SS-20 dosage and evidence
Written by Aaron CuhaReviewed Sep 2026
The short answer
SS-20 is the sister of SS-31, the peptide that became the approved drug elamipretide. SS-20 cannot mop up free radicals, the unstable molecules that damage cells. That made it a useful test case, and it worked anyway in rats and mice. There is no human study and no registered trial.
Evidence grade for SS-20: Animal or lab only. The rule: only animal or lab studies on this page. No study in people yet. The sum on this page: 4 animal studies, 1 lab study, no human study. A grade counts how much has been done to people, not whether it works.
- People given it
- 0
- Human studies
- 0
- Found nothing
- 0
Dose
No human dose established
No published study on this page has given this compound to people and reported a result.
4 animal studies, 1 lab study, no human study
6 effects reported, 4 unwanted, 2 wanted, by people using it, not a trial
Goal pages: Ageing and longevity, Injury, healing and recovery, Heart and circulation, Bone and joints
In plain English
In plain English, from Aaron
This is how I would explain it to a friend. The evidence, with the numbers, is further down the page.
SS-20 is a four amino acid peptide that protects mitochondria during a heart attack or a blocked blood supply. Its close cousin became a real approved drug. This one never left the animal lab. The interesting part is that it cannot mop up free radicals at all, and it still works in rats.
What people take it for
- Protecting the heart and kidneys under stress.
- More energy, on the theory that better mitochondria means more fuel.
- Nerve pain from chemotherapy.
- General anti aging, since aging and mitochondria get linked together.
What studies in people showed
No human has been given it and no trial is registered. Everything below is animals. In rats with a blocked heart artery, the damaged area was 47.1 percent of the tissue at risk on this peptide, against 59.9 percent with nothing. Its cousin, the one that can mop up free radicals, did slightly worse at 53.9 percent. Eight rats per group. In rat kidneys it stretched how long the organ could go without blood from 30 minutes to 45. In mice on a chemotherapy drug it stopped the nerve pain and brought the nerve fibres back to normal. The reason it works is that it sits on a fat in the mitochondria and keeps one key protein from falling apart. In a starved rat kidney the damaged form of that protein rose 17 times, and this peptide stopped that.
What people report
Reports, not study results
The good
- There is nothing to report. This peptide is barely sold and almost nobody has used it.
- Its cousin is now a real prescription drug, which is the only human track record this chemistry has.
The bad
- No human safety data at all. The animal studies measured whether it worked, not whether it was safe.
- The lab that made it holds a financial stake, and nearly all the research comes from that one group.
- Its cousin went through real trials and mostly missed the target, which is not a good sign for the family.
- Anything sold under this name is unregulated with no purity testing.
Where these come from: All of it is published animal work from one research group and its partners. There are no user reports to speak of, and no trial data of any kind.
My bottom line
The rat data is clean and the mechanism is genuinely interesting. But the company owned both peptides and picked the other one. That one ran real trials and mostly came up short. I would not be the first human to try this.
An opinion, not a finding. I am a coach, not a doctor.
What it has been measured to do
Animal and lab work, not yet tested in people
Real results, but from animals or cells, not people. What works in a mouse often does not work the same way in a person. Nobody can patent this, so nobody would ever earn back the cost of a study in people. That is usually why there is none. The record on this one is set out below.
- Kidney function1 animal or lab study
- Pain1 animal or lab study
- Cell energy and mitochondria1 animal or lab study
33 of the 36 indexed goals have no study of any kind behind SS-20
No study in people, animals or cells on this page reports a result for these. That does not prove SS-20 does nothing for them. It does mean anything you have heard about SS-20 and one of these did not come from a study cited here.
Show full evidence
What is SS-20?
SS-20 is the sister of SS-31, the peptide that became the approved drug elamipretide. SS-20 cannot mop up free radicals, the unstable molecules that damage cells. That made it a useful test case, and it worked anyway in rats and mice. There is no human study and no registered trial.
SS-20 is a tiny peptide of four amino acids, Phe-D-Arg-Phe-Lys-NH2. It is one of the Szeto-Schiller peptides made at Weill Cornell in New York. What makes it interesting is what it lacks.
Nobody has tested it in people. It never went into human trials. Its sister did.
SS-31, which became the drug elamipretide, has a part that mops up free radicals, the unstable oxygen molecules that damage cells. SS-20 does not have that part and cannot mop anything up. So scientists tested the two against each other. They wanted to know if the heart protection seen in this family came from mopping up free radicals, or from something else.
In rats, they tied off a heart artery for 60 minutes to cause a heart attack. Both peptides, given as a shot into the belly at 3 milligrams per kilogram, shrank the damaged area. The damage covered 53.9 percent of the area at risk with SS-31 and 47.1 percent with SS-20, against 59.9 percent in rats given nothing. Both cut damage to fats in cells and made heart rhythm problems less severe. The peptide that cannot mop up did at least as well as the one that can.
How SS-20 works came out later. It sticks to cardiolipin, a fat in the inner wall of mitochondria. There, it protects a key link inside cytochrome c, a protein that passes energy along. In rat kidneys starved of blood, that link breaks. A damaged form of cytochrome c rises 17-fold, the folds inside mitochondria collapse, and cytochrome c leaks out. SS-20 prevented all of it.
The real results follow from that. In rats, a dose 30 minutes before blood flow to a kidney was cut raised how long the kidney could cope without blood, from 30 to 45 minutes. It also cut later scarring. In mice given the cancer drug oxaliplatin every week, a steady supply of SS-20 prevented nerve pain. It also brought the number of tiny nerve fibres in the skin back to normal. In mice given MPTP, a toxin used to mimic Parkinson's disease, SS-20 clearly protected the brain cells that make dopamine, even though it cannot mop up free radicals.
Every one of those is an animal.
How does SS-20 work?
SS-20 goes to the inner wall of mitochondria and sticks to cardiolipin, a fat found there. That protects cytochrome c, a protein that passes energy along the chain inside mitochondria. When blood flow stops, a key link inside cytochrome c breaks. The broken protein clogs the energy chain. It also starts damaging cardiolipin, which breaks down another protein, OPA1, and lets cytochrome c leak out. By keeping that link intact, SS-20 keeps the energy chain running smoothly. That is why it looks like an antioxidant even though it has no mopping-up chemistry. It cuts how many harmful oxygen molecules get made, instead of cleaning them up afterwards.
What have studies in people found about SS-20?
SS-20 has never been given to a person in a published study. There is no study in people, no test of how the body handles it, no case report and no registered trial. Everything on record is in rats, mice, or mitochondria (the power plants inside cells) taken from animals.
- The nearest human evidence is for a different molecule. SS-31, called elamipretide, went through a full drug programme. It won fast-track US approval for Barth syndrome, a rare inherited disease, in 2025. That approval rested on a follow-on study where everyone got the drug and nobody got a dummy, after studies against a dummy in other mitochondrial diseases missed their main goals. None of that carries over to SS-20. SS-20 lacks the part of SS-31 that mops up harmful oxygen molecules, so it is a different compound thought to work a different way.
- No trial of SS-20, or of this peptide family under that name, is listed on ClinicalTrials.gov at any stage.
- The full published record is animals. In rats having a heart attack, SS-20 at 3 mg/kg, shot into the belly, left damage in 47.1 percent of the area at risk, against 59.9 percent in untreated rats. In rats, a dose before kidney surgery let the kidneys go without blood flow for 45 minutes instead of 30. In mice, it was tested for nerve pain from the cancer drug oxaliplatin and in a Parkinson's model. Mitochondria taken from rat kidneys were used to study how it works. No human anywhere.
What this does not tell you: There is no human dose, route, blood level, half-life or safety observation of any kind. The animal work used shots into the belly, a steady drip, or a dose 30 minutes before a planned surgical injury. None of those matches how anyone would use this compound. A dose given before an injury tests prevention, and cannot be read as a treatment result. And the bad news a human programme turns up, the goals that are missed and the side effects that pile up, cannot appear in a record where no programme was ever run.
The state of the research
The useful comparison is with what happened to its sister. SS-31, now elamipretide, went all the way through drug testing. In 2025, the US gave it fast-track approval for Barth syndrome, a rare inherited disease. That approval rested on a follow-on study where everyone got the drug and there was no comparison group. Before that, studies in other mitochondrial diseases, tested against a dummy drug, missed their main goals. So that is the best this chemistry has done in people so far: an approval for a very rare disease on weak evidence, next to failed results in more common conditions.
SS-20 never went down that road. Read next to its sister's record, the missing SS-20 trials are not a gap waiting to be filled with good news. A company that held both peptides chose one. It took that one through trials that mostly failed, and left the other in animals.
One note about who did this research. The SS peptides are licensed to a company. The senior author, co-authors and Cornell all have money at stake, and the papers say so. That does not make the findings wrong. It does mean almost all SS-20 research comes from one lab and its partners.
The evidence, in charts
Fig. 1a · how many people
0people have taken this in any study cited here
0 people · 0 studies in people
What this page cites instead is 4 animal studies and 1 lab study in a dish. None of them gave the compound to a person.
Counted from the list of sources on this page. We draw this chart only when a study in people is cited. An empty one is the answer, not a gap in the page.
Fig. 1b · evidence mix
None of the 5 sources here are studies in people.
- Animal study · done in animals480%
- Lab (cells in a dish) · cells or tissue120%
Counted from the list of sources on this page. It counts only what we cite, so there may be more studies out there. A review counts once, however many studies it sums up.
Fig. 2 · evidence over time
The studies cover 4 different years, 2007 to 2018, counted from the list of sources on this page. The newest source on file is from 2018, more than five years ago. Research on it may have gone quiet.
Fig. 3 · legal status at a glance
US
Not approved
UK
Not approved
AU
Not approved
CA
Not approved
Not approved in any of the four countries shown. This is what the law says, not a verdict on the science. See Legal status below for the full text and any notes.
Fig. 4 · how much does what
Nobody has tested different amounts in people
This chart would show how the effect changes as the amount goes up. For this compound, nobody has measured that in people. So we leave it empty. We will not borrow an animal chart and pretend it works the same in people.
Fig. 5 · what the molecule is
- Kind of compound
- Peptide
- Molecule weight
- About 611 Da for the tetrapeptide amide.
- Half-life
- Stated in words, not a numbersee the exact wording below
- Chain length
- None on file
Half-life as stated on file: Not established. No pharmacokinetic study in humans exists, and the animal work used pretreatment or continuous infusion schedules rather than single-dose kinetics.
No amino acid sequence is on file for SS-20, so none is drawn rather than guessed from a name.
The studies we cite
- Animal study2007Potent mitochondria-targeted peptides reduce myocardial infarction in rats.
In rats. Scientists caused heart attacks in rats and gave SS-20, SS-31 or nothing. Both peptides shrank the heart damage and calmed heart rhythm problems. SS-20 did at least as well, even though it cannot mop up free radicals. The authors think it stops them being made instead. The database tags this as a clinical trial, but it was in rats.
Rats, 8 per group, randomised to SS-31, SS-20 or placebo at 3 milligrams per kilogram intraperitoneally 30 minutes before a 60 minute left anterior descending ligation and again 5 minutes before reperfusion. Infarct area as a fraction of area at risk was 53.9 percent with SS-31 and 47.1 percent with SS-20 against 59.9 percent in controls. Both reduced lipid peroxidation and arrhythmia severity, with Lambeth scores of 5 and 3 against 13 in controls. Since SS-20 does not scavenge reactive oxygen species, the authors conclude it most likely reduces their production instead. Rats. The PubMed record carries a Clinical Trial publication type tag, which is a database artefact: the study is in rats.
- Animal study2015Improving mitochondrial bioenergetics under ischemic conditions increases warm ischemia tolerance in the kidney.
In rats. A dose of SS-20 before blood flow was cut let the kidney cope longer without it. It kept kidney cells and their mitochondria in better shape, and cut scarring later on. This is about a surgery window in rats. It is not a treatment for kidney disease in people.
Rats. Pretreatment with SS-20 thirty minutes before warm ischaemia raised tolerated ischaemia time from 30 to 45 minutes. It reduced cytoskeletal breakdown, cell swelling and mitochondrial matrix swelling, preserved cristae, improved state 3 respiration and respiratory control ratio in isolated kidney mitochondria, and reduced later interstitial fibrosis when given after ischaemia. A surgical-window result in rats, not a chronic kidney disease treatment in people.
- Animal study2018Protective Effect of a Mitochondria-Targeted Peptide against the Development of Chemotherapy-Induced Peripheral Neuropathy in Mice.
In mice. Mice on a weekly cancer drug got nerve pain and lost tiny nerve fibres in their paws. A steady supply of SS-20 prevented the pain and kept the nerve fibres normal. It was given to prevent the damage, not to treat it. The authors declare a money interest, and nobody has followed this up in people.
Mice given weekly oxaliplatin developed neuropathic pain and lost intraepidermal nerve fibres in the hind paw. Continuous SS-20 prevented the pain and returned nerve fibre density to normal levels. The authors note that SS-31 was the inventor's compound and declare that competing interest. Mice, prevention rather than treatment, and no human follow-up has been located.
- Animal study2009Mitochondria targeted peptides protect against 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine neurotoxicity.
In mice. Mice were given a toxin that mimics Parkinson's disease. SS-31 fully protected their dopamine brain cells at higher doses. SS-20, which cannot mop up free radicals, also gave real protection. Both kept mitochondria working in lab tests.
MPTP-treated mice, a Parkinson's model. SS-31 gave dose-dependent complete protection against loss of striatal dopamine and of tyrosine hydroxylase positive neurons in the substantia nigra. SS-20, which the paper states has no intrinsic ability to scavenge reactive oxygen species, also showed significant neuroprotection. Both prevented MPP+ induced inhibition of oxygen consumption, ATP production and mitochondrial swelling in isolated mitochondria. Mice and cultured cells.
- Lab (cells in a dish)2015Disruption of cytochrome c heme coordination is responsible for mitochondrial injury during ischemia.
In rat kidney tissue in the lab. When blood flow stopped, a key energy protein got damaged and the inside of the mitochondria fell apart. SS-20 prevented all of it. The authors say they, and Cornell, have money at stake in these peptides.
The mechanism paper, using mitochondria isolated from ischaemic rat kidneys. Ischaemia raised methionine-sulfoxide cytochrome c 17-fold and caused dramatic cristae collapse with OPA1 degradation and cytochrome c loss. SS-20 selectively targets cardiolipin, protects the methionine 80 to iron ligation, and prevented all of those changes. The authors disclose that the SS peptides are licensed to Stealth Peptides Inc and that they and Cornell hold financial interests.
Where to buy SS-20
No seller we track lists SS-20 yet. We read sellers’ public product lists every week, and this section fills in as soon as one does. Every seller, graded
Common questions
Has SS-20 been tested in people?
Not in any study cited here. SS-20 is the sister of SS-31, the peptide that became the approved drug elamipretide. SS-20 cannot mop up free radicals, the unstable molecules that damage cells. That made it a useful test case, and it worked anyway in rats and mice. There is no human study and no registered trial.
What is the SS-20 dosage?
No human dose established. No published study on this page has given this compound to people and reported a result. 4 animal studies, 1 lab study, no human study
Is SS-20 FDA-approved?
Not approved, and never sent to a regulator. Its sister drug SS-31, elamipretide, got US accelerated approval in 2025, a faster route based on early signs of benefit, for Barth syndrome, a rare inherited disease. SS-20 has no legal status of any kind.
Has SS-20 been tested in humans?
No. There is no human study and no registered clinical trial. All the work is in rats, mice and mitochondria taken out of cells.
How is SS-20 different from SS-31?
SS-31, which became elamipretide, has a part that mops up free radicals, the unstable oxygen molecules that damage cells. SS-20 lacks that part and cannot mop anything up. Instead, SS-20 sticks to cardiolipin, a fat in mitochondria, and protects a key link in cytochrome c. That cuts how many free radicals get made in the first place.
If SS-20 works without scavenging, is the antioxidant story wrong?
That is close to the point the rat heart attack study was built to make. Both peptides shrank heart damage and cut damage to fats in cells. The one that cannot mop up did at least as well. The authors read it this way: making fewer free radicals matters more than cleaning them up.
Why was SS-31 developed and not SS-20?
That was a company choice, not a published comparison, so any answer is a guess. Here is what is on record. SS-31 went through trials against a dummy drug that missed their main goals. Then in 2025 it got fast-track approval for Barth syndrome, based on a follow-on study with no comparison group. SS-20 stayed in animals.
Is SS-20 safe?
There is no human safety data. The animal studies looked at whether it worked, not at safety testing. Nothing is known at any human dose.