Clinical Overview

MOTS-C (Mitochondrial ORF of the 12S rRNA type-C) is a mitochondria-encoded regulatory peptide investigated for its role in cellular energy homeostasis and adaptive stress signaling. In research models, MOTS-C modulates metabolic gene programs and supports studies of nutrient sensing, insulin signaling, and exercise-like stress responses across skeletal muscle, hepatic, and adipose systems.

Mechanism of Action

Origin: Short ORF within mitochondrial 12S rRNA yields a 16-aa peptide implicated in mito-nuclear communication.
Pathways: Activation of AMPK and downstream effectors (e.g., ACC phosphorylation) → enhanced fatty-acid oxidation, glucose uptake, and mitochondrial efficiency in preclinical paradigms.
Gene Programs: Under metabolic stress, MOTS-C has been reported to translocate to the nucleus and influence stress-response transcriptional networks that coordinate substrate utilization and proteostasis.
Functional Notes: Research focuses on insulin signaling, GLUT4 trafficking, and attenuation of nutrient-excess stress signals without directly acting as a classic incretin or adrenergic agent.

Research Applications

AMPK-centered metabolic control • Substrate switching (lipid ↔ carbohydrate) • Skeletal-muscle performance and mitochondrial biogenesis assays • Hepatic glucose production studies • Adipocyte lipid handling • Mito-nuclear stress communication and redox homeostasis.

Purity & Quality Assurance

Revitalized Health peptides are produced under cGMP-aligned conditions with pharmaceutical-grade inputs. Each MOTS-C lot is confirmed at ≥99% purity by HPLC, with structure/identity verified via LC-MS/MS. Lots undergo appearance/solubility checks and microbial/endotoxin screening to research-grade specifications. Batch-level Certificates of Analysis document analytical methods, parameters, and results.

Storage & Stability

Store lyophilized vials at 2–8 °C, protected from light and moisture. Following reconstitution with bacteriostatic water, maintain at 2–8 °C and utilize within 20 days. Avoid repeated freeze–thaw cycles to preserve peptide integrity and receptor/target engagement fidelity.

Research Disclaimer

For laboratory research use only. Not intended for human consumption, therapeutic, or diagnostic application. Supplied exclusively to qualified professionals conducting controlled scientific investigations.

Formulated for research applications. Purity, identity, and lot analytics available per batch. Not medical advice.

Mechanism Strength
88/100
Mito-derived peptide • AMPK/FAO signaling
Metabolic/Performance Impact
85/100
↑ insulin sensitivity • ↑ exercise capacity (models)
Evidence Level
74/100
Robust preclinical + early human data
Safety & Tolerability
91/100
Common: mild ISR/headache; good short-term tolerability
PK / PD
Plasma t½ (peptide)
Onset (AMPK Activation)
Glucose Uptake / Insulin Sensitivity
Fatty-Acid Oxidation / Mito Programs
Mechanism & Testing

Identity: MOTS-c, a 16–amino acid mitochondria-encoded peptide (12S rRNA region), stress-responsive myo-/hepatokine.
Mode: Activates AMPK and downstream metabolic reprogramming (↑ glucose uptake, ↑ fatty-acid oxidation), interfaces with folate/purine biosynthesis nodes under energetic stress, and can translocate to the nucleus in models to influence adaptive gene expression. In animals, improves insulin sensitivity, exercise tolerance, and metabolic flexibility; early human work suggests exercise- and age-linked dynamics.
Analytics: Identity/purity by HPLC/LC-MS; peptide content & counter-ion profile; stability (accelerated/real-time). PD readouts: phospho-AMPK/ACC, glucose disposal (OGTT/IVGTT), indirect calorimetry (RER/RMR), VO₂ metrics, acyl-carnitine profiling, and transcript panels for oxidative metabolism. Monitoring: local injection site reactions, BP/HR, glucose trends; avoid disease treatment claims.

Educational, research-style content about a mitochondria-derived peptide. Not medical advice or a treatment claim.