SS-31 Peptide (Elamipretide): Mitochondrial Research Guide
SS-31, also known in the scientific literature as elamipretide, MTP-131, or Bendavia, is a synthetic aromatic-cationic tetrapeptide developed for research on mitochondrial membranes, cardiolipin biology, oxidative phosphorylation, and cellular responses to bioenergetic stress. Unlike conventional antioxidant compounds that act mainly through nonspecific radical scavenging, SS-31 has been studied for its ability to partition at the inner mitochondrial membrane and interact with the anionic phospholipid cardiolipin.
Hanpro Peptides supplies SS-31 as a lyophilized material for laboratory, analytical, in-vitro, and appropriately authorized preclinical research. Current catalog variations include 10mg × 10 vials and 50mg × 10 vials. The catalog amount is a packaging specification, not a recommended concentration or dose. This research product is not the FDA-approved finished drug Forzinity and is not intended for human or veterinary administration, self-experimentation, diagnosis, treatment, or prevention of disease.
SS-31 molecular characteristics
| Research name | SS-31 peptide |
|---|---|
| Literature synonyms | Elamipretide, MTP-131, Bendavia |
| Peptide class | Aromatic-cationic tetrapeptide; Szeto-Schiller peptide |
| Condensed sequence | H-D-Arg-Dmt-Lys-Phe-NH2, where Dmt is 2,6-dimethyltyrosine |
| Peptide length | 4 amino-acid residues |
| Molecular formula | C32H49N9O5 for elamipretide free base; verify the supplied salt form on the lot documentation |
| Approximate molecular mass | 639.8 g/mol for elamipretide free base |
| CAS number | 736992-21-5 for elamipretide free base |
| Catalog specifications | 10mg × 10 vials and 50mg × 10 vials; confirm the selected variation |
| Intended use | Laboratory research and analytical use only |
The exact molecular mass of a supplied vial can differ from the free-base value when a counterion, salt, solvent, or water content is present. Researchers should use the lot-specific certificate of analysis and product label for identity, form, purity, and quantitative calculations. The abbreviations SS-31 and elamipretide are often used interchangeably in papers, but they do not make every commercial research preparation equivalent to a regulated drug product.
How SS-31 is studied at the mitochondrial membrane
1. Membrane partitioning and cardiolipin interaction
SS-31 carries both aromatic and positively charged features. Biophysical studies indicate that it partitions into the interfacial region of negatively charged lipid membranes, with binding influenced by membrane surface charge. Cardiolipin is enriched in the inner mitochondrial membrane and helps organize respiratory-chain complexes, cristae structure, and cytochrome c function. SS-31 has therefore become a useful probe for experiments that connect membrane composition with mitochondrial physiology.
2. Cytochrome c and electron-transfer research
Cardiolipin-associated cytochrome c participates in electron transfer, while altered cardiolipin interactions can also support peroxidase activity during cellular stress. In isolated membrane and mitochondrial systems, SS-31 has been reported to modulate the cardiolipin–cytochrome c interaction, preserve electron-carrier behavior, and influence respiration and ATP synthesis. These results are mechanistic observations from defined experimental systems and should not be converted into broad therapeutic promises.
3. Membrane electrostatics and ion distribution
More recent biophysical work suggests that SS-31 can alter surface electrostatics and lipid packing without simply disrupting the bilayer. Changes at the membrane interface may affect the local distribution of calcium and other ions, as well as the behavior of positively charged proteins. This provides researchers with testable hypotheses beyond the simplified label of “mitochondrial antioxidant.” Liposome composition, ionic strength, pH, and cardiolipin content should all be controlled when comparing results.
4. Reactive oxygen species and redox-sensitive endpoints
SS-31 is frequently evaluated in models that show elevated mitochondrial reactive oxygen species. Useful endpoints include mitochondrial superoxide indicators, lipid-peroxidation products, protein carbonyls, glutathione status, antioxidant-enzyme activity, and oxidative damage to mitochondrial components. Fluorescent probes can produce artifacts, so orthogonal measurements and probe-only controls are important. A reduction in one fluorescence signal is not by itself proof of direct radical scavenging or restored mitochondrial function.
5. Mitochondrial permeability, membrane potential, and cell death
Preclinical studies have measured SS-31-associated changes in mitochondrial membrane potential, cytochrome c release, permeability transition, caspase activation, and apoptosis or necrosis markers. These pathways are interconnected. A rigorous design should pair membrane-potential measurements with viability, ATP, respiratory, and morphological assays, rather than relying on a single dye or endpoint.
Common SS-31 research applications
Mitochondrial bioenergetics: SS-31 can be used in experimental systems that quantify oxygen-consumption rate, respiratory-control ratio, ATP production, proton leak, spare respiratory capacity, and respiratory-complex behavior. Isolated mitochondria, permeabilized cells, intact cells, and tissue preparations answer different questions and should not be treated as interchangeable.
Ischemia–reperfusion models: renal, cardiac, skeletal-muscle, and vascular models have examined mitochondrial structure, ATP recovery, inflammation, oxidative stress, and cell injury after temporary interruption and restoration of blood flow. Published positive findings are preclinical and model-specific. They do not establish that an unapproved research preparation is safe or effective in people.
Aging and tissue energetics: investigators use SS-31 to explore whether membrane organization, mitochondrial efficiency, and redox balance contribute to age-associated functional decline. Suitable endpoints may include muscle energetics, fatigue-related cellular phenotypes, mitochondrial ultrastructure, proteomics, metabolomics, and stress resistance. Chronological age, biological sex, tissue source, and baseline mitochondrial function are important covariates.
Neuroscience models: cell and animal studies have investigated SS-31 in the context of mitochondrial trafficking, synaptic function, protein-aggregation stress, and neuroinflammation. For example, studies using amyloid-related neuronal models have measured mitochondrial movement, fission and fusion proteins, synaptic markers, and cell survival. These systems model selected disease mechanisms; they do not reproduce an entire human neurodegenerative disorder.
Kidney and metabolic-stress research: ischemic kidney models have assessed mitochondrial morphology, respiration, ATP recovery, tubular injury, oxidative stress, and inflammatory responses. Other experimental work examines insulin resistance, lipid overload, or altered substrate utilization. Researchers should define the metabolic state of the system and include matched nutrient, vehicle, and time controls.
Membrane-biophysics and formulation studies: SS-31 can serve as a model aromatic-cationic peptide in liposome, bicelle, surface-charge, binding, and lipid-packing experiments. These studies help distinguish sequence-specific effects from general charge or hydrophobicity. Comparison peptides, scrambled controls, and membranes with and without cardiolipin improve interpretability.
Experimental design and controls
Start with a clearly defined research question: membrane binding, bioenergetic recovery, redox signaling, cell survival, or another mechanistic endpoint. Select concentration ranges from peer-reviewed work performed in the same model, then conduct a pilot concentration-response and time-course study. Include untreated, vehicle, positive, and negative controls. When feasible, add a sequence-related comparator or cardiolipin-deficient system to test whether the effect depends on the proposed mechanism.
Confirm that an apparent mitochondrial effect is not caused by changes in cell number, general toxicity, optical interference, or solvent composition. For cell experiments, combine a viability or cell-count measurement with at least two independent mitochondrial readouts. For isolated mitochondria, report substrate, respiratory state, temperature, oxygen range, normalization method, and preparation quality. Blinding and randomized sample order can reduce measurement bias in imaging and plate-based assays.
SS-31 research may involve both acute signaling and longer adaptive responses. Sampling only one time point can miss transient effects or confuse an early physicochemical event with later transcriptional remodeling. Record the timing of preparation, exposure, washing, harvesting, and measurement. When interpreting multi-omics data, validate key findings with targeted biochemical or functional methods.
Laboratory handling and analytical verification
Review the current label, safety documentation, and lot-specific certificate before use. Establish a qualified method for solvent selection, pH, target concentration, mixing, container material, storage temperature, and permitted hold time. Do not infer solubility or stability from another supplier’s formulation or from the branded finished drug. Salt form, excipients, concentration, and container can materially alter handling behavior.
Use calibrated equipment and document the vial identifier, lot, operator, preparation time, solvent lot, calculation, container, and storage history. Gentle mixing may help limit foaming or surface exposure, but the laboratory should validate recovery. If aliquoting is used to reduce repeated freeze-thaw exposure, determine acceptable cycle limits with a stability-indicating method. Prepare only what is needed for the authorized experiment and dispose of residual material according to institutional procedures.
Fit-for-purpose quality assessment can include reversed-phase HPLC or UPLC for purity and degradation profiling, LC-MS or high-resolution MS for identity, and water or counterion assessment when accurate mass balance is required. A chemical purity value does not demonstrate biological activity. Functional verification may use cardiolipin-containing membrane models, respiration assays, ATP measurements, or another assay relevant to the intended experiment.
Regulatory distinction: research SS-31 versus Forzinity
In September 2025, the U.S. FDA granted accelerated approval to Forzinity (elamipretide) injection for improving muscle strength in adult and pediatric patients with Barth syndrome who weigh at least 30 kg. The approval applies to that regulated prescription product, labeled indication, manufacturing system, formulation, and supply chain. Continued approval may depend on verification of clinical benefit in a confirmatory trial.
This Hanpro Peptides catalog item is a separate research material. It is not Forzinity, is not a substitute or generic version, and is not offered for any clinical use. FDA approval of a branded formulation does not authorize human administration of laboratory peptide material. Researchers should also note that a phase 3 trial in primary mitochondrial myopathy did not meet its primary 6-minute-walk or fatigue endpoints, underscoring why disease-specific evidence must not be generalized.
Frequently asked questions
Is SS-31 the same molecule as elamipretide?
SS-31 is the research code commonly associated with elamipretide, an aromatic-cationic tetrapeptide. However, molecular naming does not make a research vial equivalent to a finished prescription medicine. Researchers must verify the exact salt form, purity, identity, and intended use of the supplied material.
Does SS-31 directly scavenge all reactive oxygen species?
No broad conclusion should be made from the nickname “mitochondrial antioxidant.” Research supports interactions with mitochondrial membranes and cardiolipin, with downstream effects on electron transfer, membrane electrostatics, redox balance, and bioenergetics in specific systems. The mechanism should be tested in the chosen model with orthogonal assays.
What SS-31 concentration should a laboratory use?
There is no universal research concentration. It depends on the model, endpoint, exposure time, matrix, peptide form, and assay sensitivity. Select an initial range from peer-reviewed studies using a closely matched system, then validate it with concentration-response, recovery, and viability controls. Hanpro Peptides does not provide human or animal dosing instructions.
Can SS-31 be used in animal studies?
Only appropriately qualified institutions should decide whether and how to conduct in-vivo research. Any such work requires scientific justification, ethics approval, trained personnel, compliant procurement, and institution-approved protocols. This product page does not provide an administration route or dose.
How should SS-31 activity be confirmed?
Choose a functional assay that matches the hypothesis. Options include cardiolipin-containing membrane assays, mitochondrial respiration, ATP recovery, membrane potential, redox endpoints, or cytochrome c-related measurements. Combine functional results with chemical identity and purity data and include suitable positive, negative, and vehicle controls.
Is SS-31 approved by the FDA?
The branded prescription product Forzinity received FDA accelerated approval in 2025 for a narrow Barth syndrome indication. This laboratory research product has not been approved as a drug and must not be administered to humans or animals. The distinction between an approved finished drug and a research chemical is essential.
How should lyophilized SS-31 be stored?
Follow the current product label and lot-specific certificate. Protect unopened material from moisture and unnecessary light exposure. Once prepared in solution, stability depends on solvent, concentration, pH, container, temperature, and freeze-thaw history; establish these conditions experimentally rather than assuming a universal shelf life.
Related mitochondrial and cellular research products
- MOTS-c – mitochondrial-derived peptide for metabolic and stress-signaling research.
- Humanin – mitochondrial-derived peptide studied in cellular stress and survival models.
- NAD+ – research material for redox, metabolic, and enzyme-system studies.
- VIP – neuropeptide for VPAC receptor and neuroimmune research.
- LL-37 – host-defense peptide for controlled membrane and immune-signaling research.
For comparison of distinct catalog identities, also review reduced glutathione, 5-Amino-1MQ, and AICAR. These links are for research navigation, not recommendations to combine materials or evidence of interchangeable mechanisms. Each product requires its own documentation and suitability assessment.
Selected scientific and regulatory references
- PubChem record for elamipretide structure, formula, molecular weight, and synonyms.
- Study of SS-31, cardiolipin, cytochrome c, electron transport, and ATP synthesis.
- Biophysical study of SS-31 membrane partitioning and surface electrostatics.
- Preclinical study of ATP recovery and ischemic kidney injury.
- Cellular study of mitochondrial transport and synaptic endpoints in an amyloid-related model.
- MMPOWER-3 randomized trial in primary mitochondrial myopathy.
- FDA announcement of Forzinity accelerated approval for Barth syndrome.
Research-use disclaimer
SS-31 from Hanpro Peptides is supplied strictly for laboratory research and analytical use. It is not a medicine, dietary supplement, cosmetic ingredient for consumer application, or veterinary product. It is not Forzinity and must not be used for human or animal consumption, administration, diagnosis, treatment, or disease prevention. Purchasers are responsible for determining legal eligibility, institutional approval, safe handling, storage, experimental suitability, and disposal.




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