PubMed
MOTS-c is an ancient mitochondrial-encoded regulator of metabolic homeostasis
Lee et al., 2015
Mitochondrial ORF of 12S rRNA type-c
MOTS-c is a 16-amino acid mitochondria-derived peptide (MDP) encoded within the 12S rRNA region of the mitochondrial genome — one of only a few proteins known to be encoded by mitochondrial DNA. Early human studies and animal research show it activates AMPK signaling, improves insulin sensitivity, enhances exercise capacity, and reduces age-related metabolic decline. Research only.
Overall check-ins
Trackers & reports
Overview
MOTS-c is a 16-amino acid mitochondria-derived peptide (MDP) encoded within the 12S rRNA region of the mitochondrial genome — one of only a few proteins known to be encoded by mitochondrial DNA. Early human studies and animal research show it activates AMPK signaling, improves insulin sensitivity, enhances exercise capacity, and reduces age-related metabolic decline. Research only.
Community
From check-in ratings — separate from side effects logged below. Side effects are logged separately from overall experience. A favorable check-in can still include nausea, fatigue, or injection-site reactions.
Favorable 17% · Mixed 2% · Unfavorable overall 81%
Benefits users selected when logging a favorable or mixed check-in.
Side effects are logged separately from overall experience. A favorable check-in can still include nausea, fatigue, or injection-site reactions.
Median bucket: 2–3 mg · Most common: 5+ mg
Reports span 0.01 to ≥ 5 mg (open-ended top bucket)
Anonymized self-reports from PeptIQ users — not prescribing guidance. Buckets group similar logged amounts; open-ended top buckets mean “at least” that dose.
Among repeat reporters, 56% said they felt similar to their last entry, 31% more positive, and 13% more negative.
Overall, repeat reporters leaned more positive than their previous entry.
Median gap between entries: 44 days · Based on 45 repeat reporters
Research
PubMed
Lee et al., 2015
PubMed
Reynolds et al., 2021
PubMed
Kim et al., 2019
ClinicalTrials.gov
ClinicalTrials.gov, 2024
PubMed
Zheng et al., 2023
PubMed
Lee et al., 2016
Tools
More ways to learn about MOTS-c from observational PeptIQ data.
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This page summarizes 111 anonymized self-reports from PeptIQ users who track MOTS-c, including commonly reported effects and co-tracked peptides. These are observational patterns, not clinical outcomes.
PeptIQ separates overall check-in ratings (favorable, mixed, or unfavorable) from logged side effects like nausea or fatigue. Users often report benefits and side effects in the same check-in — a high experience score does not mean zero side effects were noted.
6 sources are linked on this page, including PubMed articles, clinical trial registries, and FDA labels where applicable. Citations describe published research — not recommendations.
This wiki does not assess safety or recommend use. MOTS-c is listed as Research Only. Consult a licensed clinician for personal medical decisions.
Research, primarily in animal models, suggests MOTS-c may have a wide range of therapeutic potentials due to its ability to promote angiogenesis (formation of new blood vessels), stimulate collagen synthesis, and modulate inflammatory responses.
SourceMOTS-c is not approved by the FDA for any human use. There is no legal basis for selling it as a drug, food, or dietary supplement in the United States. The FDA has classified MOTS-c as a Category 2 bulk drug substance, which explicitly prohibits licensed compounding pharmacies from using it in compounded medications.
SourceThe safety and effectiveness of MOTS-c have not been thoroughly evaluated in humans through rigorous clinical trials. This lack of human data means that safe dosages, short-term side effects, and long-term health consequences are largely unknown.
SourceWhile there are over 200 published studies on MOTS-c, the vast majority are animal or in vitro (cell) studies. These preclinical studies consistently show positive results across various tissue types. However, there is a significant lack of comprehensive human clinical trial data.
Source