Informational only. Not medical advice.INFORMATIONAL PLATFORM ONLY — NOT MEDICAL ADVICE, DIAGNOSIS, OR TREATMENT
Informational only. Not medical advice.INFORMATIONAL PLATFORM ONLY — NOT MEDICAL ADVICE, DIAGNOSIS, OR TREATMENT
Head-to-head comparison of Humanin and MOTS-c — mechanism, dosing, side effects, legal status, and pricing.
Humanin is a mitochondrial-derived peptide encoded within the 16S ribosomal RNA gene. It was discovered through its ability to protect neurons from Alzheimer's disease-related toxicity and is studied for neuroprotection, metabolic regulation, and anti-aging applications.
MOTS-c is a 16-amino-acid mitochondrial-derived peptide (MDP) encoded within the mitochondrial 12S rRNA, discovered by Lee and Cohen at USC in 2015 (sequence: MRWQEMGYIFYPRKLR). It is an investigational, research-only peptide studied as a metabolic regulator; it has not been approved by the FDA for any indication.
Humanin
MOTS-c
Category
Legal Status
Mechanism
Dose Range
Route
Frequency
COA-verified vendors · trust score ≥70 required · single-vial price — bulk/bundle deals may be lower
Humanin
MOTS-c
COA corpus from Disclosed Labs — independently tested batches only.
Humanin
3
COAs
99.5%
Avg purity
2
Labs
MOTS-c
193
COAs
99.5%
Avg purity
16
Labs
Hashimoto et al. (2001) discovered humanin through functional screening for neuroprotective factors against amyloid-beta toxicity. Yen et al. characterized the S14G-Humanin analog (HNG) as 1000x more potent. Muzumdar et al. demonstrated that humanin improves insulin sensitivity and reduces visceral fat in animal models. Circulating humanin levels decline with age and correlate inversely with Alzheimer's biomarkers. Cohen et al. showed humanin's role in the GH/IGF-1 axis through IGFBP-3 interaction. No human clinical trials have been conducted — all dosing is extrapolated from preclinical data.
Key references
Lee et al. (Cell Metabolism, 2015; PMID 25738459) identified MOTS-c and showed that exogenous administration in mice prevented diet-induced obesity and insulin resistance via AMPK activation in skeletal muscle. Kim et al. (Cell Metabolism, 2018; PMID 29983246) demonstrated that MOTS-c translocates to the nucleus under metabolic stress and regulates antioxidant response element (ARE) genes. Reynolds et al. (Nature Communications, 2021; PMID 33473109) reported that exercise induces MOTS-c in human skeletal muscle and that MOTS-c treatment improved physical capacity in young, middle-aged, and aged mice. Human clinical data are limited to CohBar's Phase 1a/1b study of the analog CB4211 in healthy volunteers and obese NAFLD subjects, which reported acceptable tolerability and exploratory signals on ALT/AST and glucose; CohBar wound down the program in 2023. No completed Phase 2 or Phase 3 trials exist for MOTS-c or its analogs, and grey-market dosing (typically ~10 mg SubQ 2-3x/week) is not clinically validated.
Key references
Humanin (Cognitive) and MOTS-c (Metabolic) are in different categories and target different biological pathways. This is a common pattern in multi-compound research protocols. Researchers should monitor the biomarkers from both profiles and watch for interactions listed in each compound’s contraindications. Consult a licensed healthcare provider before combining any research compounds.
This platform provides informational tools only, not medical advice. This comparison is for educational purposes only. Consult a licensed provider.
Dosing Notes
Half-life
Side Effects
Contraindications
Lab Testing
Disclosed Labs