SS-31 (Elamipretide)

The row below carries a price per mg figure: listed price divided by stated peptide content, excluding shipping and codes. It is the same calculation applied on every compound page, so a figure here is directly comparable to one anywhere else on the site.

We currently track a single listing for this compound. When a second vendor is added the rows are ordered by measured $/mg, and the flags for testing and shipping are computed from the data shown. Each row carries its own verification date.

Mitochondria-targeting tetrapeptide (D-Arg-Dmt-Lys-Phe-NH₂) that binds cardiolipin on the inner mitochondrial membrane. FDA-approved as FORZINITY for Barth syndrome. Studied for cardioprotection, aging muscle, and neurodegenerative disease research.

A synthetic 4-residue peptide (D-Arg-Dmt-Lys-Phe-NH₂) engineered to concentrate more than a thousand-fold at the inner mitochondrial membrane, where it binds cardiolipin in in-vitro assays. FDA-approved as FORZINITY (2025) for Barth syndrome. For laboratory characterisation only.

SS-31 (elamipretide) is a mitochondria-targeting tetrapeptide that binds cardiolipin on the inner mitochondrial membrane. FDA-approved for Barth syndrome (FORZINITY). 2025-2026 preclinical data shows neuroprotection: upregulates mitochondrial biogenesis against Aβ in Alzheimer's models, protects dopaminergic neurons in Parkinson's, and improves retinal survival in diabetic models. AMD trials slowed progressive ellipsoid zone degradation.

SS-31 is a synthetic cell-permeable tetrapeptide (D-Arg-Dmt-Lys-Phe-NH2) engineered to concentrate more than a thousand-fold inside the inner mitochondrial membrane. It has molecular formula C32H49N9O5 and mass 639.76 Da. Common synonyms in the literature include Elamipretide, Bendavia, MTP-131, and FORZINITY. SS-31's defining feature is a rationally designed alternating aromatic–cationic motif — a 2′,6′-dimethyltyrosine residue paired with D-arginine — that exploits the negative membrane potential of energized mitochondria (Δψₘ ≈ −180 mV) to selectively accumulate at the cristae, where it binds reversibly to cardiolipin, a phospholipid unique to mitochondrial membranes.

Research into SS-31 is clinical-investigational, with several completed and ongoing human trials. It became the first mitochondria-targeted therapeutic to receive FDA approval when Bendavia/FORZINITY was cleared in 2025 for Barth syndrome, a rare paediatric cardiomyopathy driven by cardiolipin dysfunction. Beyond that indication, published work referencing SS-31 spans Barth syndrome (FDA approved): Clinical trials demonstrated improved energy production, protein complex assembly, and exercise tolerance in Barth syndrome patients. Participants showed functional improvements such as walking 1 mile without breaks. FDA approval was granted based on these meaningful clinical benefits in this rare mitochondrial disorder, Primary mitochondrial myopathy trials: Phase 1/2 IV dose-escalation trial (Class I evidence) showed dose-dependent 6-minute walk test improvement (+51.2 meters at highest dose vs. +3.0 meters placebo, p=0.0297). Phase 3 MMPOWER-3 trial (NCT03323749) evaluated subcutaneous dosing with mixed results on primary endpoints, and Heart failure research: Studies in heart failure models showed improved stroke volume, ejection fraction, cardiac output, and reduced left ventricular end-diastolic pressure. Biomarkers including natriuretic peptides were reduced. Normalized bioenergetics observed in failing cardiac tissue. Proposed mechanisms cited across the primary literature include Cardiolipin interaction: binds reversibly to cardiolipin, stabilizing content and preventing peroxidation/oxidation, Cristae protection: maintains cristae structure and prevents destabilization during apoptosis, and mPTP regulation: inhibits mitochondrial permeability transition pore opening, promotes electron transfer while reducing electron leakage. A defining property, replicated across multiple in-vitro and animal models, is selectivity: SS-31 restores function in stressed, aged, or diseased mitochondria while leaving healthy mitochondria unchanged — a pharmacological profile rarely seen in bioenergetic research tools. None of this material describes therapeutic outcomes for buyers, and No vendor listed here provides dosing guidance for SS-31 outside laboratory research.

For the full mechanistic profile, published references, cardiolipin-binding structural detail, and constraint notes on SS-31, see the SS-31 (Elamipretide) research page. For a deeper mechanism-focused review covering the tetrapeptide's cardioprotection, neuromuscular, and age-Related compounds studied alongside it include MOTS-c, studied for exercise-mimetic signalling and metabolic health. All references cited on the research pages are peer-reviewed primary literature.

Binding and functional-assay data for SS-31 (Elamipretide), from peer-reviewed in-vitro pharmacology publications. Values are receptor activity parameters — not clinical outcomes.

Study designs referencing this compound in the published literature. Descriptions cover framework only — phase, participant count, duration, and citation — not outcomes. Click a card to review the source directly.

Two published mitochondrial-targeted peptides with distinct primary targets in the inner mitochondrial membrane. Reference chemistry only.