Research peptides
SS-31
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SKUSS31
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Product details
Overview
SS-31, also known as elamipretide, is a synthetic tetrapeptide of the Szeto–Schiller family. Its sequence alternates cationic and aromatic residues studied in relation to mitochondrial-membrane interactions. Research considers cardiolipin, lipid-bilayer organisation, bioenergetic proteins, and cellular stress responses.
Structure and technical data
Technical data
Format: 30 mg. Explicit reference sequence: D-Arg–Dmt–Lys–Phe–NH2, where Dmt denotes 2′,6′-dimethyltyrosine. RXKF alone does not represent stereochemistry and amidation.
- Sequence
- D-Arg–Dmt–Lys–Phe–NH2
- Molecular formula
- C32H49N9O5
- Reported molecular mass
- 639.8 g/mol
- CAS number
- 736992-21-5
- PubChem CID
- 11764719
- Reported synonyms
- Elamipretide; SS-31; MTP-131
Reference molecular data.
View the PubChem record — PubChem CID 11764719
Dmt denotes 2′,6′-dimethyltyrosine; D-Arg specifies the first residue’s configuration and NH2 the C-terminal amidation. The molecular record excludes any salt or other formulation components.
Research context
The sections distinguish biophysical membrane experiments, cell cultures, animal models, and clinical studies with defined formulations. Membrane potential, ATP, reactive oxygen species, and organ function are different endpoints.
Membranes, cardiolipin, and electrostaticsLipid organisation and calciumMitochondrial proteins and ATP productionOxidative stress, enzymes, and cytokinesHeart, sepsis, and ischaemia–reperfusionEncephalopathy: Drp1, NLRP3, and microgliaLung and experimental inflammatory injuryAtherosclerosis and ApoE−/− modelsAgeing, microvessels, and muscleClinical research and retinal-source verification
Membranes, cardiolipin, and electrostatics
The 2020 biophysical paper compares model and mitochondrial membranes using experimental and computational approaches. The peptide partitions into the interfacial region; affinity and binding density depend on surface charge. Cardiolipin contributes to the inner membrane’s anionic environment. The proposed model concerns interfacial physical properties, not simply direct radical neutralisation.
Lipid organisation and calcium
In the same study, binding changes lipid packing without destabilising the bilayer under the tested conditions. Calcium experiments examine divalent-cation distribution at the interface and the energetic burden of mitochondrial stress. Surface-charge changes can affect ions and proteins; they do not imply that every membrane function changes in the same way.
Mitochondrial proteins and ATP production
The PNAS study uses chemical cross-linking and mass spectrometry to identify mitochondrial protein interactions with SS-31. Identified proteins mainly concern oxidative phosphorylation and 2-oxoglutarate processes and are associated with cardiolipin. Detected molecular proximity helps formulate mechanisms; it does not itself measure greater energy or performance in an organism.
Oxidative stress, enzymes, and cytokines
In the LPS-induced cardiac model, the 2019 study examines IL-6, IL-1β, and TNF-α alongside malondialdehyde, superoxide dismutase, and glutathione peroxidase. Cellular energy and mitochondrial potential are also considered. Oxidative damage, enzyme activity, and inflammatory transcripts describe different response levels; agreement is more informative than one isolated measurement.
Heart, sepsis, and ischaemia–reperfusion
Cardiac research includes H9C2 cells and LPS-exposed mice, alongside a pig model of haemorrhagic shock with aortic occlusion. The pig model compares cardiac, renal, inflammatory, and resuscitation indicators; not all outcomes change alike. Systemic-inflammatory injury and injury from interrupted and restored flow are different experimental conditions.
Encephalopathy: Drp1, NLRP3, and microglia
The sepsis-associated-encephalopathy study combines a mouse model with BV-2 microglial cells. It examines mitochondrial Drp1 translocation, fission, NLRP3 inflammasome activity, and recruitment of gasdermin-D’s N-terminal fragment. Mouse cognition and survival are also assessed. Cellular analyses seek links with mitochondrial dynamics without replacing human clinical evaluation.
Lung and experimental inflammatory injury
A 2024 primary paper studies LPS-induced lung injury through histology, transcriptomics, and S100A8/NLRP3/GSDMD pathway analyses. Inflammatory and cell-death endpoints are compared with tissue injury. This clarifies the pulmonary research context without equating LPS exposure, clinical sepsis, and every form of respiratory failure.
Atherosclerosis and ApoE−/− models
The PLOS ONE paper uses Western-diet-fed ApoE−/− mice, not rats. It examines plaque area and composition, oxidative markers, inflammatory mediators, and cholesterol-entry proteins such as CD36 and LOX-1. Plaque changes do not equal lower plasma lipids; compartments and endpoints must remain distinct when interpreting findings.
Ageing, microvessels, and muscle
The aged-mouse cerebral-microvessel abstract considers proteomic changes and mitochondrial components. The muscle review discusses mitochondrial capacity, insulin sensitivity, and muscle function across different targeted antioxidants. ROS also participate in physiological signalling; lowering an oxidative marker does not mean that more antioxidant activity is always better or that lifespan extension is established.
Clinical research and retinal-source verification
The small 2017 randomised heart-failure trial primarily examines tolerability and short-term echocardiographic changes; it does not alone establish lasting efficacy. The 2022 ARPE-19 retinal-cell paper was retracted: it is identified accordingly in the bibliography and does not support product conclusions. Preprints and conference abstracts are also distinguished from full papers.
References
- Nhu N. T. et al. (2022). Neuroprotective Effects of a Small Mitochondrially-Targeted Tetrapeptide Elamipretide in Neurodegeneration. Frontiers in Integrative Neuroscience. DOI: 10.3389/fnint.2021.747901
- Sabbah H. N. (2022). Elamipretide for Barth syndrome cardiomyopathy: gradual rebuilding of a failed power grid. Heart Failure Reviews, 27(5), 1911–1923. DOI: 10.1007/s10741-021-10177-8
- Daubert M. A. et al. (2017). Novel Mitochondria-Targeting Peptide in Heart Failure Treatment: A Randomized, Placebo-Controlled Trial of Elamipretide. Circulation: Heart Failure, 10(12). DOI: 10.1161/CIRCHEARTFAILURE.117.004389
- Patel N. et al. (2023). Elamipretide mitigates ischemia-reperfusion injury in a swine model of hemorrhagic shock. Scientific Reports, 13(1). DOI: 10.1038/s41598-023-31374-5
- Mitochondrial protein interaction landscape of SS-31
- Elamipretide Improves Mitochondrial Function
- SS31 Ameliorates Sepsis-Induced Heart Injury by Inhibiting Oxidative Stress and Inflammation
- SS-31 Improves Cognitive Function in Sepsis-Associated Encephalopathy by Inhibiting the Drp1-NLRP3 Inflammasome Activation
- The mitochondria-targeted peptide SS-31 binds lipid bilayers and modulates surface electrostatics as a key component of its mechanism of action
- Molecular Mechanism of Action of Mitochondrial Therapeutic SS-31 (Elamipretide): Membrane Interactions and Effects on Surface Electrostatics
- The beneficial effects of SS-31 on aging mice cerebral microvasculature
- [Retracted] Mitochondrial‐Targeted Antioxidant Peptide SS31 Prevents RPE Cell Death under Oxidative Stress
- SS31 alleviates LPS-induced acute lung injury by inhibiting inflammatory responses through the S100A8/NLRP3/GSDMD signaling pathway
- Chronic administration of mitochondrion-targeted peptide SS-31 prevents atherosclerotic development in ApoE knockout mice fed Western diet
- Mitochondria-Targeted Antioxidants and Skeletal Muscle Function
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