Key Takeaways

SS-31 is no longer just an investigational peptide. In the U.S., it can be classified as the "Forzinity elamipretide hydrochloride injection," approved under accelerated approval for a single rare disease indication in Barth syndrome.
That is not insignificant, but it does not convert the wider SS-31 literature into proof for broad mitochondrial, cardiology, ophthalmology, exercise, or aging claims.
The most defensible position is that Barth syndrome muscle-strength language is label-backed; most other commonly circulated uses remain investigational, mixed, or preclinical.

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[FDA label, 2025; Reuters, 2025a; Reuters, 2025b; NCATS, 2026]

SS-31: now marketed in the United States as elamipretide hydrochloride under the brand Forzinity, a mitochondria-targeting tetrapeptide and cardiolipin binder; legacy names include SS-31, MTP-131, and Bendavia. The canonical free-base sequence commonly cited in scientific materials is D-Arg-2′,6′-dimethylTyr-Lys-Phe-NH2.

What it is

SS-31 is the legacy development name for the peptide now generally referred to as elamipretide. Official and quasi-official identity sources reviewed here connect SS-31 with the sequence D-Arg-2′,6′-dimethyltyrosine-Lys-Phe-NH2, with the approved product supplied as elamipretide hydrochloride. The FDA label describes Forzinity as containing elamipretide hydrochloride, a mitochondrial cardiolipin binder, with molecular formula C32H49N9O5·3HCl and molecular weight 749.2 for the hydrochloride salt. NCATS Inxight Drugs lists the neutral formula C32H49N9O5 and molecular weight 639.7888 for elamipretide itself, underscoring the common but important distinction between the free base and the labeled hydrochloride form. [FDA label, 2025; NCATS, 2026]

In the published and legacy-development literature, the molecule may appear as SS-31, MTP-131, Bendavia, or elamipretide, and different databases may still present it through an older investigational lens. In current U.S. regulatory practice, however, the operative marketed drug is Forzinity elamipretide hydrochloride injection. Do not assume that every historical SS-31 data point maps cleanly onto the currently approved labeled product without naming the form, route, and indication. [FDA label, 2025; NCATS, 2026; Reuters, 2025b]

Material	What it is	Why it can't be collapsed into "SS-31"
SS-31	Legacy development/scientific name for the peptide.	Too imprecise for regulatory or clinical copy unless paired with current identity and context.
Elamipretide	Current generic/INN-style name used in current regulatory and identity materials.	Broader than the finished approved drug product unless the salt/formulation is also named.
Elamipretide hydrochloride	The salt named in the FDA label for the marketed drug product.	Salt-specific labeling matters for product identity; do not treat as identical to unspecified legacy material without saying so.
Forzinity	The approved branded injectable product.	Brand-specific evidence belongs to the labeled product and labeled use.
MTP-131 / Bendavia	Older development aliases used in earlier literature and clinical programs.	Older-name data may use different programs, stages, or contexts; not all such data equal current label-backed evidence.
Non-injectable or alternate-route SS-31 claims	Market or speculative representations not established by the current FDA label reviewed here.	Current label reviewed here is for subcutaneous injection; route transfer should not be assumed.

How it's proposed to work

The best-supported mechanistic backbone comes from a convergent mix of the FDA label, NCATS identity summaries, and preclinical literature: elamipretide is described as a mitochondrial cardiolipin binder that localizes to the inner mitochondrial membrane and improves mitochondrial morphology and function. That is the most defensible mechanistic anchor, because it appears directly in the approved prescribing information rather than only in a promotional or speculative source. [FDA label, 2025]

NCATS further summarizes the peptide as a membrane-penetrant, mitochondria-targeting compound that binds reversibly to cardiolipin and has been associated in preclinical and clinical-study contexts with improved mitochondrial respiration, electron-transport-chain function, ATP production, and reduced pathogenic reactive oxygen species. [NCATS, 2026]

The preclinical literature adds more specificity. Birk et al. adds color on ischemic mitochondria and cardiolipin interaction, Thomas et al. on prevention of mitochondrial depolarization and apoptosis in islet-transplantation contexts, and Brown et al. and Shi et al. on reperfusion injury, mitochondrial energy metabolism, and border-zone fibrosis after myocardial infarction. These are mechanistically informative, but they are still just preclinical anchors unless and until the exact disease, route, formulation, and endpoint are confirmed in humans. [Birk et al., 2013; Thomas et al., 2007; Brown et al., 2014; Shi et al., 2015]

Common forms in circulation

In the current U.S. regulatory materials reviewed here, the relevant form is Forzinity elamipretide injection for subcutaneous use, supplied as elamipretide hydrochloride in single-patient-use vials. [FDA label, 2025]

Legacy scientific and compound-identity materials continue to circulate under SS-31, MTP-131, and Bendavia, and NCATS still reflects older investigational framing sourced from pre-approval trial data. [NCATS, 2026; Reuters, 2025a; Reuters, 2025b]

Names and aliases

Names and aliases include SS-31, elamipretide, elamipretide hydrochloride, MTP-131, Bendavia, and Forzinity. Also note generic phrases like "mitochondrial peptide," "cardiolipin binder," and "mitochondrial protective peptide," because they often invite evidence transfer into broader claims. [FDA label, 2025; NCATS, 2026]

No controlled same-molecule evidence reviewed here supports claims about specific multi-peptide "stacks." If SS-31 is paired rhetorically with broader mitochondrial or peptide categories, treat that as market-style framing, not combination-efficacy evidence. [NCATS, 2026; Reuters, 2025b]

Regulatory status

In the U.S., Forzinity elamipretide injection received accelerated approval in September 2025 to improve muscle strength in adult and pediatric Barth syndrome patients weighing at least 30 kg. The label states that the approval was based on improvement in knee extensor muscle strength, described as an intermediate clinical endpoint, and that continued approval may depend on confirmatory evidence. [FDA label, 2025; Reuters, 2025a]

The approval history is unusually important because it shapes what can and cannot be said. Reuters and The Guardian report that elamipretide's approval path included years of review, an October 2024 advisory-committee vote reportedly recommending approval 10–6, a May 2025 complete response letter/resubmission cycle, and then September 2025 accelerated approval. Reuters also reported that the approval was contentious inside FDA review, with disagreements about the adequacy of efficacy evidence. That history does not negate approval, but it does reinforce why non-label extrapolation should be handled carefully. [Reuters, 2025a; Reuters, 2025b; The Guardian, 2025]

Evidence base

Evidence tier	What qualifies	What it does not justify
Clinical trial / label-backed	Same-molecule human interventional evidence, especially the Barth syndrome program reflected in the FDA label.	Broad non-Barth efficacy claims, route equivalence, or "clinically proven mitochondrial therapy" language.
Animal model	In vivo studies in ischemia-reperfusion, heart-failure, aging, transplantation, or related models using SS-31/elamipretide.	Human efficacy, validated dose translation, or disease-agnostic "repair" claims.
Mechanistic hypothesis	Cardiolipin binding, inner-membrane localization, mitochondrial morphology/function, ATP/ROS pathway work.	Proof that patients in unrelated conditions will improve clinically.
Anecdotal or commercial	Legacy naming, generalized mitochondrial-health narratives, disease-advocacy anecdotes, or market-style "mitochondrial support" logic.	Regulatory status, efficacy, safety, or validated route/dose claims.

Purported benefits, by evidence

Purported benefit	What the evidence supports	What it does not support	Source
Improve muscle strength in Barth syndrome	The FDA label supports a Barth syndrome claim limited to improved muscle strength in patients weighing at least 30 kg, under accelerated approval.	Unrelated mitochondrial-disease claims or "reverses Barth syndrome."	[FDA label, 2025; Reuters, 2025a]
Improve exercise tolerance or symptoms in primary mitochondrial myopathy	NCATS identifies a placebo-controlled PMM trial program and that line of study is scientifically relevant.	Approved or clinically proven efficacy in PMM based on the reviewed materials here.	[NCATS, 2026]
Support mitochondrial function	Cardiolipin binding and inner-membrane localization support careful mechanism language.	Generalized patient-facing claims like "fixes mitochondrial dysfunction."	[FDA label, 2025; NCATS, 2026; Birk et al., 2013]
Protect the heart / improve heart failure	Preclinical cardiovascular studies in reperfusion and dog heart-failure models support preclinical plausibility.	"Treats heart failure" or "improves cardiac function in patients" in current copy.	[Brown et al., 2014; Shi et al., 2015; Sabbah et al., 2016]
Reduce oxidative stress	Mechanistic and preclinical sources support careful discussion of ROS-related effects in models.	"Detoxes oxidative stress" or broad anti-aging language in people.	[NCATS, 2026; Thomas et al., 2007; Birk et al., 2013]
Help dry AMD or optic disease	NCATS notes investigations in dry AMD and LHON-related development contexts.	Established efficacy in dry AMD, LHON, or general vision preservation from the reviewed materials here.	[NCATS, 2026]
Anti-aging / energy / longevity peptide	Aging-related preclinical work and mitochondrial rhetoric explain why the claim circulates.	"Anti-aging treatment," "longevity peptide," or "energy restoration" as a clinically validated claim.	[NCATS, 2026; Whitson et al., 2020]
Broadly safe or well tolerated	The label supports discussion of frequent injection-site reactions and highlights hypersensitivity and benzyl-alcohol precautions.	Blanket "safe," "low risk," or "minimal side effects" language across all uses and populations.	[FDA label, 2025]

Key literature

Thomas DA, Stauffer C, Zhao K, et al. Mitochondrial targeting with antioxidant peptide SS-31 prevents mitochondrial depolarization, reduces islet cell apoptosis, increases islet cell yield, and improves posttransplantation function. J Am Soc Nephrol. 2007. Early evidence that SS-31 can affect mitochondrial depolarization and apoptosis in a transplantation-related setting.

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. Strong support for the cardiolipin-centered mechanistic story.

Sabbah 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. Circ Heart Fail. 2016;9(2):e002206. Supports preclinical heart-failure plausibility.

Whitson JA, Bitto A, Zhang H, et al. SS-31 and NMN: Two paths to improve metabolism and function in aged hearts. Aging Cell. 2020;19(10):e13213. Helps explain why longevity-oriented narratives cluster around SS-31.

Elamipretide in the Management of Barth Syndrome: Current Evidence and a Case Report. Mol Genet Metab. 2025. Review and case report on the Barth syndrome evidence landscape near approval.

References

U.S. Food and Drug Administration. FORZINITY (elamipretide) injection, for subcutaneous use: Highlights of Prescribing Information / Full Prescribing Information. Revised September 2025.
National Center for Advancing Translational Sciences. Inxight Drugs. ELAMIPRETIDE.
Reuters. US FDA approves first treatment for rare, life-threatening disease in males. September 19, 2025.
Reuters. US FDA asks Stealth BioTherapeutics to resubmit application for rare genetic condition therapy. May 29, 2025.
Reuters. US FDA cleared pricey rare disease drug over reviewer objections. November 5, 2025.
The Guardian. Patients with ultra-rare diseases worry FDA approach will leave them without treatment. July 6, 2025.
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.
Brown DA, Hale SL, Baines CP, et al. Reduction of early reperfusion injury with the mitochondria-targeting peptide bendavia. Journal of Cardiovascular Pharmacology and Therapeutics. 2014;19(1):121-132.
Shi J, Dai W, Hale SL, et al. Bendavia restores mitochondrial energy metabolism gene expression and suppresses cardiac fibrosis in the border zone of the infarcted heart. Life Sciences. 2015;141:170-178.

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SS-31 (Elamipretide)