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Mitochondrial-derived peptide encoded within the mitochondrial genome itself. Discovered in 2015. Modulates metabolic homeostasis, exercise capacity, and insulin sensitivity through pathways that bridge mitochondrial and nuclear function — distinct from most other peptide therapeutics.

At a glance:

  • 2 mg/mL · 10 mg per 5mL vial
  • 99.0% HPLC
  • Subcutaneous bacteriostatic water — pre-mixed
  • ~ 2 hr plasma
$350 USD / vial
  • Acetate buffer — q.s.
  • Mannitol — 5 mg / vial
  • MOTS-C — 10 mg per 5mL vial

Precision inside a bottle.

Acetate buffer

Maintains reconstituted solution at pH 5.0–5.5 — the range in which the peptide is most chemically stable. Degrades to water and acetate; renally cleared.

pH 5.0 – 5.5q.s.

Mannitol

USP-grade bulking agent used during lyophilization. Produces a uniform cake, prevents peptide collapse during reconstitution, and has no pharmacologic activity at the doses used.

Pharmacopeial5 mg / vial

MOTS-C

16-amino-acid peptide encoded within the mitochondrial 12S rRNA gene — making it one of the few human peptides not encoded in the nuclear genome. Discovered in 2015 and characterized as an exercise-mimetic and metabolic regulator. Acts primarily through AMPK pathway activation and direct nuclear gene expression effects during metabolic stress.

MW · 2174.5 g/mol10 mg per 5mL vial
Vegan
Transparent ingredients
Physician-backed Rx certification
Scientifically bonded peptides
Personalized formulations
Board-certified accreditation
Science-backed bio-hacking
Third-party tested

MOTS-C in action.

MOTS-C (Mitochondrial-derived peptide encoded by ORF of the 12S rRNA-c) is one of the most recently discovered peptides in clinical practice — first characterized by Lee et al. in 2015. It's encoded within the mitochondrial genome itself rather than the nuclear genome, making it part of an emerging class of mitochondrial-derived peptides (MDPs) that bridge mitochondrial signaling with broader cellular and metabolic pathways.

Functionally, MOTS-C modulates AMPK signaling — the cellular energy sensor that responds to low energy states by promoting glucose uptake, fatty acid oxidation, and mitochondrial biogenesis. The peptide also translocates to the nucleus during metabolic stress, directly modulating gene expression involved in metabolic adaptation. These dual mitochondrial-nuclear signaling effects are unusual and continue to be characterized in research.

Clinical evidence is preclinical-heavy with growing human pilot studies. The peptide is most often used for metabolic optimization, exercise performance support, insulin sensitivity, and age-related metabolic decline. The compound provided here is not FDA-approved. Elite HRT's clinicians determine appropriateness based on individual patient assessment.

01

AMPK pathway activation

MOTS-C activates AMP-activated protein kinase (AMPK) — the central cellular energy sensor that responds to low ATP states. AMPK activation promotes glucose uptake into cells, increases fatty acid oxidation, and stimulates mitochondrial biogenesis. The same pathway is activated by exercise and metformin, leading to MOTS-C being characterized as an "exercise mimetic."

02

Insulin sensitivity & glucose homeostasis

Through AMPK and downstream effects, MOTS-C improves insulin sensitivity in skeletal muscle and adipose tissue in animal models. Effects on glucose disposal and post-prandial glucose response have been documented in preclinical studies and small pilot human trials. Most relevant in metabolic syndrome contexts and age-related insulin resistance.

03

Exercise capacity & mitochondrial biogenesis

MOTS-C levels naturally increase with exercise. Supplementing the peptide may amplify exercise-induced mitochondrial biogenesis and improve metabolic flexibility. Animal studies show enhanced exercise capacity, improved metabolic response to exercise, and increased mitochondrial density in muscle tissue with MOTS-C administration.

04

Nuclear gene expression effects

Distinct from most peptides, MOTS-C translocates to the cell nucleus during metabolic stress and directly affects gene expression — particularly genes involved in metabolic adaptation. This dual mitochondrial-nuclear signaling role is unusual among peptides and is an active area of research. The mechanism explains some of MOTS-C's broader systemic metabolic effects.

MOTS-C

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