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 Cardarine (GW-501516) and MOTS-c — mechanism, dosing, side effects, legal status, and pricing.
Cardarine (GW-501516) is a synthetic small-molecule PPARδ agonist — not a SARM and not a peptide, despite gray-market marketing that groups it with SARMs. Developed by GSK and taken into human lipid trials, its clinical development was discontinued around 2007 after rodent carcinogenicity findings. It has no regulatory approval anywhere, is WADA-prohibited at all times, and is sold only 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.
Cardarine (GW-501516)
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
Cardarine (GW-501516)
MOTS-c
COA corpus from Disclosed Labs — independently tested batches only.
Cardarine (GW-501516)
2
COAs
99.7%
Avg purity
1
Labs
MOTS-c
193
COAs
99.5%
Avg purity
16
Labs
Completed GSK-sponsored human trials in low-HDL/dyslipidemia subjects (2.5–10 mg/day, 12 weeks) improved lipids (HDL-C +16.9%, triglycerides −16.9%, LDL −7.3%; Sprecher et al., 2012). GSK halted development around 2007 after a 2-year rodent carcinogenicity study reported tumors across multiple organs; a 2019 mouse study found GW-501516 accelerated colitis-associated colorectal cancer. A published human case report documented severe rhabdomyolysis and hepatotoxicity from self-administration. Never approved for any indication; not a peptide.
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
Cardarine (GW-501516) 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