MOTS-c vs SLU-PP-332
MOTS-c (Mitochondrial-derived peptide) and SLU-PP-332 (Small-molecule ERR agonist (exercise mimetic)) are documented as co-studied in the PeptiDex library. This page puts the two entries side by side on class, molecular weight, half-life, origin, mechanism and studied research areas — every value taken from the entry it belongs to.
Why these two are co-studied
Cross-referenced for research context — not a usage or combination recommendation.
At a glance
| Attribute | MOTS-c | SLU-PP-332 |
|---|---|---|
| Compound class | Mitochondrial-derived peptide | Small-molecule ERR agonist (exercise mimetic) |
| Research category | Metabolic & Mitochondrial | Metabolic & Mitochondrial |
| Length (amino acids) | 16 amino acids | Not documented |
| Molecular weight | ~2174 g/mol | ~290.3 g/mol (C18H14N2O2, CAS 303760-60-3) |
| Half-life | Not documented | Not documented |
| Origin | MOTS-c (Mitochondrial ORF of the 12S rRNA type-c) is a 16-amino-acid mitochondrial-derived peptide encoded within the MT-RNR1 (12S rRNA) region of mitochondrial DNA. It was described in 2015 and is one of a small family of mitochondrial-derived peptides. | SLU-PP-332 is a synthetic small-molecule compound reported by academic researchers (Saint Louis University) as an agonist of the estrogen-related receptors (ERRs). It is not a peptide. It has been studied as a candidate exercise-mimetic research compound. |
“Not documented” means the PeptiDex entry records no value for that field. Nothing on this page is estimated, and no figure is carried over from one compound to the other.
How MOTS-c works
MOTS-c is reported to regulate metabolic homeostasis, in part via activation of the AMPK pathway and modulation of the folate-methionine cycle and de novo purine biosynthesis. It has been described to translocate to the nucleus under metabolic stress and influence stress-response gene expression. Preclinical work links it to improved insulin sensitivity and glucose uptake in skeletal muscle; it is also described as exercise-responsive.
How SLU-PP-332 works
SLU-PP-332 is reported to act as a pan-agonist of the estrogen-related receptors (ERRalpha, ERRbeta, ERRgamma), nuclear receptors that regulate mitochondrial biogenesis, oxidative metabolism, and energy expenditure. In preclinical models, ERR activation has been associated with increased mitochondrial activity, fatty-acid oxidation, and endurance-type metabolic adaptations, prompting its description as an exercise mimetic.
Mechanistic descriptions reflect published research-literature understanding and are quoted from each compound's own entry. Much peptide research is preclinical (in-vitro or animal-model); mechanism in humans may differ and is not established for many compounds.
Where each one appears in the literature
The research contexts each entry documents. Listing a research area is not a claim of efficacy or a therapeutic indication, and the two lists are not scored against each other.
MOTS-c
SLU-PP-332
What sets each apart
MOTS-c
Unlike the GH-derived fragments here, MOTS-c is endogenously encoded in the mitochondrial genome and acts as a broad metabolic regulator rather than a targeted lipolytic fragment.
SLU-PP-332
Unlike the peptides here, SLU-PP-332 is a nuclear-receptor-targeting small molecule; unlike AICAR (which activates AMPK), it works upstream at the ERR transcription-factor level.
Frequently asked questions
What is MOTS-c and where does it come from?
MOTS-c (Mitochondrial Open-reading-frame of the Twelve-S rRNA type-c) is a 16-amino-acid mitochondrial-derived peptide (MDP) encoded within the 12S rRNA region of mitochondrial DNA, rather than by the nuclear genome. First described in 2015, it is studied as a regulator of metabolic homeostasis. Its sequence and MDP origin make it structurally distinct from most catalog peptides.
What is MOTS-c studied for?
MOTS-c is studied in models of metabolic homeostasis, insulin sensitivity, exercise capacity, and aging. Research reported that MOTS-c levels rise with exercise and that exogenous MOTS-c improved glucose tolerance, insulin sensitivity, and running endurance in aged mice. It is thought to act partly via AMPK-linked metabolic signaling.
How is MOTS-c thought to work mechanistically?
MOTS-c is reported to translocate to the nucleus under metabolic stress and influence adaptive gene-expression programs, and it engages the AMPK pathway and folate/one-carbon metabolism to promote glucose uptake and fatty-acid oxidation. This positions it as a signaling peptide linking mitochondrial state to whole-body metabolism in preclinical models.
Is the catalog name 'SLU-PP-322' correct?
The correct compound name is SLU-PP-332 (the '322' spelling is a common transposition error). SLU-PP-332 is a synthetic pan-ERR (estrogen-related receptor) agonist studied as an exercise-mimetic and metabolic compound. All information here refers to SLU-PP-332.
Is SLU-PP-332 a peptide?
No. SLU-PP-332 is a small molecule, not a peptide. Its molecular formula is C18H14N2O2 (MW ~290.3, CAS 303760-60-3), and it has no amino-acid sequence. It is grouped with metabolic peptides in catalogs because of its fat-oxidation/exercise-mimetic research context.
What is the mechanism of SLU-PP-332?
SLU-PP-332 is a pan-agonist of the estrogen-related receptors, with reported EC50 values around 98 nM (ERRalpha), 230 nM (ERRbeta), and 430 nM (ERRgamma), i.e. most potent at ERRalpha. Activating ERRalpha upregulates PGC-1alpha, driving mitochondrial biogenesis and fatty-acid oxidation, which is why it is described as an exercise mimetic.
Answers are the ones published on each compound's own PeptiDex entry. They are educational summaries of research-literature context and are not medical advice.