Component

Elevation of alanine and aspartate aminotransferase

Elevation of alanine and aspartate aminotransferase. Species, exposure and limitations are retained in each linked claim.

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

How nutrients influence it

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

How nutrients reach it in more than one step

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

Tracing routes…

What it does

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

Recorded relationships

What acts on it

  1. In 24 patients with newly diagnosed high-grade glioma given mebendazole with adjuvant temozolomide, four patients at 200 milligrams per kilogram per day developed elevated grade 3 alanine aminotransferase or aspartate transaminase after one month which reversed with lower dosing or discontinuation, plasma levels were variable but generally increased with dose, and mebendazole at doses up to 200 milligrams per kilogram demonstrated long-term safety and acceptable toxicity.

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

    Mebendazole: the tubulin it binds, why that is selective, the crystal form that decides whether any of it works, and the off-target that became an oncology programme (2026-09-22) · lines 576–587

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

    ### mbz-human-dose-escalation In 24 patients with newly diagnosed high-grade glioma given mebendazole with adjuvant temozolomide, four patients at 200 milligrams per kilogram per day developed elevated grade 3 alanine aminotransferase or aspartate transaminase after one month which reversed with lower dosing or discontinuation, plasma levels were variable but generally increased with dose, and mebendazole at doses up to 200 milligrams per kilogram demonstrated long-term safety and acceptable toxicity. Condition category: normal nutrient_topic: Mebendazole research collection; topical membership is not evidence of a direct clinical effect, and mebendazole is recorded separately from albendazole, from the benzimidazole class and from its own crystal forms. plain_language: At the highest dose one patient in six developed liver enzyme rises that reversed on stopping. organism: Human tissue_or_cell_type: Brain experimental_model: Single-centre dose-escalation and safety study in 24 patients with newly diagnosed high-grade glioma limitations: The only human oncology record here. It is a single-arm dose-escalation and safety study without a control group, so the survival figures cannot be read as efficacy. exposure: Oral mebendazole at 25, 50, 100 and 200 milligrams per kilogram per day with adjuvant temozolomide, with trough plasma levels at 4, 8 and 16 weeks evidence_span: {"source_cache": "artifacts/mebendazole-research/33506200.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "ab5f2c1d14ccb7fa9f690201326bdbfcab3e07758bc78b76ff9adec2ca774ec6", "start_char": 0, "end_char": 1712, "text_sha256": "ab5f2c1d14ccb7fa9f690201326bdbfcab3e07758bc78b76ff9adec2ca774ec6"} [mbz-p33506200] Mebendazole and temozolomide in patients with newly diagnosed high-grade gliomas: results of a phase 1 clinical trial. (2021). https://pubmed.ncbi.nlm.nih.gov/33506200/ DOI: 10.1093/noajnl/vdaa154
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. One patient developed a dose-limiting toxicity of transient self-limiting hepatic transaminase elevation 5 days after starting beta-glucan at 120 milligrams per kilogram per day, overall 1, 3, 12 and 24 evaluable patients had complete response, partial response, stable and progressive disease respectively at the end of treatment, positive human anti-mouse antibody response and dectin-1 rs3901533 polymorphism were associated with better overall survival, and beta-glucan dose level and serum beta-glucan levels did not correlate with response.

    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/glucan-research/34944886.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "ebbaee1e57b37044ff51d85d98d519101169e09a734d420c8bce53faab1d19f0", "start_char": 0, "end_char": 1471, "text_sha256": "ebbaee1e57b37044ff51d85d98d519101169e09a734d420c8bce53faab1d19f0"}
    experimental_model
    Phase I dose escalation of oral yeast glucan with an anti-GD2 antibody across cohorts of three to six patients
    exposure
    Oral yeast beta-glucan escalated from 10 to 200 milligrams per kilogram per day for 17 days with intravenous 3F8 antibody
    limitations
    A single-arm phase I with no control for the antibody alone, so the glucan contribution to any response cannot be isolated. Forty-four patients completed 141 cycles and forty were evaluable at end of treatment.
    nutrient_topic
    Beta-glucan research collection; topical membership is not evidence of a direct clinical effect, and each preparation is recorded as its own entity with no family link joining any pair. · Beta-glucan
    organism
    Human
    plain_language
    Across a twentyfold range of doses, how much was taken did not predict who responded; a receptor gene variant did.
    primary_references
    [bg-p34944886] Phase I Trial of Oral Yeast-Derived β-Glucan to Enhance Anti-GD2 Immunotherapy of Resistant High-Risk Neuroblastoma. (2021). https://pubmed.ncbi.nlm.nih.gov/34944886/ DOI: 10.3390/cancers13246265
    tissue_or_cell_type
    Relapsed or refractory high-risk neuroblastoma

    Beta-glucan: a structural family rather than an agent, what decides whether a bound glucan actually signals, the complement route that a cereal and a yeast preparation share, and the unequal human evidence behind each (2026-09-22) · lines 346–357

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Phase I dose escalation of oral yeast glucan with an anti-GD2 antibody across cohorts of three to six patients · source_derived_draft · unverified_draft

    ### bg-dose-did-not-track-response One patient developed a dose-limiting toxicity of transient self-limiting hepatic transaminase elevation 5 days after starting beta-glucan at 120 milligrams per kilogram per day, overall 1, 3, 12 and 24 evaluable patients had complete response, partial response, stable and progressive disease respectively at the end of treatment, positive human anti-mouse antibody response and dectin-1 rs3901533 polymorphism were associated with better overall survival, and beta-glucan dose level and serum beta-glucan levels did not correlate with response. Condition category: normal nutrient_topic: Beta-glucan research collection; topical membership is not evidence of a direct clinical effect, and each preparation is recorded as its own entity with no family link joining any pair. plain_language: Across a twentyfold range of doses, how much was taken did not predict who responded; a receptor gene variant did. organism: Human tissue_or_cell_type: Relapsed or refractory high-risk neuroblastoma experimental_model: Phase I dose escalation of oral yeast glucan with an anti-GD2 antibody across cohorts of three to six patients limitations: A single-arm phase I with no control for the antibody alone, so the glucan contribution to any response cannot be isolated. Forty-four patients completed 141 cycles and forty were evaluable at end of treatment. exposure: Oral yeast beta-glucan escalated from 10 to 200 milligrams per kilogram per day for 17 days with intravenous 3F8 antibody evidence_span: {"source_cache": "artifacts/glucan-research/34944886.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "ebbaee1e57b37044ff51d85d98d519101169e09a734d420c8bce53faab1d19f0", "start_char": 0, "end_char": 1471, "text_sha256": "ebbaee1e57b37044ff51d85d98d519101169e09a734d420c8bce53faab1d19f0"} [bg-p34944886] Phase I Trial of Oral Yeast-Derived β-Glucan to Enhance Anti-GD2 Immunotherapy of Resistant High-Risk Neuroblastoma. (2021). https://pubmed.ncbi.nlm.nih.gov/34944886/ DOI: 10.3390/cancers13246265
    Complete structured claim and evidence
  2. In a 47-year-old woman with multiple hydatid cysts of the liver in whom hepatitis developed after mebendazole treatment, clinical manifestations of hypersensitivity were absent and a correlation was found between serum mebendazole concentrations and the degree of cytolysis, which is compatible with a direct hepatotoxic effect of mebendazole.

    Experimental context and source evidence
    availability_state
    biomarker_context Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/mebendazole-research/3692093.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "dd4fb3feac1314a99fa05d5d06bd35a25350bcfed9e8570a1b0c5dc702e835b1", "start_char": 0, "end_char": 379, "text_sha256": "dd4fb3feac1314a99fa05d5d06bd35a25350bcfed9e8570a1b0c5dc702e835b1"}
    experimental_model
    Case report of hepatitis after mebendazole treatment with serial serum concentrations
    exposure
    Mebendazole treatment for multiple hepatic hydatid cysts
    limitations
    A single case. The correlation between drug concentration and cytolysis within one patient is what distinguishes a direct toxic effect from hypersensitivity, and hypersensitivity features were absent.
    nutrient_topic
    Mebendazole research collection; topical membership is not evidence of a direct clinical effect, and mebendazole is recorded separately from albendazole, from the benzimidazole class and from its own crystal forms. · Mebendazole
    organism
    Human
    plain_language
    The liver damage tracked the drug level rather than looking like an allergy, which points at the drug itself.
    primary_references
    [mbz-p3692093] Hepatotoxicity of mebendazole. Relationship with serum concentrations of the drug. (1987). https://pubmed.ncbi.nlm.nih.gov/3692093/
    tissue_or_cell_type
    Liver
    trigger_kind
    biomarker_context Imported condition classification; unverified.

    Mebendazole: the tubulin it binds, why that is selective, the crystal form that decides whether any of it works, and the off-target that became an oncology programme (2026-09-22) · lines 641–652

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

    ### mbz-dose-related-hepatotoxicity In a 47-year-old woman with multiple hydatid cysts of the liver in whom hepatitis developed after mebendazole treatment, clinical manifestations of hypersensitivity were absent and a correlation was found between serum mebendazole concentrations and the degree of cytolysis, which is compatible with a direct hepatotoxic effect of mebendazole. Condition category: biomarker_context nutrient_topic: Mebendazole research collection; topical membership is not evidence of a direct clinical effect, and mebendazole is recorded separately from albendazole, from the benzimidazole class and from its own crystal forms. plain_language: The liver damage tracked the drug level rather than looking like an allergy, which points at the drug itself. organism: Human tissue_or_cell_type: Liver experimental_model: Case report of hepatitis after mebendazole treatment with serial serum concentrations limitations: A single case. The correlation between drug concentration and cytolysis within one patient is what distinguishes a direct toxic effect from hypersensitivity, and hypersensitivity features were absent. exposure: Mebendazole treatment for multiple hepatic hydatid cysts evidence_span: {"source_cache": "artifacts/mebendazole-research/3692093.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "dd4fb3feac1314a99fa05d5d06bd35a25350bcfed9e8570a1b0c5dc702e835b1", "start_char": 0, "end_char": 379, "text_sha256": "dd4fb3feac1314a99fa05d5d06bd35a25350bcfed9e8570a1b0c5dc702e835b1"} [mbz-p3692093] Hepatotoxicity of mebendazole. Relationship with serum concentrations of the drug. (1987). https://pubmed.ncbi.nlm.nih.gov/3692093/
    Complete structured claim and evidence

In the sources

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

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

    Evidence, AI assistance and curation standards