Valtrax Research is opening — leave your email and we'll ping you the moment the first compounds are listed.
Your cart is empty
16-mer · mitochondrial-encoded peptide
A 16-residue peptide encoded inside the mitochondrial 12S rRNA gene rather than the nuclear genome. Supplied as a lyophilized powder for research purposes only.
Catalog opens shortly. Leave your address and we will ping you the moment this compound is orderable.
Tested lot by lot at ≥99% purity. The Janoshik certificate for your lot is emailed with the order.
Everything Valtrax Research ships is bench material for in-vitro work. None of it is a drug, a supplement, a cosmetic, or a medical device, and none of it is intended for human or animal use, ingestion, or administration. Placing an order is your confirmation that you are a qualified researcher buying for lawful research, under every Canadian law and regulation that applies to you.
A 16-residue peptide whose coding sequence sits not in the nuclear genome but inside the mitochondrial 12S rRNA gene — an open reading frame the organelle carries itself. That address is the whole point: MOTS-c is something the mitochondrion encodes, which casts the organelle as a source of signals, not only a generator of ATP.
Where it goes under stress is the rest of the point. Metabolic pressure sends the peptide to the nucleus, where it alters gene expression — which is why the bench work converges on AMPK, the folate–methionine cycle, and the cell’s adaptive metabolic program.
The findings group into three. The founding cluster sits on AMPK and the folate–methionine–purine axis, with insulin sensitivity and obesity endpoints attached. A mechanistic cluster tracks stress-triggered movement into the nucleus and the transcriptional shift that follows. A physiological cluster, from the exercise literature, measures circulating MOTS-c against age-related physical decline.
The founding result is Lee’s 2015 paper, which linked MOTS-c to AMPK activation, the folate–methionine–purine cycle, and recovered insulin sensitivity in metabolically stressed tissue. What made it notable was the source: a bioactive peptide written into mitochondrial DNA, acting back on the metabolism of the whole cell.
Reynolds widened the picture toward physiology. Circulating MOTS-c was found to climb with physical activity and to fall along with age-related muscle decline — pulling the readouts out of pure metabolism and into exercise and aging.
The peptide entered the record in 2015, when scans of the mitochondrial genome for small open reading frames turned up a coding sequence inside the 12S rRNA gene. It landed alongside humanin in what was then a fresh category — the mitochondrial-derived peptides.
The finding carried a larger claim than a single molecule. It recast the mitochondrion as a signaling hub that answers back to the nucleus, and the studies that followed traced that exchange across metabolism, the stress response, and aging.
Lee, C. et al. (2015). The mitochondrial-derived peptide MOTS-c promotes metabolic homeostasis and reduces obesity and insulin resistance.
PubMedKim, S.J. et al. (2017). Mitochondrially derived peptides as novel regulators of metabolism.
PubMedReynolds, J.C. et al. (2021). MOTS-c is an exercise-induced mitochondrial-encoded regulator of age-dependent physical decline and muscle homeostasis.
PubMedCobb, L.J. et al. (2016). Naturally occurring mitochondrial-derived peptides are age-dependent regulators of apoptosis, insulin sensitivity, and inflammatory markers. Aging (Albany NY) 8(4):796–809.
PubMedMerry, T.L. et al. (2020). Mitochondrial-derived peptides in energy metabolism.
PubMedThe certificate for your lot reports measured identity, purity, and net content, and is sent by email.
Janoshik Analytical, a laboratory Valtrax does not own, runs the testing — identity by mass spectrometry, purity by RP-HPLC at ≥99%. The certificate covering the lot you receive is also emailed with your order.
Same Shelf