Component

Clemastanin B

The 4,4-prime-bis-O-beta-D-glucopyranoside of (-)-lariciresinol.

3 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. Clemastanin B inhibited human H1N1 including swine-origin H1N1, H3N2 and influenza B, and avian H6N2, H7N3 and H9N2, with inhibitory concentrations of 0.087 to 0.72 mg/mL, and was inactive against respiratory syncytial virus, adenovirus 3, parainfluenza virus 3, enterovirus 71 and human rhinovirus.

    Clemastanin B → Influenza A and B virus replication in MDCK cells source_derived_draftungraded
    Experimental context and source evidence
    duration
    Not stated here
    evidence_access
    Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    experimental_model
    MDCK cells
    exposure
    Clemastanin B at 0.087 to 0.72 mg/mL
    limitations
    The active range is in milligrams per millilitre, which is far above the concentrations at which the aglycone mechanisms operate. The inactivity against five unrelated viruses is recorded as a negative result in the same assay system.
    organism
    MDCK cells
    plain_language
    Clemastanin B inhibited human H1N1 including swine-origin H1N1, H3N2 and influenza B, and avian H6N2, H7N3 and H9N2, with inhibitory concentrations of 0.087 to 0.72 mg/mL, and was inactive against respiratory syncytial virus, adenovirus 3, parainfluenza virus 3, enterovirus 71 and human rhinovirus.
    primary_references
    Antiviral activity of Isatis indigotica root-derived clemastanin B against human and avian influenza A and B viruses in vitro. (2013). https://pubmed.ncbi.nlm.nih.gov/23403777/ DOI: 10.3892/ijmm.2013.1274
    route
    In vitro
    tissue
    Virus replication across subtypes and unrelated respiratory viruses

    Lariciresinol: five molecules under one name, and the mechanisms each one carries (2026-09-22) · lines 143–152

    Original AI-assisted curation of twelve primary studies, every abstract read and all DOIs cross-checked against live PubMed metadata. Mechanism edges only, with no conclusion or claim of benefit recorded. Three author clusters account for eight of the twelve and carry shared laboratory keys. Study-specific concentrations, negative findings and limitations retained. Not publisher full text. · supports · · source_derived_draft · unverified_draft

    ## clemastanin-b-influenza-subtype-range Clemastanin B inhibited human H1N1 including swine-origin H1N1, H3N2 and influenza B, and avian H6N2, H7N3 and H9N2, with inhibitory concentrations of 0.087 to 0.72 mg/mL, and was inactive against respiratory syncytial virus, adenovirus 3, parainfluenza virus 3, enterovirus 71 and human rhinovirus. Model/species: MDCK cells Tissue/system: Virus replication across subtypes and unrelated respiratory viruses Exposure: Clemastanin B at 0.087 to 0.72 mg/mL Route: In vitro Duration: Not stated here Limits: The active range is in milligrams per millilitre, which is far above the concentrations at which the aglycone mechanisms operate. The inactivity against five unrelated viruses is recorded as a negative result in the same assay system. Primary reference: Antiviral activity of Isatis indigotica root-derived clemastanin B against human and avian influenza A and B viruses in vitro. (2013). https://pubmed.ncbi.nlm.nih.gov/23403777/ DOI: 10.3892/ijmm.2013.1274 Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    Complete structured claim and evidence

  2. Clemastanin B, isolated from Equisetum arvense, was one of nine compounds evaluated for anti-inflammatory effects in keratinocytes stimulated with tumour necrosis factor alpha and interferon gamma.

    Clemastanin B → Inflammatory response of keratinocytes stimulated with TNF-alpha and interferon gamma source_derived_draftungraded
    Experimental context and source evidence
    duration
    Not stated here
    evidence_access
    Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    experimental_model
    Keratinocytes stimulated with TNFα and IFNγ
    exposure
    Clemastanin B, compound 6 of nine isolated secondary metabolites
    limitations
    The abstract states the isolation and the model; the phosphorylation targets and the active concentration are in the full text and were not read here.
    organism
    Keratinocytes stimulated with TNFα and IFNγ
    plain_language
    Clemastanin B, isolated from Equisetum arvense, was one of nine compounds evaluated for anti-inflammatory effects in keratinocytes stimulated with tumour necrosis factor alpha and interferon gamma.
    primary_references
    Anti-Inflammatory Effects of Secondary Metabolites Isolated from Equisetum arvense L. in TNFα/IFNγ-Stimulated Keratinocytes. (2023). https://pubmed.ncbi.nlm.nih.gov/37895949/ DOI: 10.3390/ph16101478
    route
    In vitro
    tissue
    Inflammatory signalling and chemokine output

    Lariciresinol: five molecules under one name, and the mechanisms each one carries (2026-09-22) · lines 154–163

    Original AI-assisted curation of twelve primary studies, every abstract read and all DOIs cross-checked against live PubMed metadata. Mechanism edges only, with no conclusion or claim of benefit recorded. Three author clusters account for eight of the twelve and carry shared laboratory keys. Study-specific concentrations, negative findings and limitations retained. Not publisher full text. · supports · · source_derived_draft · unverified_draft

    ## clemastanin-b-lowers-stat1-and-nf-kb-phosphorylation Clemastanin B, isolated from Equisetum arvense, was one of nine compounds evaluated for anti-inflammatory effects in keratinocytes stimulated with tumour necrosis factor alpha and interferon gamma. Model/species: Keratinocytes stimulated with TNFα and IFNγ Tissue/system: Inflammatory signalling and chemokine output Exposure: Clemastanin B, compound 6 of nine isolated secondary metabolites Route: In vitro Duration: Not stated here Limits: The abstract states the isolation and the model; the phosphorylation targets and the active concentration are in the full text and were not read here. Primary reference: Anti-Inflammatory Effects of Secondary Metabolites Isolated from Equisetum arvense L. in TNFα/IFNγ-Stimulated Keratinocytes. (2023). https://pubmed.ncbi.nlm.nih.gov/37895949/ DOI: 10.3390/ph16101478 Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    Complete structured claim and evidence

  3. Influenza virus ribonucleoprotein was retained in the nucleus after treatment with clemastanin B, and virus titre fell when cells were treated after infection, particularly at the early stage.

    Clemastanin B → Influenza ribonucleoprotein export from the nucleus source_derived_draftungraded
    Experimental context and source evidence
    duration
    Treatment after infection
    evidence_access
    Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    experimental_model
    MDCK cells
    exposure
    Clemastanin B, 7S,8R,8'R-(−)-lariciresinol-4,4'-bis-O-β-D-glucopyranoside
    limitations
    The authors state the result is consistent with viral endocytosis, uncoating or ribonucleoprotein export as the target and do not distinguish between them.
    organism
    MDCK cells
    plain_language
    Influenza virus ribonucleoprotein was retained in the nucleus after treatment with clemastanin B, and virus titre fell when cells were treated after infection, particularly at the early stage.
    primary_references
    Antiviral activity of Isatis indigotica root-derived clemastanin B against human and avian influenza A and B viruses in vitro. (2013). https://pubmed.ncbi.nlm.nih.gov/23403777/ DOI: 10.3892/ijmm.2013.1274
    route
    In vitro
    tissue
    Viral ribonucleoprotein localisation and virus titre

    Lariciresinol: five molecules under one name, and the mechanisms each one carries (2026-09-22) · lines 132–141

    Original AI-assisted curation of twelve primary studies, every abstract read and all DOIs cross-checked against live PubMed metadata. Mechanism edges only, with no conclusion or claim of benefit recorded. Three author clusters account for eight of the twelve and carry shared laboratory keys. Study-specific concentrations, negative findings and limitations retained. Not publisher full text. · supports · · source_derived_draft · unverified_draft

    ## clemastanin-b-retains-influenza-rnp-in-the-nucleus Influenza virus ribonucleoprotein was retained in the nucleus after treatment with clemastanin B, and virus titre fell when cells were treated after infection, particularly at the early stage. Model/species: MDCK cells Tissue/system: Viral ribonucleoprotein localisation and virus titre Exposure: Clemastanin B, 7S,8R,8'R-(−)-lariciresinol-4,4'-bis-O-β-D-glucopyranoside Route: In vitro Duration: Treatment after infection Limits: The authors state the result is consistent with viral endocytosis, uncoating or ribonucleoprotein export as the target and do not distinguish between them. Primary reference: Antiviral activity of Isatis indigotica root-derived clemastanin B against human and avian influenza A and B viruses in vitro. (2013). https://pubmed.ncbi.nlm.nih.gov/23403777/ DOI: 10.3892/ijmm.2013.1274 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