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MOTS-c

Findings, possible implications, and reported experiences.

About MOTS-c

PeptideMitochondria

Primary research area: Mitochondria · metabolism & aging
Regulatory status: Investigational / research only
Evidence level: Preclinical · early translational
Primary mechanism: Mitochondrial-derived peptide linked to AMPK and metabolic signaling

Reference profile available · Coverage varies by section

Also known as MOTSc

MOTS-c is a 16-amino-acid peptide encoded by mitochondrial DNA. It is investigated in metabolic, exercise and aging biology, including pathways related to cellular energy sensing. [1][2]

What has been observed?

Selected source-linked reading notes, not the complete literature or a pooled conclusion.

Animal · Reading scope not recorded

Can muscle preservation occur without preventing overall weight loss?

In a C26 cancer-cachexia mouse model, MOTS-c preserved quadriceps mass relative to vehicle, without preventing overall body-weight loss.

Limits: A cancer-cachexia mouse model does not predict muscle gain in healthy people or effects during GLP-1 treatment.

Open primary source · Read interpretation separately

Explore outcomes for this compound

Uses & research: The cited foundational study reported metabolic effects in mice and described cell-level signaling. Human observations do not equal a trial of injected MOTS-c, and no approved therapeutic use is established here. [1][2]
Known half-life: No source-verified value in this profile yet. A treatment schedule or duration of an effect is not a drug half-life.
Half-life describes how quickly the measured drug concentration falls by half. It does not set a dosing interval.
Evidence & important limits: The available evidence does not establish a human half-life, a safe clinical formulation, or human effectiveness for weight, muscle, endurance or longevity outcomes. Mechanistic and animal findings require direct human testing. [1][2]

Safety & evidence boundaries

Source-specific information, not a personal safety clearance or monitoring plan.

The available evidence does not establish a human half-life, a safe clinical formulation, or human effectiveness for weight, muscle, endurance or longevity outcomes. Mechanistic and animal findings require direct human testing.

Lee et al., MOTS-c and metabolic homeostasis (2015)Cell Metabolism full article

Explore safety questions by system

These are literature filters, not claims that this compound causes each effect. A keyword match is not a confirmed adverse reaction.

Heart, blood pressure & lipids Liver injury Kidney function Glucose effects Reproductive & endocrine effects Mood & sleep Adverse effects & interactions

Interactions, rare harms, long-term effects and reversibility require separate evidence. Do not infer they are absent when the sources here do not address them.

Identity, names & formulations

Canonical compound: MOTS-c · motsc

Searchable names: MOTSc

Names share a parent research page. Different esters, salts, routes and brands are not assumed to have the same half-life, indication or exposure.

Combination evidence stays attached to the studied combination. It is not automatically assigned to each ingredient.

Understand the evidence types

Read the model and design first, then the population, outcome and limitations. These categories describe evidence, not a best-compound ranking.

Randomized human trials: Compare assigned interventions. Randomization does not by itself establish low bias or relevance to every population.
Controlled human studies: Use a comparison group; allocation and confounding still matter.
Prospective human research: Follows participants forward. It may be observational or interventional, so this is not a separate quality grade.
Observational human research: Describes associations. Confounding can explain differences.
Case reports and series: Useful for unusual events and safety signals, not reliable rates or effect sizes.
Animal research: Can test biology and function in a living model. Human exposure, benefit and safety remain separate questions.
Cell and tissue research: Tests responses in a preparation, including human-derived cells. It is not a human participant trial.
Mechanistic and computational evidence: Helps explain or predict a pathway; predictions need experimental and clinical testing.
Anecdotal reports: Self-reported experiences can generate questions. Product identity, selection bias and other interventions may be uncontrolled.

Systematic reviews synthesize studies and depend on their quality. Preprint status and abstract versus full-paper reading are separate labels. Citation popularity measures attention, not reliability. A study summary is not a formal quality appraisal.

Sources for this profile

1. Lee et al., MOTS-c and metabolic homeostasis (2015) Primary study · cell and mouse metabolic models
2. Cell Metabolism full article Full article · foundational MOTS-c study

Reference facts checked 2026-09-16. Source scope is listed above; this is not a formal quality appraisal. See each label for full prescribing information.

Browse all studies

Research outcomeResearch model

Study model describes the source. Confidence depends on methods, replication, population and outcome.

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