SS-31: The Mitochondria Peptide That Just Became an FDA-Approved Drug

Most research peptides live their whole lives in the gray zone between "interesting mouse study" and "never heard of it." SS-31 broke out. In September 2025, the FDA approved it as a prescription drug, making it the first medicine ever approved that works by repairing mitochondria from the inside.
Its official name is elamipretide, sold for one rare disease under the brand name Forzinity. In research circles it's still known by its lab code, SS-31, and it has two decades of studies behind it on aging muscle, the aging heart, and cellular energy. Here's what it is, what the research shows, and why research-grade SS-31 is still surprisingly hard to find.
What SS-31 actually does
Every cell runs on tiny power plants called mitochondria. They turn food and oxygen into ATP, the energy currency your muscles, heart, and brain spend all day. As we age, those power plants get leaky and less efficient: they make less energy and throw off more "exhaust" in the form of damaging free radicals.
Inside each mitochondrion is a folded inner wall where the actual energy-making machinery sits. That wall is held together by a special fat called cardiolipin. Think of cardiolipin as the scaffolding that keeps the assembly line lined up. When it gets damaged, the line falls out of alignment and output drops.
SS-31 is a tiny peptide, just four amino acids long, that slips into cells, heads straight for the mitochondria, and binds to cardiolipin. In effect, it props the scaffolding back up so the machinery runs closer to spec. Most antioxidants just mop up the exhaust; SS-31 is designed to fix the engine making it (Tung et al., Int J Mol Sci, 2025).
What the research found in aging animals
The most striking SS-31 work comes out of the University of Washington, where researchers have spent years testing it on old mice.
- Old muscle, young energy, in one hour (2013). A single dose given to 27-month-old mice, roughly the human equivalent of your late 70s, restored their muscle's energy production to young levels within an hour. Their muscles also tired less, and after eight days of treatment the mice ran longer (Siegel et al., Aging Cell, 2013). Young mice saw no change, which suggests SS-31 repairs damage rather than supercharging healthy cells.
- Eight weeks, more endurance (2019). Aged female mice treated daily for eight weeks had more fatigue-resistant, heavier calf muscles and could run longer on a treadmill. Interestingly, they didn't grow more mitochondria. The ones they had simply worked better (Campbell et al., Free Radical Biology & Medicine, 2019).
- The aging heart (2020). In old mice, SS-31 partly reversed the age-related stiffening that keeps the heart from relaxing and refilling properly. Paired with NMN, an NAD+ booster, the combination brought old hearts closest to their young state (Whitson et al., Aging Cell, 2020).
That last finding is worth noting for anyone already researching NAD+: the two compounds appear to fix different parts of the same energy problem.
Human trials: one win, one miss
Unlike most research peptides, SS-31 has been tested in people, and the record is honestly mixed.
- The win: Barth syndrome. Barth syndrome is an ultra-rare genetic disease in which the body can't build cardiolipin properly, so it's almost a perfect test case for a drug that targets cardiolipin. In the TAZPOWER trial, patients stayed on elamipretide for more than three years in an extension study, and walking distance and fatigue scores improved over time (Thompson et al., Genetics in Medicine, 2024). On September 19, 2025, the FDA granted accelerated approval based on improved leg-muscle strength, making it the first approved treatment for the disease.
- The miss: mitochondrial myopathy. A larger Phase 3 trial in adults with a broader group of inherited mitochondrial muscle diseases did not beat placebo overall (Karaa et al., Neurology, 2023). A follow-up analysis found that patients with one specific type of genetic defect did improve, which is now being studied further (Karaa et al., Orphanet J Rare Dis, 2024).
The takeaway: SS-31 seems to work best where cardiolipin damage is the core problem. That's exactly why aging researchers are interested, since cardiolipin damage is one of the hallmarks of old mitochondria.
Why research-grade SS-31 is hard to find
SS-31 is missing from a lot of peptide catalogs, and there's a reason. Two of its four building blocks are not the standard amino acids found in nature. One is a mirror-image form of arginine, and the other is a specially modified tyrosine. Those unusual parts are what let it slip into mitochondria and resist breakdown, but they also make it harder and more expensive to make cleanly. Plenty of suppliers skip it.
The approved drug doesn't help researchers either. Forzinity is a prescription injection for one ultra-rare disease, distributed through a specialty channel, and it isn't available for lab work.
GL Peptides carries research-grade SS-31 in a 50 mg vial. Every batch is third-party tested by Janoshik, ships with a Certificate of Analysis, and goes out in cold-chain packaging to protect the peptide in transit. Mix-and-match vial pricing applies across the catalog: 10% at 3, 15% at 5, and 25% at 10+.
The fine print and the bottom line
The exciting aging results above are all from mice. No human trial has tested SS-31 as an anti-aging or performance compound, and the one broad mitochondrial-disease trial missed its main goal. The FDA approval covers a single rare genetic disease, and it's an accelerated approval, meaning the company still has to confirm the benefit in further studies.
Still, SS-31 occupies a rare spot. Very few research peptides have both a deep stack of aging studies and an FDA-approved version proving the molecule can be made, dosed, and tolerated in people. For anyone studying how cells lose energy with age, it's one of the most credible tools available, and one of the harder ones to source.
References
Studies retrieved via PubMed.
- Siegel MP, et al. Mitochondrial-targeted peptide rapidly improves mitochondrial energetics and skeletal muscle performance in aged mice. Aging Cell. 2013;12(5):763–71. doi:10.1111/acel.12102
- Campbell MD, et al. Improving mitochondrial function with SS-31 reverses age-related redox stress and improves exercise tolerance in aged mice. Free Radic Biol Med. 2019;134:268–281. doi:10.1016/j.freeradbiomed.2018.12.031
- Whitson JA, et al. SS-31 and NMN: two paths to improve metabolism and function in aged hearts. Aging Cell. 2020;19(10):e13213. doi:10.1111/acel.13213
- Karaa A, et al. Efficacy and safety of elamipretide in individuals with primary mitochondrial myopathy: the MMPOWER-3 randomized clinical trial. Neurology. 2023. doi:10.1212/WNL.0000000000207402
- Thompson WR, et al. Long-term efficacy and safety of elamipretide in patients with Barth syndrome: 168-week open-label extension results of TAZPOWER. Genet Med. 2024. doi:10.1016/j.gim.2024.101138
- Karaa A, et al. Genotype-specific effects of elamipretide in patients with primary mitochondrial myopathy: a post hoc analysis of the MMPOWER-3 trial. Orphanet J Rare Dis. 2024. doi:10.1186/s13023-024-03421-5
- Tung C, et al. Elamipretide: a review of its structure, mechanism of action, and therapeutic potential. Int J Mol Sci. 2025;26(3):944. doi:10.3390/ijms26030944
- U.S. Food and Drug Administration. FDA grants accelerated approval to first treatment for Barth syndrome. September 19, 2025. fda.gov
This article summarizes published preclinical research for educational purposes. It is not medical advice. Products sold by GL Peptides are intended for laboratory research use only and are not for human consumption.
