MOTS-c: what the studies show, status and safety
Summary
MOTS-c is a short peptide of 16 amino acid building blocks, and the instructions for making it sit inside the DNA of our cells' own power plants, the mitochondria. It was first described in 2015. Almost everything known about giving it as a drug comes from mice. No country has approved it as a medicine, and no verified trial has ever given the peptide itself to people. It is banned in sport at all times.
Key findings at a glance
- The finding the whole field rests on comes from mice. Mice given 5 mg/kg a day did not put on weight or become resistant to insulin on a fattening diet [1].
- No verified trial has ever given it to people. One registry entry claims a study in adults with prediabetes, but its sponsor filed further entries whose own summaries call them mock or fictional example records, so it is not counted here [2].
- No country has approved it. In July 2026 the American regulator proposed keeping both chemical forms off the list of substances pharmacies may mix [3], and it has classed the substance as carrying identified safety risks since 2023 [4].
- Banned in sport at all times. Section S4.4.1 of the 2026 prohibited list names it among substances that switch on the cell's energy sensor, an enzyme called AMP-activated protein kinase [5].
- Detectable in doping tests since 2019. A blood test for doping control was validated and can pick up concentrations as low as 100 picograms per millilitre [6].
- More of it in the blood is not better. In 26 people with a cluster of metabolic problems the level reached 315 picograms per millilitre (315 ± 27) and rose in step with the amount of fat in the liver [7].
- The only close relative that reached people was abandoned. CB4211 completed an early-stage trial in 88 participants [8], after which its maker declared the preparation unsuitable for further development [9].
What it is
MOTS-c is a peptide of 16 amino acid building blocks, written as MRWQEMGYIFYPRKLR [10]. The body reads it off a short stretch of code hidden inside a gene of the mitochondria, the tiny power plants inside our cells. Its blueprint therefore sits in the DNA of the mitochondria and not, as with almost every other protein, in the DNA of the cell nucleus [1].
Changhan Lee, Pinchas Cohen and colleagues at the University of Southern California described it in March 2015 [1]. It has neither an official international drug name nor a brand name, because no product containing it has been approved anywhere. Material sold outside licensed manufacturing is labelled as being for research use only [11].
Quick facts
| Field | Value | Ref |
|---|---|---|
| Full name | Mitochondrial open reading frame of the 12S rRNA type-c | [1] |
| Class | Mitochondrial-derived peptide | [12] |
| Sequence | MRWQEMGYIFYPRKLR, 16 amino acids | [10] |
| Gene | MT-RNR1, mitochondrial 12S rRNA | [1] |
| Formula and mass | C101H152N28O22S2, 2,174.6 g/mol | [10] |
| Half-life | Not published | — |
| Route in studies | Intraperitoneal in mice; subcutaneous for the altered relative in people | [1], [8] |
| Status | Research chemical, approved nowhere | [3], [4] |
| First described | March 2015, University of Southern California | [1] |
| CAS registry number | 1627580-64-6 | [10] |
| PubChem CID | 146675088 | [10] |
| UNII | A5CV6JFB78 | [10] |
| Wikidata | Q56377357 | [13] |
How it works
Everything below comes from cells in a dish or from animals, and none of it has been shown in a person [12].
- Switching on the cell's energy sensor. The peptide is said to block a chain of chemical reactions built around folate. A substance called AICAR then piles up, and it can switch on the enzyme that acts as the cell's fuel gauge, AMP-activated protein kinase [1].
- A message to the cell nucleus. When cultured cells were starved of sugar, MOTS-c moved into the nucleus and settled next to genes that defend the cell against chemical stress [14].
- A second enzyme. One group reported that the peptide binds directly to another enzyme in skeletal muscle, casein kinase 2, and switches it on. That route would not involve the energy sensor at all [15].
- Fighting off germs. In the test tube the peptide attacked the outer envelope of bacteria including E. coli and the resistant staph germ MRSA, and human immune cells produced more of it when alerted by an immune messenger [16].
- Two findings point the other way. Peptides of this family made worn-out cells pour out more inflammatory signals [17], and in human connective tissue cells MOTS-c weakened the ability to repair damage [18].
Its closest relative is humanin, which comes from a different mitochondrial gene. The two peptides have different sequences and are measured separately [12].
What the studies found
Metabolism and glucose (mouse)
Animal data In two strains of mice, with 6 to 8 animals per group, a daily dose of 5 mg/kg helped the animals clear sugar from the blood and made their tissues respond better to insulin, measured with the standard laboratory test. On a fattening diet they neither grew obese nor became resistant to insulin [1]. This is the result the whole field is built on. No controlled study in humans has ever repeated it.
Animal data In a mouse strain that spontaneously develops autoimmune diabetes, a daily dose of 0.5 mg/kg from week 7 delayed the onset of the disease and left fewer immune cells attacking the insulin-producing tissue, in groups of 6 to 10 animals [19]. In mice whose ovaries had been removed, 5 mg/kg daily for 12 weeks slowed the loss of bone seen on fine-resolution scans [20]. In diabetic mice, 12 weeks of continuous delivery softened the changes in the heart muscle [21].
Exercise performance (mouse)
Animal data In mice aged 2, 12 and 22 months, in groups of 5 to 10, treadmill running improved at every age. Animals that started treatment at 23.5 months, roughly old age for a mouse, performed better and stayed healthy for longer [22]. No other group has published the same result.
Animal data Four to eight weeks of running on a wheel raised the amount of the animals' own MOTS-c in their muscles by about one and a half to five times (1.5- to 5-fold). In untrained mice a single dose of 15 mg/kg lengthened how long they could run by 12 percent and how far by 15 percent [23].
Untrained mice, one injection of 15 mg/kg into the abdominal cavity, compared with untreated animals. Doses per kilogram in mice cannot be carried over to people. Source [23].
Human observational data
Observational In ten young men who took no regular exercise, hard interval training raised the amount of MOTS-c both in samples of their muscle and in their blood [22]. Nobody was given anything. The study describes the body's own peptide reacting to training.
Observational In 10 lean people and 10 people with obesity, the amount of MOTS-c in the blood was much the same in both groups, 0.48 ± 0.16 against 0.52 ± 0.15 nanograms per millilitre, a difference well within chance (p = 0.60). It did move loosely in step with two standard measures of how well the body responds to insulin, the HOMA index (r = 0.53) and the Matsuda index (r = −0.46) [24].
A snapshot comparison of 10 lean people and 10 people with obesity, in which nobody was given anything. The gap is small enough to be chance (p = 0.60), and a higher level is not a better one. Source [24].
Observational Among 125 participants in China and 34 women in Europe, the 26 who had a cluster of metabolic problems together, known as metabolic syndrome, had more MOTS-c in their blood, not less. The level was 315 picograms per millilitre (315 ± 27) and it climbed in step with the fat in their livers [7]. The authors read this as the liver signalling distress rather than as a protective effect.
Observational Across different illnesses the levels point in different directions. They were lower in type 1 diabetes [19] and in an autoimmune thyroid disease, in obstructive sleep apnoea and in long-term kidney disease [25]. In 20 physically active adults the level moved in step with how high they could jump and how much muscle they carried, but not with their fitness measured as oxygen uptake [26].
CB4211, the analogue
Phase 1 (press release only) CB4211 is a chemically altered relative built by the company CohBar, not MOTS-c itself. An early-stage trial in three parts ran in 88 participants between July 2018 and April 2021 [8]. In the third part, 20 participants with obesity and fatty liver disease were given 25 mg a day for four weeks.
Phase 1 (press release only) The company reported that the safety goal was met and that nothing serious happened. Two liver enzymes whose levels rise when the liver is under strain fell by 21 and 28 percent, against a rise of 4 percent and a fall of 11 percent on placebo, and blood sugar fell by 6 percent against no change; each of those differences was large enough to count as more than chance (p < 0.05) [27]. None of it was checked by independent experts, and no results have been posted in the trial registry [8].
Third part of the early-stage trial, 20 people with obesity and fatty liver disease, over 4 weeks; every difference shown was large enough to count as more than chance (p < 0.05). CB4211 is an altered relative, not MOTS-c, and the figures come from a company press release that no independent expert ever checked. Source [27].
Phase 1 (press release only) The programme then stopped. The company stated that the preparation used in the trial was not suitable for further development [9]. CohBar merged with Morphogenesis to form TuHURA Biosciences, and the substance is not expected to be taken any further [28].
What is still unknown
- Whether it does anything in people. No verified trial has ever given the peptide itself to people, so there is nothing to weigh [2].
- What the body does with it. For the natural peptide, nobody has published how much of an injected dose reaches the blood, how long it lasts there, or how the effect changes with the amount given.
- Immune reactions and long-term safety. Whether the body forms antibodies against the peptide has never been examined in a verified trial [2].
- Particular groups of people. There are no data at all in pregnancy, in breastfeeding, in children, or in people with damaged livers or kidneys, and none on interactions with other medicines.
- Measuring it. The two laboratory methods used to measure MOTS-c in blood give widely different answers, so results from different studies cannot be laid side by side [6].
- The findings that cut the other way. The reports of worn-out cells becoming more inflammatory and of weakened tissue repair have never been resolved [17], [18].
Side effects and safety
No verified trial has ever given MOTS-c itself to people, so there is no list of side effects for the peptide. The United States Anti-Doping Agency puts it plainly: MOTS-c "is not approved by the Food and Drug Administration (FDA) for use in humans or in compounded medications" [11].
- Reactions where the needle went in. In the four-week part of the trial of the altered relative, the only complaints affecting more than one participant in ten were short-lived, mostly mild to moderate reactions at the injection site [27].
- Reactions that lingered earlier on. Those cleared up once the preparation was changed, and the replacement was later declared unsuitable for further development [9].
- Nothing serious happened. No serious side effects were reported in any of the 88 participants of that trial [27], [8].
- Reports from outside trials. People who said they had bought MOTS-c online reported a faster heartbeat, palpitations, sleeplessness, immune reactions and fever. Nobody checked whether the substance caused any of it, and nobody analysed what the products contained [11].
- Impurities and an unclear identity. The American regulator flagged possible immune reactions depending on how the substance is given, impurities in the material, and the fact that the substance itself has not been characterised well enough [3], [4].
The gaps outweigh the findings. No regulator has examined data on the purity or the chemical identity of material produced outside licensed manufacturing [3]. There is no approved package insert, nobody has weighed benefits against risks, and no system watches for harm.
Doses used in studies
The doses below are simply what the cited studies gave, listed so that the results can be understood. They are not advice on how to use anything.
| Study | Model | Dose | Route | Duration | Ref |
|---|---|---|---|---|---|
| Lee 2015 | CD-1 mice, normal diet | 5 mg/kg/day, split in two | Intraperitoneal | 4 days | [1] |
| Lee 2015 | C57BL/6 mice, normal and high-fat diet | 5 mg/kg/day | Intraperitoneal | 7 days to 8 weeks | [1] |
| Reynolds 2021 | CD-1 mice, 12 weeks old | 5 and 15 mg/kg/day | Intraperitoneal | 2 weeks | [22] |
| Reynolds 2021 | C57BL/6N mice, from 23.5 months | 15 mg/kg/day, three times weekly | Intraperitoneal | To end of life | [22] |
| Kong 2021 | NOD mice, autoimmune diabetes | 0.5 mg/kg/day | Intraperitoneal | Week 7 to week 18 or 30 | [19] |
| Kong 2021 | C57BL/6J mice, biodistribution | 10 mg/kg, tagged peptide, single dose | Intravenous | Single | [19] |
| Ming 2016 | Ovariectomised mice | 5 mg/kg/day | Not specified in the abstract | 12 weeks | [20] |
| Hyatt 2022 | Untrained mice | 15 mg/kg, single dose | Not specified in the abstract | Single | [23] |
| Wu 2025 | Diabetic mice, streptozotocin | Not quantified in the abstract | Subcutaneous minipump | 12 weeks | [21] |
| CohBar phase 1a/1b, part C | Humans, n = 20, analogue CB4211 | 25 mg daily | Subcutaneous | 4 weeks | [27], [8] |
Doses given per kilogram of mouse cannot be converted into a dose for a person. The one human dose in the table belongs to a different molecule, in a preparation that the company which built it later abandoned [9].
Development and approval status
Programme timeline
- 2015First description in Cell Metabolism, with the mouse metabolic resultsLee and Cohen, University of Southern California, ref [1]
- 2018-2021The analogue CB4211 runs through a phase 1a/1b trialn = 88, sponsor CohBar, no results posted, ref [8]
- 2019Plasma detection method for doping control validatedLimit of detection 100 pg/ml, ref [6]
- 2021Exercise and ageing results in mice published; MOTS-c named on the WADA listRefs [22], [29]
- 2023FDA places MOTS-c in category 2; CohBar drops the formulationRefs [4], [9]
- July 2026Advisory committee votes against the agency proposal to exclude MOTS-cAdvisory only, no agency decision followed, refs [30], [31]
- September 2026No final agency decision published; category 2 classification standsRef [4]
- 2015 — the first description appears in Cell Metabolism, with the results in mice and the idea that the peptide switches on the cell's energy sensor [1].
- 2018 to 2021 — the altered relative CB4211 goes through an early-stage trial in 88 participants [8].
- 2021 — the company announces the headline results by press release [27], and MOTS-c appears on the anti-doping list among substances that switch on that energy sensor [29].
- 2023 — the American regulator classes MOTS-c as carrying identified safety risks for pharmacy mixing [4], and CohBar drops its preparation [9].
- July 2026 — an advisory committee votes against the regulator's own proposal to keep MOTS-c off the list of substances pharmacies may mix [30], [31].
- September 2026 — the regulator has published no final decision, and the earlier classification still stands [4].
| Market | Status | Note | Ref |
|---|---|---|---|
| United States | Not approved | Compounding refused | [3], [4] |
| European Union | Not approved | No authorisation | — |
| Germany | Not approved | EU route | — |
| United Kingdom | Not approved | No authorisation | — |
| Australia | Not approved | Enforcement focus | [32] |
| Canada | Not approved | No database record | [33] |
| Switzerland | Not approved | Imports seized | [34] |
Every official register behind this table was queried on 6 September 2026.
The vote in July 2026 is the item most often misread. The committee voted in favour of putting MOTS-c on the list of substances pharmacies may mix, against the regulator's own proposal [3], [30]. Lawyers who followed the meeting summed it up by noting that "nothing has legally changed yet" [31].
Which peptides do hold an approval is covered under FDA-approved peptides. The wider legal picture is under are peptides legal.
Anti-doping
MOTS-c is banned at all times, in and out of competition, and it is written into the list by name rather than merely covered by a general clause. Section S4.4.1 of the 2026 prohibited list covers "activators of the AMP-activated protein kinase (AMPK), e.g. ... AICAR, mitochondrial open reading frame of the 12S rRNA-c (MOTS-c)" [5]. Substances in this group count as the stricter kind, where an athlete cannot easily argue that the finding was accidental [29], and UK Anti-Doping points out that the additions to this section in 2026 are further examples rather than new bans [35]. An exemption on medical grounds is barely conceivable, because there is no approved medical use to base one on [11]. The wider picture is at peptides banned in sport.
Compared with related peptides
| Peptide | Mechanism | Status | Strongest result in its own record | Half-life |
|---|---|---|---|---|
| MOTS-c | AMPK activation, proposed | Research chemical, approved nowhere | Diet-induced obesity prevented in mice, 5 mg/kg/day [1] | Not published |
| Humanin | Mitochondrial-derived peptide from MT-RNR2 | Research chemical, approved nowhere | Preclinical only; described before MOTS-c [12] | Not published |
| SS-31 | Binds cardiolipin in the mitochondrial membrane | Approved in the United States for Barth syndrome, 2025 | Knee extensor strength in 12 patients [36] | Not stated here |
| AICAR | AMPK activation | Named in the same WADA section | Not assessed on this page [5] | Not stated here |
What these four have in common is the part of the cell they aim at, the mitochondria, not any family resemblance between the molecules. Only SS-31 has ever been through a regulatory review, and that approval covers a single extremely rare disease in one country [36]. Humanin and MOTS-c come from different mitochondrial genes and are measured separately [12].
Being grouped with AICAR is a matter of anti-doping bookkeeping, not chemistry. Both are on the list because of a presumed effect on the same enzyme, and their structures have nothing in common [5].
Common misconceptions
- "MOTS-c is exercise in a syringe." The documented relationship runs the other way round: exercise raises the body's own MOTS-c in muscle and blood [22], [23]. Better performance after giving the peptide has been seen only in mice.
- "The CB4211 results count as clinical evidence for MOTS-c." CB4211 is a different molecule. Its results were never checked by independent experts, never entered in the registry, and the programme ended because of problems with the preparation itself [27], [8], [9].
- "A high MOTS-c level means good health." In people with a cluster of metabolic problems the level was raised, and it rose along with the fat in their livers [7]. In other conditions it was lower [19], [25]. A measured concentration is not a score for health.
- "The vote in July 2026 cleared MOTS-c." That committee only advises, it voted against the regulator's proposal, and the regulator has issued no decision since [3], [31].
- "Calling it a research chemical settles the legal question." Swiss authorities state that such labels change nothing once an item is advertised for use in people. In one operation in June 2026 they held back 23 of 46 inspected consignments [34].
- "The m.1382A>C variant is a longevity gene." A pooled analysis of 27,527 people found that the C version went with more type 2 diabetes in men [37]. The same variant has also been linked to the mix of fibre types in muscle [38].
Frequently asked questions
What is MOTS-c?
It is a peptide of 16 amino acid building blocks. Its blueprint sits in a short stretch of code inside a gene of the mitochondria, the power plants of our cells. Researchers at the University of Southern California described it in 2015. It belongs to a small family of peptides made by the mitochondria, alongside humanin.
Is MOTS-c approved anywhere?
No. No authority anywhere has approved it, for any condition, as checked on 6 September 2026. In the United States pharmacies are not allowed to mix it into preparations either.
Has anyone given MOTS-c to people in a trial?
No verified trial has ever given it to people. One entry in the American registry claims such a study, but its sponsor filed further entries whose own summaries describe them as mock, example or fictional records, so this page does not count it. Every study in people that can be verified simply measures the peptide the body makes itself, without giving anyone a dose.
Is MOTS-c banned in sport?
Yes, at all times, in and out of competition. It is named in section S4.4.1 of the anti-doping prohibited list among substances that switch on the cell's energy sensor, an enzyme called AMP-activated protein kinase. A validated blood test for it has existed since 2019.
Is a high MOTS-c level a good sign?
It cannot be read that way. In people with a cluster of metabolic problems the level was higher, not lower, and it rose along with the fat in their livers. In several other illnesses it was lower instead. On top of that, the laboratory methods disagree with each other, so values from different studies cannot be compared.
What is CB4211, the MOTS-c analogue?
CB4211 is a chemically altered relative built by the company CohBar, not MOTS-c itself. It went through an early-stage trial in 88 participants. The company then declared the preparation unsuitable for further development, and after a merger nobody took the programme any further.
What is known about MOTS-c safety in humans?
Very little. No verified trial has ever given the peptide itself to people, so nothing has been published on how the human body handles it, on what happens over long periods, or on whether the immune system reacts to it. What observations exist come from the altered relative, and they are mostly reactions at the injection site.
Does MOTS-c replace exercise?
Nothing supports that. The documented relationship runs the other way round: exercise raises the body's own MOTS-c in muscle and blood. Better performance after giving the peptide has been seen only in mice.
Why does this page list MOTS-c doses?
Those doses are simply facts about the studies, published in the cited papers and registry entries. Most of them were given to mice and measured per kilogram of animal, which cannot be converted into a dose for a person. They are listed so the studies can be understood, not as instructions.
Sources
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- Reduced circulating or tissue MOTS-c in disease cohorts: Journal of Clinical Medicine 2026;15(11):4002, Hashimoto's thyroiditis, PMID 42278864, DOI 10.3390/jcm15114002; Sleep and Biological Rhythms 2025, obstructive sleep apnoea, PMID 40538389, DOI 10.1007/s41105-025-00578-9; American Journal of Physiology: Renal Physiology 2019;317(5):F1122-F1131, chronic kidney disease, PMID 31432706, DOI 10.1152/ajprenal.00202.2019
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- Mintz (2026). FDA's advisory committee votes on peptides: what it does and doesn't do. Viewpoint, 29 July 2026. https://www.mintz.com/insights-center/viewpoints/2146/2026-07-29-fdas-advisory-committee-votes-peptides-what-it-does-and
- Therapeutic Goods Administration. TGA strengthens compliance focus on unapproved peptide products as part of evolving risk response. Retrieved 6 September 2026. https://www.tga.gov.au/news/media-releases/tga-strengthens-compliance-focus-unapproved-peptide-products-part-evolving-risk-response
- Health Canada. Drug Product Database, active ingredient query for MOTS-c; zero records. Queried 6 September 2026. https://health-products.canada.ca/api/drug/activeingredient/
- Federal Office for Customs and Border Security, Swissmedic and Swiss Sport Integrity (2026). Joint enforcement operation on peptides, statement of 22 June 2026. https://www.bazg.admin.ch/de/newnsb/aTkecQempbtqCwVzr61G_
- UK Anti-Doping. The 2026 Prohibited List: summary of changes. Retrieved 6 September 2026. https://www.ukad.org.uk/news/2026-prohibited-list-summary-changes
- US Food and Drug Administration (2025). Approval letter, NDA 215244, accelerated approval, elamipretide injection, 19 September 2025. https://www.accessdata.fda.gov/drugsatfda_docs/appletter/2025/215244Orig1s000ltr.pdf
- Zempo H, Kim SJ, Fuku N et al. (2021). A pro-diabetogenic mtDNA polymorphism in the mitochondrial-derived peptide, MOTS-c. Aging (Albany NY) 13(2):1692-1717. PMID 33468709. DOI 10.18632/aging.202529
- Kumagai H et al. (2022). The MOTS-c K14Q polymorphism in the mtDNA is associated with muscle fiber composition and muscular performance. Biochimica et Biophysica Acta General Subjects 1866(2):130048. PMID 34728329. DOI 10.1016/j.bbagen.2021.130048
Cite this page
Facts on this page were verified on 6 September 2026, and every register query behind the status table was run on that date. How pages in this register are compiled and graded is described under methodology; the full register is at peptides.
myPeptides Research & Editing. (2026). MOTS-c: what the studies show, status and safety. Version 1.0, 6 September 2026. myPeptides Peptide Register. Retrieved from https://mypep.app/peptides/mots-c
| Version | Date | Change |
|---|---|---|
| 1.0 | 2026-09-06 | Initial publication |
Last verified: 6 September 2026. Next review: on the registration of a verifiable trial in people, on any final FDA decision on the compounding list, or on any change in the anti-doping classification.