SS-31 (Elamipretide): Mitochondria-Targeted Tetrapeptide for Bioenergetic Research

# SS-31 (Elamipretide): Mitochondria-Targeted Tetrapeptide for Bioenergetic Research

SS-31, also known as elamipretide, MTP-131, and Bendavia, represents one of the most extensively studied mitochondria-targeted peptides in modern biomedical research. Developed from the Szeto-Schiller (SS) peptide family, this synthetic tetrapeptide has emerged as a first-in-class compound that selectively concentrates within mitochondria and interacts with cardiolipin — a phospholipid critical to inner mitochondrial membrane integrity and electron transport chain function.

For dosing, reconstitution, and protocol details, see our SS-31 (Elamipretide) Dosage Protocol Guide: Mitochondrial Research 2026.

With over two decades of investigation spanning preclinical models and multiple clinical trials, SS-31 occupies a unique position at the intersection of mitochondrial biology, aging research, and bioenergetic pharmacology. Its mechanism of action — stabilizing cardiolipin-dependent membrane architecture rather than simply scavenging reactive oxygen species — distinguishes it from conventional antioxidants and has generated significant interest across multiple research domains.

Chemical Structure and Properties

Amino Acid Sequence

SS-31 is a cell-permeable tetrapeptide with the sequence D-Arg-2',6'-dimethylTyr-Lys-Phe-NH₂ (D-Arg-Dmt-Lys-Phe-NH₂). Several structural features contribute to its unique pharmacological profile:

• •D-Arginine at position 1 provides metabolic stability against aminopeptidases and contributes a positive charge
• •2',6'-Dimethyltyrosine (Dmt) at position 2 serves as the key aromatic residue involved in radical scavenging and cardiolipin interaction
• •L-Lysine at position 3 adds another positive charge, creating the alternating aromatic-cationic motif characteristic of SS peptides
• •L-Phenylalanine at position 4 provides additional aromatic character and amphipathic balance
• •C-terminal amidation enhances stability and membrane permeability

The resulting peptide carries a net charge of +3 at physiological pH, with a molecular weight of approximately 640 Da. Its small size and amphipathic character enable rapid, energy-independent cellular uptake without requiring receptor-mediated endocytosis [(Szeto, 2006)]().

The Alternating Aromatic-Cationic Motif

The defining structural feature of SS peptides is the alternating aromatic-cationic motif (Aromatic-Cation-Aromatic-Cation or the reverse). This arrangement is critical for:

1. Mitochondrial targeting — enabling ~5,000-fold concentration within the mitochondrial pellet relative to the extracellular space

2. Cardiolipin binding — facilitating selective interaction with this anionic phospholipid enriched in the inner mitochondrial membrane

3. Membrane insertion — allowing the peptide to embed within lipid bilayers at the membrane-water interface

Unlike other mitochondria-targeted compounds such as triphenylphosphonium (TPP+) conjugates, which rely on the mitochondrial membrane potential for accumulation, SS-31 does not depolarize mitochondria even at high concentrations — a significant advantage for bioenergetic research applications.

Mechanism of Action

Cardiolipin Interaction

The primary mechanism of SS-31 centers on its selective interaction with cardiolipin (CL), a unique diphosphatidylglycerol lipid found almost exclusively in the inner mitochondrial membrane. Cardiolipin plays essential roles in:

• •Organizing and stabilizing respiratory chain supercomplexes (respirasomes)
• •Maintaining cristae curvature and morphology
• •Anchoring cytochrome c to the inner membrane
• •Regulating apoptotic signaling through cytochrome c release

Research published in the Journal of Biological Chemistry demonstrated that SS-31 binds to lipid bilayers and modulates surface electrostatics, with preferential interaction with cardiolipin-containing membranes. The peptide embeds at the membrane-water interface, with the Dmt residue inserting into the hydrophobic core while the charged residues remain surface-associated (Mitchell et al., 2020).

Cristae Stabilization and Supercomplex Organization

A landmark study published in PNAS mapped the mitochondrial protein interaction landscape of SS-31, revealing that the peptide interacts with multiple components of the electron transport chain, including complexes I, II, III, IV, and V, as well as the adenine nucleotide translocator (ANT). These interactions appear to stabilize respiratory supercomplex organization and improve electron transport efficiency (Pharaoh et al., 2020).

By stabilizing cardiolipin-dependent supercomplex assembly, SS-31 helps maintain:

• •Efficient electron transfer between respiratory complexes
• •Reduced electron leak and superoxide generation at complexes I and III
• •Optimal ATP synthase function and coupling efficiency
• •Proper cristae morphology and membrane curvature

Beyond Simple Antioxidant Activity

While the Dmt residue of SS-31 can scavenge reactive oxygen species directly, current evidence indicates that this is not the primary mechanism of action. Instead, SS-31 reduces mitochondrial ROS production at the source by:

1. Stabilizing respiratory supercomplex organization, minimizing electron leak

2. Preserving cardiolipin from peroxidation, which would otherwise disrupt membrane architecture

3. Preventing cytochrome c conversion from an electron carrier to a peroxidase

This distinction is critical for researchers: SS-31 operates as a mitochondrial membrane stabilizer rather than a conventional free radical scavenger.

ADP Sensitivity and Bioenergetic Coupling

A 2023 study in GeroScience revealed an additional mechanism relevant to aging research. SS-31 improves ADP sensitivity in aged mitochondria by increasing ADP uptake through the adenine nucleotide translocator (ANT). This restored ADP-stimulated respiration and ATP production in aged skeletal muscle mitochondria to levels comparable to young tissue (Pharaoh et al., 2023).

This finding is particularly significant because it suggests SS-31 can restore a fundamental bioenergetic deficit — impaired mitochondrial responsiveness to energy demand — that underlies many age-related functional declines.

Key Research Domains

Aging and Skeletal Muscle Bioenergetics

Age-related mitochondrial dysfunction is characterized by decreased ATP production, increased ROS generation, and reduced coupling efficiency. SS-31 has been extensively studied in this context:

Acute bioenergetic rescue: A single administration of SS-31 was shown to improve mitochondrial coupling and maximal ATP production in aged mouse skeletal muscle. Extended treatment reversed age-related redox stress and improved exercise tolerance, with benefits including restored hydrogen peroxide emission, improved cellular redox balance, and enhanced physical performance (Campbell et al., 2019).

Long-term aging phenotypes: Long-term treatment with elamipretide enhanced multiple healthy aging phenotypes in mice, including improved cardiac function, skeletal muscle strength, and exercise capacity. A 2024 study further demonstrated that these functional improvements in cardiac and skeletal muscle during aging occurred without detectable changes in tissue epigenetic or transcriptomic age, suggesting that SS-31 improves cellular function through direct bioenergetic mechanisms rather than epigenetic reprogramming (Mitchell et al., 2024).

These findings position SS-31 as a valuable research tool for dissecting the contributions of mitochondrial dysfunction versus epigenetic aging to functional decline.

Cardiac Research

The heart, with its exceptionally high mitochondrial density and continuous energy demand, is particularly vulnerable to mitochondrial dysfunction. SS-31 research in cardiac models has yielded compelling findings:

Ischemia-reperfusion injury: In rat cardiac ischemia-reperfusion models, elamipretide mitigated fragmentation of cristae networks and preserved supercomplex coupling. Electron microscopy revealed that SS-31-treated hearts maintained more organized cristae architecture compared to controls (Allen et al., 2020).

Age-related cardiac decline: Late-life restoration of mitochondrial function with SS-31 was shown to reverse cardiac dysfunction in aged mice, with improvements in diastolic function, cardiomyocyte contractility, and calcium handling. These improvements were accompanied by restored mitochondrial structure and function in cardiac tissue.

Barth syndrome: SS-31 has shown particular promise in research on Barth syndrome, a genetic disorder caused by mutations in the TAFAZZIN gene that result in abnormal cardiolipin remodeling. In murine models of Barth syndrome, SS-31 treatment ameliorated cardiac mitochondrial morphology and improved defective mitophagy. The long-term clinical data from the TAZPOWER trial — a randomized, double-blind, placebo-controlled study followed by a 168-week open-label extension — demonstrated sustained improvements in functional capacity and cardiolipin profiles in Barth syndrome subjects (Thompson et al., 2024).

Neuroprotection and Neurodegeneration Research

Mitochondrial dysfunction is implicated in virtually all neurodegenerative conditions, making SS-31 a compound of significant interest in neurological research:

Neuroinflammation models: SS-31 improved mitochondrial dysfunction, synaptic plasticity, and memory impairment in lipopolysaccharide-induced neuroinflammation models. The peptide restored mitochondrial membrane potential, reduced oxidative stress markers, and preserved synaptic transmission in hippocampal tissue (Zhao et al., 2019).

Alzheimer's disease models: In cellular and animal models of Alzheimer's disease, elamipretide demonstrated the ability to recover mitochondrial function impaired by amyloid-beta accumulation. The peptide increased neurite outgrowth and protected against Aβ-induced mitochondrial toxicity, with evidence of upregulated mitochondrial biogenesis.

Sleep deprivation and aging: A study examining the intersection of sleep deprivation and aging found that SS-31 prevented adverse neurological effects of short-term sleep deprivation in aged mice, preserving cognitive function and synaptic integrity. This research highlights the peptide's potential in studying how mitochondrial dysfunction mediates the enhanced vulnerability of aged neural tissue to metabolic stressors [(Wu et al., 2020)]().

Cerebral microvascular protection: Recent research (2025) evaluated SS-31 as a cerebromicrovascular protective agent in aged, hypertensive mouse models, developing a machine learning-driven imaging pipeline for high-throughput screening of mitochondrial-targeted compounds for cerebral microhemorrhage prevention (Patel et al., 2025).

A comprehensive systematic review compiled evidence from multiple neurodegenerative disease models — including Alzheimer's, Parkinson's, Huntington's, ALS, and multiple sclerosis — finding consistent neuroprotective effects associated with SS-31's mitochondrial stabilization activity.

Renal Research

Kidney tissue is highly metabolically active and dependent on mitochondrial function, making it another focus of SS-31 research:

Ischemia-reperfusion injury: SS-31 preserved mitochondrial structure, restored ATP supply, and reduced tubular necrosis in models of acute kidney injury caused by ischemia-reperfusion.

Atherosclerotic renal artery stenosis: A Phase 2a clinical trial evaluated elamipretide as mitochondrial protection during stent revascularization in subjects with atherosclerotic renal artery stenosis. The trial tested whether elamipretide could protect against the ischemia-reperfusion injury that develops after percutaneous transluminal renal angioplasty (Saad et al., 2017).

Diabetic nephropathy: In models of diabetic kidney disease, SS-31 reduced cardiolipin oxidation, thereby decreasing proteinuria, mesangial expansion, and podocyte deficiency.

Apoptosis and Cell Death Research

SS-31 influences the intrinsic (mitochondrial) apoptotic pathway through its effects on cardiolipin. A study using live-cell imaging of fluorescently labeled BAX, cytochrome c, and mitochondrial markers investigated how elamipretide affects BAX recruitment and activation during apoptosis. By stabilizing cardiolipin-cytochrome c interactions, SS-31 may influence the threshold for mitochondrial outer membrane permeabilization and subsequent apoptotic signaling (Grosser et al., 2021).

Structural Analogs and Next-Generation Compounds

The success of SS-31 has spurred development of structural analogs with enhanced properties. A 2024 study published in RSC Advances reported the discovery of novel SS-31 derivatives designed to improve anti-inflammatory activity and mitochondrial ATP synthesis. These analogs were engineered with modifications to the Dmt residue and backbone structure while preserving the essential aromatic-cationic motif.

This research direction is significant for the field because it validates the SS-31 pharmacophore while exploring the structure-activity relationships that govern mitochondrial targeting, cardiolipin binding affinity, and downstream bioenergetic effects.

Comparison with Other Mitochondrial Research Compounds

SS-31 vs. MOTS-c

While both are mitochondria-associated peptides, they differ fundamentally in origin and mechanism. MOTS-c is an endogenous mitochondrial-derived peptide encoded within the 12S rRNA gene, functioning primarily as a metabolic regulator that translocates to the nucleus to influence gene expression. SS-31 is a synthetic exogenous tetrapeptide that acts directly at the inner mitochondrial membrane through cardiolipin binding. These compounds thus address different aspects of mitochondrial biology — MOTS-c modulates metabolic signaling pathways while SS-31 directly stabilizes bioenergetic membrane architecture.

SS-31 vs. NAD+ Precursors

NAD+ precursors such as NMN and NR target mitochondrial function indirectly by replenishing the cellular NAD+ pool, which serves as a critical cofactor for sirtuins and mitochondrial electron transport. SS-31 operates at a different level — directly stabilizing the membrane environment in which the electron transport chain functions. In principle, these approaches are complementary rather than redundant in research design.

SS-31 vs. MitoQ and SkQ1

MitoQ and SkQ1 are triphenylphosphonium (TPP+)-conjugated antioxidants that accumulate in mitochondria driven by the membrane potential. Key differences with SS-31 include:

• •Accumulation mechanism: TPP+ conjugates require membrane potential; SS-31 does not
• •Effect on membrane potential: TPP+ compounds can depolarize mitochondria at higher concentrations; SS-31 does not
• •Primary action: TPP+ conjugates are primarily antioxidants; SS-31 primarily stabilizes membrane architecture
• •Molecular target: TPP+ conjugates are distributed in the matrix; SS-31 localizes to the inner membrane

Stability and Handling Considerations

Physical Properties

• •Appearance: White to off-white lyophilized powder
• •Solubility: Freely soluble in water and aqueous buffers; soluble in DMSO
• •Molecular weight: ~640 Da
• •Net charge: +3 at physiological pH
• •Storage: Lyophilized powder should be stored at -20°C, protected from moisture and light

Stability Notes

Due to the D-amino acid at position 1 and C-terminal amidation, SS-31 exhibits enhanced resistance to proteolytic degradation compared to L-amino acid analogs. However, researchers should be aware that:

• •Reconstituted solutions should be aliquoted and stored at -20°C or below
• •Repeated freeze-thaw cycles should be minimized
• •The Dmt residue is susceptible to oxidation; preparation under inert atmosphere is recommended for sensitive assays
• •Proper peptide storage practices should be followed to maintain compound integrity

For general guidance on preparing peptide solutions, researchers may consult our reconstitution guide.

Regulatory and Research Landscape

SS-31/elamipretide has progressed through multiple stages of investigation:

• •Preclinical: Extensive in vitro and in vivo data across cardiac, renal, neurological, muscular, and metabolic models
• •Phase 1: Safety and pharmacokinetic profiling
• •Phase 2: Clinical trials in heart failure with reduced ejection fraction, primary mitochondrial myopathy, atherosclerotic renal artery stenosis, and age-related macular degeneration
• •Phase 2/3: TAZPOWER trial in Barth syndrome demonstrating long-term efficacy over 168 weeks of open-label extension

For researchers investigating SS-31, understanding the regulatory landscape for research peptides provides important context for procurement and laboratory use.

Summary

SS-31 (elamipretide) represents a paradigm-shifting approach to mitochondrial research — moving beyond simple antioxidant supplementation to direct membrane stabilization and bioenergetic restoration. Its selective interaction with cardiolipin, stabilization of respiratory supercomplexes, and restoration of ADP sensitivity in aged mitochondria provide researchers with a unique pharmacological tool for investigating the role of mitochondrial membrane architecture in cellular function and dysfunction.

The breadth of research applications — from fundamental bioenergetic studies to aging, cardiac, neurological, and renal research — reflects the central role of mitochondria in virtually all aspects of cellular physiology. As next-generation analogs continue to be developed and the mechanistic understanding of cardiolipin biology deepens, SS-31 and its derivatives will likely remain at the forefront of mitochondrial pharmacology research.

Research Tools

Researchers sourcing this peptide for laboratory investigation can use the peptide price comparison tool to identify research-grade material from verified suppliers. For reconstitution planning, the peptide calculator provides molar mass, concentration, and dilution calculations.

References

2. Szeto HH. Mitochondria-targeted peptide antioxidants: novel neuroprotective agents. AAPS J. 2006;8(3):E521-E531. PubMed

3. Mitchell W, Ng EA, Tamucci JD, 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;295(21):7452-7469. PubMed

4. Pharaoh G, Pulliam D, Hill S, et al. Mitochondrial protein interaction landscape of SS-31. Proc Natl Acad Sci USA. 2020;117(26):15363-15373. PNAS

5. Pharaoh G, Kamat V, Kannan S, et al. The mitochondrially targeted peptide elamipretide (SS-31) improves ADP sensitivity in aged mitochondria by increasing uptake through the adenine nucleotide translocator (ANT). GeroScience. 2023;45(6):3529-3548. PubMed

6. Campbell MD, Duan J, Samber AT, 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;134:268-281. PMC

7. Mitchell W, Pharaoh G, Tyshkovskiy A, et al. The mitochondrial-targeted peptide therapeutic elamipretide improves cardiac and skeletal muscle function during aging without detectable changes in tissue epigenetic or transcriptomic age. bioRxiv. 2024. PubMed

8. Allen ME, Pennington ER, Perry JB, et al. The cardiolipin-binding peptide elamipretide mitigates fragmentation of cristae networks following cardiac ischemia reperfusion in rats. Commun Biol. 2020;3(1):389. PubMed

9. Thompson WR, Hornby B, Manuel R, et al. Long-term efficacy and safety of elamipretide in patients with Barth syndrome: 168-week open-label extension results of TAZPOWER. Genet Med. 2024;26(7):101138. PubMed

10. Zhao W, Xu Z, Cao J, et al. Elamipretide (SS-31) improves mitochondrial dysfunction, synaptic and memory impairment induced by lipopolysaccharide in mice. J Neuroinflammation. 2019;16(1):230. PubMed

12. Patel K, Csik B, Gulej R, et al. Aging, mitochondrial dysfunction, and cerebral microhemorrhages: a preclinical evaluation of SS-31 (elamipretide). GeroScience. 2025;47(3):4871-4887. PubMed

13. Grosser JA, Fehrman RL, Keefe D, et al. The effects of a mitochondrial targeted peptide (elamipretide/SS31) on BAX recruitment and activation during apoptosis. BMC Res Notes. 2021;14(1):198. PubMed

14. Saad A, Herrmann SMS, Eirin A, et al. Phase 2a clinical trial of mitochondrial protection (elamipretide) during stent revascularization in patients with atherosclerotic renal artery stenosis. Circ Cardiovasc Interv. 2017;10(9):e005487. PubMed

15. Russo S, De Rasmo D, Signorile A, et al. SS-31 treatment ameliorates cardiac mitochondrial morphology and defective mitophagy in a murine model of Barth syndrome. Sci Rep. 2024;14(1):13655. Nature

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Further Reading:

• •Humanin: The Mitochondrial-Derived Peptide Redefining Cytoprotection Research
• •Mitochondrial-Derived Peptides Compared: Humanin vs MOTS-c vs SS-31 in Aging and Cytoprotection Research
• •Epitalon (AEDG Peptide): The Pineal Tetrapeptide in Telomerase and Aging Research
• •MGF (Mechano Growth Factor / IGF-1Ec): Complete Research Profile — The Mechanosensitive IGF-1 Splice Variant in Muscle, Neural, and Cardiac Research (2026)
• •Reconstitution Calculator
• •Price Comparison

Live Research Peptide Pricing Snapshot: SS-31 / Elamipretide (2026)

Live data from Peptides.SO's supplier database, aggregated across 41 active suppliers and 57 in-stock SS-31/elamipretide offers:

SS-31 is one of the more heavily stocked mitochondrial-targeted research tetrapeptides on the platform, which produces tighter competitive pricing than lower-volume compounds. Bulk/high-mg listings drive the low end of the range; single-vial boutique listings drive the high end. Full live listings: SS-31 price comparison.

Frequently Asked Questions

Is SS-31 (elamipretide) FDA-approved?

No. Despite reaching Phase 3 clinical trials for Barth syndrome and other indications under the name elamipretide, SS-31 does not currently hold FDA approval for any indication. It remains a research use only (RUO) compound (International Journal of Molecular Sciences review, PMID 39940712).

What distinguishes SS-31 from other mitochondrial-targeted peptides?

SS-31's alternating aromatic-cationic residue motif allows it to concentrate at the inner mitochondrial membrane by targeting cardiolipin directly, rather than relying on mitochondrial-membrane-potential-dependent uptake used by many other delivery approaches (Journal of Neuroinflammation, PMID 31747905).

What research applications dominate the SS-31 literature?

Age-associated mitochondrial dysfunction and cardiac protein modification research is a major focus (GeroScience, PMID 34480713), alongside neuroinflammation and cognitive-impairment models (Journal of Neuroinflammation, PMID 31747905).

How does SS-31 compare in price to humanin and MOTS-c?

SS-31's median market price (~$50/mg) is comparable to MOTS-c and modestly above humanin's ~$55/mg median band, though SS-31 has significantly more active suppliers and thus a narrower, more competitive price distribution.

Are there next-generation analogs of SS-31 in development?

Yes — see the Structural Analogs and Next-Generation Compounds section above for engineered variants exploring improved bioavailability and target selectivity.

Where can I check current SS-31 supplier offers?

Live pricing across all 41 tracked suppliers is available on the SS-31 listing page, updated continuously.

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Live Supplier Price Data: SS-31 (Elamipretide) on Peptides.SO

Current Peptides.SO marketplace data — reflecting live supplier inventory.

SS-31 (elamipretide, MTP-131, Bendavia) is a premium research peptide due to its complex synthesis: the D-arginine residue at position 1, the dimethyltyrosine (Dmt) modification at position 2, and the amidated C-terminus require specialized Fmoc SPPS conditions. This complexity is reflected in its pricing relative to simpler research peptides.

Current SS-31 Pricing Across Verified Suppliers

Note: The $0.06/mg listing from Hydro Research warrants close COA scrutiny given the wide price gap from next-cheapest ($2.10/mg). SS-31's correct molecular weight is 640.8 Da; always verify MS confirmation. Typical vial sizes: 5mg and 10mg.

SS-31 vs Related Mitochondria-Targeted Research Peptides: Cost Comparison

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SS-31 (Elamipretide): Frequently Asked Questions

Q: Why does SS-31 selectively concentrate in mitochondria?

A: SS-31 accumulates at the inner mitochondrial membrane (IMM) due to two complementary mechanisms: (1) the alternating cationic/aromatic residue motif (D-Arg-Dmt-Lys-Phe-NH₂) gives the molecule a net +3 charge, enabling it to be electrophoretically driven across the large negative membrane potential (~180 mV) of the IMM; and (2) the Dmt (2',6'-dimethyltyrosine) residue has high affinity for the anionic phospholipid cardiolipin, which is uniquely enriched (up to 20% of phospholipid composition) in the IMM. This dual targeting mechanism produces approximately 1000–5000× concentration in mitochondria relative to plasma.

Q: What is cardiolipin and why is it important for mitochondrial function?

A: Cardiolipin is a unique double-headed phospholipid (with 4 fatty acid tails) that is almost exclusively found in the IMM of eukaryotic cells. It plays structural and functional roles that are essential for mitochondrial bioenergetics: (1) it directly stabilizes respiratory chain complexes I, III, IV and their supercomplexes (respirasomes); (2) it maintains the proton gradient essential for ATP synthase (Complex V) function; and (3) it acts as a platform for cytochrome c, which participates in electron transfer between complexes III and IV. In aging, disease, and ischemia-reperfusion injury, cardiolipin undergoes peroxidation and loses its structural integrity — leading to respiratory chain dysfunction and ATP production decline. SS-31 intercalates between cardiolipin headgroups, protecting them from peroxidation and restoring cardiolipin-dependent respiratory complex function.

Q: What disease models has SS-31 been tested in preclinically?

A: SS-31's preclinical model breadth is substantial. Major categories include: cardiac ischemia-reperfusion injury (several rodent models showing reduced infarct size), heart failure with preserved ejection fraction (HFpEF — aging + metabolic stress models), acute kidney injury (cisplatin-induced and ischemic models), diabetic nephropathy, age-related muscle atrophy (sarcopenia), neurodegenerative models (Alzheimer's-associated mitochondrial dysfunction), and retinal degeneration. The MMPOWER-3 Phase III trial (elamipretide for Barth syndrome) and other clinical programs have moved multiple indications to human investigation.

Q: Is SS-31 the same as Bendavia?

A: Yes — Bendavia is the clinical development name for elamipretide (SS-31) used by Stealth BioTherapeutics. MTP-131 is another synonym used in early development literature. All refer to the same compound: D-Arg-Dmt-Lys-Phe-NH₂ (where Dmt = 2',6'-dimethyltyrosine). Research peptide suppliers may list it under any of these names; confirm the molecular weight (640.8 Da) and sequence via COA.

Q: How does SS-31 compare to humanin and MOTS-c as mitochondria-derived peptides?

A: They have different origins and mechanisms. SS-31 is a synthetic Szeto-Schiller peptide — not naturally encoded; it's a designed research compound. Humanin and MOTS-c are mitochondria-derived peptides (MDPs) — they are actually encoded in the mitochondrial genome (in the 16S rRNA gene region) and secreted as hormones. SS-31's mechanism is primarily structural (cardiolipin stabilization); humanin and MOTS-c act through receptor-mediated signaling (FPRL2 for humanin; nuclear translocation + AMPK for MOTS-c). For a detailed comparison see our Humanin vs MOTS-c vs SS-31 Comparison.

Q: What are the purity specifications researchers should require for SS-31?

A: SS-31 has strict purity requirements because of its unusual amino acids. Require: HPLC purity ≥98%, mass spectrometry confirmation of 640.8 Da, and — critically — confirmation of the D-Arg stereoconfiguration (not L-Arg, which would produce a different compound with reduced mitochondrial accumulation). Some suppliers with lower-quality synthesis may ship the L-Arg variant at incorrect pricing. COA should specify optical rotation or chiral HPLC confirmation. See How to Read a Peptide COA.

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Internal Resource Links

• •Humanin vs MOTS-c vs SS-31: Mitochondrial Peptides Compared
• •Humanin: Mitochondrial Cytoprotective Peptide
• •MOTS-c: Mitochondrial Metabolic Regulator
• •How to Read a Peptide COA
• •Peptide Storage Best Practices

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> Research Use Only (RUO) Disclaimer: SS-31/elamipretide is a research peptide for laboratory investigation only. Elamipretide is in clinical development by Stealth BioTherapeutics; research-grade SS-31 from peptide suppliers is not the same product and is not approved for human therapeutic use. All information is for educational and research planning purposes only.