MOTS-c

Identity and specifications

MOTS-c was described from a short open reading frame within mitochondrial 12S rRNA. It is distinct from compounds that change NAD+ availability or act directly at incretin receptors.

What the selected studies examined

Lee and colleagues investigated cellular metabolism and mouse physiology. Reynolds and colleagues examined mouse experiments alongside human exercise-related measurements of endogenous MOTS-c.

Limitations and open questions

Measuring a naturally occurring peptide after exercise is different from administering it to humans. These publications do not establish longevity, exercise-performance or clinical benefits of ECL material.

These publications describe the materials and experimental conditions used by their authors. They do not establish the identity, composition, stability, safety or performance of East Coast Labs material. A reference list is a selected starting point, not a systematic review.

Interpreting a supplied material

Check the exact product and selected size, then read its documentation status. A laboratory report describes the named sample at the stated date; it does not establish a match to current stock. Read Testing & quality for the distinction between document authenticity and a documented lot relationship.

Handling, solvent compatibility and stability require material-specific information and a validated laboratory protocol. Published biological findings do not establish storage conditions or suitability for a particular experiment.

Primary references

• Lee et al. (2015). The mitochondrial-derived peptide MOTS-c promotes metabolic homeostasis and reduces obesity and insulin resistance.
• Reynolds et al. (2021). MOTS-c is an exercise-induced mitochondrial-encoded regulator of age-dependent physical decline and muscle homeostasis.