532, "text_sha256": "091ba3ac445b68112bac29dec56d0d1a48e0d258714ebdbe090b5e7728e6ceaa"} [mbz-p7877171] Beta-tubulin genes from the parasitic nematode Haemonchus contortus modulate drug resistance in Caenorhabditis elegans. (1995). https://pubmed.ncbi.nlm.nih.gov/7877171/ DOI: 10.1006/jmbi.1994.0102
Complete structured claim and evidence
Albendazole-resistant Giardia lines showed major chromosome rearrangements and differences in the cytoskeleton, particularly the median body, implicating the cytoskeleton in the mechanism of resistance, but sequence data spanning the region encoding phenylalanine at position 200 demonstrated that the beta-tubulin gene did not carry a mutation at that codon, suggesting that phenylalanine at position 200 is not necessary for benzimidazole resistance.
Resistance to benzimidazole anthelmintics → Beta-tubulin carrying phenylalanine at position 200 source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mebendazole-research/9158790.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "b1e25da8738886a9f416bb8411755eca925e232495786f938ef8f9afac40de30", "start_char": 0, "end_char": 1295, "text_sha256": "b1e25da8738886a9f416bb8411755eca925e232495786f938ef8f9afac40de30"}
experimental_model
Albendazole resistance induced in three Giardia cultures by stepwise drug exposure, with beta-tubulin sequencing
exposure
Growth in successively increasing albendazole, with immunofluorescence and PCR across codon 200
limitations
A counterexample obtained with albendazole rather than mebendazole, in a protozoan rather than a nematode. It is recorded because it tests the codon-200 rule directly and the rule fails.
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
Giardia
plain_language
Resistant parasites that never touched the famous mutation, so it cannot be the only route.
primary_references
[mbz-p9158790] Albendazole resistance in Giardia is correlated with cytoskeletal changes but not with a mutation at amino acid 200 in beta-tubulin. (1996). https://pubmed.ncbi.nlm.nih.gov/9158790/ DOI: 10.1089/mdr.1996.2.303
tissue_or_cell_type
Cytoskeleton and beta-tubulin gene
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 277–288
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Albendazole resistance induced in three Giardia cultures by stepwise drug exposure, with beta-tubulin sequencing · source_derived_draft · unverified_draft
### mbz-resistance-without-codon-200 Albendazole-resistant Giardia lines showed major chromosome rearrangements and differences in the cytoskeleton, particularly the median body, implicating the cytoskeleton in the mechanism of resistance, but sequence data spanning the region encoding phenylalanine at position 200 demonstrated that the beta-tubulin gene did not carry a mutation at that codon, suggesting that phenylalanine at position 200 is not necessary for benzimidazole 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: Resistant parasites that never touched the famous mutation, so it cannot be the only route. organism: Giardia tissue_or_cell_type: Cytoskeleton and beta-tubulin gene experimental_model: Albendazole resistance induced in three Giardia cultures by stepwise drug exposure, with beta-tubulin sequencing limitations: A counterexample obtained with albendazole rather than mebendazole, in a protozoan rather than a nematode. It is recorded because it tests the codon-200 rule directly and the rule fails. exposure: Growth in successively increasing albendazole, with immunofluorescence and PCR across codon 200 evidence_span: {"source_cache": "artifacts/mebendazole-research/9158790.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "b1e25da8738886a9f416bb8411755eca925e232495786f938ef8f9afac40de30", "start_char": 0, "end_char": 1295, "text_sha256": "b1e25da8738886a9f416bb8411755eca925e232495786f938ef8f9afac40de30"} [mbz-p9158790] Albendazole resistance in Giardia is correlated with cytoskeletal changes but not with a mutation at amino acid 200 in beta-tubulin. (1996). https://pubmed.ncbi.nlm.nih.gov/9158790/ DOI: 10.1089/mdr.1996.2.303
Complete structured claim and evidence
Three beta-tubulin cDNAs were cloned from Haemonchus contortus, two differing at only 23 nucleotides giving 4 amino acid changes and a third representing a different isotype class differing extensively in the carboxy terminus; comparison with mammalian beta-tubulins identified several regions of consistent difference whose functional significance has not been defined, and sequences very similar or identical to two of the clones were present in both benzimidazole-sensitive and benzimidazole-resistant populations although resistant organisms may differ in the presence of a gene product related to the third.
Nematode beta-tubulin → Resistance to benzimidazole anthelmintics source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mebendazole-research/1741017.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5dfdd18b65ab4df953ac012978b5c922824de051db3b5fab15bac4b97abbfb5c", "start_char": 0, "end_char": 1425, "text_sha256": "5dfdd18b65ab4df953ac012978b5c922824de051db3b5fab15bac4b97abbfb5c"}
experimental_model
Cloning and sequencing of three beta-tubulin cDNAs from Haemonchus contortus
exposure
Sequence comparison across nematode and mammalian beta-tubulins and across sensitive and resistant populations
limitations
Sequence work only. It states plainly that the molecular basis of the nematode versus mammalian difference is not known, which is still the open question in this chapter.
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 worm has several versions of this protein, and the differences from ours are known but not explained.
primary_references
[mbz-p1741017] Three beta-tubulin cDNAs from the parasitic nematode Haemonchus contortus. (1992). https://pubmed.ncbi.nlm.nih.gov/1741017/ DOI: 10.1016/0166-6851(92)90227-b
tissue_or_cell_type
Beta-tubulin genes
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 290–301
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cloning and sequencing of three beta-tubulin cDNAs from Haemonchus contortus · source_derived_draft · unverified_draft
### mbz-more-than-one-isotype Three beta-tubulin cDNAs were cloned from Haemonchus contortus, two differing at only 23 nucleotides giving 4 amino acid changes and a third representing a different isotype class differing extensively in the carboxy terminus; comparison with mammalian beta-tubulins identified several regions of consistent difference whose functional significance has not been defined, and sequences very similar or identical to two of the clones were present in both benzimidazole-sensitive and benzimidazole-resistant populations although resistant organisms may differ in the presence of a gene product related to the third. 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 has several versions of this protein, and the differences from ours are known but not explained. organism: Nematode tissue_or_cell_type: Beta-tubulin genes experimental_model: Cloning and sequencing of three beta-tubulin cDNAs from Haemonchus contortus limitations: Sequence work only. It states plainly that the molecular basis of the nematode versus mammalian difference is not known, which is still the open question in this chapter. exposure: Sequence comparison across nematode and mammalian beta-tubulins and across sensitive and resistant populations evidence_span: {"source_cache": "artifacts/mebendazole-research/1741017.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5dfdd18b65ab4df953ac012978b5c922824de051db3b5fab15bac4b97abbfb5c", "start_char": 0, "end_char": 1425, "text_sha256": "5dfdd18b65ab4df953ac012978b5c922824de051db3b5fab15bac4b97abbfb5c"} [mbz-p1741017] Three beta-tubulin cDNAs from the parasitic nematode Haemonchus contortus. (1992). https://pubmed.ncbi.nlm.nih.gov/1741017/ DOI: 10.1016/0166-6851(92)90227-b
Complete structured claim and evidence
Changing Saccharomyces cerevisiae beta-tubulin residue phenylalanine 167 to tyrosine produced at least 3 to 4 fold decreased sensitivity to carbendazim and nocodazole and the mutant was cold sensitive, implying a direct effect on benzimidazole binding rather than a nonspecific increase in microtubule stability, but surprisingly the mutant had 8 fold increased sensitivity to benomyl, which is structurally identical to carbendazim except at position 1, suggesting that residue 167 interacts with benzimidazoles in the vicinity of the 1 position.
Beta-tubulin carrying tyrosine at position 167 → Resistance to benzimidazole anthelmintics source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/mebendazole-research/8641470.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "35145959fc480be6039e088de374d7549dddc6f298511a41d2a760e7fdb8f455", "start_char": 0, "end_char": 917, "text_sha256": "35145959fc480be6039e088de374d7549dddc6f298511a41d2a760e7fdb8f455"}
experimental_model
Site-directed mutagenesis and gene replacement of Saccharomyces cerevisiae beta-tubulin residue 167
exposure
Phenylalanine 167 changed to tyrosine, then tested against carbendazim, nocodazole and benomyl
limitations
A clean genetic test in a tractable organism, and the cold sensitivity argues the effect is on binding rather than on general microtubule stability. Yeast beta-tubulin is not nematode beta-tubulin.
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
Yeast
plain_language
The same mutation that resists one compound makes the organism more vulnerable to its near twin.
primary_references
[mbz-p8641470] Site-directed mutagenesis of Saccharomyces cerevisiae beta-tubulin: interaction between residue 167 and benzimidazole compounds. (1996). https://pubmed.ncbi.nlm.nih.gov/8641470/ DOI: 10.1016/0014-5793(96)00334-1
tissue_or_cell_type
Beta-tubulin
trigger_kind
machinery_impairment 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 303–314
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Site-directed mutagenesis and gene replacement of Saccharomyces cerevisiae beta-tubulin residue 167 · source_derived_draft · unverified_draft
### mbz-tyr167-and-negative-effect Changing Saccharomyces cerevisiae beta-tubulin residue phenylalanine 167 to tyrosine produced at least 3 to 4 fold decreased sensitivity to carbendazim and nocodazole and the mutant was cold sensitive, implying a direct effect on benzimidazole binding rather than a nonspecific increase in microtubule stability, but surprisingly the mutant had 8 fold increased sensitivity to benomyl, which is structurally identical to carbendazim except at position 1, suggesting that residue 167 interacts with benzimidazoles in the vicinity of the 1 position. Condition category: machinery_impairment 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 mutation that resists one compound makes the organism more vulnerable to its near twin. organism: Yeast tissue_or_cell_type: Beta-tubulin experimental_model: Site-directed mutagenesis and gene replacement of Saccharomyces cerevisiae beta-tubulin residue 167 limitations: A clean genetic test in a tractable organism, and the cold sensitivity argues the effect is on binding rather than on general microtubule stability. Yeast beta-tubulin is not nematode beta-tubulin. exposure: Phenylalanine 167 changed to tyrosine, then tested against carbendazim, nocodazole and benomyl evidence_span: {"source_cache": "artifacts/mebendazole-research/8641470.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "35145959fc480be6039e088de374d7549dddc6f298511a41d2a760e7fdb8f455", "start_char": 0, "end_char": 917, "text_sha256": "35145959fc480be6039e088de374d7549dddc6f298511a41d2a760e7fdb8f455"} [mbz-p8641470] Site-directed mutagenesis of Saccharomyces cerevisiae beta-tubulin: interaction between residue 167 and benzimidazole compounds. (1996). https://pubmed.ncbi.nlm.nih.gov/8641470/ DOI: 10.1016/0014-5793(96)00334-1
Complete structured claim and evidence
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
Fumarate reductase activity in a thiabendazole-resistant Haemonchus contortus strain was significantly lower than in a susceptible strain, but activity in a mebendazole-resistant strain did not differ from the susceptible strain even though it was cross-resistant to thiabendazole, and on reassessment two American strains resistant to thiabendazole and to cambendazole had activities indistinguishable from corresponding susceptible strains, so that benzimidazole resistance cannot be generally correlated with diminished fumarate reductase activity although it may be a contributory factor in the specific Australian thiabendazole-resistant strains.
Fumarate reductase of Haemonchus contortus → Resistance to benzimidazole anthelmintics source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mebendazole-research/6877276.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "59837d0bc8f0d0c120dd9d647dcd86cd046545768ec6ab198e2262d381aafbf7", "start_char": 0, "end_char": 1052, "text_sha256": "59837d0bc8f0d0c120dd9d647dcd86cd046545768ec6ab198e2262d381aafbf7"}
experimental_model
Fumarate reductase activity compared across benzimidazole-susceptible and resistant Haemonchus contortus strains, with reassessment of published reports
exposure
Thiabendazole-resistant, mebendazole-resistant and susceptible strains
limitations
A proposed resistance mechanism tested across strains and largely rejected. The reassessment of other laboratories’ published values is the useful part.
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
A once-popular explanation for resistance, checked across strains and found not to hold.
primary_references
[mbz-p6877276] Observations on the fumarate reductase system in Haemonchus contortus and their relevance to anthelmintic resistance and to strain variations of energy metabolism. (1983). https://pubmed.ncbi.nlm.nih.gov/6877276/ DOI: 10.1016/0166-6851(83)90011-7
tissue_or_cell_type
Mitochondrial electron transport
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 329–340
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Fumarate reductase activity compared across benzimidazole-susceptible and resistant Haemonchus contortus strains, with reassessment of published reports · source_derived_draft · unverified_draft
### mbz-fumarate-reductase-retired Fumarate reductase activity in a thiabendazole-resistant Haemonchus contortus strain was significantly lower than in a susceptible strain, but activity in a mebendazole-resistant strain did not differ from the susceptible strain even though it was cross-resistant to thiabendazole, and on reassessment two American strains resistant to thiabendazole and to cambendazole had activities indistinguishable from corresponding susceptible strains, so that benzimidazole resistance cannot be generally correlated with diminished fumarate reductase activity although it may be a contributory factor in the specific Australian thiabendazole-resistant strains. 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 once-popular explanation for resistance, checked across strains and found not to hold. organism: Nematode tissue_or_cell_type: Mitochondrial electron transport experimental_model: Fumarate reductase activity compared across benzimidazole-susceptible and resistant Haemonchus contortus strains, with reassessment of published reports limitations: A proposed resistance mechanism tested across strains and largely rejected. The reassessment of other laboratories’ published values is the useful part. exposure: Thiabendazole-resistant, mebendazole-resistant and susceptible strains evidence_span: {"source_cache": "artifacts/mebendazole-research/6877276.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "59837d0bc8f0d0c120dd9d647dcd86cd046545768ec6ab198e2262d381aafbf7", "start_char": 0, "end_char": 1052, "text_sha256": "59837d0bc8f0d0c120dd9d647dcd86cd046545768ec6ab198e2262d381aafbf7"} [mbz-p6877276] Observations on the fumarate reductase system in Haemonchus contortus and their relevance to anthelmintic resistance and to strain variations of energy metabolism. (1983). https://pubmed.ncbi.nlm.nih.gov/6877276/ DOI: 10.1016/0166-6851(83)90011-7
Complete structured claim and evidence
Steady-state pool sizes of glucose and metabolic intermediates including adenine nucleotides and end products revealed no differences between adult Haemonchus contortus resistant or susceptible to benzimidazoles, all three strains had similar levels of total lipid, protein and free amino acid and produced a similar sum total of end products, and although the mebendazole-resistant strain showed a diversion of carbon flow to the ethanol-producing pathway and greater cyanide-sensitive aerobic carbon dioxide output, the extent to which these metabolic differences may be related to benzimidazole resistance is not readily apparent.
Carbohydrate and energy metabolism of the parasite → Resistance to benzimidazole anthelmintics source_derived_draftungraded
Experimental context and source evidence
evidence_span
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experimental_model
Biochemical comparison of susceptible, mebendazole-resistant and thiabendazole-resistant Haemonchus contortus in vitro
exposure
Steady-state metabolite pools, end products and labelled carbon dioxide over 30 to 60 minute and 18 hour incubations
limitations
A broad metabolic survey across matched resistant and susceptible strains. Its own authors state the relationship to resistance is not apparent.
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
Resistant and susceptible worms handle sugar much the same, so metabolism is not where resistance lives.
primary_references
[mbz-p6427605] Energy metabolism of adult Haemonchus contortus in vitro: a comparison of benzimidazole-susceptible and -resistant strains. (1984). https://pubmed.ncbi.nlm.nih.gov/6427605/ DOI: 10.1016/0166-6851(84)90031-8
tissue_or_cell_type
Whole adult worms
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 342–353
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Biochemical comparison of susceptible, mebendazole-resistant and thiabendazole-resistant Haemonchus contortus in vitro · source_derived_draft · unverified_draft
### mbz-metabolism-does-not-explain-resistance Steady-state pool sizes of glucose and metabolic intermediates including adenine nucleotides and end products revealed no differences between adult Haemonchus contortus resistant or susceptible to benzimidazoles, all three strains had similar levels of total lipid, protein and free amino acid and produced a similar sum total of end products, and although the mebendazole-resistant strain showed a diversion of carbon flow to the ethanol-producing pathway and greater cyanide-sensitive aerobic carbon dioxide output, the extent to which these metabolic differences may be related to benzimidazole resistance is not readily apparent. 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: Resistant and susceptible worms handle sugar much the same, so metabolism is not where resistance lives. organism: Nematode tissue_or_cell_type: Whole adult worms experimental_model: Biochemical comparison of susceptible, mebendazole-resistant and thiabendazole-resistant Haemonchus contortus in vitro limitations: A broad metabolic survey across matched resistant and susceptible strains. Its own authors state the relationship to resistance is not apparent. exposure: Steady-state metabolite pools, end products and labelled carbon dioxide over 30 to 60 minute and 18 hour incubations evidence_span: {"source_cache": "artifacts/mebendazole-research/6427605.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4834a68834e7916938d61b08f8dc38fb00085c0b43761372c8ef883da0d8cbf8", "start_char": 0, "end_char": 1809, "text_sha256": "4834a68834e7916938d61b08f8dc38fb00085c0b43761372c8ef883da0d8cbf8"} [mbz-p6427605] Energy metabolism of adult Haemonchus contortus in vitro: a comparison of benzimidazole-susceptible and -resistant strains. (1984). https://pubmed.ncbi.nlm.nih.gov/6427605/ DOI: 10.1016/0166-6851(84)90031-8
Complete structured claim and evidence
Testing the biological activity of the three polymorphic forms of mebendazole called A, B and C by median lethal dose in mice after oral and intraperitoneal administration and by anthelmintic effect against the enteral and parenteral phases of Trichinella spiralis, the polymorphic form A was the least toxic and the least effective, and use of polymorph C was judged advisable for oral treatment given its lower toxicity than form B and similar anthelmintic effect.
Mebendazole polymorph A → Cure rate and egg reduction rate in treated infection source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mebendazole-research/3608627.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "cf4b94d7b266abf376ded706272be7f440f6f46b82db5ee9c36d2c34af6e8825", "start_char": 0, "end_char": 608, "text_sha256": "cf4b94d7b266abf376ded706272be7f440f6f46b82db5ee9c36d2c34af6e8825"}
experimental_model
Median lethal dose and anthelmintic efficacy of three mebendazole polymorphs in mice
exposure
Polymorphs A, B and C given orally and intraperitoneally, against enteral and parenteral phases of infection
limitations
Tests toxicity and efficacy of the three solid forms in the same animals. Numerical values for the median lethal doses are not given in the abstract and are not assumed 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
One crystal form of the same molecule barely poisons the mouse and barely touches the worm.
primary_references
[mbz-p3608627] Experimental chemotherapy and toxicity in mice of three mebendazole polymorphic forms. (1987). https://pubmed.ncbi.nlm.nih.gov/3608627/ DOI: 10.1159/000238506
tissue_or_cell_type
Whole body and Trichinella spiralis infection
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 355–366
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Median lethal dose and anthelmintic efficacy of three mebendazole polymorphs in mice · source_derived_draft · unverified_draft
### mbz-polymorph-a-is-inert Testing the biological activity of the three polymorphic forms of mebendazole called A, B and C by median lethal dose in mice after oral and intraperitoneal administration and by anthelmintic effect against the enteral and parenteral phases of Trichinella spiralis, the polymorphic form A was the least toxic and the least effective, and use of polymorph C was judged advisable for oral treatment given its lower toxicity than form B and similar anthelmintic effect. 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 crystal form of the same molecule barely poisons the mouse and barely touches the worm. organism: Mouse tissue_or_cell_type: Whole body and Trichinella spiralis infection experimental_model: Median lethal dose and anthelmintic efficacy of three mebendazole polymorphs in mice limitations: Tests toxicity and efficacy of the three solid forms in the same animals. Numerical values for the median lethal doses are not given in the abstract and are not assumed here. exposure: Polymorphs A, B and C given orally and intraperitoneally, against enteral and parenteral phases of infection evidence_span: {"source_cache": "artifacts/mebendazole-research/3608627.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "cf4b94d7b266abf376ded706272be7f440f6f46b82db5ee9c36d2c34af6e8825", "start_char": 0, "end_char": 608, "text_sha256": "cf4b94d7b266abf376ded706272be7f440f6f46b82db5ee9c36d2c34af6e8825"} [mbz-p3608627] Experimental chemotherapy and toxicity in mice of three mebendazole polymorphic forms. (1987). https://pubmed.ncbi.nlm.nih.gov/3608627/ DOI: 10.1159/000238506
Complete structured claim and evidence
In 958 children randomly allocated to seven treatment groups, the efficacy of single-dose 300 milligrams of polymorph A was not different from the placebo control at the 0.05 level in both hookworm and Trichuris infections, while the egg reduction and cure rates of 300 and 500 milligrams of polymorph C were similar to each other though inferior to the standard 100 milligrams twice daily for three days.
Mebendazole polymorph A → Cure rate and egg reduction rate in treated infection source_derived_draftungraded
Experimental context and source evidence
availability_state
biomarker_context Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/mebendazole-research/7939946.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "972b8bb36b68b1f40fba5f7bdb38668e9d1c40cba27ddeb19db16a3bcf29053d", "start_char": 0, "end_char": 698, "text_sha256": "972b8bb36b68b1f40fba5f7bdb38668e9d1c40cba27ddeb19db16a3bcf29053d"}
experimental_model
Randomised seven-arm trial in 958 schoolchildren in Southern Thailand
exposure
Single doses of 300 milligrams polymorph A, 300 and 500 milligrams polymorph C, against placebo and against 100 milligrams polymorph C twice daily for three days
limitations
The only human record here that varies the crystal form, with a placebo arm. It is a single-dose comparison and does not follow reinfection.
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 children, a full dose of the wrong crystal form worked no better than a sugar pill.
primary_references
[mbz-p7939946] Efficacy of single-dose mebendazole, polymorphic forms A and C, in the treatment of hookworm and Trichuris infections. (1993). https://pubmed.ncbi.nlm.nih.gov/7939946/
tissue_or_cell_type
Hookworm and Trichuris infection
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 368–379
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomised seven-arm trial in 958 schoolchildren in Southern Thailand · source_derived_draft · unverified_draft
### mbz-polymorph-a-equals-placebo In 958 children randomly allocated to seven treatment groups, the efficacy of single-dose 300 milligrams of polymorph A was not different from the placebo control at the 0.05 level in both hookworm and Trichuris infections, while the egg reduction and cure rates of 300 and 500 milligrams of polymorph C were similar to each other though inferior to the standard 100 milligrams twice daily for three days. 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: In children, a full dose of the wrong crystal form worked no better than a sugar pill. organism: Human tissue_or_cell_type: Hookworm and Trichuris infection experimental_model: Randomised seven-arm trial in 958 schoolchildren in Southern Thailand limitations: The only human record here that varies the crystal form, with a placebo arm. It is a single-dose comparison and does not follow reinfection. exposure: Single doses of 300 milligrams polymorph A, 300 and 500 milligrams polymorph C, against placebo and against 100 milligrams polymorph C twice daily for three days evidence_span: {"source_cache": "artifacts/mebendazole-research/7939946.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "972b8bb36b68b1f40fba5f7bdb38668e9d1c40cba27ddeb19db16a3bcf29053d", "start_char": 0, "end_char": 698, "text_sha256": "972b8bb36b68b1f40fba5f7bdb38668e9d1c40cba27ddeb19db16a3bcf29053d"} [mbz-p7939946] Efficacy of single-dose mebendazole, polymorphic forms A and C, in the treatment of hookworm and Trichuris infections. (1993). https://pubmed.ncbi.nlm.nih.gov/7939946/
Complete structured claim and evidence
In an accelerated stability study, form C was converted to the thermodynamically stable and least soluble form A with increased temperature and moisture, the transformation was significantly increased at constant temperature and humidity when trace amounts of form A were already present, four of the seven products tested contained trace amounts of form A, in some tablets transformation was so quick that it reduced shelf life to less than one month, and tablet dissolution of those products was reduced to the extent that it did not comply with USP and FDA specifications.
Mebendazole polymorph C → Mebendazole polymorph A source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mebendazole-research/19691117.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6005cbf9afb4151467910164f873d0956382c3bcc10cac8514326385b32e32b1", "start_char": 0, "end_char": 1296, "text_sha256": "6005cbf9afb4151467910164f873d0956382c3bcc10cac8514326385b32e32b1"}
experimental_model
Accelerated stability study of mebendazole tablets under ICH storage conditions
exposure
Storage at 30 degrees with 65% relative humidity and at 40 degrees with 75% relative humidity
limitations
Solid-state kinetics on marketed products, modelled with the Johnson-Mehl-Avrami-Erofeyev-Kolmogorov equation. It measures dissolution rather than patient 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
Pharmaceutical product
plain_language
The working form of the drug turns into the useless form on the shelf, faster if a trace of the useless form is already there.
primary_references
[mbz-p19691117] Characterization of polymorph transformations that decrease the stability of tablets containing the WHO essential drug mebendazole. (2010). https://pubmed.ncbi.nlm.nih.gov/19691117/ DOI: 10.1002/jps.21899
tissue_or_cell_type
Tablets
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 381–392
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Accelerated stability study of mebendazole tablets under ICH storage conditions · source_derived_draft · unverified_draft
### mbz-crystal-form-sets-solubility In an accelerated stability study, form C was converted to the thermodynamically stable and least soluble form A with increased temperature and moisture, the transformation was significantly increased at constant temperature and humidity when trace amounts of form A were already present, four of the seven products tested contained trace amounts of form A, in some tablets transformation was so quick that it reduced shelf life to less than one month, and tablet dissolution of those products was reduced to the extent that it did not comply with USP and FDA specifications. 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 working form of the drug turns into the useless form on the shelf, faster if a trace of the useless form is already there. organism: Pharmaceutical product tissue_or_cell_type: Tablets experimental_model: Accelerated stability study of mebendazole tablets under ICH storage conditions limitations: Solid-state kinetics on marketed products, modelled with the Johnson-Mehl-Avrami-Erofeyev-Kolmogorov equation. It measures dissolution rather than patient outcome. exposure: Storage at 30 degrees with 65% relative humidity and at 40 degrees with 75% relative humidity evidence_span: {"source_cache": "artifacts/mebendazole-research/19691117.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6005cbf9afb4151467910164f873d0956382c3bcc10cac8514326385b32e32b1", "start_char": 0, "end_char": 1296, "text_sha256": "6005cbf9afb4151467910164f873d0956382c3bcc10cac8514326385b32e32b1"} [mbz-p19691117] Characterization of polymorph transformations that decrease the stability of tablets containing the WHO essential drug mebendazole. (2010). https://pubmed.ncbi.nlm.nih.gov/19691117/ DOI: 10.1002/jps.21899
Complete structured claim and evidence
Of four raw materials of mebendazole examined, three were polymorph C and the other was polymorph A or a mixture of forms A and B, with X-ray powder diffractometry and infrared spectroscopy indicating form B while the much slower powder dissolution suggested polymorph A; the literature prescribes use of polymorph C pharmaceutically, generic manufacturers should be aware that forms other than C are still available on the market, and all four mebendazole tablets then available in South Africa contained polymorph C.
Mebendazole polymorph A → Aqueous solubility and dissolution rate of the solid drug source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mebendazole-research/9876612.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c0cb5ad093307edd2cbaee474418c3086cd524c606eaddd1cae7186ed962fd26", "start_char": 0, "end_char": 666, "text_sha256": "c0cb5ad093307edd2cbaee474418c3086cd524c606eaddd1cae7186ed962fd26"}
experimental_model
Preformulation analysis of four mebendazole raw materials and four marketed tablets
exposure
X-ray powder diffractometry, infrared spectroscopy and powder dissolution
limitations
A small survey in one country at one time. It also shows the analytical methods disagreeing with each other on one sample, which is recorded.
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
Pharmaceutical product
plain_language
The inactive form is still sold as raw material, and the tests used to tell the forms apart do not always agree.
primary_references
[mbz-p9876612] Identification of the mebendazole polymorphic form present in raw materials and tablets available in South Africa. (1998). https://pubmed.ncbi.nlm.nih.gov/9876612/ DOI: 10.3109/03639049809085647
tissue_or_cell_type
Raw material and tablets
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 394–405
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Preformulation analysis of four mebendazole raw materials and four marketed tablets · source_derived_draft · unverified_draft
### mbz-wrong-form-reaches-market Of four raw materials of mebendazole examined, three were polymorph C and the other was polymorph A or a mixture of forms A and B, with X-ray powder diffractometry and infrared spectroscopy indicating form B while the much slower powder dissolution suggested polymorph A; the literature prescribes use of polymorph C pharmaceutically, generic manufacturers should be aware that forms other than C are still available on the market, and all four mebendazole tablets then available in South Africa contained polymorph C. 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 inactive form is still sold as raw material, and the tests used to tell the forms apart do not always agree. organism: Pharmaceutical product tissue_or_cell_type: Raw material and tablets experimental_model: Preformulation analysis of four mebendazole raw materials and four marketed tablets limitations: A small survey in one country at one time. It also shows the analytical methods disagreeing with each other on one sample, which is recorded. exposure: X-ray powder diffractometry, infrared spectroscopy and powder dissolution evidence_span: {"source_cache": "artifacts/mebendazole-research/9876612.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c0cb5ad093307edd2cbaee474418c3086cd524c606eaddd1cae7186ed962fd26", "start_char": 0, "end_char": 666, "text_sha256": "c0cb5ad093307edd2cbaee474418c3086cd524c606eaddd1cae7186ed962fd26"} [mbz-p9876612] Identification of the mebendazole polymorphic form present in raw materials and tablets available in South Africa. (1998). https://pubmed.ncbi.nlm.nih.gov/9876612/ DOI: 10.3109/03639049809085647
Complete structured claim and evidence
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
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.
A meal containing fat, taken with the dose → 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/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
Complete structured claim and evidence
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
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.
Mebendazole → Methyl 5-(alpha-hydroxybenzyl)-2-benzimidazole carbamate, the hydroxy metabolite 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
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
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
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
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
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
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
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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
Polymorph B and polymorph C both increased survival in a GL261 glioma model with B exhibiting greater toxicity, polymorph A showed no benefit, B and C both reached brain concentrations exceeding the GL261 half-maximal inhibitory concentration 29-fold, polymorph C demonstrated a 24-hour brain-to-plasma area-under-curve ratio of 0.82 while B showed higher plasma exposure and a lower ratio, polymorph A presented markedly lower levels in both plasma and brain, and combination with elacridar significantly improved the efficacy of polymorph C in glioma and medulloblastoma models.
Mebendazole polymorph C → Brain to plasma exposure ratio source_derived_draftungraded
Experimental context and source evidence
availability_state
biomarker_context Imported condition classification; unverified.
evidence_span
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experimental_model
Polymorph content of marketed and custom tablets measured by infrared spectroscopy, then tested in orthotopic mouse glioma and medulloblastoma models with LC/MS pharmacokinetics
exposure
Polymorphs A, B and C, alone and with the transporter inhibitor elacridar
limitations
Carries the polymorph distinction across from the anthelmintic use into the oncology use and finds it decides brain exposure. Mouse models, and elacridar is an experimental tool rather than a co-therapy.
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 same crystal form that works against worms is the one that gets into the brain; the inert form stays out of the blood entirely.
primary_references
[mbz-p25862759] Brain Penetration and Efficacy of Different Mebendazole Polymorphs in a Mouse Brain Tumor Model. (2015). https://pubmed.ncbi.nlm.nih.gov/25862759/ DOI: 10.1158/1078-0432.ccr-14-2681
tissue_or_cell_type
Brain 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 524–535
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Polymorph content of marketed and custom tablets measured by infrared spectroscopy, then tested in orthotopic mouse glioma and medulloblastoma models with LC/MS pharmacokinetics · source_derived_draft · unverified_draft
### mbz-polymorph-decides-brain-levels Polymorph B and polymorph C both increased survival in a GL261 glioma model with B exhibiting greater toxicity, polymorph A showed no benefit, B and C both reached brain concentrations exceeding the GL261 half-maximal inhibitory concentration 29-fold, polymorph C demonstrated a 24-hour brain-to-plasma area-under-curve ratio of 0.82 while B showed higher plasma exposure and a lower ratio, polymorph A presented markedly lower levels in both plasma and brain, and combination with elacridar significantly improved the efficacy of polymorph C in glioma and medulloblastoma models. 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 same crystal form that works against worms is the one that gets into the brain; the inert form stays out of the blood entirely. organism: Mouse tissue_or_cell_type: Brain and plasma experimental_model: Polymorph content of marketed and custom tablets measured by infrared spectroscopy, then tested in orthotopic mouse glioma and medulloblastoma models with LC/MS pharmacokinetics limitations: Carries the polymorph distinction across from the anthelmintic use into the oncology use and finds it decides brain exposure. Mouse models, and elacridar is an experimental tool rather than a co-therapy. exposure: Polymorphs A, B and C, alone and with the transporter inhibitor elacridar evidence_span: {"source_cache": "artifacts/mebendazole-research/25862759.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7545a89b4d17461bbe2d8ac8c7f3093b6ae0ce2f20307ab57b524d91f4f827c3", "start_char": 0, "end_char": 1682, "text_sha256": "7545a89b4d17461bbe2d8ac8c7f3093b6ae0ce2f20307ab57b524d91f4f827c3"} [mbz-p25862759] Brain Penetration and Efficacy of Different Mebendazole Polymorphs in a Mouse Brain Tumor Model. (2015). https://pubmed.ncbi.nlm.nih.gov/25862759/ DOI: 10.1158/1078-0432.ccr-14-2681
Complete structured claim and evidence
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
Mebendazole was determined to interfere with vascular endothelial growth factor receptor 2 kinase by competing with ATP, selectively inhibited tumour angiogenesis but not the normal brain vasculature in orthotopic medulloblastoma models, suppressed the kinase in vivo, and significantly extended survival of medulloblastoma models derived from different molecular backgrounds including a PTCH1-mutant tumour with acquired resistance to the smoothened inhibitor vismodegib.
Mebendazole → Vascular endothelial growth factor receptor 2 / KDR source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mebendazole-research/25253417.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "96333adbb3bce735b14f3c51317229543279992c3cd170760cc494566e49a169", "start_char": 0, "end_char": 1798, "text_sha256": "96333adbb3bce735b14f3c51317229543279992c3cd170760cc494566e49a169"}
experimental_model
Autophosphorylation and cell-free kinase assays with orthotopic medulloblastoma allograft and xenograft models
exposure
Mebendazole in PTCH1-mutant allografts, a group 3 xenograft and a vismodegib-resistant model
limitations
Identifies a third mechanism, kinase inhibition, with a defined competition mode. Whether this operates at achievable human concentrations is not established here.
nutrient_topic
Mebendazole research collection; topical membership is not evidence of a direct clinical effect, and mebendazole is recorded separately from albendazole, from the benzimidazole class and from its own crystal forms. · Mebendazole
organism
Mouse
plain_language
It also blocks the receptor that grows new tumour blood vessels, and spares the normal ones.
primary_references
[mbz-p25253417] Effective treatment of diverse medulloblastoma models with mebendazole and its impact on tumor angiogenesis. (2015). https://pubmed.ncbi.nlm.nih.gov/25253417/ DOI: 10.1093/neuonc/nou234
tissue_or_cell_type
Medulloblastoma and tumour vasculature
Mebendazole: the tubulin it binds, why that is selective, the crystal form that decides whether any of it works, and the off-target that became an oncology programme (2026-09-22) · lines 550–561
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Autophosphorylation and cell-free kinase assays with orthotopic medulloblastoma allograft and xenograft models · source_derived_draft · unverified_draft
### mbz-vegfr2-atp-competition Mebendazole was determined to interfere with vascular endothelial growth factor receptor 2 kinase by competing with ATP, selectively inhibited tumour angiogenesis but not the normal brain vasculature in orthotopic medulloblastoma models, suppressed the kinase in vivo, and significantly extended survival of medulloblastoma models derived from different molecular backgrounds including a PTCH1-mutant tumour with acquired resistance to the smoothened inhibitor vismodegib. Condition category: normal nutrient_topic: Mebendazole research collection; topical membership is not evidence of a direct clinical effect, and mebendazole is recorded separately from albendazole, from the benzimidazole class and from its own crystal forms. plain_language: It also blocks the receptor that grows new tumour blood vessels, and spares the normal ones. organism: Mouse tissue_or_cell_type: Medulloblastoma and tumour vasculature experimental_model: Autophosphorylation and cell-free kinase assays with orthotopic medulloblastoma allograft and xenograft models limitations: Identifies a third mechanism, kinase inhibition, with a defined competition mode. Whether this operates at achievable human concentrations is not established here. exposure: Mebendazole in PTCH1-mutant allografts, a group 3 xenograft and a vismodegib-resistant model evidence_span: {"source_cache": "artifacts/mebendazole-research/25253417.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "96333adbb3bce735b14f3c51317229543279992c3cd170760cc494566e49a169", "start_char": 0, "end_char": 1798, "text_sha256": "96333adbb3bce735b14f3c51317229543279992c3cd170760cc494566e49a169"} [mbz-p25253417] Effective treatment of diverse medulloblastoma models with mebendazole and its impact on tumor angiogenesis. (2015). https://pubmed.ncbi.nlm.nih.gov/25253417/ DOI: 10.1093/neuonc/nou234
Complete structured claim and evidence
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
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.
Mebendazole → Elevation of alanine and aspartate aminotransferase source_derived_draftungraded
Experimental context and source evidence
evidence_span
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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
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.
Mebendazole → Progression-free survival in high-grade glioma source_derived_draftungraded
Experimental context and source evidence
evidence_span
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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
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
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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
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
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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
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
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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
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.
Mebendazole → Drug-induced hepatitis and hepatocellular cytolysis source_derived_draftungraded
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

Availability and dependencies

Each situation shows the normal role first, then what the sources report under a specific condition. A shortfall in the diet, a fault in the machinery, and a low blood reading are kept separate because they are not the same thing.

When the worm carries tyrosine at position 200

Condition: machinery_impairment · A single phenylalanine to tyrosine substitution at position 200 of beta-tubulin isotype 1.

Normal role: Benzimidazoles bind beta-tubulin, and a phenylalanine at position 200 of isotype 1 is part of what they bind to.

Recorded consequence: Constructs encoding Phe200 restored susceptibility to a resistant host while Tyr200 constructs did not, identifying the substitution as the cause of resistance rather than a marker of it.

Scope: Caenorhabditis elegans expressing Haemonchus contortus alleles

When resistance to one benzimidazole increases sensitivity to another

Condition: machinery_impairment · A phenylalanine to tyrosine substitution at position 167.

Normal role: Benzimidazoles bind beta-tubulin at a site that residue 167 helps form, near the 1 position of the ring.

Recorded consequence: Sensitivity to carbendazim and nocodazole falls 3 to 4 fold while sensitivity to benomyl rises 8 fold, so resistance within the class is not uniform.

Scope: Saccharomyces cerevisiae gene replacement

When the tablet contains the wrong crystal form

Condition: biomarker_context · A product made with polymorph A rather than polymorph C.

Normal role: Mebendazole is barely soluble, so the rate at which the solid dissolves sets how much drug is absorbed at all.

Recorded consequence: Single-dose 300 milligram polymorph A performed no differently from placebo against hookworm and Trichuris in 958 children, while the same dose of polymorph C worked.

Scope: Randomised trial in Thai schoolchildren

When the dose is swallowed without fat

Condition: biomarker_context · Taking the dose on an empty stomach rather than with a fatty meal.

Normal role: Mebendazole is absorbed poorly because it barely dissolves, and dietary fat helps carry it into solution.

Recorded consequence: Measurable plasma concentrations appeared in volunteers only when the drug was given together with a fatty meal, so a systemic indication such as echinococcosis can fail on administration alone.

Scope: Three volunteers given 1.5 gram doses

When hepatic oxidation is inhibited

Condition: biomarker_context · Co-administration of cimetidine, which inhibits hepatic microsomal oxidation.

Normal role: Mebendazole that is absorbed is cleared by hepatic oxidative metabolism, and little of it survives to circulate.

Recorded consequence: Maximum serum mebendazole concentrations rose significantly, the fall in oxidative capacity correlated with the rise in drug concentration, and previously unresponsive hydatid cysts resolved completely.

Scope: Eight patients over 30 days

When the plasma level actually gets high

Condition: biomarker_context · High-dose long-term treatment for echinococcosis, or anything else that raises the plasma level such as cimetidine or cholestasis.

Normal role: Mebendazole is absorbed so poorly that systemic exposure is usually low, which is why it is well tolerated for gut-lumen infections.

Recorded consequence: Severe reversible neutropenia from marrow suppression appeared alongside striking cyst shrinkage in the same patient, and grade 3 transaminase elevation appeared at the highest oncology doses, so the benefit and the harm arrive together.

Scope: Case reports and a dose-escalation study in humans

The sources

Every document behind this chapter is preserved word for word. Open one to read it in full with its recorded conflicts marked in place.

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)AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · unverified_draftRead preserved source

Recorded disagreements

Where two sources say different things, both are kept and the difference is explained. You can discuss a disagreement or propose a mechanism that might account for it.

Do differences in parasite energy metabolism account for benzimidazole resistance?Two proposals were put and both were tested against matched resistant and susceptible Haemonchus contortus strains. Fumarate reductase activity was lower in one thiabendazole-resistant strain but unchanged in a mebendazole-resistant strain that was nonetheless cross-resistant to thiabendazole, and on reassessment two further resistant strains had activities indistinguishable from susceptible controls. A broader survey found no differences in glucose or metabolic intermediate pools, in lipid, protein or free amino acid, or in the total of end products, with the strain differences that did appear leaving their own authors unable to say whether they related to resistance. Both records qualify the metabolic account rather than supporting it, while the beta-tubulin records in this collection show a substitution that reverses the phenotype outright. The metabolic findings are retained because the same enzymes are proposed elsewhere in this collection as the drug target.Read the recorded disagreement
Does tighter binding to parasite tubulin explain why mebendazole spares the host?Measured against Ascaris suum embryonic tubulin, mebendazole bound 250 to 400 times more tightly than to bovine brain tubulin, and that ratio is the standard explanation for the drug being safe in the host. Measured against tubulin purified from the Ascaris intestine, the tissue the drug visibly destroys, the difference against porcine brain tubulin was about twofold, and those authors concluded that interference with the parasite microtubular system cannot on its own explain selective toxicity, proposing differential pharmacokinetics instead. The two studies used different parasite tissues, different mammalian sources and different purification, and one reports mebendazole as noncompetitive with colchicine on nematode tubulin while the other reports it as competitive on intestinal tubulin. Two later records in this collection offer a third answer, that the selectivity is kinetic and temperature dependent rather than a matter of equilibrium affinity. Which reading is correct is not settled here.Read the recorded disagreement
Is the phenylalanine to tyrosine change at codon 200 what makes a parasite resistant?Putting Haemonchus contortus beta-tubulin alleles into resistant Caenorhabditis elegans showed the phenotype following the codon exactly: Phe200 restored susceptibility, Tyr200 did not, which makes the substitution causal in that species. Albendazole-resistant Giardia lines selected in culture carried no mutation at codon 200 at all, and their authors concluded that phenylalanine at position 200 is not necessary for resistance; what those lines did show was chromosome rearrangement and a visibly altered cytoskeleton. A third record found three beta-tubulin cDNAs in Haemonchus contortus with sequences similar or identical to two of them present in both sensitive and resistant populations, so more than one gene product is in play even in the species where the codon rule was established. The organisms differ, a nematode against a protozoan, and the selecting drug differs. Codon 200 is one route to resistance and these records do not make it the only one.Read the recorded disagreement
Is the target tubulin, or the enzymes of parasite carbohydrate metabolism?The tubulin account is supported by direct binding measurements in several nematode species, by electron microscopy showing fewer and shorter microtubules, by the correlation between tubulin inhibition and egg hatch inhibition across the chemical series, and by a 1975 ultrastructural study in which the first change seen in the parasite gut is secretory granules stranded in the Golgi, which is what a transport failure looks like. Against that, mebendazole was the most potent of four benzimidazoles against purified helminth malate dehydrogenase, and in live infected mice it inhibited Echinococcus cyst wall pyruvate kinase by 85 to 88% and phosphoenolpyruvate carboxykinase by 90 to 92%, more than albendazole did. Those authors name these enzymes as the important site of attack. The records are not directly comparable: the tubulin work measures binding constants and the metabolic work measures percentage inhibition at administered doses, and neither set establishes what concentration reaches the enzyme in a treated human. Both are recorded; the loss of glycogen in the 1975 study is consistent with either.Read the recorded disagreement

Open questions in this collection

Questions the curators could not answer from the sources in front of them, kept here with the reason each one is still open. These are gaps in this collection, not findings or proof that no one has studied them.

Whether the crystal form of the mebendazole a patient actually receives is known at the point of use.Single-dose polymorph A performed no better than placebo in 958 children, the inactive form was still sold as raw material in 1998, and an accelerated stability study found four of seven products carrying trace form A with some tablets failing dissolution specifications within a month. No record here reports the polymorph content of products in current use.
Whether the oncology doses can be reached reliably given solubility-limited absorption.Bioavailability from solution was 17% in one man, absorption is limited by solubility so that a twentyfold dose increase raised exposure only 1.4-fold for the sister compound, plasma levels varied thirtyfold between patients on the same milligram-per-kilogram dose, and in the one human oncology study plasma levels were described as variable while grade 3 transaminase elevation appeared at the top dose.
Whether mebendazole inhibits parasite carbohydrate-metabolism enzymes at concentrations reached in a treated host.Mebendazole inhibited Echinococcus cyst wall pyruvate kinase by 85 to 88% at administered doses in mice and was the most potent of four benzimidazoles against purified helminth malate dehydrogenase, but no record here relates those inhibitions to a measured drug concentration at the enzyme.
What at the molecular level makes nematode beta-tubulin different from ours.Several regions of consistent difference between nematode and mammalian beta-tubulins were identified by sequence comparison in 1992 and their functional significance was explicitly not defined. The kinetic and temperature-dependence records in this collection describe the consequence of the difference rather than its structural basis.
Whether the developmental toxicity seen in vitro matters at the doses used.Benzimidazoles inhibited rat embryo cell growth and differentiation at nanomolar concentrations with a potency order matching their mammalian tubulin inhibition, while a prospective cohort of 192 pregnancies found no excess of major malformations at pinworm doses. No record here covers pregnancy at the high doses used for echinococcosis or oncology.

Chapters are assembled from supplied drafts and curated literature summaries. Statements remain unverified against the primary studies, and the ledger is not medical advice.

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