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Study · Not a test of the peptide alone · 2025

2 results

Pegmolesatide ameliorates indoxyl sulfate-induced cardiomyocyte hypertrophy through modulating the EPOR-CD131-dependent JAK2/STAT3 signaling pathway.

Zhang X, Li S, Lin T, Gan L, Zhu L, Zuo L

International immunopharmacology14 Oct 2025

Summary

The text of this summary is not shown here, because the article license does not allow reuse. Read it at the source (opens in a new tab)

Text rights: Publisher copyright. Results still quote short attributed sentences.

Results from this study2

No result from this study comes from a test of the peptide.

Studies that did not test the peptide alone2

In this study, Cibinetide (ARA-290) was a lab tool or a carrier, part of a mix, or the subject of a lab method. These results are not evidence about taking Cibinetide (ARA-290).

  1. 01LabNot a test of Cibinetide (ARA-290) aloneIn vitro (cells)Mechanism

    In indoxyl sulfate-treated H9c2 cardiomyocytes, the CD131 agonist ARA290 reversed the cardioprotective effects of pegmolesatide.

    In plain wordsIn cells, ARA290 used as a tool reversed the protective effect of another drug, pegmolesatide.

    Outcome
    DecreaseReversal of pegmolesatide cardioprotection by ARA290
    Study

    n: not reported in source

    H9c2 cardiomyocytes with indoxyl sulfate-induced hypertrophy
    Outcome group
    Receptor activity and mechanism · Cardiovascular

    Source sentences

    Summary
    Functional rescue experiments showed that the cardioprotective effects of Pegmolesatide were reversed by CD131 agonist ARA290 or STAT3 activator Colivelin.
    2 context sentences
    Summary · context
    H9c2 cardiomyocytes were assigned to different treatment groups (vehicle, IS, IS+P, P) and RNA sequencing was performed to identify dysregulated signaling pathways.
    Summary · context
    Mechanistic exploration groups supplemented with CD131 agonist ARA290, STAT3 activator Colivelin, or STAT3 inhibitor Stattic for rescue experiments.

    In this study, Cibinetide (ARA-290) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking Cibinetide (ARA-290).

  2. 02LabNot a test of Cibinetide (ARA-290) aloneIn vitro (cells)Mechanism

    In indoxyl sulfate-treated H9c2 cardiomyocytes, combined ARA290 and the STAT3 inhibitor Stattic partially restored the anti-hypertrophic activity of pegmolesatide.

    In plain wordsIn cells, ARA290 with Stattic partly restored the anti-growth effect of another drug, pegmolesatide.

    Outcome
    IncreaseRestoration of anti-hypertrophic activity by ARA290 with Stattic
    Study

    n: not reported in source

    H9c2 cardiomyocytes with indoxyl sulfate-induced hypertrophy
    Outcome group
    Receptor activity and mechanism · Cardiovascular

    Source sentences

    Summary
    Notably, combined treatment with ARA290 and STAT3 inhibitor Stattic partially restored its anti-hypertrophic activity.
    2 context sentences
    Summary · context
    H9c2 cardiomyocytes were assigned to different treatment groups (vehicle, IS, IS+P, P) and RNA sequencing was performed to identify dysregulated signaling pathways.
    Summary · context
    Mechanistic exploration groups supplemented with CD131 agonist ARA290, STAT3 activator Colivelin, or STAT3 inhibitor Stattic for rescue experiments.

    In this study, Cibinetide (ARA-290) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking Cibinetide (ARA-290).

AI wrote and checked these results. AI can make mistakes, so check important results against the source.

Version history

PepBank keeps every version of the data on this study. Status changes from Retraction Watch, Europe PMC and Crossref are listed with their source.

  1. Version 3Current

    27 Oct 2026, 16:32 UTC

    Study data updated · source update from Europe PMC

  2. Version 2

    10 Oct 2026, 10:21 UTC

    Study results updated

  3. Version 1

    9 Oct 2026, 03:13 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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