Peptide Library

Human study PLS-00137

Hypomethylation of thymosin β4 promoter is associated with glucocorticoid therapy in patients with acute-on-chronic hepatitis B-induced liver failure.

Case-control study · Not reported participants enrolled · not included in the assessments (wrong compound)

Version 1 · published November 8, 2026 · evidence through November 8, 2026 · research snapshot 2026.1.1 · methodology ev-1 · Automated assessment by AI (claude-opus-5-5 and claude-sonnet-5-5), not reviewed by a person.

Only the abstract was available. Essential methods may be missing, which limits what can be judged.

Reports of this study

Every publication, registration and abstract describing this one study. Participants are counted once.

  • Hypomethylation of thymosin β4 promoter is associated with glucocorticoid therapy in patients with acute-on-chronic hepatitis B-induced liver failure.primary · International health · 2023-01-01 · PMID 35150577 · DOI

Design and participants

Design
Case-control study
Population
Patients with acute-on-chronic hepatitis B liver failure (ACHBLF), patients with chronic hepatitis B, and healthy controls, retrospectively enrolled
Conditions
Acute-on-chronic hepatitis B liver failure, Chronic hepatitis B
Planned enrollment (registry)
Not reported
Enrolled
Not reported
Randomized
Not reported
Completed follow-up
Not reported

Intervention and comparator

What each group received. Related peptides, analogs and combinations are never treated as the compound itself.

    What the authors reported

    As stated in the sources. This is the authors’ account, not Peptide Library’s assessment.

    Adverse events

    None reported. That is not evidence of safety, and how safety was monitored isn’t described.

    The authors concluded (paraphrased): ACHBLF patients with low Tβ4 promoter methylation may respond more favorably to glucocorticoid treatment.

    Peptide Library’s assessment

    An automated assessment, made by AI separately from the authors’ conclusions and not reviewed by a person. How risk of bias is assessed.

    Limitations

    • other: Tβ4 was not given to participants; it was measured only as an endogenous gene methylation and expression biomarker.
    • abstract only: Only the PubMed abstract is available in the record, so methods and results details are limited.
    • selection bias: Participants were retrospectively enrolled, which raises concern about selection and confounding.
    • confounding: The retrospective comparison of methylation groups was not described as adjusted for disease severity or other prognostic factors.
    • inappropriate endpoint: Tβ4 was only measured as an endogenous biomarker and not administered, so the study gives no evidence on the effects or safety of Tβ4 as a treatment.

    No risk-of-bias assessment has been published for this study’s results.

    Claims this study informs

    Where each value comes from

    • arms: PMID 35150577, abstract (Methods, sentences 1 and 3) · extracted by AI (automated, not verified by a person) · abstract only
    • author_conclusion: PMID 35150577, abstract (Conclusions, sentence 1) · extracted by AI (automated, not verified by a person) · abstract only
    • design: PMID 35150577, abstract (Methods, sentence 1) · extracted by AI (automated, not verified by a person) · abstract only
    • population: PMID 35150577, abstract (Methods, sentence 1) · extracted by AI (automated, not verified by a person) · abstract only

    • Version 1 · published November 8, 2026 · evidence through November 8, 2026 · research snapshot 2026.1.1 · methodology ev-1 · Automated assessment by AI (claude-opus-5-5 and claude-sonnet-5-5), not reviewed by a person.

    These assessments describe published research. Records marked automated were produced by AI under the published methodology and have not been reviewed by a person; they can contain errors. None of this is medical advice, not a statement about any product’s safety for human use, and not a regulatory approval. Peptide Library’s vendor and partner relationships play no part in them (editorial independence).