Most peptides on this shelf suffer from having almost no human data. SS-31 has the opposite problem, and it is a more interesting one. It has been through a phase 3 trial, published in a major neurology journal, and the trial did not work. That result is more useful than anything written on a product page, and it is the reason this page exists. It sits under the longevity goal, where the mitochondrial claims are made.
What SS-31 is
SS-31 is a short synthetic peptide that concentrates in mitochondria and binds cardiolipin, a lipid in the inner mitochondrial membrane that is required for the machinery of energy production to hold its shape. Under the name elamipretide it has been developed as a drug, and under the names MTP-131 and Bendavia it appears in the older trial records. A vial sold as SS-31 and a syringe used in a hospital trial of elamipretide are the same molecule described by different vocabularies.
The phase 3 that missed
MMPOWER-3 is the trial to know [1]. It was a phase 3, randomized, double-blind, placebo-controlled study in people with genetically confirmed primary mitochondrial myopathy: the disease elamipretide was designed for, in the patients most likely to respond. Participants (N = 218) were randomized one to one, 109 to 40 mg a day of subcutaneous elamipretide and 109 to placebo, for 24 weeks. Mean age was 45.6 years and 64% were women. At baseline the group walked 336.7 ± 81.2 meters on the six-minute walk test.
It missed both primary endpoints. The difference between elamipretide and placebo in distance walked at week 24 was -3.2 meters, with a 95% confidence interval from -18.7 to 12.3 and p = 0.69. On the fatigue score the difference was -0.07, confidence interval -0.10 to 0.26, p = 0.37. The point estimate on walking distance slightly favored placebo. The drug was well tolerated, with most adverse events mild to moderate, which is worth saying: this is a well-behaved molecule that did not do the thing it was given for.
The Barth syndrome result, and how it gets misquoted
TAZPOWER tested elamipretide in Barth syndrome, a genetic disorder of the same cardiolipin metabolism the drug acts on [2]. Part one was a randomized, double-blind, placebo-controlled crossover in 12 subjects: 40 mg a day for 12 weeks, a 4-week washout, then the opposite arm. Neither primary endpoint was met.
Ten subjects then continued into an open-label extension, and at 36 weeks the paper reports significant improvements: +95.9 meters on the six-minute walk test (p = 0.024) and -2.1 points on the symptom scale (p = 0.031). A 168-week extension followed [3].
The study closest to what it is sold for
Sellers pitch SS-31 for energy and aging rather than for a rare genetic disease, and there is one randomized trial close to that question [4]. Thirty-nine healthy older adults aged 60 to 85, 46% female, were enrolled specifically because their mitochondria were functioning poorly, and given a single two-hour infusion of elamipretide or placebo. Mitochondrial capacity was measured non-invasively by magnetic resonance and optical spectroscopy.
Immediately after the infusion the treated group's mitochondrial capacity was higher than placebo, marginally: p = 0.055 on the absolute change and p = 0.045 on the percentage change. By day 7 there was no difference, which the authors attribute to the half-life of the drug in blood. A single dose moved a laboratory measure for less than a week. That is a real finding, and it is not a claim about how anyone felt or what they could do.
A randomized placebo-controlled trial in heart failure found no improvement in the endpoint it set either[5], and an active phase 3 in a different indication was still listed as recruiting-complete on ClinicalTrials.gov at the time of writing.
Where it stands with the FDA
Neither SS-31 nor elamipretide appears in the 503A bulk drug substances categories, updated May 14, 2026, or in the 503B categories, updated March 21, 2025. A compounding pharmacy has no lawful route to prepare it. A molecule being an investigational drug elsewhere does not create one; if anything it is the reason there is no route, because the compound is inside a development program rather than outside it.
For how that framework decides what a pharmacy may prepare, see what makes a peptide legal to prescribe. For compounds at the other end of the evidence range, see semax and KPV.