Component

Avermectin

Parent macrocyclic lactone family from which ivermectin is derived; findings recorded against avermectin are not interchangeable with ivermectin.

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

Read recorded mechanisms Open recursive mind map

How nutrients influence it

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

How nutrients reach it in more than one step

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

Tracing routes…

What it does

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

Recorded relationships

What it acts on

  1. Avermectin inhibited NF-kappa-B p65 translocation into the nucleus and inhibited JNK and p38 phosphorylation in lipopolysaccharide-stimulated mouse macrophages.

    Avermectin → NF-kappa-B p65 nuclear translocation in RAW 264.7 macrophages source_derived_draftungraded
    Experimental context and source evidence
    duration
    30 minutes after lipopolysaccharide
    evidence_access
    Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    experimental_model
    Mouse RAW 264.7 macrophages
    exposure
    Avermectin 0.625, 1.25 or 5 mg/L for one hour before 1 mg/L lipopolysaccharide
    limitations
    The compound tested was avermectin, the parent macrocyclic lactone, not ivermectin, and tumour necrosis factor alpha, interleukin-1 beta and interleukin-10 were regulated while interleukin-6 was not significantly affected.
    organism
    Mouse RAW 264.7 macrophages
    plain_language
    Avermectin inhibited NF-kappa-B p65 translocation into the nucleus and inhibited JNK and p38 phosphorylation in lipopolysaccharide-stimulated mouse macrophages.
    primary_references
    Avermectin exerts anti-inflammatory effect by downregulating the nuclear transcription factor kappa-B and mitogen-activated protein kinase activation pathway. (2009). https://pubmed.ncbi.nlm.nih.gov/19453757/ DOI: 10.1111/j.1472-8206.2009.00684.x
    route
    In vitro
    tissue
    NF-kappa-B and MAP kinase signalling, cytokine output

    Ivermectin: mechanism of action across parasite, host barrier and mammalian targets (2026-09-22) · lines 222–231

    Original AI-assisted curation of sixteen primary studies resolved by PubMed title search and cross-checked against live PubMed metadata. Study-specific citations, concentrations, negative findings and limitations retained. Not publisher full text. · supports · · source_derived_draft · unverified_draft

    ## avermectin-nfkb-mapk-inflammation Avermectin inhibited NF-kappa-B p65 translocation into the nucleus and inhibited JNK and p38 phosphorylation in lipopolysaccharide-stimulated mouse macrophages. Model/species: Mouse RAW 264.7 macrophages Tissue/system: NF-kappa-B and MAP kinase signalling, cytokine output Exposure: Avermectin 0.625, 1.25 or 5 mg/L for one hour before 1 mg/L lipopolysaccharide Route: In vitro Duration: 30 minutes after lipopolysaccharide Limits: The compound tested was avermectin, the parent macrocyclic lactone, not ivermectin, and tumour necrosis factor alpha, interleukin-1 beta and interleukin-10 were regulated while interleukin-6 was not significantly affected. Primary reference: Avermectin exerts anti-inflammatory effect by downregulating the nuclear transcription factor kappa-B and mitogen-activated protein kinase activation pathway. (2009). https://pubmed.ncbi.nlm.nih.gov/19453757/ DOI: 10.1111/j.1472-8206.2009.00684.x Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    Complete structured claim and evidence

  2. An avermectin-sensitive glutamate-gated chloride channel was cloned from Caenorhabditis elegans and shown to be a new member of the ligand-gated ion channel superfamily.

    Avermectin → Caenorhabditis elegans glutamate-gated chloride channel alpha / GluCl source_derived_draftungraded
    Experimental context and source evidence
    duration
    Acute
    evidence_access
    Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    experimental_model
    Caenorhabditis elegans complementary DNAs expressed in Xenopus oocytes
    exposure
    Avermectin applied to the expressed channel
    limitations
    The same report notes that avermectins also interact with vertebrate and invertebrate GABA receptors, so an invertebrate-only target cannot be inferred from this channel alone.
    organism
    Caenorhabditis elegans complementary DNAs expressed in Xenopus oocytes
    plain_language
    An avermectin-sensitive glutamate-gated chloride channel was cloned from Caenorhabditis elegans and shown to be a new member of the ligand-gated ion channel superfamily.
    primary_references
    Cloning of an avermectin-sensitive glutamate-gated chloride channel from Caenorhabditis elegans. (1994). https://pubmed.ncbi.nlm.nih.gov/7935817/ DOI: 10.1038/371707a0
    route
    In vitro
    tissue
    Expression cloning and electrophysiology of a glutamate-gated chloride channel

    Ivermectin: mechanism of action across parasite, host barrier and mammalian targets (2026-09-22) · lines 13–22

    Original AI-assisted curation of sixteen primary studies resolved by PubMed title search and cross-checked against live PubMed metadata. Study-specific citations, concentrations, negative findings and limitations retained. Not publisher full text. · supports · · source_derived_draft · unverified_draft

    ## ivermectin-glucl-cloning An avermectin-sensitive glutamate-gated chloride channel was cloned from Caenorhabditis elegans and shown to be a new member of the ligand-gated ion channel superfamily. Model/species: Caenorhabditis elegans complementary DNAs expressed in Xenopus oocytes Tissue/system: Expression cloning and electrophysiology of a glutamate-gated chloride channel Exposure: Avermectin applied to the expressed channel Route: In vitro Duration: Acute Limits: The same report notes that avermectins also interact with vertebrate and invertebrate GABA receptors, so an invertebrate-only target cannot be inferred from this channel alone. Primary reference: Cloning of an avermectin-sensitive glutamate-gated chloride channel from Caenorhabditis elegans. (1994). https://pubmed.ncbi.nlm.nih.gov/7935817/ DOI: 10.1038/371707a0 Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    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