SS-31 Peptide Dosage Chart: Reconstitution Units, Protocol Sheet & the Elamipretide FDA Label

SS-31 at a glance

What it is

A synthetic mitochondria-targeting tetrapeptide, D-Arg-Dmt-Lys-Phe-NH2 (Dmt = 2',6'-dimethyltyrosine). C32H49N9O5, average molecular weight 639.8 Da, PubChem CID 11764719. Known across its development history as SS-31, MTP-131, Bendavia and elamipretide; the approved product is Forzinity.

Approval status

FDA-approved in 2025 (Forzinity, elamipretide hydrochloride injection, Stealth BioTherapeutics) to improve muscle strength in adult and paediatric patients with Barth syndrome weighing at least 30 kg. This is an accelerated approval based on an intermediate endpoint, with continued approval contingent on confirmatory trials.

Mechanism, per the label

"A mitochondrial cardiolipin binder that localizes to the inner mitochondrial membrane and improves mitochondrial morphology and function." That is the FDA-approved mechanism statement verbatim, not a paraphrase.

Approved dose

40 mg subcutaneously once daily, at the same time each day, in patients weighing at least 30 kg; reduced in severe renal impairment. Research-community discussion typically reports far lower figures - see the dosage section for why that gap matters.

What the trial found

The randomised crossover trial in 12 Barth syndrome patients did not beat placebo on either primary endpoint (6-minute walk distance and Total Fatigue Score). Approval rests on knee extensor muscle strength, a secondary endpoint, and gains appeared only during the open-label extension rather than the randomised period.

Pharmacokinetics

From the label: exposure is dose-proportional from 2 to 80 mg with minimal accumulation; Tmax 0.5-1 hour; absolute subcutaneous bioavailability approximately 92%; volume of distribution ~0.5 L/kg; plasma protein binding ~39%; roughly 100% of the dose recovered in urine within 48 hours.

Half-life

The label does not state one. It gives Tmax, bioavailability, distribution, metabolism and complete urinary recovery by 48 hours, but no elimination half-life figure - so numbers quoted elsewhere are not coming from the label.

Formulation contrast

The approved product is a ready-to-use 80 mg/mL aqueous solution preserved with benzyl alcohol, discarded 8 days after first puncture. Research-market SS-31 ships lyophilised and has to be reconstituted, which is why the arithmetic on this page exists.

Research-market status

SS-31 sold as a lyophilised research vial is not the approved product, is not approved for any use in that form, and is supplied for research and educational use only.

Reported ranges from research/community — examples, not recommendations.

What it is / mechanism

SS-31 is a tetrapeptide with an unusual design brief: get into the inner mitochondrial membrane and stay there. Its sequence is D-Arg-Dmt-Lys-Phe-NH2, where Dmt is 2',6'-dimethyltyrosine, and the alternating aromatic-cationic pattern is the point rather than an accident. The molecule carries a net positive charge that draws it toward the strongly negative membrane potential inside mitochondria, and the aromatic residues give it enough lipophilicity to partition into the membrane once it arrives. The D-arginine at the N-terminus is there for stability: swapping in the D-isomer makes the peptide substantially more resistant to the aminopeptidases that would otherwise chew it from that end. Molecular weight is 639.8 Da (C32H49N9O5), which is large for a tetrapeptide because of the dimethylated tyrosine. The FDA-approved label states the mechanism in one sentence: elamipretide is "a mitochondrial cardiolipin binder that localizes to the inner mitochondrial membrane and improves mitochondrial morphology and function." It is worth pausing on how unusual it is to be able to quote a regulator-reviewed mechanism statement for a compound in this market. Almost every other peptide on a research-supplier site has a mechanism section assembled from primary papers and inference. This one has a mechanism section that a regulatory agency reviewed and permitted. Cardiolipin is what makes the target specific. It is a phospholipid found essentially only in the inner mitochondrial membrane, where it makes up a large fraction of the lipid content and does structural work that ordinary phospholipids do not. Cardiolipin stabilises the cristae - the folds that give the inner membrane its enormous surface area - and it physically organises the respiratory chain complexes, holding them in the supercomplex arrangements that make electron transport efficient. It also anchors cytochrome c to the membrane. When cardiolipin is damaged by oxidation or is abnormal in structure, cristae architecture degrades, respiratory supercomplexes disassemble, electron transport becomes leakier, and cytochrome c is released more readily. SS-31 binds cardiolipin and, on the model the development programme was built around, restores that architecture rather than adding an antioxidant or a substrate. Barth syndrome is why this mechanism found a clinical home. It is a rare X-linked disorder caused by mutations in the tafazzin gene, whose product remodels cardiolipin into its mature form. Patients therefore have structurally abnormal cardiolipin from birth, along with cardiomyopathy, skeletal muscle weakness and neutropenia. A drug whose entire mechanism is cardiolipin binding and cristae stabilisation is about as mechanistically targeted at that disease as a molecule can be, which is why the indication that ultimately succeeded was this one rather than the larger populations the programme originally pursued. The compound's name history is worth untangling, because it causes real confusion in supplier listings and search results. It originated in academic work as SS-31 - the Szeto-Schiller series, hence the SS - was developed clinically as MTP-131, carried the trade name Bendavia during its cardiovascular reperfusion-injury phase, was renamed elamipretide as its international non-proprietary name, and is marketed as Forzinity. Five names, one molecule. A research supplier listing "SS-31" and a pharmacy dispensing "Forzinity" are referring to the same peptide, though not to the same product - the formulations are entirely different, as the reconstitution section explains. One thing the mechanism does not do is generalise as easily as it reads. A molecule that improves mitochondrial membrane architecture sounds as though it should help any condition with mitochondrial involvement, and that is precisely the reasoning the clinical programme tested at scale across primary mitochondrial myopathy, cardiovascular reperfusion injury, heart failure and retinal disease. The results of those trials are covered in the evidence and dosage sections, and they are a useful lesson in how far a clean mechanism carries on its own.

Researched effects

The effect claims for SS-31 are best read in two columns: what the approved label supports, and what the wider trial programme actually produced. The label supports one thing, narrowly. Forzinity is indicated to improve muscle strength in adult and paediatric Barth syndrome patients weighing at least 30 kg, and the approval is an accelerated one based on knee extensor muscle strength measured by handheld dynamometry - explicitly described in the label as an intermediate clinical endpoint, with continued approval contingent on verification of clinical benefit in confirmatory trials. That is a real, regulator-reviewed efficacy finding in a rare disease, and it is the only approved effect claim that exists for this molecule anywhere. The registration trial itself is worth describing honestly, because it is more complicated than "approved for Barth syndrome" implies and no commercial page seems to say so. It enrolled 12 patients, aged 12 to 35, with genetically confirmed Barth syndrome, in a double-blind placebo-controlled crossover design: 12 weeks of elamipretide, a 4-week washout, 12 weeks of placebo, or the reverse order. The primary endpoints were distance walked in a 6-minute walk test and Total Fatigue Score on the Barth Syndrome Symptom Assessment. The label states plainly that Forzinity was not superior to placebo on those primary endpoints. Ten patients completed and entered an open-label extension; eight reached Week 168 and three reached Week 192. Knee extensor strength - a secondary endpoint - showed no increase during the randomised trial, and increases were observed during the extension period. Median baseline strength was 124 newtons (range 92 to 176). So the approved effect rests on a secondary endpoint that moved in an uncontrolled open-label extension rather than in the randomised comparison, in a total population of twelve people. That is not a reason to dismiss it - in an ultra-rare disease with no alternative, regulators weigh evidence differently, and the accelerated-approval pathway exists precisely for this situation, with the confirmatory-trial requirement as the safeguard. It is a reason to be accurate about what has and has not been demonstrated, especially when the same molecule is sold as a research chemical to people extrapolating from the word "approved." Outside Barth syndrome, the record is largely one of well-designed trials that did not deliver. The clinical programme was broad and serious: a Phase 3 trial in primary mitochondrial myopathy, terminated; earlier intravenous work on reperfusion injury in patients undergoing angioplasty under the Bendavia name, terminated; multiple Phase 1/2 studies in mitochondrial myopathy and skeletal muscle function; and topical ophthalmic formulations tested in Phase 2. A Phase 3 study of subcutaneous elamipretide in retinal disease remains active. The pattern across that programme is the substantive finding: a compound with a clean, specific, well-characterised mechanism repeatedly failed to convert it into endpoint-level benefit in larger populations, and succeeded only in the rare disease where the mechanism maps onto the causal defect directly. What gets reported in research-community settings - improved endurance, faster recovery, subjective energy - has no controlled data behind it at all. It is not supported by the label, which makes no such claim, and it is not supported by the failed trials, several of which were specifically powered to detect exactly that kind of functional improvement in people with genuine mitochondrial impairment. Anyone reading anecdotal reports of an energy effect should weigh them against a 6-minute walk test that did not separate from placebo. Nothing here is a claim that SS-31 treats, prevents or improves any condition outside its single approved indication, and nothing here is medical advice.

Dosage — reported ranges (overview)

SS-31 is one of the rare cases where an approved human dose exists, which makes the dosage discussion both easier and more awkward than usual. The approved dose is 40 mg subcutaneously once daily for patients weighing at least 30 kg, administered at the same time each day. If a dose is missed, the label directs skipping it rather than doubling up. The dose is reduced in adults with severe renal impairment, for a reason the pharmacokinetics make plain: elamipretide and its two metabolites are cleared almost entirely in urine, with roughly 100% of a dose recovered there by 48 hours, and exposure rises by 125% in patients with creatinine clearance below 30 mL/min. This is a renally cleared molecule and the label treats it as one. The research community commonly reports figures around 5 to 10 mg once daily - roughly a quarter to an eighth of the approved dose. That gap is worth sitting with rather than glossing over, because it is unusual. In most peptide categories the community figure exceeds anything a regulator would sanction. Here it is dramatically lower, and there is no published rationale for the lower figure: no dose-ranging study identified 5 to 10 mg as a threshold of activity, no trial tested it, and the label's own pharmacokinetic data show linear, dose-proportional exposure with minimal accumulation all the way from 2 mg to 80 mg, which means there is no exposure ceiling being avoided in that range. The most plausible explanation for the community figure is cost - at research-market prices, 40 mg per day is a great deal of peptide - rather than any evidence that a lower amount does the same thing. That should cut in a specific direction when reading community reports. If someone reports no effect at 5 mg per day, that is not evidence about the compound, because the only dose ever shown to do anything in a controlled setting is eight times larger. And if someone reports a large effect at 5 mg per day, it is worth remembering that 40 mg per day in genuinely mitochondrially impaired patients did not beat placebo on a 6-minute walk test. The trial regimen provides the only durable frequency data. Dosing in the registration programme was once daily, at a consistent time, sustained over 12 weeks in the randomised phase and continued for up to 192 weeks in the extension - a genuinely long exposure record for a peptide, and the source of the only long-term tolerability information that exists. There is no cycling in the approved regimen. The community habit of running peptides in four-to-eight-week blocks with breaks has no counterpart in how this compound was actually studied, where continuous daily administration for years is the pattern the evidence describes. One administration detail from the label is worth carrying over because it answers a question people ask constantly and rarely get sourced: subcutaneous exposure was comparable whether the injection went into the thigh or the abdomen. That is a measured pharmacokinetic finding rather than a rule of thumb, and it is specific to this molecule rather than a general principle. Finally, the formulation difference makes a dose figure less transferable than it looks. The approved product is a solution at 80 mg/mL; the approved 40 mg dose is therefore 0.5 mL of a manufactured, preservative-containing, quality-controlled solution. Research-market SS-31 is a lyophilised powder of unverified content that the buyer reconstitutes. The number 40 mg means something different in those two contexts, and the reconstitution section deals with the arithmetic side of that. Everything above describes an approved regimen and what has been reported, for educational purposes. It is not a recommendation, and SS-31 purchased as a research chemical is not the approved product and is not approved for use in any person.

A printable protocol sheet with a reconstitution reference and an injection log comes with All-Access Lifetime.

Reconstitution — bac-water math

There is a formulation difference here that most guides skip, and it changes what reconstitution means for this compound. The FDA-approved product does not require any: Forzinity ships as a clear, colourless-to-yellow aqueous solution at 80 mg/mL in 280 mg / 3.5 mL single-patient-use vials, preserved with benzyl alcohol, ready to draw. Research-market SS-31 is the opposite - a lyophilised powder, commonly in 50 mg vials, which has to be reconstituted with bacteriostatic water before anything can be measured out of it. The arithmetic below applies to the research format, not to the approved one. The method is standard: concentration in mg per mL is the vial's mg divided by the mL of bacteriostatic water added, and syringe units are (target mg / concentration in mg per mL) x 100, since a U-100 insulin syringe holds 1 mL across 100 units. The table works a 50 mg vial at four volumes against the 5 mg and 10 mg amounts commonly discussed in research settings - shown as arithmetic examples, not as recommendations. It is worth running the same check on the approved dose for perspective: 40 mg fits a single 1 mL U-100 syringe only at the most concentrated preparation below (0.8 mL, or 80 units, at 50 mg/mL), and would need 1.6 mL at 25 mg/mL and 4 mL at 10 mg/mL - which is one reason the manufactured product is supplied at 80 mg/mL rather than as a powder. The calculator on this page will run the same computation for any vial size and volume.

This is concentration math, not a dose recommendation.

Injection / administration basics

The approved label gives an unusually complete picture of how this molecule is administered in clinical practice, and it is a better reference than anything reconstructed from community discussion. Forzinity is given by subcutaneous injection into the abdomen - at least two inches from the navel - or the outer thigh, rotating the site daily. The label instructs patients not to inject where skin is tender, bruised, red or hard, and to avoid scars and stretch marks. It requires aseptic technique, directs visual inspection of each vial for particulate matter and cloudiness before use with instructions not to use cloudy or particulate-containing solution, and specifies that the product is single-patient-use and must not be mixed with other products in the same syringe. Dosing is once daily at the same time each day. The product is explicitly not approved for intravenous use. Injection-site reactions - erythema, pain, induration, pruritus, bruising or urticaria - are the most common adverse reactions, and the label notes they can be treated with antihistamines or topical corticosteroids. Two of these details are more informative than they first appear. The thigh-versus-abdomen equivalence is a pharmacokinetic finding, not a convenience statement: the label reports comparable exposure at both sites, which means site selection for this molecule is genuinely a matter of rotation and comfort rather than absorption. And the instruction to discard the vial 8 days after first opening is a preservative-driven in-use limit, discussed further in the storage section. Where research-market SS-31 is used subcutaneously after reconstitution, the general handling pattern is the same - U-100 insulin syringe, aseptic technique, subcutaneous site, daily rotation, avoiding compromised tissue - with the important difference that a self-reconstituted vial has none of the manufacturing controls behind the approved solution. A worked step-by-step version, a printable protocol sheet and a blank injection log come with All-Access Lifetime. This section describes an approved product's labelled administration and general handling concepts for educational purposes. It is not an administration protocol, it does not apply to research-market material, and nothing here is medical advice. Forzinity is a prescription medicine and a qualified professional should direct any actual use.

Half-life & frequency rationale

The FDA-approved label does not state an elimination half-life for elamipretide. That is worth saying explicitly, because it is a genuinely unusual gap in an otherwise detailed pharmacokinetics section, and because half-life figures for SS-31 do circulate without attribution. What the label does provide is substantial, and in practice more useful than a single number. Exposure increases proportionally across a dose range of 2 to 80 mg with daily subcutaneous injection, and accumulation is minimal - which is itself the most practically relevant half-life statement available, since a compound that does not accumulate on once-daily dosing is clearing substantially within the dosing interval. Maximum concentrations are reached 0.5 to 1 hour after subcutaneous administration, so absorption is fast. Absolute subcutaneous bioavailability is approximately 92%, which is high, and exposure is comparable between thigh and abdominal injection. Distribution is throughout total body water at a volume of approximately 0.5 L/kg, with low plasma protein binding of around 39%. Elimination is characterised in structural terms rather than temporal ones. Elamipretide is metabolised by sequential C-terminal degradation to an M1 tripeptide and an M2 dipeptide, neither of which has pharmacological activity, and parent plus both metabolites are excreted in urine, with approximately 100% of the dose recovered there by 48 hours in patients with normal renal function. Complete urinary recovery within 48 hours puts a real outer bound on how long the molecule and its fragments persist, even without a stated t-half. The practical reading is that this behaves as a rapidly absorbed, rapidly and renally cleared peptide dosed once daily without accumulation, and that once-daily dosing in the approved regimen reflects that profile rather than a long duration of action. If you encounter a specific half-life figure for SS-31, it did not come from the approved label - which is the most authoritative pharmacokinetic source that exists for this compound - and the useful question is which study did produce it.

Stacking — overview

SS-31 sits awkwardly in stack discussion, and the reason is worth understanding rather than working around. Most peptide stacking logic is about combining signalling pathways - a growth-hormone secretagogue with a releasing hormone, a repair peptide with an anti-inflammatory one. SS-31 does not signal. Its mechanism is structural: it binds a phospholipid and stabilises membrane architecture. There is no receptor to collide with, no axis to saturate, and no feedback loop to blunt, which means the usual class-collision reasoning simply does not apply to it in either direction. What that produces in practice is a compound that gets paired with metabolic and mitochondrial peptides on thematic grounds rather than mechanistic ones. Pairings with MOTS-c and with NAD+ precursors appear in community discussion built around a general mitochondrial-function theme; the honest description is that these combinations share a subject matter, not a demonstrated interaction. No controlled study has tested SS-31 alongside any other peptide, and the clinical programme studied it as a monotherapy throughout. The more useful framing for anyone reading stack content about this compound is the one the trial record supplies. Elamipretide was tested at a properly powered scale in populations with genuine mitochondrial dysfunction and did not produce endpoint-level functional benefit outside Barth syndrome. A combination rationale that starts from "SS-31 improves mitochondrial function, so add it to anything metabolic" is starting from a premise the Phase 3 programme did not support. That is not an argument against the compound; it is an argument for reading combination claims about it with the trial record in view. The cross-compound Stacking Guide covers combination logic, class collisions and blend arithmetic across the library. Paid access to this guide adds the SS-31 Stacking Module alongside the printable protocol sheet and injection log.

For how combinations are grouped by research context, the named blends, and why a pre-mixed blend vial cannot be calculated from its total milligrams, see the peptide stacks guide.

Storage & handling

• The approved product's storage tells you what the molecule tolerates: Forzinity is stored refrigerated at 2-8 C and must not be frozen. After the first dose, the opened vial may be kept refrigerated or at room temperature between 20-25 C.
• Discard 8 days after first opening. This in-use limit is set by the benzyl alcohol preservative rather than by peptide stability, and it is a useful calibration point for anyone judging how long a reconstituted multi-dose vial should be trusted.
• Research-market SS-31 lyophilised and unopened: store cold and dark, typically at -20 C for long-term storage, with refrigeration generally described as adequate for shorter periods. Keep the vial in its carton.
• After reconstitution with bacteriostatic water: refrigerate at roughly 2-8 C and do not freeze. Freeze-thaw cycling degrades peptides in solution and is the most common avoidable handling error.
• Add bacteriostatic water slowly down the inside wall of the vial rather than onto the powder, swirl rather than shake, keep the stopper clean and use a fresh needle for each withdrawal. Mechanical agitation causes aggregation, and no preservative compensates for repeated entry with a contaminated needle.

Evidence File

The SS-31 Evidence File: 29 Trials and Four Traced Numbers

Elamipretide has been registered on ClinicalTrials.gov under five different names, and the registry does not cross-index them, so a search on the international non-proprietary name alone returns an incomplete programme. It also has something almost no research-market peptide has: a registry results database entry for fourteen of its trials, in which the sponsor posted the actual arm-by-arm numbers, including for the trials that failed. Those posted tables are a separate document from any journal publication and are rarely quoted anywhere. This module works from them, trial by trial, and traces the figures that circulate about this compound back to the documents they came from.

• 29 interventional trials of this molecule enumerated
• 9 studies an INN-only registry search does not return
• 4 circulating claims traced, one of them to no source at all
• 456 subjects of completed but unreported trial data

Sourcing File

The SS-31 Sourcing File: Salt Form, Stereochemistry and the Certificate Gap

Elamipretide is registered with the FDA's substance registry twice - once as a free base and once as a salt, each with its own registry identifier, its own CAS number and its own molecular weight. The approved brand name is attached to the salt. That distinction is invisible on a research-vial label and invisible to a purity figure, and it changes what a stated milligram amount means before any question of quality is asked. This module works through the identity numbers as registered, the arithmetic that follows from them, the impurities and look-alikes that are specific to this sequence, and which of them a standard certificate can and cannot exclude.

• 2 substances registered with the FDA under this molecule's name
• 1.53-fold spread in actual peptide from one 50 mg label
• 4 mass offsets separating SS-31 from its analogs and its likeliest degradant
• 2 chiral tests that would settle the D-arginine, neither standard on a certificate

Benefit & Outcome Review

The SS-31 Benefit and Outcome Review: 14 Claims Against the Human Record

Most peptides in this market are judged against rodent studies because nothing else exists. SS-31 is the unusual case where that is not necessary: elamipretide has been tested in randomised, placebo-controlled human trials in mitochondrial myopathy, Barth syndrome, heart failure, reperfusion injury, renal artery stenosis and macular degeneration, and most of those trials posted their numbers. This review takes the claims made for the compound one at a time, separates human data from animal data, states the effect size against the actual comparator rather than against baseline, and says plainly which claims have no human study behind them at all.

• 14 marketed claims judged against the human record
• 4 randomised trials measured six-minute walk distance
• 6 claims with no human study located
• 1 claim accepted by a regulator, on an intermediate endpoint

Guide FAQ

Quick answers about guide scope, access, and educational use context.