Informational only. Not medical advice.INFORMATIONAL PLATFORM ONLY — NOT MEDICAL ADVICE, DIAGNOSIS, OR TREATMENT
Head-to-head comparison of GW-0742 and MOTS-c — mechanism, side effects, legal status, and pricing.
GW-0742 is a synthetic small-molecule PPARδ (PPAR-beta/delta) agonist developed by GlaxoSmithKline as a phenoxyacetic-acid/thiazole derivative—not a peptide or hormone. It exhibits ~1000-fold selectivity for human PPARδ (EC50 = 1.1 nM) over PPARα and PPARγ. Never advanced past preclinical development, GW-0742 has no approved human therapeutic use and no registered clinical trials. It is prohibited at all times under WADA as a member of the banned PPARδ-agonist class (Hormone and Metabolic Modulators), though not individually named on the list.
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.
GW-0742
MOTS-c
Category
Legal Status
Mechanism
Half-life
Side Effects
COA-verified vendors · trust score ≥70 required · single-vial price — bulk/bundle deals may be lower
GW-0742
MOTS-c
COA corpus from Disclosed Labs — independently tested batches only.
GW-0742
3
COAs
99.6%
Avg purity
2
Labs
MOTS-c
193
COAs
99.5%
Avg purity
16
Labs
No human efficacy or safety data exist; the only identified human exposure is a single 15 mg oral dose administered to volunteers solely to characterize urinary metabolites for an anti-doping detection assay—a bioanalytical study yielding no therapeutic or safety information. Preclinical rodent findings include: oral GW-0742 (30 mg/kg/day × 3 weeks) reduced right ventricular hypertrophy and systolic pressure in rats with chronic hypoxia-induced pulmonary hypertension but did not prevent pulmonary vascular remodeling; intraperitoneal GW-0742 (0.1 mg/kg) improved survival and reduced intestinal injury, leukocyte activation, cytokines, and apoptosis markers in a mouse gut ischemia/reperfusion model; and GW-0742 ameliorated hepatic steatosis, ER stress, and lung inflammation in various mouse models. Critically, mouse studies also demonstrated hepatomegaly, hepatic/skeletal-muscle peroxisome proliferation, and skeletal myopathy driven predominantly by off-target PPARα cross-activation, indicating mechanism-based toxicity risk.
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.
GW-0742 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.
Contraindications
Lab Testing
Key references