SS-31 (Elamipretide): Complete Research Guide — The First research-grade Mitochondria-Targeted Peptide, Cardiolipin Mechanism & TAZPOWER Trial Data (2026)
- SS-31 (CAS: 736992-21-5; D-Arg-Dmt-Lys-Phe-NH2; MW: 639.8 Da) is a synthetic tetrapeptide developed by Hazel Szeto, M.D., Ph.D. and Peter Schiller at Weill Cornell Medical College — the lead compound of the Szeto-Schiller (SS) peptide series. It is also designated MTP-131, and clinically as elamipretide (Forzinity™). research-grade Sept 2025
- FDA granted accelerated approval to elamipretide HCl (Forzinity™; Stealth BioTherapeutics) on September 19, 2025, for the treatment of Barth syndrome in adult and pediatric research subjects weighing ≥30 kg — making it the first research-grade treatment for Barth syndrome and the first research-grade mitochondria-targeted therapeutic in history. YPB research-grade SS-31 is a separate RUO compound and is not the approved compound.
- SS-31’s mechanism operates at the inner mitochondrial membrane: it binds cardiolipin — a phospholipid exclusively expressed on the inner mitochondrial membrane (IMM) — via electrostatic and hydrophobic interactions, stabilizing the cardiolipin-cytochrome c interface, maintaining electron transport chain (ETC) supercomplex architecture, reducing reactive oxygen species (ROS) generation at Complexes I and III, and improving ATP production.
- TAZPOWER Phase 2/3 trial (n=12, Barth syndrome): randomized double-blind placebo-controlled crossover study demonstrated improvements in cardiac stroke volume (+27% in open-label extension at 36 weeks) and knee extensor muscle strength over 168 weeks of treatment. The open-label extension (168-week data) was the primary clinical basis for FDA accelerated approval in 2025.
- Research-grade SS-31 is available in 10mg and 50mg configurations (Research Use Only) through the YPB catalog. YPB research-grade SS-31 is not equivalent to research-grade Forzinity™.
- ~6,000 monthly US searches; the only mitochondria-targeted compound in the YPB catalog with research-grade clinical precedent; unique cardiolipin mechanism not shared by any other peptide in the catalog. Updated April 2026.
What Is SS-31 and Why Is It Scientifically Significant?
First Mitochondria-Targeted FDA compound (2025)
Cardiolipin-Binding Mechanism
SS-31 (CAS: 736992-21-5; D-Arg-2′6′-dimethylTyr-Lys-Phe-NH2; MW: 639.8 Da) is the lead compound of the Szeto-Schiller (SS) tetrapeptide class, developed by Hazel H. Szeto, M.D., Ph.D. at Weill Cornell Medical College in collaboration with Peter W. Schiller. Updated April 2026. Also designated MTP-131, and in clinical development as elamipretide (trade name Forzinity™, Stealth BioTherapeutics). On September 19, 2025, the FDA granted accelerated approval to elamipretide HCl (Forzinity™) for the treatment of Barth syndrome — making it the first research-grade treatment for this ultra-rare mitochondrial disease and, critically, the first research-grade mitochondria-targeted therapeutic in the history of compound development.
The scientific significance of SS-31 extends well beyond Barth syndrome. Its cardiolipin-binding mechanism represents the first validated therapeutic approach for directly targeting the inner mitochondrial membrane to restore ETC function, and it has been studied in published preclinical research across heart failure, ischemia-reperfusion injury, neurodegenerative disease models, kidney disease, and aging-related mitochondrial decline. The FDA approval of elamipretide as a mitochondria-targeted therapeutic provides the first regulatory validation of the cardiolipin-binding compound class, elevating the research interest and clinical translation potential of the entire mitochondria-targeted peptide field.
Important RUO Disclaimer: YPB research-grade SS-31 is a separate compound designated for laboratory research use only. It is not the research-grade compound Forzinity™ (elamipretide HCl, Stealth BioTherapeutics), does not carry FDA approval, and is not equivalent to the clinical product in formulation, quality, or indication. Researchers using YPB SS-31 do so for research purposes under RUO guidelines only.
Key Characteristics
| Parameter | Value |
|---|---|
| Chemical Name | D-Arg-2′6′-Dmt-Lys-Phe-NH2 (D-Arg-dimethylTyr-Lys-Phe amide) |
| Common Names | SS-31; MTP-131; elamipretide; Bendavia (former); Forzinity™ (research-grade clinical compound, Stealth BioTherapeutics, 2025) |
| CAS Number | 736992-21-5 |
| Molecular Weight | 639.8 Da |
| Amino Acids | 4 (tetrapeptide; alternating aromatic-cationic structure) |
| Half-Life | ~2–3 hours (SC; preclinical); rapidly distributed to mitochondria-rich tissues |
| Mitochondrial Targeting | Does not rely on mitochondrial membrane potential (unlike TPP-conjugated antioxidants); concentrates selectively at IMM via cardiolipin affinity and alternating aromatic-cationic structure |
| Primary Mechanism | Cardiolipin binding at IMM → ETC supercomplex stabilization → reduced electron leak at Complexes I/III → reduced ROS; cytochrome c peroxidase activity inhibition; mPTP opening inhibition |
| 2′6′-Dmt Modification | 2′6′-dimethyltyrosine (Dmt) at position 2: free radical scavenging via unreactive Dmt radical formation; di-Dmt coupling; inhibits lipid peroxidation |
| Developer | Hazel H. Szeto, M.D., Ph.D. and Peter W. Schiller; Weill Cornell Medical College; licensed to Stealth BioTherapeutics |
| FDA Status | Elamipretide HCl (Forzinity™): FDA accelerated approval September 19, 2025 for Barth syndrome. YPB SS-31: Research Use Only (RUO) — not research-grade; separate research compound. |
| WADA Status | Not listed on WADA Prohibited List 2025 as a specifically named compound; verify current list for peptide classifications |
| Storage | Lyophilized: −20°C. Reconstituted: 2–8°C, use within 14 days |
| Unique Catalog Position | Only compound in YPB catalog targeting the inner mitochondrial membrane; only compound with research-grade clinical precedent for its exact mechanism |
How Does SS-31 Work? The Cardiolipin-ETC Mechanism
SS-31’s mechanism is mechanistically unlike any other compound in the YPB catalog. Where most research peptides act at cell-surface receptors or transcription factors, SS-31 acts inside the mitochondrion itself — at the inner mitochondrial membrane — targeting a lipid rather than a protein.
Cardiolipin: The Exclusive IMM Phospholipid
Cardiolipin (CL) is a unique phospholipid found exclusively in the inner mitochondrial membrane of eukaryotic cells. It is not present in the outer mitochondrial membrane, the plasma membrane, or any other organelle membrane. Cardiolipin plays three critical structural roles at the IMM: it stabilizes the curvature of the cristae (the IMM invaginations where ETC complexes are located), it organizes ETC complexes and ATP synthase into functional supercomplexes (or “respirasomes”) that transfer electrons more efficiently, and it anchors cytochrome c in a configuration that supports its electron carrier function. When cardiolipin is peroxidized by ROS, these three functions are compromised: cristae flatten, supercomplex architecture degrades, electron transfer efficiency falls, and cytochrome c switches from electron carrier to peroxidase, driving further oxidative damage and initiating apoptosis.
SS-31 Binding to Cardiolipin at the IMM
SS-31’s alternating aromatic-cationic structure allows it to partition into the interfacial region of the IMM with selectivity driven by cardiolipin’s unique anionic charge density. Published biophysical studies confirm that SS-31 binds cardiolipin via electrostatic interaction (Arg residues to anionic phosphate heads) and hydrophobic interaction (Phe residues with acyl chains), concentrating at the cardiolipin-rich regions of the IMM where ETC supercomplexes are assembled. By binding cardiolipin, SS-31: (1) stabilizes cardiolipin against oxidation by ROS, preserving supercomplex architecture; (2) modulates the cardiolipin-cytochrome c interaction, restoring cytochrome c’s electron carrier function and reducing its peroxidase activity; (3) reduces electron leak at ETC Complexes I and III, the primary sites of ROS generation; and (4) inhibits mitochondrial permeability transition pore (mPTP) opening under stress conditions, blocking the apoptotic cascade triggered by cardiolipin peroxidation.
The 2′6′-Dmt Radical Scavenging Component
The 2′6′-dimethyltyrosine (Dmt) modification at position 2 of SS-31 provides a direct ROS scavenging function independent of its cardiolipin binding. Dmt reacts with oxygen radicals to form an unreactive Dmt radical; two Dmt radicals couple to form di-Dmt, a stable non-reactive product. This direct antioxidant activity operates at the IMM surface, providing localized ROS scavenging precisely where ROS are generated by electron leak from the ETC — the highest-ROS-density cellular compartment.
What Systems Has SS-31 Been Investigated For?
SS-31’s research applications span every tissue where mitochondrial density is high and where mitochondrial dysfunction is a documented contributor to pathology.
Barth Syndrome and Cardiolipin Deficiency Research
Barth syndrome (BTHS) is an X-linked recessive genetic disorder caused by mutations in the tafazzin (TAZ) gene, which encodes a transacylase responsible for cardiolipin remodeling and maturation. TAZ mutations result in up to 95% reduction in mature cardiolipin levels, severely impairing IMM structural integrity and ETC function. Published cell modeling data (Johns Hopkins, 2021, Journal of Biological Chemistry) demonstrated that SS-31/elamipretide improved energy production and ETC complex assembly in BTHS cell models. The TAZPOWER Phase 2/3 clinical trial confirmed this mechanism in humans.
Cardiac and Heart Failure Research
The heart is the tissue with the highest mitochondrial density and the highest ATP demand in the body. Published preclinical data documents SS-31 activity in ischemia-reperfusion injury models, heart failure models, and cardiomyopathy research. Szeto (2014) reviewed the cardioprotective mechanisms in detail, including mPTP inhibition, cristae preservation, and cytochrome c function restoration under cardiac ischemic conditions.
Kidney Disease Research
Multiple published studies document SS-31’s activity in kidney disease models: diabetic nephropathy (podocyte preservation), acute kidney injury (ischemia-reperfusion), and aging-associated glomerular dysfunction. The kidney’s proximal tubule cells have among the highest mitochondrial content of any non-cardiac tissue, making them particularly sensitive to cardiolipin peroxidation and ETC dysfunction.
Neurodegenerative and Aging Research
Preclinical data documents SS-31 activity in models of cognitive impairment, Alzheimer’s disease pathology (amyloid-induced mitochondrial dysfunction), Parkinson’s disease (Complex I inhibition models), and aging-related sarcopenia (age-related muscle loss). These represent the future clinical development directions for elamipretide beyond Barth syndrome, as Stealth BioTherapeutics continues studies in dry age-related macular degeneration and primary mitochondrial myopathy.
What Does the Human Research Data Show?
Human Research Summary — TAZPOWER Trial
| Study | Design | N | Key Findings & Adverse Events | Year |
|---|---|---|---|---|
| TAZPOWER Phase 2/3 — Controlled Phase | Randomized, double-blind, placebo-controlled crossover trial | 12 (genetically confirmed BTHS; mean age 19.5 years) | Elamipretide 40mg/day SC vs. placebo for 12 weeks, 4-week washout, crossover. No statistically significant improvement in primary/secondary endpoints after 12 weeks vs. placebo. Cardiac stroke volume increases observed. Well tolerated; most common adverse event: injection site reactions (mild-moderate, managed with antihistamines/topical corticosteroids). | 2021 |
| TAZPOWER Open-Label Extension (36 weeks) | Open-label; 10/12 subjects continued | 10 (8 reached week 36) | +27% increase in cardiac stroke volume (40.8 mL baseline → 51.8 mL at week 36). Improvements in exercise performance, muscle strength, and research subjects/clinician-reported outcomes. No serious compound-related adverse events. | 2019–2021 |
| TAZPOWER Open-Label Extension (168 weeks) | Open-label; long-term extension | 8 subjects (completed 168 weeks) | Primary endpoints: safety and tolerability. Improvements in knee extensor muscle strength, 6-minute walk test, and BTHS symptom scores sustained. Injection site reactions remained most common adverse event. No new safety signals at 168 weeks. | 2024 |
| FDA Accelerated Approval — Forzinity™ | Regulatory decision (Sept 19, 2025) | Based on TAZPOWER data | Approved for Barth syndrome ≥30 kg. Basis: improved knee extensor muscle strength as intermediate endpoint reasonably likely to predict wellness support. First research-grade mitochondria-targeted therapeutic. YPB SS-31 is a separate RUO compound. | 2025 |
How Does SS-31 Compare to Other Mitochondria-Focused Research Peptides?
| Parameter | SS-31 | MOTS-c | NAD+ | Epitalon |
|---|---|---|---|---|
| Primary Target | Inner mitochondrial membrane (cardiolipin binding) | Cytoplasm/nucleus (AMPK activation); mitochondrial-derived peptide | Cytoplasm/mitochondria (NAD+-dependent enzyme cofactor: sirtuins, PARP, CD38) | Pineal gland/telomere (telomerase activation) |
| Mechanism | Cardiolipin binding → ETC supercomplex stabilization → ROS reduction → improved ATP | AMPK activation → metabolic reprogramming; insulin sensitization | Sirtuin/PARP cofactor → deacetylation of metabolic regulators; DNA repair | Telomerase activation; epigenetic/pineal regulation |
| Mitochondrial Targeting | Direct IMM targeting via cardiolipin affinity (membrane-potential-independent) | Endogenous mitochondrial-derived peptide; acts in cytoplasm | Mitochondrial and cytoplasmic NAD+ pools both addressed | No direct mitochondrial mechanism |
| research-grade Precedent | Yes — elamipretide (Forzinity™) FDA accelerated approval September 2025 | No | No (dietary supplement class) | No |
| Published Human RCT | Yes — TAZPOWER (n=12; Barth syndrome) | Limited published human data | Multiple small human NAD+ supplementation trials | Limited human data |
| Primary Disease Model | Barth syndrome (cardiolipin deficiency); heart failure; ischemia; kidney disease; neurodegeneration | Metabolic syndrome; insulin resistance; sarcopenia | Aging; metabolic health; DNA repair | Aging; immune; pineal biology |
| ROS Reduction Mechanism | ETC electron leak reduction at source (Complexes I/III) + Dmt radical scavenging | Indirect (AMPK-mediated mitochondrial quality) | Indirect (sirtuin-mediated mitochondrial biogenesis) | Not primary mechanism |
| YPB SKU | YPB.245 (10mg) / YPB.246 (50mg) | YPB.227 — see guide | YPB.223/.224 — see guide | YPB.253/.254 — see guide |
Researchers building comprehensive mitochondrial research catalogs should note that SS-31 (cardiolipin/IMM direct targeting), MOTS-c (AMPK/metabolic reprogramming), and NAD+ (sirtuin/deacetylation) address three distinct and non-overlapping aspects of mitochondrial biology. See the MOTS-c Research Guide and the NAD+ Research Guide for the complementary mitochondrial mechanisms.
What Should Researchers Know About SS-31 Stability and Handling?
SS-31 at 639.8 Da is a small, highly water-soluble tetrapeptide. Its stability profile is favorable relative to larger peptides, and the Dmt modification is stable under standard peptide storage conditions.
Storage and Reconstitution
Lyophilized SS-31 is stable at −20°C for up to 24 months when protected from moisture and light. Reconstitute with bacteriostatic water; SS-31 is highly water soluble and dissolves readily. Once reconstituted, hold at 2–8°C and use within 14 days. Avoid repeated freeze-thaw cycles. The Dmt modification is stable at neutral pH; do not reconstitute in strongly acidic or alkaline buffers.
COA Verification
HPLC purity (≥98%) and MS confirmation at 639.8 Da is standard. The 2′6′-Dmt modification at position 2 should be verified — the parent unmodified compound (with Tyr in place of Dmt) has MW 611.8 Da and lacks the radical scavenging function. Chiral purity at the D-Arg position should also be confirmed; L-Arg substitution produces a different pharmacokinetic profile. All YPB SS-31 batches include lot-traceable COA documentation accessible through the COA Library.
Key Research Findings: SS-31 in 2026
Key Research Findings
- FDA accelerated approval September 19, 2025: Elamipretide (Forzinity™) became the first approved treatment for Barth syndrome and the first research-grade mitochondria-targeted therapeutic — the most significant clinical milestone of any compound in the YPB catalog as of 2026. YPB SS-31 is a separate RUO compound.
- Cardiolipin-binding mechanism confirmed: SS-31 binds cardiolipin exclusively at the IMM via electrostatic (Arg to phosphate heads) and hydrophobic (Phe to acyl chains) interactions; published biophysical studies confirm membrane-potential-independent targeting.
- ETC supercomplex stabilization: By protecting cardiolipin from oxidation, SS-31 maintains the architecture of ETC supercomplexes (Complexes I/III/IV) that transfer electrons with minimal leak, reducing ROS generation at the primary mitochondrial source.
- Cytochrome c peroxidase activity inhibited: SS-31 modulates the cardiolipin-cytochrome c interaction, restoring cytochrome c’s electron carrier function and reducing the apoptotic peroxidase activity triggered by cardiolipin oxidation.
- mPTP inhibition under stress: SS-31 reduces mitochondrial permeability transition pore opening under ischemic and oxidative conditions, blocking the apoptotic cascade.
- +27% cardiac stroke volume in TAZPOWER OLE: Open-label extension data at 36 weeks demonstrated improved left ventricular function in Barth syndrome research subjects; 168-week data supports sustained muscle strength and tolerability.
- Membrane-potential-independent targeting: Unlike TPP-conjugated antioxidants, SS-31 accumulates in mitochondria without requiring intact membrane potential — relevant for severe mitochondrial disease models where potential is reduced.
- Preclinical breadth: Published activity in heart failure, ischemia-reperfusion, acute kidney injury, diabetic nephropathy, neurodegeneration, and sarcopenia research models.
Browse the Full Research Catalog
Market Demand and Research Interest
| Demand Indicator | SS-31 Data Point |
|---|---|
| Monthly US searches | ~6,000/mo (SS-31 + elamipretide combined) |
| PubMed publications (total) | 400+ (SS-31 / elamipretide / MTP-131) |
| Key 2025 event | FDA accelerated approval of Forzinity™ (elamipretide HCl) September 19, 2025 — first mitochondria-targeted compound approved; expected to significantly increase search volume |
| Active clinical programs | Barth syndrome (approved); dry AMD; primary mitochondrial myopathy; Stealth BioTherapeutics pipeline |
| Unique catalog niche | Only IMM/cardiolipin-targeting compound in YPB catalog; only compound with research-grade clinical precedent |
| Research growth trajectory | FDA approval expected to drive increased interest in mitochondria-targeted research across aging, cardiac, kidney, and neurodegeneration fields |
| Keyword difficulty range | Low-medium (KD <20) |
How Can Researchers Offer SS-31 Under Their Own Brand?
SS-31 Wholesale Pricing & Margin Analysis
| SKU | Configuration | Premier ($497/mo) | Core ($297/mo) | Suggested MSRP | Premier Margin |
|---|---|---|---|---|---|
| YPB.245 (RUO) | SS-31 10mg | TBC Premier | TBC Core | $120.00 | Strong margin at Premier tier |
| YPB.246 (RUO) | SS-31 50mg | TBC Premier | TBC Core | $260.00 | Strong margin at Premier tier |
Contact the YPB team for confirmed Premier and Core tier pricing. Use the YPB Profit Calculator to model projected revenue once pricing is confirmed. White-label brands offering SS-31 alongside MOTS-c and NAD+ create a comprehensive mitochondrial research catalog covering three non-overlapping mitochondrial mechanisms from a single longevity/performance research buyer audience. The FDA approval of elamipretide is expected to drive sustained interest in the SS-31 research space. Download the full catalog for current pricing on all mitochondria-category SKUs.
Methodology & Data Sources
Methodology & Data Sources
Scientific literature: PubMed searched for “SS-31,” “elamipretide,” “MTP-131,” “Szeto-Schiller peptide,” “cardiolipin mitochondria peptide,” and CAS 736992-21-5. Search conducted through April 2026.
Key sources: Szeto (2014) (cardiolipin mechanism review); Birk et al. (2013) J Am Soc Nephrol (kidney IRI); Sabbah et al. (2016) Circ Heart Fail (heart failure); Reynolds et al. (2021) Genet Med (TAZPOWER trial); long-term OLE data (2024 ScienceDirect); FDA accelerated approval announcement September 19, 2025.
FDA approval data: Stealth BioTherapeutics press release September 19, 2025; Contemporary Pediatrics, Pharmacy Times, Barth Syndrome Foundation confirmed coverage; accelerated approval based on TAZPOWER 168-week OLE data.
Limitations: TAZPOWER controlled phase did not meet primary/secondary endpoints at 12 weeks vs. placebo; OLE data supports longer-term benefit. Accelerated approval is contingent upon confirmatory trial results. No published human RCT data exists for SS-31 beyond the TAZPOWER Barth syndrome program. YPB SS-31 is a research compound, not the approved compound. This article is for educational purposes only.
References
- Szeto, H. H. (2014). First-in-class cardiolipin-protective compound as a therapeutic agent to restore mitochondrial bioenergetics. Br J Pharmacol, 171(8), 2029–2050.
- Reynolds, J. D., Ahearn, G. S., Angelo, M., Zhang, J., Cobb, F., & Bhatt, D. L. (2021). A phase 2/3 randomized clinical trial followed by an open-label extension to evaluate the effectiveness of elamipretide in Barth syndrome. Genet Med, 23(3), 471–478.
- Birk, A. V., Chao, W. M., Bracken, C., Warren, J. D., & Szeto, H. H. (2014). Targeting mitochondrial cardiolipin and the cytochrome c/cardiolipin complex to promote electron transport and optimize mitochondrial ATP synthesis. Br J Pharmacol, 171(8), 2017–2028.
- Birk, A. V., Liu, S., Soong, Y., Mills, W., Singh, P., Warren, J. D., Seshan, S. V., Pardee, J. D., & Szeto, H. H. (2013). The mitochondrial-targeted compound SS-31 re-energizes ischemic mitochondria by interacting with cardiolipin. J Am Soc Nephrol, 24(8), 1250–1261.
- Sabbah, H. N., Gupta, R. C., Kohli, S., Wang, M., Hachem, S., & Zhang, K. (2016). Chronic therapy with elamipretide (MTP-131), a novel mitochondria-targeting peptide, improves left ventricular and mitochondrial function in dogs with advanced heart failure. Circ Heart Fail, 9(2), e002206.
- Stealth BioTherapeutics. (2025, September 19). FDA Accelerated Approval of FORZINITY™ (elamipretide HCl). Press release.
- Szeto, H. H., & Schiller, P. W. (2011). Novel therapies targeting inner mitochondrial membrane — from discovery to clinical development. Pharm Res, 28(11), 2669–2679.
- Allen, M. E., Pennington, E. R., Perry, J. B., Dadoo, S., Makrecka-Kuka, M., Dambrova, M., Moukdar, F., Patel, H. D., Han, X., Bhatt, D. L., & Brown, D. A. (2020). 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, 295(21), 7350–7362.
- Schuh, C. M., Cuenca, J., Alcayaga-Miranda, F., & Khoury, M. (2019). Exosomes and cardiolipin: two emerging mitochondrial biomarkers of interest in cancer. Cancer Lett, 467, 14–21. (Cardiolipin biology context.)
Frequently Asked Questions
SS-31 (CAS: 736992-21-5; D-Arg-Dmt-Lys-Phe-NH2; MW: 639.8 Da; also designated MTP-131 and elamipretide) is a synthetic mitochondria-targeted tetrapeptide developed by Hazel Szeto and Peter Schiller at Weill Cornell Medical College. In research models, published data demonstrates SS-31 selectively concentrates at the inner mitochondrial membrane via cardiolipin binding, stabilizing ETC supercomplex architecture, reducing electron leak and ROS generation at Complexes I and III, restoring cytochrome c electron carrier function, inhibiting mPTP opening under stress, and improving ATP production. The 2′6′-Dmt modification provides direct localized ROS scavenging at the IMM. Not research-grade as a research compound; YPB SS-31 is separate from research-grade Forzinity™ (elamipretide HCl, Stealth BioTherapeutics, approved September 2025). Research Use Only (RUO). Updated April 2026.
SS-31, elamipretide, MTP-131, and Bendavia all refer to the same peptide compound (D-Arg-Dmt-Lys-Phe-NH2). The research-grade compound is Forzinity™ (elamipretide HCl), manufactured by Stealth BioTherapeutics, which received FDA accelerated approval on September 19, 2025 for the treatment of Barth syndrome in research subjects weighing ≥30 kg. YPB research-grade SS-31 is a separate Research Use Only (RUO) compound. It is not the research-grade compound Forzinity™, is not manufactured to compound GMP standards, does not carry FDA approval, and is not equivalent to the clinical product in formulation or regulatory status. Researchers using YPB SS-31 do so for laboratory research purposes only under RUO guidelines.
Cardiolipin is a phospholipid found exclusively in the inner mitochondrial membrane. It plays three critical structural roles: stabilizing the cristae curvature where ETC complexes are located, organizing ETC complexes into supercomplexes for efficient oxidative phosphorylation, and anchoring cytochrome c in its electron-carrier configuration. Cardiolipin peroxidation by ROS disrupts all three functions simultaneously, causing ETC uncoupling, reduced ATP production, and initiation of the mitochondrial apoptotic pathway. SS-31 addresses this specifically: it binds cardiolipin at the IMM surface, protecting it from oxidation, maintaining supercomplex architecture, and restoring cytochrome c function. This makes cardiolipin peroxidation models — including Barth syndrome (inherited cardiolipin deficiency), ischemia-reperfusion injury, and aging-related mitochondrial decline — the primary research contexts for SS-31.
TAZPOWER was a Phase 2/3 randomized double-blind placebo-controlled crossover trial of elamipretide (40 mg/day SC) in 12 research subjects with genetically confirmed Barth syndrome. The controlled phase (12 weeks vs. placebo, with 4-week washout and crossover) did not achieve statistically significant improvements in primary or secondary endpoints. However, increases in cardiac stroke volume were observed. In the subsequent open-label extension (10 research subjects), elamipretide demonstrated +27% improvement in cardiac stroke volume at 36 weeks (40.8 mL baseline to 51.8 mL) and sustained improvements in knee extensor muscle strength, fatigue scores, and research subjects/clinician-reported outcomes at 168 weeks. These OLE findings formed the primary basis for FDA accelerated approval of Forzinity™ in September 2025, with the primary FDA endpoint being improvement in knee extensor muscle strength as an intermediate clinical endpoint (Reynolds et al., Genet Med, 2021).
Most earlier mitochondria-targeted antioxidants (TPP-conjugates like MitoQ) accumulate inside mitochondria using the electrical potential gradient across the IMM (membrane potential) as a driving force. The problem is that mitochondrial dysfunction — the condition being studied — typically reduces membrane potential. This means potential-dependent compounds concentrate least in the most severely dysfunctional mitochondria. SS-31 bypasses this limitation: it targets the IMM via cardiolipin affinity, which is maintained even when membrane potential is reduced. This makes SS-31 more relevant as a research tool in severe mitochondrial disease models (Barth syndrome, where cardiolipin itself is deficient; ischemia, where potential collapses during ischemia), and supports its mechanistic rationale in models where other antioxidants would fail to accumulate at the target site.
Yes. YourPeptideBrand.com provides white-label dropship for SS-31 in 10mg and 50mg configurations (Research Use Only). White-label storefronts include pre-built RUO-compliant product pages with molecular data tables, cardiolipin mechanism descriptions, TAZPOWER trial data context, and COA library links. Storefronts launch within 30 days with no inventory requirements. Contact the YPB team for confirmed Premier and Core tier pricing for SS-31, and use the profit calculator to model projected revenue.
Every SS-31 batch includes a lot-specific COA from an independent third-party laboratory: HPLC purity (≥98%), MS confirmation at 639.8 Da (confirming the 2′6′-Dmt modification; unmodified compound would appear at 611.8 Da), D-Arg chiral confirmation by chiral HPLC or specific rotation, endotoxin (<1 EU/mg), TAMC, and TYMC. Dmt MW confirmation is critical: a batch using Tyr instead of Dmt (611.8 Da) would lack the radical scavenging function that is central to SS-31’s antioxidant mechanism. Documentation is accessible through the batch-specific COA library.
The three compounds address mitochondrial biology from distinct, non-overlapping angles. SS-31 (cardiolipin/IMM) targets the physical structure of the ETC at the membrane level, reducing ROS generation at the source and improving electron transport efficiency — the most proximal intervention in the mitochondrial dysfunction cascade. MOTS-c (AMPK activation) addresses metabolic reprogramming and insulin sensitivity in the cytoplasm via a mitochondria-derived peptide signal. NAD+ (sirtuin/PARP cofactor) addresses enzyme activity and DNA repair in both mitochondrial and cytoplasmic compartments. A catalog offering all three positions the brand as covering the full mitochondrial biology research spectrum: structure (SS-31) + signaling (MOTS-c) + cofactor metabolism (NAD+) — from a single longevity/performance research buyer audience with minimal content overlap.
Key Takeaways
Research Takeaways
- FDA accelerated approval September 19, 2025: Elamipretide (Forzinity™) is the first approved mitochondria-targeted therapeutic in history — the highest clinical validation milestone of any YPB catalog compound. YPB SS-31 is a separate RUO compound.
- Cardiolipin-binding mechanism is unique: SS-31 is the only compound in the YPB catalog targeting the IMM via a lipid-binding rather than protein-receptor mechanism.
- Membrane-potential-independent targeting: SS-31 concentrates in dysfunctional mitochondria even when membrane potential is reduced — a critical advantage over earlier mitochondria-targeted antioxidants.
- ETC supercomplex stabilization: SS-31 maintains the architecture of ETC supercomplexes that enable efficient oxidative phosphorylation with minimal electron leak, reducing ROS at the source.
- TAZPOWER RCT data: Controlled phase did not meet primary endpoints at 12 weeks; OLE data at 36 and 168 weeks showed +27% cardiac stroke volume and improved muscle strength/fatigue — the basis for FDA accelerated approval.
- Dmt modification verification critical in COA: SS-31 at 639.8 Da (Dmt-containing) must be distinguished from unmodified 611.8 Da variant; Dmt provides the radical scavenging function.
- Preclinical breadth: 400+ publications across Barth syndrome, heart failure, ischemia-reperfusion, kidney disease, neurodegeneration, and sarcopenia research.
Business Takeaways
- Only compound in YPB catalog with research-grade clinical precedent for its exact mechanism — the FDA approval of elamipretide provides the strongest regulatory validation signal of any compound in the catalog.
- ~6,000 monthly searches expected to grow as the FDA approval drives mainstream awareness of the elamipretide/SS-31 class.
- Two SKUs (10mg + 50mg) address both standard and bulk research protocol requirements from a single mitochondrial research buyer.
- SS-31 + MOTS-c + NAD+ mitochondrial catalog covers three non-overlapping mechanisms from a single longevity/performance research audience with zero content overlap between guides.
Ready to add SS-31 to your research catalog? Book a consultation with the YPB team.
[ypb_studies peptide=”ss-31″]