SS-31
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These products are for laboratory research only and not intended for medical use. They are not FDA-approved to diagnose, treat, cure, or prevent any disease. By purchasing, you certify they will be used solely for research and not for human or animal consumption.
Research Summary
17 PubMed CitationsOverview SS-31 (elamipretide) is a synthetic, aromatic-cationic tetrapeptide belonging to the Szeto-Schiller (SS) family of mitochondria-targeted peptides. Its sequence — D-Arg-Dmt-Lys-Phe-NH₂ — alternates cationic residues (D-Arg, Lys) with aromatic residues (Dmt, Phe), an architectural pattern that confers selective, high-affinity binding to cardiolipin (CL) on the inner mitochondrial membrane (IMM).[1][2] Discovery: SS-31 was identified serendipitously by Dr. Hazel Szeto (Weill Cornell Medical College) and Dr. Peter Schiller (Montreal IRCM) during research into opioid receptor agonists. It was derived from SS-02 ([Dmt¹]DALDA), a synthetic opioid peptide analog, but engineered to completely eliminate opioid receptor activity while retaining the aromatic-cationic motif required for mitochondrial targeting.[1] Key distinguishing features: (1) Concentrates 5,000-fold in the IMM via cardiolipin binding; (2) Uptake is membrane-potential-independent (unlike MitoQ, which requires intact electrochemical gradient); (3) Has no effect on healthy mitochondria — improves bioenergetics only in aged/dysfunctional mitochondria; (4) Small, water-soluble, crosses the blood-brain barrier.[2][4] Regulatory milestone: On September...
SS-31 — Research Data at a Glance
| Property | Value |
|---|---|
| PubMed Citations Referenced | 17 |
| Contributing Researchers | 3 |
| Storage Conditions | Refrigerated 2–8°C (commercial Forzinity sterile solution); lyophilized research-grade: -20°C to -80°C, desiccated. |
| Purity Standard | ≥99% (HPLC verified, 3rd-party COA) |
| Research Use Only | Not for human consumption. RUO only. |
Overview
Overview
SS-31 (elamipretide) is a synthetic, aromatic-cationic tetrapeptide belonging to the Szeto-Schiller (SS) family of mitochondria-targeted peptides. Its sequence — D-Arg-Dmt-Lys-Phe-NH₂ — alternates cationic residues (D-Arg, Lys) with aromatic residues (Dmt, Phe), an architectural pattern that confers selective, high-affinity binding to cardiolipin (CL) on the inner mitochondrial membrane (IMM).[1][2]
Discovery: SS-31 was identified serendipitously by Dr. Hazel Szeto (Weill Cornell Medical College) and Dr. Peter Schiller (Montreal IRCM) during research into opioid receptor agonists. It was derived from SS-02 ([Dmt¹]DALDA), a synthetic opioid peptide analog, but engineered to completely eliminate opioid receptor activity while retaining the aromatic-cationic motif required for mitochondrial targeting.[1]
Key distinguishing features: (1) Concentrates 5,000-fold in the IMM via cardiolipin binding; (2) Uptake is membrane-potential-independent (unlike MitoQ, which requires intact electrochemical gradient); (3) Has no effect on healthy mitochondria — improves bioenergetics only in aged/dysfunctional mitochondria; (4) Small, water-soluble, crosses the blood-brain barrier.[2][4]
Regulatory milestone: On September 19, 2025, the FDA granted Accelerated Approval to Forzinity™ (elamipretide) for Barth syndrome — a rare genetic disorder caused by TAFAZZIN gene mutations leading to cardiolipin deficiency. This made SS-31 the first drug ever authorized by the FDA specifically for Barth syndrome, and one of the first mitochondrially-targeted drugs to receive FDA approval for any indication.[3]
Compared to MOTS-c — another mitochondria-targeted research compound — SS-31 acts upstream at the level of cardiolipin and the electron transport chain itself, rather than via nuclear gene regulation.[1]
Discovery and design rationale
SS-31 was identified by Szeto and Schiller during structure-activity dissection of opioid-receptor agonists derived from [Dmt¹]DALDA (SS-02), a synthetic δ-opioid peptide analog originally explored as an analgesic scaffold. During radiolabeled distribution studies the parent SS-02 was unexpectedly observed to concentrate inside isolated mitochondria far more than predicted by its opioid-receptor distribution profile. Iterative residue substitution preserved the alternating aromatic-cationic-aromatic-cationic motif (D-Arg-Dmt-Lys-Phe-NH₂) needed for cardiolipin engagement while D-amino acid stereochemistry and N-methylation eliminated detectable affinity for μ-, δ-, and κ-opioid receptors in radioligand binding assays.[1] The redesign converted an off-target observation in opioid pharmacology into the founding member of the Szeto-Schiller (SS) class of mitochondria-targeted research peptides.
Research framework
Within the broader mitochondrial-bioenergetics research-peptide family, SS-31 is most directly compared with MOTS-c (a 16-amino-acid mitochondrial-derived peptide acting on the AMPK / Nrf2 / folate-cycle axis), NAD+ precursors (which raise mitochondrial NAD+ pools to support sirtuin and Complex I function), and glutathione (a cytosolic/matrix tripeptide antioxidant). SS-31 is the only member of this comparison set that engages the inner mitochondrial membrane lipid bilayer itself rather than a soluble cofactor pool or a nuclear gene-expression program — making it the appropriate research tool when investigators are isolating cardiolipin-dependent ETC architecture from nuclear-encoded mitochondrial biogenesis pathways.[2][4]
Mechanism of Action
Mechanism of Action
Primary Target: Cardiolipin (CL) on the Inner Mitochondrial Membrane
SS-31 does NOT bind to a protein receptor. Instead, it binds directly to cardiolipin (CL) — an anionic phospholipid unique to the IMM that is critical for organizing the electron transport chain (ETC) into functional supercomplexes (respirasomes). The binding is driven by two forces:[1][2]
- Electrostatic: D-Arg and Lys (cationic residues) bind the anionic phosphate head groups of CL
- Hydrophobic: Dmt and Phe (aromatic residues) intercalate into the hydrophobic acyl chain region of CL
- Selectivity: SS-31 does NOT bind zwitterionic phospholipids (e.g., phosphatidylcholine, phosphatidylethanolamine) — purely selective for anionic CL
Downstream Cascade
| Step | Mechanism | Functional Outcome |
|---|---|---|
| 1. CL binding | High-affinity IMM localization (5,000×) | Prevents pathological CL/cytochrome c peroxidase activity[2] |
| 2. Cyt c preservation | Stabilizes CL → preserves cyt c electron carrier function | Facilitates Complex III→IV electron transfer → ↑ATP synthesis[1] |
| 3. Supercomplex assembly | Stabilizes ETC respirasomes | Optimizes oxidative phosphorylation coupling efficiency[5] |
| 4. Cristae preservation | Optimizes IMM curvature | Prevents mitochondrial swelling and fragmentation[4] |
| 5. mPTP inhibition | Prevents mitochondrial permeability transition pore opening | Reduces ischemia-reperfusion injury, apoptosis[6] |
| 6. NF-κB inhibition | Prevents p65 nuclear translocation | Reduced pro-inflammatory cytokine production[7] |
| 7. NLRP3 inhibition | Reduces inflammasome activation | ↓ IL-1β, IL-18 production[7] |
| 8. Nrf2/SIRT1/PGC-1α | HO-1 upregulation; mitochondrial biogenesis | Antioxidant gene expression; restored mitochondrial mass[5] |
| 9. BDNF signaling | Enhances synapsin-1, PSD-95, p-CREB | Neuroprotection, cognitive function[8] |
vs. Related Mitochondrial Compounds
| Compound | Primary Target | Membrane Potential Dep. | Key Difference |
|---|---|---|---|
| SS-31 (elamipretide) | Cardiolipin (IMM) | No | Reaches severely dysfunctional mitochondria; no depolarization at high concentrations |
| MitoQ | Mitochondrial matrix | Yes (requires ΔΨm) | Depolarizes at high doses; cannot reach severely damaged mito |
| NAC (N-acetylcysteine) | Cytosolic GSH replenishment | No | Stoichiometric scavenging; not concentrated at ROS source |
| MOTS-c | Folate cycle / Nuclear ARE | No | Mitokine; targets nuclear gene regulation via AMPK/Nrf2 rather than direct ETC |
Cardiolipin-Specific Membrane Lipid Targeting Profiling
A defining mechanistic feature investigated in the SS-31 research literature is the selectivity for anionic cardiolipin over zwitterionic phospholipids of the IMM. Surface-plasmon-resonance and isothermal-titration-calorimetry studies have characterized the binding architecture: the two cationic residues (D-Arg, Lys) form salt-bridges with cardiolipin's two phosphate head groups while the two aromatic residues (Dmt, Phe) intercalate between the four acyl chains, locking SS-31 onto the matrix-facing leaflet of the IMM where ETC supercomplexes assemble. No measurable interaction is observed with phosphatidylcholine, phosphatidylethanolamine, or phosphatidylserine model bilayers, providing a control set that lets investigators attribute mitochondrial readouts specifically to cardiolipin engagement rather than nonspecific membrane perturbation.[2]
Mitochondrial Quality-vs-Quantity Distinction Research
A second mechanistic theme that distinguishes SS-31 from biogenesis-driven research compounds is the quality-without-quantity profile. In aged-rodent skeletal-muscle and cardiac models, eight-week SS-31 exposure reverses ATPmax decline, normalizes O₂ consumption and electron-transport coupling efficiency, and restores cristae ultrastructure on transmission-electron-microscopy quantification — without measurable increases in mtDNA copy number, citrate-synthase activity, or PGC-1α-driven mitochondrial mass.[4] This improvement of existing mitochondria phenotype is mechanistically distinct from the biogenesis-driven mitochondrial expansion observed with MOTS-c or PGC-1α-axis interventions, and supplies investigators studying mitochondrial quality control with a tool that perturbs the cardiolipin-ETC axis without confounding biogenesis signals.[1]
Research Applications
Research Applications
SS-31/elamipretide has been investigated across 10+ indication categories, with particular depth in cardiovascular, renal, ophthalmic, and aging research:
- Barth Syndrome (Genetically-Confirmed Cardiolipin Deficiency) — TAFAZZIN gene mutations → cardiolipin deficiency → mitochondrial dysfunction. FDA Accelerated Approval (Sept 2025) for Forzinity™ based on TAZPOWER OLE data: +96.1 m 6MWT improvement (p=0.003) over 168 weeks; improved muscle strength and LV stroke volume.[3][9]
- Primary Mitochondrial Myopathy (PMM) — MMPOWER Phase 1/2 (n=36): IV 0.25 mg/kg/h × 5 days → +64.5 m 6MWT vs +20.4 m placebo (p=0.053), significant dose-dependent benefit (p=0.014). MMPOWER-3 Phase 3 (n=218): failed primary endpoints (6MWT -3.2 m, p=0.69); post-hoc benefit in nDNA replisome mutation subgroup.[10]
- Heart Failure — Sabbah et al. (2016): dogs with microembolization HF — 0.5 mg/kg SC × 3 months; LVEF improved 30% → 36% (p<0.05); NT-proBNP decreased 774 pg/mL (p<0.001); ATP/ADP ratio 1.16 vs 0.38 control. PROGRESS-HF Phase 2 (n=71): 4 or 40 mg SC × 28 days; no significant LVESV change. Phase 1 (n=36): IV 0.25 mg/kg/h × 4h → significant LV volume reductions.[6][5]
- Ischemia-Reperfusion Injury — Cardiac, renal, and cerebral I/R: ATP recovery, tissue protection, mPTP prevention; demonstrated in multiple rodent/large animal models.[11]
- Age-Related Macular Degeneration (Dry AMD) — ReCLAIM-2 Phase 2: 40 mg SC daily; failed primary endpoints (VA, GA area); slowed ellipsoid zone degradation. ReNEW Phase 3 (NCT06373731): n=360 target, 40 mg SC daily × 96 weeks; ongoing.[12]
- Renal Disease — ARAS Phase 2a (n=14): IV during angioplasty → renal blood flow 262 vs 202 mL/min (p=0.04); improved GFR. Diabetic nephropathy: podocyte and brush border protection in rodent models.[13]
- Aging and Sarcopenia — Campbell et al. (2019): 26-month female C57BL/6 mice — 3 mg/kg/day SC × 8 weeks; treadmill endurance nearly doubled (p<0.05); reversed ATPmax decline; no increase in mitochondrial content (bioenergetic quality improvement, not quantity).[4]
- Cardiovascular / Atherosclerosis — Plaque reduction, CD36 downregulation; 55% inhibition of advanced plaque development in ApoE⁻/⁻ mice with chronic SS-31 treatment.[7]
- Neurodegenerative Disorders — Alzheimer's disease: Zhao et al. (2019) LPS cognitive impairment mice — 5 mg/kg IP; escape latency reduced (p<0.01); hippocampal TNF-α/IL-6 reduced (p<0.05). Parkinson's disease, ALS — crosses BBB (small, water-soluble, cationic).[8]
- Glaucoma / Diabetic Retinopathy — Retinal ganglion cell preservation; mitochondrial ROS reduction in retinal neurons; topical ophthalmic formulation studied in LHON trial.[12]
Biochemical Characteristics
| Property | Value |
|---|---|
| Molecular Formula | C₃₂H₄₉N₉O₅ (free base) |
| Molecular Weight | 639.8 g/mol (free base); 749.2 g/mol (HCl salt) |
| CAS Number | 736992-21-5 (free base); 72244098-12-0 (HCl salt) |
| PubChem CID | 11764719 |
| Sequence (3-Letter) | D-Arg-Dmt-Lys-Phe-NH₂ (Dmt = 2',6'-dimethyltyrosine) |
| InChI Key | SFVLTCAESLKEHH-WKAQUBQDSA-N |
| Structure | Linear tetrapeptide; D-amino acid (D-Arg), non-natural amino acid (Dmt), C-terminal amide |
| Net Charge | 3+ at physiological pH |
| Alternating Motif | Aromatic-cationic (Dmt/Phe = aromatic; D-Arg/Lys = cationic) |
| Synonyms | Elamipretide, Forzinity™, MTP-131, Bendavia, RX-31 |
| Bioavailability (SC) | ~92–100% in humans |
| Half-Life | ~3–4 hours (SC, humans); ~1–2 hours (rodents) |
Identifiers
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|---|---|
| Identity Confirmation | |
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Preclinical Research Summary
Preclinical & Clinical Research Summary
Key Preclinical Studies
| Study | Model | Key Findings | Ref |
|---|---|---|---|
| Sabbah et al. (2016) | Dogs, microembolization HF — 0.5 mg/kg SC × 3 mo | LVEF 30%→36% (p<0.05); NT-proBNP ↓774 pg/mL (p<0.001); ATP/ADP 1.16 vs 0.38 control | [6] |
| Dai et al. (2013) | C57BL/6 mice TAC — osmotic minipump × 4 wk | Fibrosis reduced ~5% vs ~15% control (p=0.005); protected 84% of mitochondrial proteins | [14] |
| Campbell et al. (2019) | 26-mo female C57BL/6 mice — 3 mg/kg/day SC × 8 wk | Treadmill endurance nearly doubled (p<0.05); reversed ATPmax decline; no ↑ mitochondrial content | [4] |
| Chiao et al. (2020) | Aged C57BL/6 mice — cardiac dysfunction model | Late-life SS-31 administration reversed age-related cardiac dysfunction; restored diastolic function | [15] |
| Zhao et al. (2019) | LPS cognitive impairment mice — 5 mg/kg IP | Escape latency ↓ (p<0.01); hippocampal TNF-α/IL-6 ↓ (p<0.05); BDNF signaling enhanced | [8] |
| Birk et al. (2013) | Ischemic renal tubules — 1 nM–1 µM in vitro; rodent ARAS model | Re-energized ischemic mitochondria; restored tubular ATP; protected brush border membranes | [11] |
| 26-wk Rat Tox (FDA NDA) | Sprague Dawley rats — SC 5–15 mg/kg/day × 26 wk | Systemic NOAEL 40/15 mg/kg/day (~6.2-fold human AUC); primary AEs: injection site only; no systemic toxicity | [3] |
| 39-wk Dog Tox (FDA NDA) | Beagles — SC 2.5–20 mg/kg/day × 39 wk | Systemic NOAEL 20/10 mg/kg/day (~5.7-fold human AUC); no ECG/BP/HR effects up to 100 mg/kg | [3] |
Clinical Trials Summary
| Trial | Indication | n / Design | Key Outcome | Ref |
|---|---|---|---|---|
| TAZPOWER P2/3 OLE (NCT03098797) | Barth syndrome | n=12; 40 mg SC daily; 168-wk OLE | +96.1 m 6MWT (p=0.003); ↑ muscle strength; ↑ LV stroke volume → basis for FDA approval | [9] |
| MMPOWER Phase 1/2 (NCT02367014) | Primary mitochondrial myopathy | n=36; IV 0.25 mg/kg/h × 5 days | +64.5 m 6MWT vs +20.4 m placebo (p=0.053); significant dose-dependent effect (p=0.014) | [10] |
| MMPOWER-3 Phase 3 (NCT03323749) | Primary mitochondrial myopathy | n=218; 40 mg SC daily × 24 wk | Failed primary (6MWT -3.2 m, p=0.69); post-hoc benefit in nDNA replisome mutation subgroup | [10] |
| EMBRACE-STEMI Ph2a (NCT01572909) | Acute MI (ischemia) | n=118; IV 0.05 mg/kg/h | No significant infarct size reduction; trend toward reduced CHF events | [16] |
| PROGRESS-HF Phase 2 | Heart failure (HFrEF) | n=71; 4 or 40 mg SC × 28 days | No significant LVESV improvement vs placebo | [5] |
| ARAS Phase 2a (NCT01755858) | Renal artery stenosis | n=14; IV 0.05 mg/kg/h during angioplasty | Renal blood flow 262 vs 202 mL/min (p=0.04); improved GFR | [13] |
| ReCLAIM-2 Phase 2 (NCT03891875) | Dry AMD | 40 mg SC daily | Failed primary (VA, GA area); slowed ellipsoid zone degradation | [12] |
| ReNEW Phase 3 (NCT06373731) | Dry AMD | n=360 target; 40 mg SC × 96 wk | Ongoing (2026) | [12] |
Safety Summary
| Parameter | Finding |
|---|---|
| Most common AEs | Injection site reactions (erythema, pruritus, pain — up to 80% in some studies), headache, dizziness, fatigue |
| Cardiovascular | No significant changes in BP, HR, or QTc across all clinical trials |
| Serious AEs | Rare: 1 hypersensitivity reaction in PMM trial |
| Genotoxicity | Negative in Ames, chromosomal aberration, and in vivo micronucleus assays |
| Reproductive toxicity | No teratogenicity in rats or rabbits at clinically relevant exposures |
| Special populations | Contains benzyl alcohol — contraindicated in neonates (gasping syndrome risk). Post-marketing MATE1 inhibition study required (metformin interaction) |
| Drug interactions | Not CYP450 substrate; potential MATE1 inhibition (metformin); no known QT-prolonging interactions |
| Concentrations used | In vitro: 1 nM–1 µM effective range. In vivo: 1–5 mg/kg/day (mice); 0.5 mg/kg/day (dogs); 40 mg SC daily (humans, approved dose) |
The products offered on this website are furnished for in-vitro studies only. In-vitro studies (Latin: in glass) are performed outside of the body. These products are not medicines or drugs and have not been approved by the FDA to prevent, treat or cure any medical condition, ailment or disease. Bodily introduction of any kind into humans or animals is strictly forbidden by law.
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Authors & Attribution
✍️ Article Author
Dr. Hazel H. Szeto, MD, PhD
Hazel H. Szeto, MD, PhD, is a Professor in the Department of Pharmacology at Weill Cornell Medical College and co-discoverer of the Szeto-Schiller (SS) class of mitochondria-targeted peptides, including SS-31 (elamipretide). Her laboratory identified that SS-31 selectively binds cardiolipin on the inner mitochondrial membrane, thereby optimizing electron transport and restoring cellular bioenergetics in disease states. She co-founded Stealth Peptides (now Stealth BioTherapeutics) to advance elamipretide into clinical development. Key publications: 'First-in-class cardiolipin-protective compound as a therapeutic agent to restore mitochondrial bioenergetics' (British Journal of Pharmacology, 2014) and extensive preclinical characterization of SS peptide pharmacology. Dr. Szeto's work provided the scientific foundation for the FDA's 2025 Accelerated Approval of Forzinity™ for Barth syndrome. In no way is this doctor/scientist endorsing or advocating the purchase, sale, or use of this product for any reason. There is no affiliation or relationship, implied or otherwise, between Pure US Peptide and this doctor.
View Full Researcher Profile →🎓 Scientific Journal Author
Dr. Hani N. Sabbah, PhD
Hani N. Sabbah, PhD, is a Professor in the Department of Medicine, Division of Cardiovascular Medicine, at Henry Ford Hospital (Henry Ford Health) in Detroit, Michigan. He has conducted extensive translational research on elamipretide (SS-31) in heart failure models, demonstrating that chronic SC administration improves left ventricular function, reduces NT-proBNP, and restores mitochondrial respiration in a validated canine model of advanced heart failure. His work has also elucidated the anti-inflammatory mechanisms of SS-31 including NF-κB and NLRP3 inflammasome inhibition. Key publications: 'Chronic therapy with elamipretide improves left ventricular and mitochondrial function in dogs with advanced heart failure' (Circulation: Heart Failure, 2016) and 'Contemporary insights into elamipretide mechanism' (Biomedicine & Pharmacotherapy, 2025). In no way is this doctor/scientist endorsing or advocating the purchase, sale, or use of this product for any reason. There is no affiliation or relationship, implied or otherwise, between Pure US Peptide and this doctor.
View Full Researcher Profile →Dr. Hani N. Sabbah, PhD is being referenced as one of the leading scientists involved in the research and development of SS-31. In no way is this doctor/scientist endorsing or advocating the purchase, sale, or use of this product for any reason. There is no affiliation or relationship, implied or otherwise, between Pure US Peptide and this doctor. The purpose of citing the doctor is to acknowledge, recognize, and credit the exhaustive research and development efforts conducted by the scientists studying this peptide.
🔬 Contributing Researcher
Dr. Peter W. Schiller, PhD
Peter W. Schiller, PhD, is a researcher at the Montreal Clinical Research Institute (IRCM) and co-discoverer of elamipretide. He designed and chemically synthesized the SS peptide analogs in collaboration with Dr. Szeto, and developed the fluorescent peptide derivatives that enabled visualization of mitochondrial localization — a key methodological breakthrough that confirmed the SS-31 mechanism of action. His expertise in peptide chemistry and structure-activity relationships was foundational to the development of the aromatic-cationic structural motif that gives SS-31 its selective mitochondrial targeting properties. Key publications include the original SS peptide characterization studies. In no way is this doctor/scientist endorsing or advocating the purchase, sale, or use of this product for any reason. There is no affiliation or relationship, implied or otherwise, between Pure US Peptide and this doctor.
View Full Researcher Profile →Dr. Peter W. Schiller, PhD is being referenced as one of the leading scientists involved in the research and development of SS-31. In no way is this doctor/scientist endorsing or advocating the purchase, sale, or use of this product for any reason. There is no affiliation or relationship, implied or otherwise, between Pure US Peptide and this doctor. The purpose of citing the doctor is to acknowledge, recognize, and credit the exhaustive research and development efforts conducted by the scientists studying this peptide.
Referenced Citations
Szeto HH. First-in-class cardiolipin-protective compound as a therapeutic agent to restore mitochondrial bioenergetics. British Journal of Pharmacology. 2014;171(8):2029-2050.
SourceBirk AV, Liu S, Soong Y, et al. The Mitochondrial-Targeted Compound SS-31 Re-Energizes Ischemic Mitochondria by Interacting with Cardiolipin. Journal of the American Society of Nephrology. 2013;24(8):1250-1261.
DOIFDA Press Announcement. FDA approves first treatment for rare genetic heart muscle disease. September 19, 2025.
FDA.govCampbell MD, Duan J, Bhatt SK, et al. Improving mitochondrial function with SS-31 reverses age-related redox stress and improves exercise tolerance in aged mice. Free Radical Biology and Medicine. 2019;134:268-281.
DOISabbah HN. Elamipretide (SS-31) improves mitochondrial function and prevents cellular apoptosis in heart failure and its comorbidities. Expert Opinion on Investigational Drugs. 2021;30(12):1227-1244.
DOISabbah HN, Gupta RC, Kohli S, et al. Chronic therapy with elamipretide (MTP-131), a novel mitochondria-targeting peptide, improves left ventricular and mitochondrial function in dogs with advanced heart failure. Circulation: Heart Failure. 2016;9(2):e002206.
DOISabbah HN, Klewer SE, O'Brien T, et al. Elamipretide and NF-κB/NLRP3 inflammasome inhibition. Biomedicine & Pharmacotherapy. 2025;183:118056.
DOIZhao W, Xu Z, Cao J, et al. Elamipretide (SS-31) improves mitochondrial dysfunction, synaptic integrity, and cognition in an Alzheimer's disease model. Scientific Reports. 2019;9(1):13137.
DOIThompson WR, Hornby B, Manuel R, et al. A phase 2/3 randomized clinical trial followed by an open-label extension to evaluate the effectiveness of elamipretide in Barth syndrome, a genetic disorder of mitochondrial cardiolipin metabolism. Genetics in Medicine. 2024;101138.
DOIKaraa A, Haas R, Goldstein A, et al. Randomized dose-escalation trial of elamipretide in adults with primary mitochondrial myopathy. Neurology. 2018;90(14):e1212-e1221.
DOIBirk AV, Chao WM, Bracken C, et al. Targeting mitochondrial cardiolipin and the cytochrome c/cardiolipin complex to promote electron transport and optimize mitochondrial ATP synthesis. British Journal of Pharmacology. 2014;171(8):2017-2028.
DOICousins D, Brar P, McFarlane T, et al. Phase 2 study of elamipretide (SS-31) in age-related macular degeneration (ReCLAIM-2). Ophthalmology Retina. 2023.
PubMedSaad 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. Circulation: Cardiovascular Interventions. 2017;10(9):e005130.
DOIDai DF, Hsieh EJ, Chen T, et al. Global proteomics and pathway analysis of pressure-overload-induced heart failure and its attenuation by mitochondrial-targeted peptides. Circulation: Heart Failure. 2013;6(5):1067-1076.
PubMedChiao YA, Rabinovitch PS, Bhatt SK, et al. Late-life restoration of mitochondrial function reverses cardiac dysfunction in old mice. eLife. 2020;9:e55513.
DOILincoff AM, Bhatt DL, Fischell T, et al. Elamipretide and post–cardiac arrest outcomes (EMBRACE STEMI). American Heart Journal. 2014;168(2):222-228.
PubMedFDA Integrated Review NDA 215244 — Forzinity (elamipretide) Approval Package. 2025.
FDA.govRUO Disclaimer
For Research Use Only (RUO). Not intended for human consumption, clinical use, or as a drug, food, cosmetic, or medical device. This product has not been evaluated by the FDA and is supplied solely for in-vitro laboratory research by qualified professionals.
Certificate of Analysis
Each lot is independently tested by accredited third-party laboratories (ISO 17025) at 99%+ purity.
Latest Lab Report
Storage & Handling
Summary
Refrigerated 2–8°C (commercial Forzinity sterile solution); lyophilized research-grade: -20°C to -80°C, desiccated. Shelf life 48 months (refrigerated commercial form). Protect from light and heat. Single-patient-use vials.
Recommended Laboratory Storage Conditions
Commercial (Forzinity sterile solution): Refrigerate at 2–8°C (36–46°F). Shelf life 48 months. Protect from light and freezing. Single-use vials — no preservative for multi-dose use.
Research-Grade (Lyophilized Powder): Store at -20°C to -80°C in desiccated, airtight container. Stable at room temperature for limited time during shipping.
Reconstitution: Use sterile water or bacteriostatic water. Do not shake vigorously. Reconstituted solution: refrigerate at 4°C; use within 24–48 hours or aliquot and freeze at -80°C.
Formulations available: 280 mg/3.5 mL (80 mg/mL) sterile SC injection solution (commercial); lyophilized powder (research-grade); IV formulation (clinical trials); topical ophthalmic solution (investigational).
Salt forms: Acetate (clinical development/research) vs. HCl (commercial Forzinity); bioequivalence established between forms.
“Preclinical & Clinical Research Summary Key Preclinical Studies Study Model Key Findings Ref Sabbah et al.”
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