MOTS-c (Mitochondrial Peptide)

MOTS-c CAS Number and Chemical Identity

JMWritten & reviewed by Jack Muncaster · Founder, UK PeptidesLast reviewed 2026-08-232 cited sources

MOTS-c carries CAS Registry Number 1627580-64-6, PubChem CID 146675088 and UNII A5CV6JFB78, with molecular formula C101H152N28O22S2 and molecular weight 2,174.6 Da. These identifiers are what let a certificate of analysis be cross-referenced against published literature, since supplier naming varies considerably.

Key facts

CAS Registry Number
1627580-64-6
PubChem CID
146675088
UNII
A5CV6JFB78
Molecular formula
C101H152N28O22S2
Molecular weight
2,174.6 Da
Sequence
H-MRWQEMGYIFYPRKLR-OH
Common salt form
Trifluoroacetate (TFA)

Why identifiers matter more than names

Peptide naming is inconsistent across suppliers and literature — MOTS-c appears as MOTS-c, MOTSc, MOTS c and 'mitochondria-derived peptide MOTS-c'. A CAS number, a PubChem CID and a UNII are unambiguous. When checking whether a certificate of analysis describes the compound a paper studied, the identifier is the thing to compare, not the label.

The salt form and what it does to mass

Synthetic peptides purified by reverse-phase HPLC are usually isolated as trifluoroacetate salts, and PubChem lists MOTS-c in that form. TFA content is not inert accounting: it contributes to the total weight of the powder, so a vial's net peptide content is lower than its gross weight. A certificate that reports peptide content separately from gross weight is describing this correctly.

Research material referenced

MOTS-C 10mg — third-party HPLC tested

View — £24.99

Confirming identity analytically

Mass spectrometry is the identity check. The observed monoisotopic or average mass should correspond to the theoretical value for MRWQEMGYIFYPRKLR. Because the sequence carries two methionines, oxidised species appear at +16 and +32 Da, and their presence in a trace indicates oxidative degradation rather than a different compound.

Confirming purity analytically

Reverse-phase HPLC quantifies how much of the sample is the target peptide against everything else present — truncated sequences from incomplete coupling, deletion sequences, and oxidation products. A purity figure with no chromatogram behind it is an assertion. The trace is what makes it a measurement.

Extended research context

The MOTS-c (Mitochondrial Peptide) deep dive

Deep dive: why a peptide encoded in mitochondrial DNA is unusual

The human mitochondrial genome is 16,569 base pairs encoding 37 genes, and was considered fully characterised by the 1980s: thirteen respiratory-chain proteins, twenty-two transfer RNAs, two ribosomal RNAs. MOTS-c is encoded by a short open reading frame nested inside the 12S rRNA gene — sequence already annotated as doing something else, which is exactly why it went unnoticed. Humanin, found in 2001 inside the 16S rRNA gene, established that the genome held more than its annotation suggested; MOTS-c was found in 2015 by looking deliberately. The implication is that the mitochondrion encodes and releases signalling molecules of its own, rather than only executing instructions sent from the nucleus.

Deep dive: AMPK activation without touching AMPK

AMPK is normally activated when AMP and ADP bind its gamma subunit, making it a direct sensor of the AMP-to-ATP ratio. MOTS-c does not raise that ratio and does not bind the kinase. It inhibits the folate cycle, the one-carbon pathway feeding de novo purine biosynthesis, and the intermediate AICAR accumulates as a result. AICAR is an AMP mimetic — phosphorylated to ZMP, it binds the same regulatory site AMP occupies. So the peptide reaches a cytosolic energy sensor through one-carbon metabolism and a diffusible small molecule, which is a materially different architecture from a receptor-ligand interaction, and different again from metformin's inhibition of complex I.

Deep dive: reading a preclinical literature honestly

Roughly 250 indexed papers exist, and the overwhelming majority are cell and rodent studies. Where humans appear, the work is generally observational: measuring circulating concentrations and correlating them with age, fitness or metabolic state. The 2021 Nature Communications paper is the clearest example of the structure — the human arm measured MOTS-c before and after exercise, finding roughly a 12-fold rise in skeletal muscle against 1.6-fold in circulation, while the interventional work was done in mice. Two inferences the secondary literature routinely makes and the primary literature does not support: that a correlation between low concentrations and poor metabolic health establishes direction, and that a molecule which rises during exercise would reproduce exercise if administered.

Research applications

  • Study of mitochondrial-derived peptides and retrograde signalling
  • AMPK pathway research through non-canonical activation
  • One-carbon and folate-cycle metabolism models
  • Exercise physiology and mitochondrial bioenergetics research
  • Ageing biology and mitochondrial genome expression studies

Handling checklist

  • Store lyophilised material cold, dry and protected from light
  • Expect methionine oxidation as the primary degradation route (+16 Da per residue)
  • No reducing agent needed — the sequence contains no cysteine
  • Introduce diluent gently against the vial wall; swirl rather than shake
  • Aliquot to avoid repeated freeze-thaw cycles
  • Check mass spectrometry for +16 and +32 satellites before relying on a batch

Common research-handling mistakes

Learnt from thousands of researcher orders across our UK labs.

Reading exercise induction as proof that administration mimics exercise

Fix: The papers report that exercise raises MOTS-c. The reverse inference is not supported and is not claimed.

Treating human observational data as interventional evidence

Fix: Human work measures endogenous concentrations; administration studies were conducted in mice.

Assuming MOTS-c has a cell-surface receptor like humanin

Fix: No receptor is established. Its characterised activity is intracellular.

Storing reconstituted material as though it were as stable as the powder

Fix: Solution-phase material is subject to hydrolysis and oxidation; the lyophilised form is far more stable.

Overlooking WADA status in athlete-adjacent research

Fix: MOTS-c is on the prohibited list; this is relevant to any research context involving competitors.

Continue researching

Peer-reviewed guides, comparators and matched reference materials.

Related questions researchers ask

  • What is MOTS-c?
  • What does MOTS-c stand for?
  • How does MOTS-c activate AMPK?
  • What is a mitochondrial-derived peptide?
  • How is MOTS-c different from humanin?
  • Does exercise increase MOTS-c?

Frequently asked questions

What is the CAS number for MOTS-c?
1627580-64-6. PubChem CID 146675088 and UNII A5CV6JFB78 identify the same compound.
Why does the vial weight not equal the peptide content?
Synthetic peptides are typically trifluoroacetate salts, and the counter-ion contributes to gross weight. Net peptide content is lower and should be stated separately.
What mass should mass spectrometry show?
A mass corresponding to C101H152N28O22S2, approximately 2,174.6 Da. Peaks 16 or 32 Da higher indicate methionine oxidation.

Primary sources & clinical trials

Peer-reviewed research and registered trials from PubMed, ClinicalTrials.gov, PubChem, FDA and NIH. All links open in a new tab and point to the primary source, so every claim can be verified at origin.

JM

Written and reviewed by

Jack Muncaster · Founder, UK Peptides

Jack founded UK Peptides in Manchester after repeatedly receiving research compounds with missing or recycled paperwork. He is responsible for supplier selection, batch release decisions and the content published in this research library. Every article here is sourced to primary literature and every product page to a signed third-party certificate.

More MOTS-c (Mitochondrial Peptide) articles

Popular across the research hub

One flagship guide from every other research category — keep exploring.

Research use only. The information above is provided for scientific and educational reference. Compounds referenced are not approved for human use and are supplied for in vitro research or reference-material purposes only. No efficacy, safety, or therapeutic claims are made.