Mitochondrial+ blend
SS-31 with TB-500 and MOTS-c (Mitochondrial+ blend vial)
Written by Aaron CuhaReviewed Sep 2026
Also known as: Mito plus, SS-31 TB-500 MOTS-c blend
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.
A big 55 mg vial with three peptides in it: 9 mg SS-31, 16 mg TB-500 and 30 mg MOTS-c. Do the division and the product flips. The one with a real drug trial behind it is the smallest part. The one with no human data is the biggest.
What people take it for
- Energy and stamina.
- Long term fatigue.
- Recovery from training.
What the trials actually showed
Nobody has tested the three together. SS-31 is 16.4 percent of the powder. Its phase 3 trial in a mitochondrial muscle disease did not show a real benefit in the group it studied. Some genetic subgroups did better on a walking test. MOTS-c is 54.5 percent of the powder and has no human trial at all. Its work is in fat mice. TB-500 is 29.1 percent and has no human study by any route. A drug testing lab found the product is a 7 amino acid piece of a 43 amino acid protein. And here is the odd bit. TB-500 is a healing peptide. It has nothing to do with mitochondria. No published paper explains why it is nearly a third of a mitochondria product. The math: mix 55 mg with 5 mL and every unit mark carries 60 micrograms of MOTS-c, 32 of TB-500 and 18 of SS-31.
What people report
Reports, not trial results
The good
- More energy and better exercise tolerance in the first weeks.
- Better recovery from training, which people credit to the healing peptide rather than the mitochondria ones.
The bad
- Nothing at all.
- Sore shot sites.
- Complaints about cost, since the part people want is the smallest slice.
- One plunger moves all three, and the three do not share a schedule.
Where these come from: Peptide forums and seller product pages. People talking, using unverified material, usually alongside other things.
My bottom line
You are buying this for the SS-31 and getting mostly something else. When a vial gives you least of the thing with the best evidence, that tells you who the vial was designed for.
An opinion, not a finding. I am a coach, not a doctor.
Overview
A 55 mg three-peptide vial, sold at 9 mg SS-31, 16 mg TB-500 and 30 mg MOTS-c. MOTS-c is more than half the powder and has no human trial; the SS-31 component with an actual phase 3 programme is the smallest share at 16.4%; and the third component is a repair peptide with no mitochondrial rationale at all.
This vial is the clearest case in the batch of the arithmetic changing what the product is.
The split is 9 mg SS-31, 16 mg TB-500 and 30 mg MOTS-c, 55 mg of powder. That is MOTS-c at 54.5%, TB-500 at 29.1% and SS-31 at 16.4%. Reconstitute with 5 mL and you have 11 mg/mL of total powder: 6 mg/mL of MOTS-c, 3.2 mg/mL of TB-500 and 1.8 mg/mL of SS-31. One unit on a 100 unit insulin syringe carries 60 micrograms of MOTS-c, 32 micrograms of TB-500 and 18 micrograms of SS-31.
So the component with a completed phase 3 development programme is the one you get least of, and the component with no human trial is the one you get most of. Whatever a buyer came for, by mass this is mostly a MOTS-c vial.
The third ingredient is the odd one. TB-500 is a repair peptide with no mitochondrial mechanism, characterised by a doping control laboratory as Ac-LKKTETQ, the seven amino acid acetylated fragment of thymosin beta 4 rather than the 43 amino acid protein. It has no human study by any route. Its presence in a product sold for mitochondrial function is unexplained by any published rationale, and it is nearly a third of the powder.
On the evidence: elamipretide's phase 3 trial in primary mitochondrial myopathy did not demonstrate a significant benefit in its overall population, with post hoc subgroup improvements in people carrying specific nuclear DNA variants. MOTS-c has mouse data only. TB-500 has none.
The schedules are also incompatible in the usual way. People running the repair fragment alone describe milligram loading doses then weekly maintenance; the two mitochondrial peptides are used on their own patterns. One plunger sets all three.
Mechanism of action
SS-31 binds cardiolipin in the inner mitochondrial membrane and is described as stabilising it. MOTS-c is a mitochondrially encoded peptide described as activating AMPK. The Ac-LKKTETQ fragment binds actin and has no described mitochondrial role. Two of the three components share a target organelle; the third does not, and no publication explains its inclusion.
Human evidence
The smallest component by mass is the only one with a clinical trial, and that trial did not meet its primary analysis. The largest component has no human data and the middle one has none either.
- The blend: no published study, no registered trial.
- SS-31, 16.4% of the vial: phase 3 trial did not demonstrate significant benefit overall, with post hoc subgroup improvements in specific genetic diagnoses.
- MOTS-c, 54.5% of the vial: no human trial. Mouse metabolomics only.
- TB-500, 29.1% of the vial: no human study by any route, and the material is a seven amino acid fragment of a 43 amino acid protein.
What this does not tell you: Nothing is known about what three peptides do together, and nothing in the published record explains why a repair fragment is in a mitochondrial product at nearly a third of its mass.
What it has been measured to do
Measured in people
Goals Mitochondrial+ blend has been measured for in a human being, most people first. Counts come from the study lines on this page and deliberately undercount.
- Getting strongerno headcount stated · 1 study
Measured in animals or cells, not yet in people
Real results that answer a different question from a trial. Where a human trial is missing on a compound nobody can patent, the reason is usually that no sponsor would ever recover the cost of running one. The record on this one is set out below.
- Blood sugar and insulin1 preclinical study
What people using it report
Uncontrolled and self-selected, so it cannot show that anything works. It is still the best guide on this page to what people actually do with Mitochondrial+ blend, what they expect, and what goes wrong. The full account, including the negative reports, is below.
34 of the 36 indexed goals have no study of any kind behind Mitochondrial+ blend
No trial, no animal work, no cell work on this page reports a result for these. That is an absence of evidence rather than evidence of absence, but it does mean anything you have been told about Mitochondrial+ blend and one of these did not come from a study cited here.
Reading the research record
The ratio is the finding on this page. A vial sold on the strength of a drug that reached phase 3 delivers that drug as the smallest of three components, and delivers the untested one as the largest. That pattern recurs across this whole category, and it is invisible unless someone does the division.
The presence of the repair fragment is the second thing. No published work connects Ac-LKKTETQ to mitochondrial function, and the fragment has no human study by any route. Adding it increases the mass, the price and the number of unknowns without adding a rationale anyone has written down.
The evidence, charted
Fig. 1a · evidence scale
1human study cited, participant count not stated
participants not stated
No participant total is drawn, because none of the human citations on this page gives one. Read the citations below for what each study measured.
Participant counts are read from the citation lines on this page. Where a line states no number, nothing is counted for it rather than estimated.
Fig. 1b · evidence mix
1 of 4 citations here is human work, the rest are not.
- Human · given to people125%
- Animal · given to animals125%
- In vitro · cells, tissue or a dish125%
- Review · summarises other work125%
Counted from the citation list on this page, typed as this page types it. It understates any literature larger than the sources we cite, and a review counts once however many studies it covers.
Fig. 2 · evidence over time
Evidence spans 4 distinct years, 2012 to 2025, counted from the citation list on this page.
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 jurisdictions shown. A jurisdiction's classification is a regulatory fact, not a verdict on the science; see Legal status below for the full text and any notes.
Fig. 4 · dose response
No human dose response curve exists
We draw this figure where the data supports it. For this compound in humans it does not, so the panel stays empty rather than borrowing an animal curve and implying it transfers.
Fig. 5 · molecular identity
- Modality
- Blend
- Molecular weight
- A mixture. MOTS-c is a 16 amino acid peptide, SS-31 a tetrapeptide, and the fragment sold as TB-500 about 889 Da.
- Half-life
- Stated in words, not a number
- Sequence length
- None on file
see the exact wording below
Half-life as stated on file: Not defined for the blend. Three components with different clearance and no pharmacokinetic study of the mixture.
No amino acid sequence is on file for Mitochondrial+ blend, which is expected: a blend is not built from residues.
Fig. 6 · what is in the vial
54.5%of a 55 mg Mitochondrial+ blend vial is MOTS-c
- MOTS-c30 mg54.5%
- TB-50016 mg29.1%
- SS-31 (elamipretide)9 mg16.4%
Label mass from a standard vial, not a dose, and not an assay. The ratio is fixed by the seller, so a draw that hits the amount you want of one component sets the amount of every other component with it. No study has tested this combination in any species.
Key studies & citations
- Human2024
Genotype-specific effects of elamipretide in patients with primary mitochondrial myopathy: a post hoc analysis of the MMPOWER-3 trial
MMPOWER-3 as published did not demonstrate a significant benefit of elamipretide in a genotypically diverse adult population with primary mitochondrial myopathy. Post hoc, the mitochondrial DNA replisome cohort improved 25.2 metres on the six-minute walk against 2.0 metres on placebo at p = 0.06, and the chronic progressive external ophthalmoplegia subset improved 37.3 metres against a 8.0 metre decline at p = 0.0024.
Orphanet Journal of Rare Diseases - Animal2019
The mitochondrial-derived peptide MOTS-c is a regulator of plasma metabolites and enhances insulin sensitivity
In diet-induced obese mice, MOTS-c reduced sphingolipid, monoacylglycerol and dicarboxylate metabolism pathways, which are upregulated in obesity and diabetes models, with the paper describing improved insulin sensitivity and increased beta oxidation. Mice. The senior author discloses a consulting and stockholding interest in a mitochondrial peptide company.
Physiological Reports - In vitro2012
Synthesis and characterization of the N-terminal acetylated 17-23 fragment of thymosin beta 4 identified in TB-500, a product suspected to possess doping potential
A doping control laboratory ran the TB-500 product through high performance liquid chromatography and high resolution mass spectrometry and identified the contents as Ac-LKKTETQ, the acetylated 17 to 23 fragment of thymosin beta 4. Seven amino acids, not the 43 amino acid protein the marketing names.
Drug Testing and Analysis - Review2025
Emerging Use of BPC-157 in Orthopaedic Sports Medicine: A Systematic Review
544 articles screened, 36 included, of which 35 were preclinical and one was clinical. That single clinical study was a retrospective series in which 7 of 12 patients reported relief beyond six months after intra-articular BPC-157 for unspecified chronic knee pain. The review puts the half-life at under 30 minutes.
HSS Journal
What users report
Self-reported experiences, not evidence. Nothing below was measured under controlled conditions, and reports like these cannot separate a real effect from placebo, from the training or diet change that accompanied it, or from what the product actually contained. They are here because knowing what people describe, including what goes wrong, is worth reading alongside the studies.
- More energy and better exercise tolerance in the first weeks.
- Improved recovery from training, which people attribute to the repair fragment rather than the mitochondrial components.
- Nothing at all.
- Injection site reactions.
- Complaints about cost, since the vial is large by peptide standards and the component people want is the smallest share of it.
Sources: Peptide forums and vendor product pages. Uncontrolled self-reports from people using unverified material, frequently alongside other compounds.
Frequently asked questions
What fraction of the vial is each component?
On the 55 mg vial, MOTS-c is 54.5%, TB-500 is 29.1% and SS-31 is 16.4%. Reconstituted with 5 mL, one unit carries 60 micrograms of MOTS-c, 32 micrograms of TB-500 and 18 micrograms of SS-31.
Why is a repair peptide in a mitochondrial blend?
No published rationale explains it. The fragment sold as TB-500 has no described mitochondrial mechanism and no human study by any route, and it is nearly a third of the powder.
Which component has the best evidence?
SS-31, which is elamipretide, and it is the smallest share of the vial. Its phase 3 trial did not demonstrate a significant benefit in its overall population, with post hoc improvements in specific genetic subgroups.
Has the three-way combination been studied?
No, in any species.
Can I adjust one component?
No. One plunger moves all three, and their single-agent schedules are not compatible with each other.