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Study · In vitro (cells) · 2026

6 results

Therapeutic Peptide SS-31 Modulates Membrane Binding and Aggregation of α-Synuclein and Restores Impaired Mitochondrial Function.

Stefaniak E, Cui B, Yan X, Sun K, Teng X, Ying L

Chemical biology & drug design1 Jun 2026

PMID42219795 (opens in a new tab)DOI10.1111/cbdd.70332 (opens in a new tab)PepBankPUB-42219795
Publisher pagePubMedAsk about this study
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Summary

Membrane binding and aggregation properties of α-synuclein are closely associated with Parkinson's disease and a class of related syndromes named as synucleinopathy. This study explored the potential of SS-31 (Elamipretide), a therapeutic tetrapeptide with alternating cationic and aromatic residues and known properties of mitochondrial inner membrane binding and oxidative stress reduction, in modulating α-synuclein interaction with the lipid membranes and mitigating the impairment of mitochondrial function induced by α-synuclein oligomers. It was demonstrated by both fluorescence correlation spectroscopy and fluorescence anisotropy that SS-31 displaces both wild-type and N-terminal acetylated α-synuclein from negatively charged small unilamellar vesicles in a dose-dependent manner. Thioflavin-T assay and transmission electron microscopy showed that SS-31 inhibits membrane-induced α-synuclein aggregation and alters the morphology of α-synuclein fibrils. Moreover, MTT assay and Seahorse Mito Stress Test indicated that SS-31 enhances cell viability and restores impaired mitochondrial function in α-synuclein oligomer-treated neuroblastoma cells. Finally, confocal imaging revealed that SS-31 hinders cellular uptake of α-synuclein oligomers, possibly by modifying cell membrane electrostatics. These findings suggest that SS-31 potentially attenuates α-synuclein induced mitochondrial impairment via its interaction with the lipid membranes, justifying further development of a peptide-based intervention against α-synuclein mediated pathology.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study6

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

  1. 01LabIn vitro (cells)Efficacy outcome

    In neuroblastoma cells treated with α-synuclein oligomers, SS‑31 enhanced cell viability.

    In plain wordsIn nerve-type cells exposed to toxic α-synuclein, SS‑31 improved cell survival.

    Peptide
    Elamipretide (SS-31)
    Outcome
    IncreaseCell viability with alpha-synuclein oligomers
    Study

    n: not reported in source

    Neuroblastoma cells treated with alpha-synuclein oligomers
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Moreover, MTT assay and Seahorse Mito Stress Test indicated that SS-31 enhances cell viability and restores impaired mitochondrial function in α-synuclein oligomer-treated neuroblastoma cells.
    1 context sentence
    Summary · context
    This study explored the potential of SS-31 (Elamipretide), a therapeutic tetrapeptide with alternating cationic and aromatic residues and known properties of mitochondrial inner membrane binding and oxidative stress reduction, in modulating α-synuclein interaction with the lipid membranes and mitigating the impairment of mitochondrial function induced by α-synuclein oligomers.
  2. 02LabIn vitro (cells)Mechanism

    In neuroblastoma cells treated with α-synuclein oligomers, SS‑31 restored impaired mitochondrial function.

    In plain wordsIn nerve-type cells exposed to toxic α-synuclein, SS‑31 restored mitochondrial function.

    Peptide
    Elamipretide (SS-31)
    Outcome
    IncreaseMitochondrial function with alpha-synuclein oligomers
    Study

    n: not reported in source

    Neuroblastoma cells treated with alpha-synuclein oligomers
    Outcome group
    Mitochondrial function · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Moreover, MTT assay and Seahorse Mito Stress Test indicated that SS-31 enhances cell viability and restores impaired mitochondrial function in α-synuclein oligomer-treated neuroblastoma cells.
    1 context sentence
    Summary · context
    This study explored the potential of SS-31 (Elamipretide), a therapeutic tetrapeptide with alternating cationic and aromatic residues and known properties of mitochondrial inner membrane binding and oxidative stress reduction, in modulating α-synuclein interaction with the lipid membranes and mitigating the impairment of mitochondrial function induced by α-synuclein oligomers.
  3. 03LabIn vitro (cells)Mechanism

    In neuroblastoma cells, SS‑31 hindered cellular uptake of α-synuclein oligomers, possibly by modifying cell membrane electrostatics.

    In plain wordsIn nerve-type cells, SS‑31 reduced how much toxic α-synuclein entered the cells.

    Peptide
    Elamipretide (SS-31)
    Outcome
    DecreaseCellular uptake of alpha-synuclein oligomers
    Study

    n: not reported in source

    Neuroblastoma cells treated with alpha-synuclein oligomers
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Finally, confocal imaging revealed that SS-31 hinders cellular uptake of α-synuclein oligomers, possibly by modifying cell membrane electrostatics.
    1 context sentence
    Summary · context
    This study explored the potential of SS-31 (Elamipretide), a therapeutic tetrapeptide with alternating cationic and aromatic residues and known properties of mitochondrial inner membrane binding and oxidative stress reduction, in modulating α-synuclein interaction with the lipid membranes and mitigating the impairment of mitochondrial function induced by α-synuclein oligomers.
  4. 04LabIn vitro (cell-free)Mechanism

    In lab tests, SS‑31 displaced wild-type and N-terminal acetylated α-synuclein from negatively charged small unilamellar vesicles in a dose-dependent manner.

    In plain wordsIn lab tests, SS‑31 pushed the protein α-synuclein off fat-membrane particles, more so at higher doses.

    Peptide
    Elamipretide (SS-31)
    Outcome
    DecreaseDisplacement of alpha-synuclein from lipid vesicles
    Study

    n: not reported in source

    Negatively charged small unilamellar vesicles
    Outcome group
    Receptor activity and mechanism · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    It was demonstrated by both fluorescence correlation spectroscopy and fluorescence anisotropy that SS-31 displaces both wild-type and N-terminal acetylated α-synuclein from negatively charged small unilamellar vesicles in a dose-dependent manner.
    1 context sentence
    Summary · context
    This study explored the potential of SS-31 (Elamipretide), a therapeutic tetrapeptide with alternating cationic and aromatic residues and known properties of mitochondrial inner membrane binding and oxidative stress reduction, in modulating α-synuclein interaction with the lipid membranes and mitigating the impairment of mitochondrial function induced by α-synuclein oligomers.
  5. 05LabIn vitro (cell-free)Mechanism

    In lab tests, SS‑31 inhibited membrane-induced α-synuclein aggregation.

    In plain wordsIn lab tests, SS‑31 reduced clumping of the protein α-synuclein on membranes.

    Peptide
    Elamipretide (SS-31)
    Outcome
    DecreaseMembrane-induced alpha-synuclein aggregation
    Study

    n: not reported in source

    Alpha-synuclein with lipid membranes
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Thioflavin-T assay and transmission electron microscopy showed that SS-31 inhibits membrane-induced α-synuclein aggregation and alters the morphology of α-synuclein fibrils.
    1 context sentence
    Summary · context
    This study explored the potential of SS-31 (Elamipretide), a therapeutic tetrapeptide with alternating cationic and aromatic residues and known properties of mitochondrial inner membrane binding and oxidative stress reduction, in modulating α-synuclein interaction with the lipid membranes and mitigating the impairment of mitochondrial function induced by α-synuclein oligomers.
  6. 06LabIn vitro (cell-free)Mechanism

    In lab tests, SS‑31 altered the morphology of α-synuclein fibrils.

    In plain wordsIn lab tests, SS‑31 changed the shape of fibres formed by the protein α-synuclein.

    Peptide
    Elamipretide (SS-31)
    Outcome
    Not applicableAlpha-synuclein fibril morphology
    Study

    n: not reported in source

    Alpha-synuclein fibrils
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Thioflavin-T assay and transmission electron microscopy showed that SS-31 inhibits membrane-induced α-synuclein aggregation and alters the morphology of α-synuclein fibrils.
    1 context sentence
    Summary · context
    This study explored the potential of SS-31 (Elamipretide), a therapeutic tetrapeptide with alternating cationic and aromatic residues and known properties of mitochondrial inner membrane binding and oxidative stress reduction, in modulating α-synuclein interaction with the lipid membranes and mitigating the impairment of mitochondrial function induced by α-synuclein oligomers.

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

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Terms as the source lists them.

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