GW-501516 is a PPAR agonist (Peroxisome Proliferator-Activated Receptor) originally developed for hyperlipidemia, obesity, metabolic dysfunction and heart disease by GlaxoSmithKline, a multinational pharmaceutical company. The compound is also known by other names such as Endurobol and Cardarine and is often cited in scientific studies as a PPARδ agonist.

Several studies have shown that GW-501516 affects fatty acid metabolism, skeletal muscle endurance, and glucose and insulin balance.

Since PPARδ plays a critical role in mitochondrial respiration, temperature regulation, inflammation mediation, skin and muscle repair, skeletal reprogramming and keratinocyte differentiation, it can be assumed that GW-501516 may also impact these additional areas. Read more here.

One mouse study explicitly showed the effect of GW-501516 on the endurance of both trained and untrained mice. After three weeks of treatment with GW-501516, trained rats showed a 31.2% increase in their total walking distance, while untrained rats improved their total distance by 68.6%. Even one week of treatment with GW-501516 increased walking distance by 48.6% compared to the control group.

The group of rats that received both Cardarine and had previously been trained to run showed higher utilization of longer saturated fatty acids and triglycerides, likely due to increased fatty acid metabolism following PPARδ activation, affecting PDK4 and other mediating pathways of fatty acid oxidation. Read more here.

Molecular analyzes revealed that PPARδ is involved in exercise-induced muscle fiber reprogramming and skeletal muscle metabolism by regulating the expression of genes associated with contractile proteins, mitochondrial biogenesis and lipid oxidation.

Another study confirmed the above by administering GW-501516 to mice on a high-fat diet. The treated group showed only a slight weight reduction, but metabolic markers such as reduced insulin resistance, increased metabolism, increased mitochondrial activity and reduced lipids in skeletal muscle were noted. Furthermore, both plasma glucose and blood insulin were reduced in genetically obese mice. Read more here.

One study indicated that GW-501516 may also play a role in reducing inflammation, particularly in the liver. In rats fed a diet high in fructose, GW-501516 reduced inflammatory markers ACE/AT1r axis. In addition, the genes that regulate beta oxidation were increased and the genes that regulate fat cell production and glucose were reduced. Read more here.

Similar results were observed in primate studies. Research in middle-aged, overweight to obese rhesus monkeys indicated that HDL cholesterol was increased and LDL decreased, along with fasting triglycerides and fasting insulin levels. Researchers believe that GW-501516 could be a major breakthrough for cardiovascular diseases such as atherosclerosis and could reduce the severity of metabolic syndromes. Read more here.

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