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SS-31: Benefits, side effects, dosage details, and how it works

We present the science behind SS-31’s benefits for longevity and quality of life.

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Last updated: Sep 16th, 2025
SS 31 Peptide

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Sooner or later, we all feel the effects of aging: aching bodies, faltering memories, and appointments with cardiologists who say to be more careful about what we eat. Staying ahead of the aging process is simple in theory — exercise the mind, work out the body, and listen to those cardiologists — but simple doesn’t mean easy.

Peptides may offer a way to make it easier. With their broad spectrums of activity, several of them have earned attention for supporting longevity. One peptide in particular, called SS-31, has shown a compelling amount of promise in slowing or mitigating aging-related changes. What’s more, its full potential has yet to be established.

In this guide, we explain what the SS-31 peptide is, what it can do to improve your quality of life, and how you might go about trying it yourself.

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Over the past two decades, Innerbody Research has helped tens of millions of readers make more informed decisions about staying healthy and living healthier lifestyles.

As a team, we’ve put in close to 2,000 hours of research and writing on the subject of therapeutic peptides, and the number continues to grow. Through our close readings of scientific studies and reviews, as well as our relationships with clinicians and patients, we’ve been able to produce comprehensive profiles of even obscure peptide therapies.

Additionally, like all health-related content on this website, this guide was thoroughly vetted by one or more members of our Medical Review Board for accuracy and will continue to be monitored for updates by our editorial team.

What is SS-31?

SS-31 is a synthetic tetrapeptide. It’s alternatively known as MTP-131 and is currently being developed by Stealth BioTherapeutics under the trademarks Elamipretide and Bendavia.

It’s specifically designed to target mitochondria. On entering the body, SS-31 binds with high affinity to cardiolipin, a phospholipid uniquely found in the inner mitochondrial membrane and known to interact with a protein called cytochrome c. This interaction determines whether cytochrome c becomes either an electron carrier or a peroxidase, and SS-31 promotes conversion to the former instead of the latter. As an electron carrier, cytochrome c drives the synthesis of adenosine triphosphate (ATP), our primary form of cellular energy. ATP production is the principal function of mitochondria, so SS-31’s presence helps ensure that the “powerhouses of the cell” continue to carry out their critical role.

SS-31 may also inhibit the opening of a channel in the inner membrane called the mitochondrial permeability transition pore (mPTP), at least in rodents. Because mPTP opening has been implicated in neuronal death, SS-31’s inhibitory action is a potential mechanism of action for the peptide’s cognitive health benefits.

Furthermore, several studies have concluded that SS-31 is capable of scavenging mitochondrial reactive oxygen species, making it a potent antioxidant. Its antioxidant mechanism of action isn’t yet fully understood, but one group of researchers has theorized that it has to do with an ability to activate autophagy — a cellular recycling process that promotes efficient function and which is critical for mitigating oxidative stress.

Current therapeutic uses of SS-31

Clinical studies on SS-31 support its use as a treatment for multiple aging-related changes, including those related to cognition, physiology, and vision. Though the lion’s share of supportive studies were conducted in animal models, they broadly paint a positive picture of the peptide’s therapeutic potential.

Below, we summarize the scientific literature on some of SS-31’s most promising applications.

Cognitive deficits

Researchers in a mouse study from 2016 found that SS-31 administration after isoflurane treatment effectively “rescued” cognitive deficits by reversing mitochondrial dysfunction in the hippocampus, the part of the brain responsible for memory and learning. This reversal, in turn, helped regulate the signaling of brain-derived neurotrophic factor, an essential protein for neuronal function.

In a 2017 study, researchers administered SS-31 to young rats before isoflurane treatment to examine its utility as a preventive against cognitive defects. The subjects here exhibited relatively little cognitive deficit or mitochondrial dysfunction in the hippocampus, and their cognitive function was comparable to that of the control group that did not receive isoflurane.

Alzheimer’s disease

Mitochondrial dysfunction appears to be a central event in the pathogenesis of Alzheimer’s disease, so the preservation of mitochondrial health may be one of the keys to disease prevention. To that end, a 2017 study points favorably to SS-31’s use for Alzheimer’s prevention. In it, an Alzheimer’s mouse model that received intraperitoneal injections of SS-31 not only maintained its mitochondrial function but also exhibited “significantly decreased” levels of amyloid beta, a key feature of the disease.

Stroke and traumatic brain injury

After a stroke or traumatic brain injury, oxidative stress can accumulate in the brain and lead to worse health outcomes. This is known as secondary brain injury. But here, too, SS-31 can offer protection. For example, in a 2019 rat study, SS-31 administration helped normalize levels of an enzyme associated with cerebral oxidative stress after mild brain trauma, while a 2020 rat model saw decreases in a key oxidative stress biomarker, along with decreased neuronal cell death and neurological deficit, after a subarachnoid hemorrhage.

Atherosclerosis

Atherosclerosis refers to a hardening of the arteries. It results, in part, from oxidative stress that activates inflammatory cells. Once activated, these cells release chemical signals that cause fats, cholesterol, and other substances to accumulate on the arterial walls. It’s a disease believed to underlie approximately 50% of all deaths in the Western Hemisphere. But with SS-31’s antioxidant action, it can potentially decrease one’s atherosclerotic risk.

Case in point, a 2017 phase 2a clinical trial, involving 14 patients with severe atherosclerotic renal artery stenosis (atherosclerosis concerning the kidneys), exhibited increased blood flow to the kidneys and improved kidney function. These findings suggest that SS-31 may be able to attenuate vascular blockages in humans.

Muscle function

Because mitochondria generate much of the energy our muscles use, it’s probably no shock that mitochondrial dysfunction contributes to muscle disorders, including age-related losses (sarcopenia). And considering SS-31’s relationship to mitochondrial health, one might expect that it could yield benefits for muscle function. Such benefits were made evident in a 2018 study in aged mice, in which eight weeks of SS-31 treatment was able to reverse age-related decline in mitochondrial ATP production, allowing for improvements in subjects’ exercise tolerance and a restoration of redox homeostasis (a balance between pro-oxidants and antioxidants that promotes proper muscle generation and function).

Glaucoma

Glaucoma, one of the leading causes of blindness globally, is a group of eye conditions characterized by damage to the retinal ganglion cells (RGCs). Since oxidative stress and mitochondrial dysfunction appear to contribute to RGC death, researchers have looked to SS-31 as a potential glaucoma treatment. Indeed, in a 2015 review published in Medical Hypothesis, Discovery & Innovation, the authors concluded that SS-31 is “an attractive mitochondria-targeted antioxidant that can protect the mitochondria and RGCs against oxidative damage,” and designated it a “novel neuroprotective ophthalmic drug for protecting RGCs in glaucoma.”

Many other studies have assessed SS-31 as a treatment for other ailments, including but not limited to osteoarthritis, hypertension, liver cancer, and heart failure. Except for heart failure, for which SS-31 has shown mixed or inconclusive results, the peptide has had varying degrees of success in animal models. But it’s for the above health conditions for which SS-31 is most likely to be prescribed.

In addition, SS-31 is the subject of numerous active clinical trials concerning an array of health conditions, such as macular degeneration and Barth’s syndrome. We’ll be following these trials as they unfold and will update this guide with their results.

Is SS-31 safe?

The literature on SS-31 overwhelmingly describes a high safety profile. To illustrate, we can point to several double-blind, randomized controlled trials that otherwise failed to support its therapeutic potential for specific diseases. One such trial, from 2020, had inconclusive results on SS-31’s benefits for heart failure, but it described the peptide as “well tolerated” and reported no significant increases in blood pressure, heart rate, or electrocardiogram intervals. Another trial, from the same year, yielded no significant benefit for mitochondrial myopathy but found the only noteworthy adverse effects to be injection site reactions, “the majority of which were mild.”

These findings are consistent with the risks described by the clinicians we know who prescribe SS-31, though they add that some users may also experience headaches, dizziness, gastrointestinal distress, flushing, or fatigue. Other peptides, and medications in general, are known to cause similar reactions. In most cases, they’re temporary.

There’s only one other safety concern with SS-31, and it’s common to most therapeutic peptides: it’s contraindicated for women who are pregnant or breastfeeding and people with a history of cancer. That’s because there isn’t enough research to determine whether SS-31 poses a danger to a developing fetus or child, and its effects on cell function theoretically could increase the risk of cancer recurrence.

Research-grade vs. pharmaceutical-grade SS-31

When we talk about a peptide’s safety profile in humans, we always refer to the pharmaceutical-grade version of it. To be considered pharmaceutical-grade, the peptide must meet strict chemical purity tolerances and be either approved or indexed by the U.S. Food & Drug Administration.

Research-grade peptides aren’t held to the same standards. They’re allowed to contain a higher level of impurities because they’re intended exclusively for laboratory use — in animals or cell cultures. But with more impurities comes a greater risk of immunogenicity, when the body’s immune system reacts to a substance as though it were a threat. It’s like an allergic reaction, and just like an allergic reaction, the outcome can be fatal.

Meanwhile, there’s a real attraction that research-grade peptides have for consumers: they don’t require a prescription. Practically any adult can buy something like SS-31 through an online vendor (which might describe the product as “pharmaceutical-” or “USP-grade,” although it’s probably not) with nothing more than a credit card. The gentlest word we have for that path is unwise.

Please, if you have a genuine need for SS-31, go through the proper medical channels and get a prescription. We discuss the topic a little further under “Where to find SS-31” at the end of this guide.

What’s it like to use SS-31?

User expectations and experiences are hard to come by through research papers. Fortunately, our known peptide prescribers have shared with us the knowledge they’ve gained through observing patients’ health outcomes with SS-31, and so we can relay their findings to you here.

Dosing and administration

A standard dose of SS-31 is 5mg, but it may vary depending on factors such as age, weight, and health history. You can expect to take just two doses per week, much fewer than the daily or near-daily administrations common with other peptides.

SS-31 is almost always an injectable. As such, it should come as a dried powder in a vial. Normally, the powder is part of a kit that includes items you’ll need to reconstitute the powder into an injectable solution: bacteriostatic water and needle syringes. What you do is use a needle syringe to transfer a measure of water to the powder. You should gently dissolve the powder in the water, as agitation can degrade the peptide.

When you’re ready for a dose, you ought to inject the prescribed amount into an area of subcutaneous fat, such as your stomach, a thigh, or an upper arm. You should rotate your sites to avoid irritation. Morning administration is ideal so that you can take fuller advantage of SS-31’s energizing effects.

As with other peptides, SS-31 is often cycled. That is, your schedule entails a certain period of regular administration (the “on” period) followed by a shorter period of no use at all (the “off” period). A common SS-31 cycle is three months on and one month off, totaling three cycles per year.

Timeline of benefits from SS-31

The most immediate benefit of SS-31 is an energizing effect from its action on mitochondrial function. This tends to become apparent within 1-2 weeks, as patients feel less fatigued and experience greater physical endurance.

At 2-4 weeks, SS-31’s cognitive benefits begin to take effect. At this time, you might notice an increased ability to focus and remember information.

At 8-12 weeks, and thereafter, come the antioxidant benefits. Though they aren’t as apparent as the earlier effects, you might notice a general improvement in your well-being, possibly as well as some enhancements in muscle function.

SS-31 storage

Between doses, you should store your reconstituted SS-31 in a cold environment. The U.K.’s National Institute for Biological Standards and Control recommends a storage temperature of 4°C, or 39°F, so a refrigerator is the best place for it. You should have no need to wrap or otherwise cover your vial, as peptide vials usually come with a “self-healing” rubber stopper that maintains an airtight seal even after it’s punctured.

Who is (and isn’t) a candidate for SS-31?

Older people are probably the best-suited population for SS-31, as its primary therapeutic benefits relate to aging-related changes of the brain, body, and cardiovascular system. More specifically, SS-31 principally acts on the mitochondria and oxidative stress, which worsen with time. That being the case, a rule of thumb could be: you might be a prime candidate if you have concerns about cholesterol, cognition, muscle loss, and vision impairment stemming from your age.

Which isn’t to say that younger people can’t benefit from SS-31 therapy. Never has there been a bad time to enact preventive health protocols for slowing the sandfall of the biological hourglass. It’s just that a clinician might not consider a twenty- or thirtysomething to be well-indicated for this particular therapy. One may have to exhaust other options and show signs of significant mitochondrial dysfunction to qualify for a prescription.

Also poorly indicated are people whose health isn’t likely to benefit from SS-31. Someone with heart disease, for example, would be a poor candidate since relevant clinical trials haven’t met the primary endpoints for that use.

Then there are people for whom SS-31 is contraindicated: women who are pregnant or breastfeeding, and people with a history of cancer. For these populations, SS-31 could pose an undue safety risk, which is better to avoid altogether.

Where to find SS-31

The best (and probably only) place to get pharmaceutical-grade SS-31 is through a licensed clinic. It may not be an FDA-approved drug, but clinicians around the United States have prescribed it and continue to do so. And to qualify for a prescription, you may need to demonstrate that you need SS-31 to treat a relevant health condition — that is, no other, more widely available drug can do for you what SS-31 might.

We want to reiterate that you can undoubtedly find SS-31 through online vendors without a prescription, but then you’d be dealing with (a) a business with an unvalidated reputation and (b) a research-grade peptide that can put your life in danger. We strongly urge you to ignore the presence of these vendors in your web searches, and (unless you intend to carry out sanctioned laboratory experiments) always give a wide berth to research-grade peptides.

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Sources

Innerbody uses only high-quality sources, including peer-reviewed studies, to support the facts within our articles. Read our editorial process to learn more about how we fact-check and keep our content accurate, reliable, and trustworthy.

  1. Mayo Clinic Staff. (2024). Aging: What to expect. Mayo Clinic.

  2. Birk, A. V., et al. (2013). The mitochondrial-targeted compound SS-31 re-energizes ischemic mitochondria by interacting with cardiolipin. Journal of the American Society of Nephrology, 24(8), 1250-1261.

  3. Szeto, H. H. (2014). First-in-class cardiolipin-protective compound as a therapeutic agent to restore mitochondrial bioenergetics. British Journal of Pharmacology, 171(8), 2029-2050.

  4. Ramsay, R. R. (2019). Electron carriers and energy conservation in mitochondrial respiration. ChemTexts, 5(9).

  5. Wu, J., et al. (2016). BDNF pathway is involved in the protective effects of SS-31 on isoflurane-induced cognitive deficits in aging mice. Behavioural Brain Research, 305, 115-121.

  6. Kalani, K., Yan, S. F., & Yan, S. S. (2018). Mitochondrial permeability transition pore: A potential drug target for neurodegeneration. Drug Discovery Today, 23(12), 1983-1989.

  7. Cleveland Clinic. (2024). Hippocampus. Cleveland Clinic.

  8. Wu, J., et al. (2017). Elamipretide (SS-31) ameliorates isoflurane-induced long-term impairments of mitochondrial morphogenesis and cognition in developing rats. Frontiers in Cellular Neuroscience, 11, 119.

  9. Ashleigh, T., Swerdlow, R. H., & Beal, M. F. (2023). The role of mitochondrial dysfunction in Alzheimer's disease pathogenesis. Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association, 19(1), 333-342.

  10. Reddy, P. H., Manczak, M., & Kandimalla, R. (2017). Mitochondria-targeted small molecule SS31: a potential candidate for the treatment of Alzheimer's disease. Human Molecular Genetics, 26(8), 1483-1496.

  11. Allen, C. L., & Bayraktutan, U. (2009). Oxidative stress and its role in the pathogenesis of ischaemic stroke. International Journal of Stroke, 4(6), 461-470.

  12. Fesharaki-Zadeh, A. (2022). Oxidative stress in traumatic brain injury. International Journal of Molecular Sciences, 23(21), 13000.

  13. Hemphill III, J. C., & Besmertis, L. (2001). Occurrence of secondary brain insults in intracerebral hemorrhage. 32(Supplement 1).

  14. Czigler, A., et al. (2019). Hypertension exacerbates cerebrovascular oxidative stress induced by mild traumatic brain injury: Protective effects of the mitochondria-targeted antioxidative peptide SS-31. Journal of Neurotrauma, 36(23), 3309-3315.

  15. Shen, R., et al. (2020). SS31 attenuates oxidative stress and neuronal apoptosis in early brain injury following subarachnoid hemorrhage possibly by the mitochondrial pathway. Neuroscience Letters, 717, 134654.

  16. Batty, M., Bennett, M. R., & Yu, E. (2022). The role of oxidative stress in atherosclerosis. Cells, 11(23), 3843.

  17. National Heart, Lung, and Blood Institute. (2024). Atherosclerosis: Causes and risk factors. National Institutes of Health.

  18. Pahwa, R., & Jialal, I. (2023). Atherosclerosis. StatPearls [Internet].

  19. Hou, Y., et al. (2018). The antioxidant peptide SS31 prevents oxidative stress, downregulates CD36 and improves renal function in diabetic nephropathy. Nephrology Dialysis Transplantation, 33(11), 1908-1918.

  20. Yang, Q., Li, C., & Chen, Q. (2022). SS31 ameliorates oxidative stress via the restoration of autophagic flux to protect aged mice from hind limb ischemia. Frontiers in Cardiovascular Medicine, 9, 789331.

  21. Ornatowski, W., et al. (2020). Complex interplay between autophagy and oxidative stress in the development of pulmonary disease. Redox Biology, 36, 101679.

  22. Saad, A., et al. (2017). Phase 2a clinical trial of mitochondrial protection (Elamipretide) during stent revascularization in patients with atherosclerotic renal artery stenosis. Circulation: Cardiovascular Interventions, 10(9), e005487.

  23. Chen, H., et al. (2022). Mitochondrial dysfunction as an underlying cause of skeletal muscle disorders. International Journal of Molecular Sciences, 23(21), 12926.

  24. Campbell, M. D., et al. (2018). Improving mitochondrial function with SS-31 reverses age-related redox stress and improves exercise tolerance in aged mice. Free Radical Biology & Medicine, 134, 268-281.

  25. Mosca, N., et al. (2021). Redox homeostasis in muscular dystrophies. Cells, 10(6), 1364.

  26. World Health Organization. (2023). Blindness and vision impairment. WHO.

  27. Calkins, D. J. (2018). Why retinal ganglion cells are important in glaucoma. Glaucoma Research Foundation.

  28. Pang, Y., Wang, C., & Yu, L. (2015). Mitochondria-targeted antioxidant SS-31 is a potential novel ophthalmic medication for neuroprotection in glaucoma. Medical Hypothesis, Discovery & Innovation, 4(3), 120-126.

  29. Butler, J., et al. (2020). Effects of Elamipretide on left ventricular function in patients with heart failure with reduced ejection fraction: The PROGRESS-HF phase 2 trial. Journal of Cardiac Failure, 26(5), 429-437.

  30. De Groot, A. S., et al. (2023). Immunogenicity risk assessment of synthetic peptide drugs and their impurities. Drug Discovery Today, 28(10), 103714.

  31. Liu, E., et al. (2004). Preventing peptide-induced anaphylaxis: Addition of C-terminal amino acids to produce a neutral isoelectric point. The Journal of Allergy and Clinical Immunology, 114, 607-613.

  32. National Institute for Biological Standards and Control. (n.d.). Peptide handling, dissolution & storage. NIBSC.

  33. Bratic, A., & Larsson, G. (2013). The role of mitochondria in aging. The Journal of Clinical Investigation, 123(3), 951-957.

  34. Maldonado, E., Urbina, F., & Solari, A. (2023). Aging hallmarks and the role of oxidative stress. Antioxidants, 12(3), 651.

  35. Karaa, A., et al. (2020). A randomized crossover trial of elamipretide in adults with primary mitochondrial myopathy. Journal of Cachexia, Sarcopenia and Muscle, 11(4), 909-918.