The researchers who discovered SS-31 were Hazel Szeto at Weill Cornell Medical College and Peter Schiller at the Montreal Clinical Research Institute. Their collaboration began with peptides, short chains of protein building blocks, studied for pain. It led to a different question: why did these small molecules gather inside mitochondria, the parts of cells that make usable energy?
SS-31 was designed by chemists. It wasn't extracted from human tissue or discovered as a natural hormone. The mitochondrial findings were published in 2004.
Who discovered SS-31, and what were they studying?
Szeto studied how drugs affect the body at Weill Cornell in New York. Schiller worked on peptide chemistry in Montreal. His institute's account credits both scientists with designing the Szeto-Schiller peptide family and says it was first synthesized in his laboratory.
The early work concerned opioid receptors, docking sites on cells involved in pain signaling. Researchers wanted small peptides that could reach those sites and remain intact long enough to study.
A 2001 paper by Szeto, Schiller, and colleagues in the Journal of Pharmacology and Experimental Therapeutics compared opioid peptides in sheep. One was called [Dmt1]DALDA, a name for a particular modified peptide. The team measured how the compounds moved through blood and how quickly they were cleared.
That paper belongs to SS-31's family history. It studied opioid-peptide relatives, rather than SS-31 itself, and it was animal work.
The unexpected finding inside cells
The next question was where the peptides went after entering a cell. In Weill Cornell's 2014 account of the discovery, Szeto described tracking a peptide with a fluorescent label, a marker that glows under a microscope.
Its location matched the mitochondria. That observation shifted the project from pain receptors toward the cell's energy-making structures. Later versions rearranged the building blocks to remove opioid activity.
Kesheng Zhao was first author of the 2004 Journal of Biological Chemistry report, with Szeto and Schiller among the authors. It described peptides that entered cells and concentrated at the inner mitochondrial membrane, the structure's inner boundary. The experiments involved cells, isolated mitochondria, and a heart model outside the body.
Those findings opened a research direction. They weren't results from treated patients. Later work focused on cardiolipin, a fat that helps organize that membrane. Our SS-31 peptide guide explains the mechanism in more detail.
How the Szeto-Schiller peptide got its names
SS means Szeto-Schiller, after the two researchers. The number 31 identifies this member of the family. It doesn't describe its length: SS-31 contains four amino acids, the building blocks of proteins.
The same molecule collected other names as it moved into drug development:
| Name | Where it fits in the history |
|---|---|
| SS-31 | The laboratory designation in the Szeto-Schiller family. |
| MTP-131 | An earlier development code used in human studies. |
| Bendavia | An earlier development name used alongside MTP-131. |
| Elamipretide | The nonproprietary name, meaning the shared drug name rather than a brand. |
| Forzinity | The name of a specific manufactured elamipretide product. |
The first human study's registry uses MTP-131 and Bendavia together. The World Health Organization's 2015 list of proposed shared drug names, INN List 113, page 216, records elamipretide and its chemical structure.
These names help connect older papers to newer ones. A shared molecule name doesn't make every product bearing it the same preparation.
From the laboratory to the first human studies
Szeto founded Stealth Peptides in 2006, according to Weill Cornell's account. The company later became known as Stealth BioTherapeutics. Its SEC annual report records operations beginning in 2006 and an original licensing agreement with Cornell and the Montreal institute that April.
The first human study, NCT01115920, began in May 2010. The registry records 40 healthy adults and describes a trial comparing a single infusion with placebo, an inactive comparison treatment. It assessed safety and how the drug moved through the body. The record has no posted results.
An early published result came from EMBRACE STEMI, a study in people having a heart attack. Its European Heart Journal report, published online in 2015 and in a 2016 issue, found no significant reduction in its main measure of heart damage versus placebo.
Human testing therefore began well before the rare-disease label. Testing also didn't mean every hoped-for result followed. Later disease studies have their own accounts: TAZPOWER in Barth syndrome and MMPOWER-3 in inherited muscle disease.
Where elamipretide stands today
As of October 1, 2026, the day this article was written, the FDA's September 19, 2025 letter marks Forzinity's accelerated approval for improving muscle strength in Barth syndrome. This inherited disorder affects mitochondrial function. The indication covers adults and children weighing at least 30 kilograms. The current label reads “Revised: 9/2025.”
Accelerated approval allows earlier access based on a measure considered reasonably likely to predict benefit, with another trial required to confirm it. The Forzinity approval anniversary covers that decision's history.
As of October 1, 2026, the day this article was written, that follow-up has moved into treating participants. On July 8, 2026, Mighty Therapeutics, Stealth BioTherapeutics' parent company, announced that the first participant had been dosed in 4TAZPower. The planned comparison with placebo lasts 72 weeks. Starting treatment is a milestone, rather than confirmation of benefit.
SS-31 is coming soon to Promise — add me to the list. SS-31 prescribed through Promise will be dispensed by a licensed U.S. compounding pharmacy as a compounded medication, which is different from an FDA-approved product: the formulation Promise will offer is not FDA-approved. Compounded means prepared by a pharmacy for an individual prescription. A licensed provider may still prescribe — that decision is between you and your doctor.
Why MOTS-c has a different origin
MOTS-c often appears beside SS-31 in discussions of mitochondrial health. Their discovery stories are different. SS-31 came from designed peptide chemistry; MOTS-c was identified in genetic instructions already present in mitochondria.
Lee and colleagues' 2015 Cell Metabolism paper described MOTS-c as a 16-amino-acid peptide and studied how it affected fuel handling in cells and mice. It is studied as a signal, while SS-31 is studied at the membrane.
Sharing a cellular neighborhood doesn't make them interchangeable. Nor does the history establish that combining them improves an outcome in people.
What this history means for a prescription
A discovery paper explains why a molecule attracted interest. A clinical trial tests a particular product in a particular group. A prescription asks whether the evidence fits the person considering treatment.
That distinction matters when an online seller borrows elamipretide's history for a vial sold without a prescription. The name alone supplies neither a clinical review nor a pharmacy record.
At Promise, a licensed provider reviews every SS-31 request and may prescribe or decline; not everyone qualifies. Once visits open, if prescribed, a licensed U.S. compounding pharmacy will prepare and dispense the medication. The provider sets the actual dose and follow-up plan.
