Last updated: March 2026
GW-0742 is a highly selective PPARδ agonist from GlaxoSmithKline's metabolic research program — structurally related to Cardarine (GW-501516) but with greater PPARδ selectivity over PPARα. Animal studies demonstrate endurance enhancement, fat oxidation, and favorable lipid profile changes. No human clinical trials exist.
GW-0742 activates PPARδ (peroxisome proliferator-activated receptor delta), a nuclear receptor that functions as a master regulator of fatty acid oxidation, mitochondrial biogenesis, and skeletal muscle fiber type. Unlike Cardarine, GW-0742 has minimal activity at PPARα, making it a cleaner tool for isolating PPARδ-specific effects in research.
GW-0742 binds the PPARδ ligand-binding domain with high affinity and potency (EC₅₀ ~1 nM in cell assays). PPARδ is expressed highly in skeletal muscle, heart, and adipose tissue. Its activation drives transcriptional programs that shift cellular metabolism toward lipid utilization. GW-0742's selectivity ratio over PPARα is significantly higher than Cardarine's, reducing off-target PPARα signaling.
Activated PPARδ upregulates key genes in fatty acid beta-oxidation: CPT1 (carnitine palmitoyltransferase), HADHA, and ACADL. These enzymes shuttle long-chain fatty acids into the mitochondria and oxidize them for ATP. In exercising skeletal muscle, this means more fat burned relative to glycogen — the metabolic basis of the endurance effect observed in rodent studies.
PPARδ activation promotes expression of slow-twitch (Type I) oxidative muscle fiber characteristics in fast-twitch (Type II) fibers. In rodent models, chronic PPARδ agonist administration increased the proportion of oxidative, fatigue-resistant fiber markers, including myoglobin and mitochondrial density. This is the cellular basis for the dramatic endurance improvements seen in Cardarine and related compound studies.
PPARδ agonism in liver and adipose tissue affects lipoprotein metabolism. Animal and some early human trial data with related compounds show: increased HDL cholesterol ("good" cholesterol), reduced LDL, reduced VLDL triglycerides, and suppression of hepatic lipid accumulation. GW-0742 demonstrated similar lipid-improving effects in dyslipidemic animal models, though human extrapolation remains speculative.
⚠️ All data below is from animal studies (primarily rodent models). No human clinical trial data exists for GW-0742. Where Cardarine (GW-501516) data is referenced for context, it is labeled. These figures are for research reference only.
Testing and monitoring supplies for PPARδ agonist research.
Dosing schedules, interaction warnings, and cycle protocols for 50+ compounds — all in one place.
This page is for educational purposes only. It is not medical advice. GW-0742 is not FDA approved and is not intended for human use. All data referenced is from preclinical animal studies. The closely related compound Cardarine (GW-501516) was discontinued from clinical development due to carcinogenicity findings. Do not use any research chemical without consulting a qualified medical professional.