What is SS-31?
SS-31 is a synthetic tetrapeptide of the Szeto-Schiller series. It is also written SS31, and its international nonproprietary name is elamipretide. Its sequence is D-Arg-Dmt-Lys-Phe-NH2, where Dmt is 2,6-dimethyltyrosine (PubChem CID 11764719). Its design motif alternates aromatic and basic residues. This gives the molecule a net positive charge. The motif also lets SS-31 cross cell membranes and concentrate in the inner mitochondrial membrane.
There, reported levels are more than 1000-fold higher than outside the cell (Zhao et al., 2004; Szeto, 2006). Since then it has been studied in isolated mitochondria and cell culture. It has also been studied in rodent models of ischemia-reperfusion and aging, and in human clinical trials. Disguised Alpha supplies SS-31 as a lyophilized powder for laboratory research use only. Nothing on this page is guidance for use in people.
Elamipretide is a drug. In September 2025 it was granted accelerated approval in the United States, under the brand name Forzinity. Its approved indication concerns muscle strength in adult and pediatric patients with Barth syndrome. The approval covers patients who weigh at least 30 kilograms. It was the first disease-specific approval for that condition.
The approval requires a confirmatory trial (Shirley, 2026). That approval covers that pharmaceutical product for that indication only. The SS-31 sold here is research-grade lyophilized peptide for laboratory use. It is not that drug product. It is not intended for that or any clinical indication, and it is not for use in people.
SS-31 reference data
| Property | Value |
|---|---|
| Name | SS-31 |
| Aliases | Elamipretide, MTP-131, Bendavia, SS 31, Szeto-Schiller peptide (PubChem CID 11764719) |
| Sequence | D-Arg-Dmt-Lys-Phe-NH2 (D-arginyl-2,6-dimethyl-L-tyrosyl-L-lysyl-L-phenylalaninamide, PubChem CID 11764719) |
| Peptide class | Aromatic-cationic mitochondria-targeting tetrapeptide |
| Molecular formula | C₃₂H₄₉N₉O₅ |
| Molecular weight | 639.8 g/mol |
| PubChem CID | 11764719 |
| Form | Lyophilized powder |
| Sizes carried | 10MG, 50MG |
| Testing | Third-party tested, certificate published on the product page and in the COA portal |
Formula, molecular weight and sizes come from the SS-31 product page. Sequence and aliases come from PubChem (CID 11764719). The figures above describe the free peptide. Salt forms add mass. So check identity and measured content against your lot's certificate before any quantitative work.
See it beside the other compounds on this site in the peptide molecular weight reference table.
What the research covers
Published work on SS-31 falls into six areas. Each summary below states the model used. Human studies used the drug product in clinical settings. They describe that product, not the research material sold here.
Design and mitochondrial targeting
The founding study screened peptide antioxidants that can enter cells. They were built on alternating aromatic and basic residues. In N2A nerve cells, they cut intracellular reactive oxygen species and cell death caused by t-butylhydroperoxide. Half-maximal effects were in the nanomolar range. In isolated mitochondria, they lowered reactive oxygen species production. They inhibited the permeability transition and swelling. They also stopped calcium-induced cytochrome c release. Analogs lacking dimethyltyrosine did not inhibit mitochondrial reactive oxygen species or swelling (Zhao et al., 2004). A review of the series set out the targeting rationale (Szeto, 2006).
Cardiolipin binding and cristae structure
One team used a polarity-sensitive fluorescent analog. They reported that SS-31 binds tightly to cardiolipin. Cardiolipin is the anionic phospholipid of the inner mitochondrial membrane. Cristae need it to form. The team found that the SS-31 and cardiolipin complex inhibited cytochrome c peroxidase activity. It did so by protecting the heme iron of cytochrome c. In rat kidneys put under ischemia, SS-31 given beforehand preserved cristae membranes. It also prevented mitochondrial swelling (Birk et al., 2013).
A review by the same group framed cardiolipin itself as the drug target. It also summed up how SS-31 acts (Szeto, 2014). Another study looked at rat hearts after ischemia-reperfusion. It used serial block face scanning electron microscopy with 3D reconstruction. This showed that cristae networks broke apart less. The drop in complex I, II and IV activity in permeabilized ventricular fibers was smaller. Mass spectrometry showed that cardiolipin levels were not restored (Allen et al., 2020).
Biophysics and protein interactions
Biophysical and computational work used model and mitochondrial membranes. It found that the peptide partitions into the interfacial region. Its affinity there is linked to surface charge. It does not destabilize lamellar bilayers. It alters lipid packing and surface electrostatics. Divalent cation distribution changed, and calcium stress in mitochondria fell (Mitchell et al., 2020). Cross-linking mass spectrometry found the protein partners of SS-31 in mitochondria. They act in oxidative phosphorylation and 2-oxoglutarate metabolism. All are known cardiolipin binders. They were often cross-linked near cardiolipin-interacting regions (Chavez et al., 2020).
Rodent ischemia-reperfusion models
In a rat model of kidney ischemia-reperfusion, SS-31 protected mitochondrial structure and respiration during early reperfusion. It sped up ATP recovery and cut tubular apoptosis and necrosis. It also lowered markers of oxidative stress and inflammation (Szeto et al., 2011). The cardiac work above used the same model in rat hearts (Allen et al., 2020).
Aged rodent energetics
One study used young (5 month) and old (27 month) mice. SS-31 was given once at 3 milligrams per kilogram. In old mice, resting and maximal mitochondrial ATP production returned to young levels within one hour. So did coupling of oxidative phosphorylation and muscle cell energy state. These were measured by combined optical and phosphorus-31 magnetic resonance spectroscopy. There was no observable effect in young muscle (Siegel et al., 2013).
An 8-week study in 26-month-old female mice reported a reversal of the decline in maximal mitochondrial ATP production and coupling. It also found a shift in glutathione redox status. Cysteine S-glutathionylation was reversed across the muscle proteome. This came without more mitochondrial protein (Campbell et al., 2019). In old mice, 8 weeks of SS-31 reversed much of the diastolic dysfunction. It also normalized cardiomyocyte proton leak and lowered mitochondrial reactive oxygen species. It added nothing further in mice already expressing mitochondrial-targeted catalase (Chiao et al., 2020).
Human clinical program and regulatory history
Elamipretide has been tested in several placebo-controlled trials. A phase 2 crossover trial studied 30 adults with primary mitochondrial myopathy. It missed statistical significance on its primary six-minute walk endpoint (Karaa et al., 2020). The phase 3 trial in 218 participants met neither primary endpoint (Karaa et al., 2023). A phase 2 trial studied 71 patients with heart failure with reduced ejection fraction.
It found no significant change in left ventricular end systolic volume at four weeks (Butler et al., 2020). In Barth syndrome, a 12-subject crossover trial met neither primary endpoint. Its open-label extension reported gains at 36 weeks (Reid Thompson et al., 2021). The 168-week extension reported that it stayed well tolerated. Six-minute walk gains built up over time (Thompson et al., 2024). That program led to the accelerated approval above (Shirley, 2026).
Key studies
- Zhao K, et al. "Cell-permeable peptide antioxidants targeted to inner mitochondrial membrane inhibit mitochondrial swelling, oxidative cell death, and reperfusion injury." J Biol Chem. 2004. PMID 15178689. DOI 10.1074/jbc.M402999200. Neuronal cell culture, isolated mitochondria and ex vivo heart model.
- Szeto HH. "Cell-permeable, mitochondrial-targeted, peptide antioxidants." AAPS J. 2006. PMID 16796378. DOI 10.1007/BF02854898. Review of the Szeto-Schiller series and its targeting rationale.
- Szeto HH, et al. "Mitochondria-targeted peptide accelerates ATP recovery and reduces ischemic kidney injury." J Am Soc Nephrol. 2011. PMID 21546574. DOI 10.1681/ASN.2010080808. Rat kidney ischemia-reperfusion model.
- Birk AV, et al. "The mitochondrial-targeted compound SS-31 re-energizes ischemic mitochondria by interacting with cardiolipin." J Am Soc Nephrol. 2013. PMID 23813215. DOI 10.1681/ASN.2012121216. Fluorescent binding analysis, isolated mitochondria and rat renal ischemia.
- Siegel MP, et al. "Mitochondrial-targeted peptide rapidly improves mitochondrial energetics and skeletal muscle performance in aged mice." Aging Cell. 2013. PMID 23692570. DOI 10.1111/acel.12102. Young and old mice: in vivo spectroscopy of muscle energetics.
- Szeto HH. "First-in-class cardiolipin-protective compound as a therapeutic agent to restore mitochondrial bioenergetics." Br J Pharmacol. 2014. PMID 24117165. DOI 10.1111/bph.12461. Review of mechanism and the development program.
- Campbell MD, et al. "Improving mitochondrial function with SS-31 reverses age-related redox stress and improves exercise tolerance in aged mice." Free Radic Biol Med. 2019. PMID 30597195. DOI 10.1016/j.freeradbiomed.2018.12.031. Aged mice, 8 weeks: muscle energetics and thiol redox proteomics.
- Mitchell W, et al. "The mitochondria-targeted peptide SS-31 binds lipid bilayers and modulates surface electrostatics as a key component of its mechanism of action." J Biol Chem. 2020. PMID 32273339. DOI 10.1074/jbc.RA119.012094. Model membranes, isolated mitochondria and simulation.
- Chavez JD, et al. "Mitochondrial protein interaction landscape of SS-31." Proc Natl Acad Sci U S A. 2020. PMID 32554501. DOI 10.1073/pnas.2002250117. Chemical cross-linking mass spectrometry in isolated mitochondria.
- Allen ME, et al. "The cardiolipin-binding peptide elamipretide mitigates fragmentation of cristae networks following cardiac ischemia reperfusion in rats." Commun Biol. 2020. PMID 32680996. DOI 10.1038/s42003-020-1101-3. Rat heart ischemia-reperfusion: respirometry and 3D electron microscopy.
Handling and storage of lyophilized SS-31
General lab practice for this material:
- Store the powder at -20°C, away from light, until use. Storage guidance is on the product page.
- Let the sealed vial reach room temperature before opening. This keeps moisture from condensing on the powder.
- The peptide is water-soluble and strongly cationic. It partitions into anionic lipid interfaces based on charge (Mitchell et al., 2020). So anionic buffer components or plasticware can shift free concentration.
- Published work uses the free peptide as the reference form. Supplied material is often a salt. To calculate molar concentrations, use the formula and content on the certificate. Do not use the catalog label mass.
- Once the powder is dissolved, keep solutions at 2 to 8°C and away from light. Split stock into single-use aliquots to avoid freeze/thaw cycles.
- Record the lot number and keep its certificate with your notes.
Frequently asked questions
What is the SS-31 peptide?
SS-31 is a four-residue aromatic-cationic peptide, D-Arg-Dmt-Lys-Phe-NH2. It builds up in the inner mitochondrial membrane and binds cardiolipin (Zhao et al., 2004; Birk et al., 2013). It is studied in mitochondrial bioenergetics, oxidative stress and ischemia-reperfusion models.
Is SS-31 the same thing as elamipretide?
They are names for the same molecule. It also carried the development codes MTP-131 and Bendavia (PubChem CID 11764719). The distinction that matters is molecule versus product. The approved drug is made, tested and labeled for clinical use. Our SS-31 is research-grade powder for laboratory use only, and it is not that product.
Is SS-31 FDA approved?
Elamipretide received accelerated approval in the United States in September 2025. It covers one specific indication in Barth syndrome, and a confirmatory trial is required (Shirley, 2026). Earlier trials in primary mitochondrial myopathy did not meet their primary endpoints (Karaa et al., 2023). The same was true in heart failure with reduced ejection fraction (Butler et al., 2020). That approval applies to that drug product only. Disguised Alpha's SS-31 is not approved for any human use.
What does SS-31 do at the mitochondrial membrane in published models?
Reported findings include selective cardiolipin binding. Another is inhibition of cytochrome c peroxidase activity, with electron transport preserved. Others are protection of cristae structure and lower output of mitochondrial reactive oxygen species. Studies also report changes in membrane surface electrostatics (Birk et al., 2013; Szeto, 2014; Mitchell et al., 2020). All of this is cell, isolated organelle and animal work.
How should SS-31 powder be stored?
Keep the lyophilized powder at -20°C and away from light. Once dissolved, store the solution at 2 to 8°C, away from light. Avoid freeze/thaw cycles. These steps are listed on the product page.
Where can researchers buy SS-31?
Disguised Alpha sells it for laboratory research. It is third-party tested, with the certificate published on the product page: SS-31 (10MG and 50MG).
Related compounds and guides
- MOTS-c research guide and MOTS-c: a mitochondrial-derived peptide studied in overlapping metabolic models
- SS-31 & 5-Amino-1MQ and its research guide
- Mitochonic Acid-5 (MA-5) and its research guide
- Humanin (Mitochondrial Bioregulator)
- NAD+ and its research guide, plus COQ10
- COA portal: every published certificate, by lot
This product is for research use only. It has not been evaluated for safety or effectiveness in humans. Not for human consumption. All products are intended for laboratory research purposes only.