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Study · In vitro (cells) · 2021

3 results

Drp1-dependent peptide reverse mitochondrial fragmentation, a homeostatic response in Friedreich ataxia.

Johnson J, Mercado-Ayón E, Clark E, Lynch D, Lin H

Pharmacology research & perspectives1 May 2021Cited by 25 (Europe PMC)

PMID33951329 (opens in a new tab)PMCIDPMC8099044 (opens in a new tab)DOI10.1002/prp2.755 (opens in a new tab)PepBankPUB-33951329
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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: CC BY-NC-ND. Results still quote short attributed sentences.

Results from this study3

2 results from studies that gave the peptide. No result from this study comes from people.

  1. 01LabIn vitro (cells)Mechanism

    In Friedreich ataxia cellular models, SS‑31 reversed excessive mitochondrial fragmentation through a Drp1-dependent mechanism.

    In plain wordsIn lab cells from Friedreich ataxia models, SS‑31 reversed excessive splitting of mitochondria.

    Peptide
    Elamipretide (SS-31)
    Outcome
    DecreaseMitochondrial fragmentation
    Study

    humann: not reported in source

    Friedreich ataxia cellular models (patient fibroblasts)
    Outcome group
    Mitochondrial function · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    The cardiolipin-stabilizing compound SS-31 similarly reverses fragmentation through a Drp1-dependent mechanism
    1 context sentence
    Summary · context
    This paper demonstrates that frataxin deficiency causes excessive mitochondrial fragmentation that is dependent upon Drp1 activity in Friedreich ataxia cellular models.
  2. 02LabIn vitro (cells)Mechanism

    In Friedreich ataxia cellular models, SS‑31 did not affect ATP levels.

    In plain wordsIn lab cells from Friedreich ataxia models, SS‑31 did not change cell energy (ATP) levels.

    Peptide
    Elamipretide (SS-31)
    Outcome
    No significant changeATP levels
    Study

    humann: not reported in source

    Friedreich ataxia cellular models (patient fibroblasts)
    Outcome group
    Mitochondrial function · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    but it does not affect ATP levels.
    1 context sentence
    Summary · context
    This paper demonstrates that frataxin deficiency causes excessive mitochondrial fragmentation that is dependent upon Drp1 activity in Friedreich ataxia cellular models.

Studies that did not test the peptide alone1

In this study, Elamipretide (SS-31) 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 Elamipretide (SS-31).

  1. 03LabNot a test of Elamipretide (SS-31) aloneIn vitro (cells)Mechanism

    In FRDA patient fibroblasts, the combination of TAT-P110 and SS‑31 did not differ in effect from SS‑31 alone.

    In plain wordsIn lab cells, SS‑31 combined with TAT-P110 had the same effect as SS‑31 alone.

    Peptide
    Elamipretide (SS-31)
    Outcome
    No significant changeTAT-P110 plus SS-31 versus SS-31 alone in patient fibroblasts
    Study

    humann: not reported in source

    Friedreich ataxia cellular models (patient fibroblasts)
    Comparator
    SS-31 alone
    Outcome group
    Mitochondrial function · Nervous system and cognition

    Source sentences

    Summary
    The combination of TAT-P110 and SS-31 does not affect FRDA patient fibroblasts differently from SS-31 alone, suggesting that the two drugs act through the same pathway but differ in their ability to alter mitochondrial homeostasis.
    1 context sentence
    Summary · context
    This paper demonstrates that frataxin deficiency causes excessive mitochondrial fragmentation that is dependent upon Drp1 activity in Friedreich ataxia cellular models.

    In this study, Elamipretide (SS-31) 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 Elamipretide (SS-31).

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 2Current

    10 Oct 2026, 08:19 UTC

    Study results updated

  2. Version 1

    9 Oct 2026, 02:47 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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