SS-31
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Resumo da Pesquisa
17 Citacoes PubMedVisao Geral SS-31 (elamipretide) e um(a) sintetico(a), aromatic-cationic tetrapeptide pertencente a 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 que confere selective, high-affinity binding to cardiolipin (CL) no(a) inner membrana mitocondrial (IMM).[1][2] Discovery: SS-31 was identificado(a) serendipitously by Dr. Hazel Szeto (Weill Cornell Medical College) and Dr. Peter Schiller (Montreal IRCM) during research into opioid agonista do receptors. It was derivado(a) de SS-02 ([Dmt¹]DALDA), a synthetic opioid peptide analog, but projetado(a) para completely eliminate opioid receptor activity enquanto retaining the aromatic-cationic motif necessario(a) para mitochondrial targeting.[1] Key distinguishing features: (1) Concentrates 5,000-fold no(a) IMM via cardiolipin binding; (2) Uptake is membrane-potential-independent (diferentemente de MitoQ, que requer intact electrochemical gradient); (3) Has no effect on healthy mitochondria — melhora bioenergetics apenas in aged/dysfunctional mitochondria; (4) Small, water-soluble, crosses the blood-brain barrier.[2][4] Regulatory milestone: On...
SS-31 — Dados de Pesquisa em Resumo
| Propriedade | Valor |
|---|---|
| Citacoes PubMed Referenciadas | 17 |
| Pesquisadores Colaboradores | 3 |
| Condicoes de Armazenamento | Refrigered 2–8°C (commercial Forzinity solução estéril); liofilizado research-grade: -20°C to -80°C, dessecado. |
| Padrao de Pureza | ≥99% (HPLC verified, 3rd-party COA) |
| Apenas para Uso em Pesquisa | Nao destinado ao consumo humano. Apenas para uso em pesquisa. |
Visao Geral
Visao Geral
SS-31 (elamipretide) e um(a) sintetico(a), aromatic-cationic tetrapeptide pertencente a 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 que confere selective, high-affinity binding to cardiolipin (CL) no(a) inner membrana mitocondrial (IMM).[1][2]
Discovery: SS-31 was identificado(a) serendipitously by Dr. Hazel Szeto (Weill Cornell Medical College) and Dr. Peter Schiller (Montreal IRCM) during research into opioid agonista do receptors. It was derivado(a) de SS-02 ([Dmt¹]DALDA), a synthetic opioid peptide analog, but projetado(a) para completely eliminate opioid receptor activity enquanto retaining the aromatic-cationic motif necessario(a) para mitochondrial targeting.[1]
Key distinguishing features: (1) Concentrates 5,000-fold no(a) IMM via cardiolipin binding; (2) Uptake is membrane-potential-independent (diferentemente de MitoQ, que requer intact electrochemical gradient); (3) Has no effect on healthy mitochondria — melhora bioenergetics apenas 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 levando a cardiolipin deficiency. This made SS-31 the first drug ever authorized pelo(a) FDA specifically for Barth syndrome, and one do(a) primeiro(a) mitochondrially-targeted drugs to receive aprovacao da FDA for qualquer indication.[3]
Comparado(a) a MOTS-c — another mitochondria-targeted composto de pesquisa — SS-31 acts upstream at o nivel of cardiolipin e o(a) electron transport chain itself, rather do que via nuclear gene regulacao.[1]
Mecanismo de Acao
Mecanismo de Acao
Primary Target: Cardiolipin (CL) no(a) Inner Mitochondrial Membrane
SS-31 does NOT bind to a protein receptor. Instead, it binds directly to cardiolipin (CL) — an anionic phospholipid unique para o(a) IMM que is critico(a) para 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 no(a) 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 | Mecanismo | 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 → preserva cyt c electron carrier function | Facilitates Complex III→IV electron transfer → ↑ATP synthesis[1] |
| 3. Supercomplex assembly | Stabilizes ETC respirasomes | Optimizes oxidative fosforilacao coupling efficiency[5] |
| 4. Cristae preservation | Optimizes IMM curvature | Prevents mitochondrial swelling and fragmentation[4] |
| 5. mPTP inibicao | Prevents mitochondrial permeability transition pore opening | Reduces isquemia-reperfusao injury, apoptose[6] |
| 6. NF-κB inibicao | Prevents p65 nuclear translocation | Reduced pro-inflamatorio(a) cytokine production[7] |
| 7. NLRP3 inibicao | Reduces inflammasome ativacao | ↓ IL-1β, IL-18 production[7] |
| 8. Nrf2/SIRT1/PGC-1α | HO-1 upregulacao; biogenese mitocondrial | Antioxidant expressao genica; restaurou 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 alto(a) concentrations |
| MitoQ | Mitochondrial matrix | Yes (requer ΔΨm) | Depolarizes at alto(a) 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; direciona nuclear gene regulacao via AMPK/Nrf2 rather do que direto(a) ETC |
Aplicacoes de Pesquisa
Aplicacoes de Pesquisa
SS-31/elamipretide tem sido investigado(a) 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; melhorou 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-dependente benefit (p=0.014). MMPOWER-3 Phase 3 (n=218): failed desfecho primarios (6MWT -3.2 m, p=0.69); post-hoc benefit in nDNA replisome mutation subgroup.[10]
- Insuficiencia Cardiaca — Sabbah et al. (2016): dogs with microembolization HF — 0.5 mg/kg SC × 3 months; LVEF melhorou 30% → 36% (p<0.05); NT-proBNP diminuiu 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-Reperfusao Injury — Cardiac, renal, and cerebral I/R: ATP recovery, protecao tecidual, mPTP prevention; demonstrated in multiplos(as) rodent/large modelo animals.[11]
- Age-Related Macular Degeneration (Dry AMD) — ReCLAIM-2 Phase 2: 40 mg SC daily; failed desfecho primarios (VA, GA area); slowed ellipsoid zone degradacao. 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); melhorou GFR. Diabetic nefropatia: 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 downregulacao; 55% inibicao of advanced plaque development in ApoE⁻/⁻ mice with cronico(a) SS-31 treatment.[7]
- Neurodegenerative Disorders — Alzheimer's disease: Zhao et al. (2019) LPS cognitive impairment mice — 5 mg/kg IP; escape latency reduziu (p<0.01); hipocampal TNF-α/IL-6 reduziu (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; topico(a) ophthalmic formulation studied in LHON trial.[12]
Caracteristicas Bioquimicas
| Propriedade | Valor |
|---|---|
| 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-aminoacido (D-Arg), non-natural aminoacido (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) |
Identificadores
| Purity Standard | |
|---|---|
| Identity Confirmation | |
| Counter-Ion | |
| Detection Methods | |
| Metabolism | |
| Excretion |
Resumo da Pesquisa Pre-clinica
Preclinical & Clinical Research Summary
Key Preclinical Studies
| Estudo | Modelo | Principais Achados | 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 reduziu ~5% vs ~15% control (p=0.005); protegeu 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; restaurou diastolic function | [15] |
| Zhao et al. (2019) | LPS cognitive impairment mice — 5 mg/kg IP | Escape latency ↓ (p<0.01); hipocampal TNF-α/IL-6 ↓ (p<0.05); BDNF signaling aprimorou | [8] |
| Birk et al. (2013) | Ischemic renal tubules — 1 nM–1 µM in vitro; rodent ARAS model | Re-energized ischemic mitochondria; restaurou tubular ATP; protegeu 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 sistemico(a) 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
| Ensaio | Indication | n / Design | Desfecho Principal | 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 aprovacao da FDA | [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-dependente 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 (isquemia) | n=118; IV 0.05 mg/kg/h | No significant infarct size reduction; trend toward reduziu 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); melhorou GFR | [13] |
| ReCLAIM-2 Phase 2 (NCT03891875) | Dry AMD | 40 mg SC daily | Failed primary (VA, GA area); slowed ellipsoid zone degradacao | [12] |
| ReNEW Phase 3 (NCT06373731) | Dry AMD | n=360 target; 40 mg SC × 96 wk | Ongoing (2026) | [12] |
Safety Summary
| Parametro | Finding |
|---|---|
| Most common AEs | Injection site reactions (erythema, pruritus, pain — up to 80% in algum(a) studies), headache, dizziness, fatigue |
| Cardiovascular | No significant changes in BP, HR, or QTc across all ensaios clinicos |
| Serious AEs | Rare: 1 hypersensitivity reaction in PMM trial |
| Genotoxicity | Negative in Ames, chromosomal aberration, e em 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 inibicao study required (metformin interaction) |
| Drug interactions | Not CYP450 substrate; potential MATE1 inibicao (metformin); no known QT-prolonging interactions |
| Concentrations used | In vitro: 1 nM–1 µM eficaz range. In vivo: 1–5 mg/kg/day (mice); 0.5 mg/kg/day (dogs); 40 mg SC daily (humans, approved dose) |
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Apenas para Pesquisa Laboratorial. Não se destina ao uso humano, uso médico, uso diagnóstico ou uso veterinário.
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Autores e Atribuicao
✍️ Autor do Artigo
Dr. Hazel H. Szeto, MD, PhD
Hazel H. Szeto, MD, PhD, is a Professor no(a) Department of Pharmacology at Weill Cornell Medical College and co-discoverer do(a) Szeto-Schiller (SS) class of mitochondria-targeted peptides, incluindo SS-31 (elamipretide). Her laboratory identificado(a) que SS-31 liga-se seletivamente cardiolipin no(a) inner membrana mitocondrial, assim optimizing electron transport and restoring cellular bioenergetics in disease states. She co-founded Stealth Peptides (now Stealth BioTherapeutics) to advance elamipretide into desenvolvimento clinico. Key publications: 'First-in-class cardiolipin-protective compound como um(a) therapeutic agent para restaurar mitochondrial bioenergetics' (British Journal of Pharmacology, 2014) and extensive preclinical characterization of SS peptide pharmacology. Dr. Szeto's work provided the scientific foundation para o(a) FDA's 2025 Accelerated Approval of Forzinity™ for Barth syndrome. De forma alguma este(a) médico(a)/cientista endossa ou defende a compra, venda ou uso deste produto por qualquer motivo. Não existe afiliação ou relação, implícita ou de outra forma, entre a Pure US Peptide e este(a) médico(a).
Ver Perfil Completo do Pesquisador →🎓 Autor de Revista Cientifica
Dr. Hani N. Sabbah, PhD
Hani N. Sabbah, PhD, is a Professor no(a) Department of Medicine, Division of Cardiovascular Medicine, at Henry Ford Hospital (Henry Ford Health) in Detroit, Michigan. He has conducted extensive traducaoal research on elamipretide (SS-31) in insuficiencia cardiaca models, demonstrating que cronico(a) SC administration melhora left ventricular function, reduz NT-proBNP, and restaura mitochondrial respiration in a validated canine model of advanced insuficiencia cardiaca. His work tambem tem elucidated the anti-inflamatorio(a) mechanisms of SS-31 incluindo NF-κB and NLRP3 inflammasome inibicao. Key publications: 'Chronic therapy with elamipretide melhora left ventricular and funcao mitocondrial in dogs with advanced insuficiencia cardiaca' (Circulation: Heart Failure, 2016) and 'Contemporary insights into elamipretide mechanism' (Biomedicine & Pharmacotherapy, 2025). De forma alguma este(a) médico(a)/cientista endossa ou defende a compra, venda ou uso deste produto por qualquer motivo. Não existe afiliação ou relação, implícita ou de outra forma, entre a Pure US Peptide e este(a) médico(a).
Ver Perfil Completo do Pesquisador →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.
🔬 Pesquisador Colaborador
Dr. Peter W. Schiller, PhD
Peter W. Schiller, PhD, is a researcher no(a) 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 que enabled visualization of mitochondrial localization — um(a) principal methodological breakthrough que confirmou the SS-31 mecanismo de acao. His expertise in peptide chemistry and structure-activity relationships was foundational to o desenvolvimento do(a) aromatic-cationic structural motif que gives SS-31 its selective mitochondrial targeting properties. Key publications include the original SS peptide characterization studies. De forma alguma este(a) médico(a)/cientista endossa ou defende a compra, venda ou uso deste produto por qualquer motivo. Não existe afiliação ou relação, implícita ou de outra forma, entre a Pure US Peptide e este(a) médico(a).
Ver Perfil Completo do Pesquisador →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.
Citacoes Referenciadas
Szeto HH. First-in-class cardiolipin-protective compound como um(a) therapeutic agent para restaurar 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 do(a) American Society of Nephrology. 2013;24(8):1250-1261.
DOIFDA Press Announcement. FDA approves primeiro(a) treatment for rare genetic heart muscle disease. September 19, 2025.
FDA.govCampbell MD, Duan J, Bhatt SK, et al. Improving funcao mitocondrial with SS-31 reverses age-related redox stress and melhora exercise tolerance in camundongos idosos. Free Radical Biology and Medicine. 2019;134:268-281.
DOISabbah HN. Elamipretide (SS-31) melhora funcao mitocondrial and previne cellular apoptose in insuficiencia cardiaca e seu(sua) 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), um(a) novo(a) mitochondria-targeting peptide, melhora left ventricular and funcao mitocondrial in dogs with advanced insuficiencia cardiaca. Circulation: Heart Failure. 2016;9(2):e002206.
DOISabbah HN, Klewer SE, O'Brien T, et al. Elamipretide and NF-κB/NLRP3 inflammasome inibicao. Biomedicine & Pharmacotherapy. 2025;183:118056.
DOIZhao W, Xu Z, Cao J, et al. Elamipretide (SS-31) melhora mitochondrial dysfunction, sinaptico(a) 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 randomizado ensaio clinico followed by an open-label extension to evaluate o efeitoiveness of elamipretide in Barth syndrome, a genetic disorder of mitochondrial cardiolipin metabolismo. 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 e o(a) cytochrome c/cardiolipin complex para promover 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 ensaio clinico 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-induziu insuficiencia cardiaca e seu(sua) 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 funcao mitocondrial 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.govAviso de Uso em Pesquisa
Apenas para Uso em Pesquisa (RUO). Nao destinado ao consumo humano, uso clinico, ou como medicamento, alimento, cosmetico ou dispositivo medico. Este produto nao foi avaliado pelo FDA e e fornecido exclusivamente para pesquisa laboratorial in vitro por profissionais qualificados.
Certificado de Analise
Each lot is independently tested by accredited third-party laboratories (ISO 17025) at 99%+ purity.
Ultimo Relatorio de Laboratorio
Armazenamento e Manuseio
Resumo
Refrigered 2–8°C (commercial Forzinity solução estéril); liofilizado research-grade: -20°C to -80°C, dessecado. Shelf life 48 meses (refrigerado forma comercial). Protect de light e heat. Frascos de uso único por paciente.
Condições Recomendadas de Armazenamento Laboratorial
Commercial (Forzinity sterile solution): Refrigerate at 2–8°C (36–46°F). Shelf life 48 months. Proteja da luz and freezing. Single-use vials — no preservative for multi-dose use.
Research-Grade (Liofilizado Powder): Store at -20°C to -80°C in desiccated, airtight container. Estável à temperatura ambiente for limited time during shipping.
Reconstitution: Use sterile water or agua bacteriostatica. Não agite vigorosamente. Reconstituted solution: refrigerate at 4°C; use dentro de 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); liofilizado powder (research-grade); IV formulation (ensaios clinicos); topico(a) ophthalmic solution (investigacional).
Salt forms: Acetate (desenvolvimento clinico/research) vs. HCl (commercial Forzinity); bioequivalence estabeleceu between forms.
“Preclinical & Clinical Research Summary Key Preclinical Studies Estudo Modelo Principais Achados Ref Sabbah et al.”
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