◇ Compound Reference
Mitochondrial-Derived Peptide · 10mg
Mitochondrial-encoded peptide regulating systemic metabolic signaling, insulin sensitivity, and exercise capacity at the cellular level.
Mitochondrial-Derived Peptide · 10mg per vial · dispensed after a physician review.
Every 100 units are drawn from one lot and tested once. The certificate below is the one that applies to this batch - when it closes, the next opens with a new lot and a new certificate.
MOTS-c is a 16-amino-acid mitochondrial-derived peptide encoded within the mitochondrial 12S rRNA. It functions as a metabolic regulator that travels from the mitochondrion to the nucleus to modulate gene expression in response to metabolic stress.
Activates AMPK pathway, regulates insulin sensitivity, and modulates mitochondrial biogenesis. Acts as a metabolic exercise mimetic with broad effects on glucose homeostasis and lipid metabolism.
Cellular / mitochondrial - SS-31, MOTS-c, Epithalon, NAD+, V-04
These protocols target cellular energy, mitochondrial function, and markers of biological aging. Monitoring here is less about week-to-week safety and more about confirming the protocol is moving the deeper markers it is meant to.
Incremental approach. V-04 is introduced in phases (structural support first, then signaling, then a short telomere overlay) at conservative doses. Re-testing at the 6-month mark is how progress is judged.
Educational only - not medical advice or a dosing instruction. Your physician orders the tests, sets your dose, interprets results, and decides if a protocol is right for you. See the Informed Consent & Disclaimer for full terms.
| Class | Mitochondrial-derived peptide (16 aa) |
| Studied mechanism | Metabolic regulation, AMPK-pathway activity in preclinical models |
| Human pharmacokinetics | Not well-characterised in human literature |
| Evidence base | Predominantly preclinical; early human interest |
| Form | Lyophilized powder, reconstituted under clinical protocol |
| Regulatory status | Not an approved therapy; physician-supervised use only |
Foundational discovery paper from the Cohen lab at USC. Identified MOTS-c as a mitochondrially-encoded peptide that activates AMPK signalling, improves insulin sensitivity in high-fat-diet mouse models, and reduces diet-induced obesity. Established MOTS-c as a metabolic-homeostasis regulator and the first widely-studied mitochondrially-derived peptide (MDP). Findings are preclinical (mouse); controlled human outcome trials for exogenous MOTS-c administration remain pending.
View on publisher ↗In mice, late-life intermittent MOTS-c treatment (initiated at 23.5 months) increased physical capacity and healthspan markers. In humans, the authors demonstrated that exercise induces endogenous MOTS-c expression in skeletal muscle and circulation - supporting MOTS-c as an exercise-mimetic mitokine. The healthspan extension data are preclinical (mouse); the human findings are correlative (exercise induces endogenous MOTS-c), not yet outcome trials for exogenous administration.
View on publisher ↗Small human study (n=49) examining endogenous MOTS-c response to combined aerobic and resistance exercise across two ethnic groups. Post-exercise MOTS-c levels rose significantly in non-Hispanic White breast cancer survivors but not in Hispanic survivors, suggesting that endogenous MOTS-c response to exercise may be modulated by ethnic-specific mtDNA variation. Important context: this is endogenous-expression research, not a trial of exogenous MOTS-c therapy. Underlines that mechanism-to-clinic translation for exogenous MOTS-c administration is still pending.
View on publisher ↗MOTS-c is verified and lot-tested, dispensed following a Biological Audit. The Audit is complimentary for the Batch 001 cohort.
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