Preloaded Autoinjector | SS-31 (Elamipretide) | 3ml Pen | 10mg

The SS-31 pen is a preloaded 3ml research autoinjector holding elamipretide in solution at 10/3 mg/ml, giving 10mg of total peptide. What separates this molecule from most research peptides is that its approved counterpart is also a liquid: FORZINITY ships at 80 mg/ml in a preserved phosphate buffer, so the solution-format question has a published answer to argue with.

Specification Table

What Changes When The SS-31 Pen Ships Elamipretide In Solution?

Less than for almost any other peptide in this catalogue, because the manufacturer of the approved product reached the same conclusion and sells a liquid. FORZINITY is a sterile aqueous solution at 80 mg/ml, not a lyophilisate, which removes the usual argument that a dry cake is the only defensible presentation.

The chemistry behind that decision is worth stating residue by residue. Elamipretide is four residues long and carries no Asn and no Gln, so the deamidation route that dominates the shelf life of longer peptides has nothing to act on. There is no Asp-Gly or Asp-Pro bond, so no succinimide chemistry and no acid-labile cleavage site. There is no Cys, so no disulfide scrambling, and no Trp, so no indole oxidation. The C-terminus is a primary amide and the N-terminal residue is D-arginine, which blocks aminopeptidases.

One side chain is exposed. Dmt, the 2′,6′-dimethyltyrosine at position 2, carries the phenol that Zhao and colleagues identified in 2004 as the radical-scavenging group. A phenol that scavenges radicals is by definition oxidisable, and tyrosines in solution are photo-oxidised and metal-oxidised to quinone and dityrosine species. No forced-degradation study of elamipretide has been published, so the rate is unknown rather than known to be slow.

The formulation of the approved product suggests the manufacturer treated that risk as manageable but not negligible. FORZINITY is buffered with monobasic sodium phosphate to pH 4.7 to 6.1, preserved with benzyl alcohol at 20 mg/ml, stored at 2-8°C, and discarded eight days after the vial is first punctured. Three of those four decisions (acidic-to-neutral buffering, a preservative, a short in-use window) are the decisions a formulator makes when a solution is stable enough to sell and not stable enough to ignore.

The other solution-state property is electrostatic. Three cationic centres (the free N-terminal amine, the arginine guanidinium and the lysine side chain) give a net charge near +3 across the pH range from 3 to 9, with a calculated pI around 11.6. That charge is the physical basis of the mechanism, since Mitchell and colleagues showed in 2020 that binding to anionic cardiolipin bilayers is driven by surface electrostatics. It also predicts adsorption to the negatively charged silanol groups on borosilicate glass, which matters at dilute working concentrations rather than at the fill concentration. No adsorption study for this peptide has been located.

What Is SS-31 Peptide, And What Does Elamipretide Do?

SS-31 is the Szeto-Schiller laboratory code for elamipretide, a four-residue cationic-aromatic peptide that concentrates in the inner mitochondrial membrane and binds cardiolipin. It has also been published as MTP-131, Bendavia and Ocuvia, and the same molecule is the active ingredient of FORZINITY.

The alternating charge-and-aromatic motif is the whole design. Zhao 2004 showed that Dmt-containing SS peptides accumulate in the inner membrane and limit mitochondrial swelling and oxidative cell death; Birk 2013 tied that to cardiolipin binding in ischaemic kidney mitochondria; Mitchell 2020 measured the bilayer interaction directly. The FDA label describes it as a cardiolipin binder that improves mitochondrial morphology and function. It is not a receptor ligand, which is why the mechanism reads as biophysics rather than pharmacology.

Human pharmacokinetics are unusually clean for a research peptide. After subcutaneous injection, Tmax is 0.5 to 1 hour, absolute bioavailability is about 92 percent, protein binding about 39 percent, volume of distribution about 0.5 L/kg, and the half-life 3 to 4 hours. Close to 100 percent of an administered amount is recovered in urine within 48 hours as parent compound plus the M1 tripeptide and M2 dipeptide, both inactive. D-arginine at position 1 blocks attack from the N-terminus, and clearance proceeds by trimming from the other end instead.

Concentration And Increment Arithmetic For The SS-31 Pen

At 10mg in 3 ml the concentration is 10/3 mg/ml, and the molar concentration is (10/3) divided by 639.8, multiplied by 1000, which is 10 x 0.521 mM on the free-base mass. Quote the fill as trihydrochloride and the divisor becomes 749.2 instead, which shifts the molar figure by about 17 percent.

Per-increment delivery follows from the fill: 10/300 mg in 0.01 ml and 10/30 mg in 0.1 ml. A worked example makes the scale legible. A 10 mg fill gives 3.33 mg/ml, 5.21 mM, 33 micrograms per 0.01 ml and 0.33 mg per 0.1 ml.

FORZINITY is 80 mg/ml, roughly 125 mM, so a 10 mg fill in this format is about 24-fold more dilute than the approved solution. The cell literature is the opposite problem: protection against oxidative stress is reported in the 10 nanomolar to 1 micromolar range, and reaching 100 nanomolar from 5.21 mM needs a dilution of roughly 52,000-fold. The device fixes concentration; it does not shorten that dilution series. The peptide dilution calculator handles the arithmetic for a specific fill.

What The SS-31 Pen Format Suits, And What It Does Not

The SS-31 pen suits work that draws repeatedly from one lot over weeks and would otherwise reconstitute a fresh vial each time. Fixing concentration at manufacture removes diluent measurement error and adsorptive loss during transfer, an argument set out in full in the pen versus vial comparison and across the preloaded autoinjector range.

It suits this molecule better than most, for the reason given above: the degradation inventory is short, and the company holding the approval sells the compound as a solution rather than a powder.

It does not suit anyone who needs a defined salt form on paper. Free base, hydrochloride, acetate and TFA all deliver different peptide masses for the same weighed quantity, and a solution gives no cake to weigh. The FDA briefing document records that the clinical-trial material was an acetate salt while the marketed product is the hydrochloride, which is exactly the kind of substitution that a mass-based potency calculation has to account for.

What The Product Record Does Not State

Four things, and one of them is unusual to have to ask for.

The salt form is unpublished. That single value changes the peptide content of a nominal 10mg fill, and the difference between 639.8 and 749.2 g/mol is not a rounding error.

The excipient system is unpublished. Whether the solution is preserved matters for a multi-draw device, and the approved product uses benzyl alcohol at 20 mg/ml with a warning attached to it.

Solution pH is unpublished. The approved product sits between pH 4.7 and 6.1, and there is no published stability curve for elamipretide outside that window.

Fill date and stability across shelf life are unpublished. FORZINITY carries an eight-day in-use limit after first puncture, which is a manufacturer’s answer for a preserved vial under defined conditions and not a figure that transfers to a different formulation. Request all four against the certificate of analysis before quantitative work, and see the peptide storage and stability notes for what the general case looks like.

Verifying The Device And Confirming The Contents Are Intact

Inspect the solution against a white background before each draw. It should be clear and free of particulate. Elamipretide is small, hydrophilic and highly cationic, with a PubChem XLogP3 of 0, so visible haze or fibre-like material is not expected and is a reason to stop rather than to shake.

Let the SS-31 pen reach ambient temperature before actuating, since cold raises viscosity and viscosity changes delivered volume. Verify delivered mass gravimetrically once per device onto a tared vessel.

For contents rather than volume, this peptide has a usable UV handle. Dmt and Phe absorb near 280 nm, so absorbance at that wavelength tracks the aromatic residues, though it will not distinguish intact peptide from oxidised phenol. Mass spectrometry is the discriminating measurement: oxidation of the Dmt phenol adds 16 daltons, and dityrosine coupling shows as a dimer near 1277 Da against the 639.4 monoisotopic parent. Loss of Phe from the C-terminus would show as the M1 tripeptide, which is the same species the label lists as an inactive metabolite.

What The SS-31 Literature Actually Reports

A large mechanistic file and a run of missed primary endpoints. That combination is the most important thing to know before designing anything around this compound.

TAZPOWER (SPIBA-201, NCT03098797) enrolled 12 males with genetically confirmed Barth syndrome on 40 mg daily subcutaneously. The 12-week randomised double-blind placebo-controlled crossover missed both primary endpoints: the six-minute walk test moved by -0.8 m (p = 0.97) and the BTHS-SA fatigue score by +0.06 (p = 0.89). In the open-label extension the walk test rose by 95.9 m at week 36 (p = 0.024), and a 168-week extension was published in 2024.

MMPOWER (Karaa 2018) was a randomised double-blind intravenous dose-escalation study in 36 adults with primary mitochondrial myopathy; the highest dose gave +64.5 m on the walk test against +20.4 m for placebo, p = 0.053. MMPOWER-3 (Karaa 2023) was the phase 3 follow-up and did not meet its primary endpoint. EMBRACE-STEMI (Gibson 2016) infused MTP-131 during primary PCI and did not reduce infarct size. PROGRESS-HF (Butler 2020) missed its left ventricular end-systolic volume endpoint in heart failure with reduced ejection fraction. The ReCLAIM studies in dry age-related macular degeneration also failed their primary endpoints.

Animal work is ischaemia-reperfusion in rat and mouse heart and kidney, reviewed by Szeto in 2014. Nothing has been published on healthy-subject longevity, exercise performance or cognition, and no trial has used research-grade TFA or acetate material or any pen presentation.

Adverse findings from the 12-patient label population are specific. Injection-site reactions occurred in 100 percent of treated patients against 67 percent on placebo, with erythema 100 percent versus 25 percent, pain 75 percent versus 42 percent, and induration and pruritus each 67 percent versus 17 percent. Eosinophilia appeared after 30 days, peaked near day 90 at a mean rise of roughly 0.5 to 0.6 x 10^3 per microlitre, and resolved over 6 to 12 months. Two participants discontinued for injection-site reactions.

Where Do Claims About SS-31 Peptide Benefits Come From?

Marketing pages listing SS-31 peptide benefits almost always translate the mechanistic literature into outcome language that the trials did not produce. Cardiolipin binding and reduced mitochondrial swelling are measurements in isolated mitochondria and cell lines; they are not endurance, energy or age reversal in a person.

The specific inversions are easy to name. Exercise capacity was the endpoint MMPOWER-3 measured and missed. Cardiac outcome was the endpoint EMBRACE-STEMI and PROGRESS-HF measured and missed. Retinal outcome was the endpoint ReCLAIM measured and missed. A page describing SS-31 peptide benefits in those three areas is describing the hypotheses that the trials tested, not the results they returned.

SS-31 FDA Approval And Regulatory Position

The SS-31 FDA approval is real, narrow and conditional. FORZINITY (elamipretide hydrochloride) injection, 280 mg per 3.5 ml at 80 mg/ml, NDA 215244, Stealth BioTherapeutics, received accelerated approval on September 19, 2025, indicated to improve muscle strength in adult and paediatric patients with Barth syndrome weighing at least 30 kg, at 40 mg once daily. Barth syndrome affects roughly 130 people in the United States by the FDA’s count and about 150 by the sponsor’s, and the approval rests on knee-extensor strength, a median rise of about 34 to 68 newtons from baseline between weeks 12 and 48. This research preparation is not FORZINITY and has no approval anywhere.

The path there was not smooth. FDA refused to file in August 2021, an advisory committee met on October 10, 2024, and a complete response letter issued in May 2025 before the September 2025 accelerated approval. Continued approval is contingent on a confirmatory randomised placebo-controlled knee-extensor-strength trial starting March 2026, completing September 2029 and reporting March 2030, plus carcinogenicity and metformin-interaction studies.

Because the molecule is now the active ingredient of an approved drug, compounding a copy of FORZINITY is restricted under sections 503A and 503B. Elamipretide is not named on the FDA Category 2 bulk-substance page and no import alert was located. An EMA orphan designation is cited by the sponsor; no European marketing authorisation was found, and no approval was located at PMDA, the TGA or Health Canada. WADA does not name the compound individually; before approval it fell under the S0 non-approved-substances clause, and its post-approval classification is not explicitly addressed in the sources consulted.

What Does a Mitochondria-Targeting Peptide Actually Target?

Cardiolipin, and that specificity is what separates elamipretide from every other compound sold as a mitochondrial support product. Cardiolipin is a four-tailed phospholipid found almost nowhere in the cell except the inner mitochondrial membrane, where it makes up about a fifth of the lipid and where it holds the respiratory complexes in the supercomplex arrangement they need to work efficiently. The peptide’s alternating aromatic and basic residues give it a positive charge that draws it across membranes toward the negative matrix potential, and its aromatic face then associates with cardiolipin once it arrives.

The consequence is structural rather than catalytic. A mitochondrial-targeted peptide bound to cardiolipin stabilises cristae architecture and keeps cytochrome c in its electron-carrying role rather than its peroxidase role, which is the switch that begins apoptosis. Electron flow through the electron transport chain improves where it had been disrupted, ATP production rises toward normal, and the electron leak that generates reactive oxygen species falls. That last point is worth stating precisely: the reduction in oxidative stress follows from better-coupled respiration rather than from radical scavenging, so calling this an antioxidant misdescribes the mechanism. Oxidative stress here is an output of broken coupling, not an independent target.

Because the effect is corrective rather than stimulatory, the published work shows most benefit where mitochondrial dysfunction is already present and little where it is not. Ischemia-reperfusion injury models, in heart and in kidney, are where the largest effects appear, since reperfusion is exactly the setting in which cardiolipin peroxidation and cristae collapse dominate. That pattern is consistent across the preclinical literature and it shapes what claims are reasonable.

Where Do the Broader Claims Come From?

From the preclinical breadth rather than from clinical results. Animal work has covered heart failure, acute kidney injury, neurodegeneration, retinal disease, sarcopenia and age-related decline in exercise tolerance, and reports of improved mitochondrial function in aged skeletal muscle are the basis for most anti-aging framing around the compound, and anti-aging is the heading it is most often sold under. Neuroprotection appears in stroke and Parkinson models. Those are real published results in animals.

The human record is narrower and more mixed than that list suggests. The Barth syndrome approval described above rests on knee-extensor strength in an ultra-rare disease. The larger primary mitochondrial myopathy programme missed its primary endpoint in a phase three trial despite promising earlier data, and work in geographic atrophy has progressed without an approval. Anyone reading mitochondrial health or mitochondrial protection claims for this molecule should separate the animal literature, which is substantial, from the human evidence, which is one narrow accelerated approval and a set of mixed trials.

Reported side effects come from those trials rather than from case reports, which is a meaningful difference from most compounds in this catalogue. Injection site reactions were the commonest finding, frequent enough to be dose-limiting for some participants, along with headache and gastrointestinal upset. That is a real adverse event profile generated under monitoring, and it applies to the approved formulation rather than to a research preparation.

What Should a Purchaser Check, and What Does the Format Change?

Ask for a lot-specific CoA giving purity by HPLC with the gradient described, an accurate mass, water content and the counter-ion percentage. The counter-ion question is sharper here than usual: the approved product is a hydrochloride, and material supplied as an acetate or trifluoroacetate salt differs in mass per milligram and, for trifluoroacetate, carries its own cytotoxicity in cell work at concentrations that matter. A CoA that omits the counter-ion is omitting a number that changes the molar concentration.

On format, a vial arrives dry, is reconstituted with bacteriostatic water at the bench, and lets the concentration follow the experiment while the solid keeps. A peptide pen fixes the concentration at 10/3 mg/ml and starts ageing from a fill date the record does not state. For work at defined molar concentrations across a dose range, peptide pens are the wrong format and a vial is the right one; for repeated identical volumes, the reverse holds.

Two framing points. This material is supplied research use only, and research use only is a legal status rather than a formality: it means the preparation may not be given to humans or animals, regardless of the approved drug’s existence. And peptide therapy providers listing this compound alongside GHK-Cu and BPC-157 are grouping by claimed benefit rather than by evidence, since one of the three has an approved product behind it and the other two do not. Peptide therapy protocols for this molecule are not derived from the trials that produced its approval.

Published Literature

References below were checked against Crossref, PubMed listings or the publisher’s own record before being listed here.

1. Szeto HH. First-in-class cardiolipin-protective compound as a therapeutic agent to restore mitochondrial bioenergetics. Br J Pharmacol. 2014;171(8):2029-2050. DOI: 10.1111/bph.12461. PMID: 24117165
2. Birk AV, Liu S, Soong Y, et al. The mitochondrial-targeted compound SS-31 re-energizes ischemic mitochondria by interacting with cardiolipin. J Am Soc Nephrol. 2013;24(8):1250-1261. DOI: 10.1681/ASN.2012121216. PMID: 23813215
3. Zhao K, Zhao GM, Wu D, et al. Cell-permeable peptide antioxidants targeted to inner mitochondrial membrane inhibit mitochondrial swelling, oxidative cell death, and reperfusion injury. J Biol Chem. 2004;279(33):34682-34690. DOI: 10.1074/jbc.M402999200. PMID: 15178689
4. 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. DOI: 10.1074/jbc.RA119.012094. PMID: 32273339
5. Reid Thompson W, 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. Genet Med. 2021;23(3):471-478. DOI: 10.1038/s41436-020-01006-8. PMID: 33077895
6. Karaa 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. DOI: 10.1212/WNL.0000000000005255. PMID: 29500292
7. Karaa A, Bertini E, Carelli V, et al. Efficacy and safety of elamipretide in individuals with primary mitochondrial myopathy: the MMPOWER-3 randomized clinical trial. Neurology. 2023;101(3):e238-e252. DOI: 10.1212/WNL.0000000000207402. PMID: 37268435
8. Gibson CM, Giugliano RP, Kloner RA, et al. EMBRACE STEMI study: a Phase 2a trial to evaluate the safety, tolerability, and efficacy of intravenous MTP-131 on reperfusion injury in patients undergoing primary percutaneous coronary intervention. Eur Heart J. 2016;37(16):1296-1303. DOI: 10.1093/eurheartj/ehv597. PMID: 26586786

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