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 BAM15 and MOTS-c — mechanism, dosing, side effects, legal status, and pricing.
BAM15 is a synthetic small-molecule mitochondrial uncoupler (protonophore) — not a peptide — studied preclinically for obesity and metabolic disease as a potentially safer alternative to DNP. It has never been tested in humans, has no regulatory approval, and was added to the WADA Prohibited List as an AMPK activator. It is sold as a gray-market research chemical.
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.
BAM15
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
BAM15
MOTS-c
COA corpus from Disclosed Labs — independently tested batches only.
BAM15
3
COAs
99.1%
Avg purity
1
Labs
MOTS-c
193
COAs
99.5%
Avg purity
16
Labs
In diet-induced obese mice, BAM15 reduced fat mass and improved insulin sensitivity without changing food intake or lean mass (Nature Communications 2020); other mouse work shows benefit in diabetes, and in sepsis/acute kidney injury. Rodent PK is ~67% oral bioavailability with a ~1.7 h half-life; there is no human PK, safety, or dosing data. Not approved; not a peptide.
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.
BAM15 and MOTS-c are both in the Metabolic category and may have overlapping mechanisms. Researchers should review both profiles carefully, understand the mechanisms of action, and monitor the relevant biomarkers when combining compounds in the same class. As always, consult a licensed healthcare provider before making any decisions about combining 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