A practical reference on GW501516: what it is, how it behaves, what the literature reports, and where the honest uncertainties sit.
Reviewed 2026-04-29. Anything still debated is marked as such rather than presented as settled.
Cardarine is a common name for the investigational chemical GW501516, also written GW-1516. It was developed as a peroxisome proliferator-activated receptor delta agonist for metabolic conditions such as dyslipidemia. Early research focused on lipid handling and energy use in skeletal muscle and other tissues. The compound was never approved as a medicine. In public discussion, it is often grouped with performance-enhancing substances, although its receptor target differs from that of anabolic steroids or selective androgen receptor modulators. Regulatory and health authorities have issued warnings about its use.
GW501516 acts on PPARδ, a nuclear receptor that helps regulate fatty acid oxidation and energy homeostasis. In animal studies, activation of this receptor was associated with increased endurance and changes in lipid metabolism. Human trials examined effects on blood lipids and other metabolic markers, but the compound did not advance to approval. Rodent studies later reported tumors in multiple tissues at doses used in those experiments. Whether those findings translate to human risk remains uncertain, and the clinical relevance of the animal data is still debated.
Cardarine is the common name for GW501516, a synthetic compound studied as a peroxisome proliferator-activated receptor delta agonist. Researchers developed it to explore treatments for lipid disorders and metabolic conditions. It is not an approved medicine in any country. Early clinical work examined changes in HDL cholesterol and triglycerides, but development was discontinued after animal studies raised concerns about cancer. The compound remains available as a research chemical and appears in discussions of performance enhancement.
At the molecular level, GW501516 binds and activates PPARδ, a nuclear receptor that regulates transcription. Activation shifts expression of genes involved in fatty acid oxidation, energy expenditure, and lipid transport in skeletal muscle and liver. Animal studies report increased endurance and altered lipid profiles after exposure. Human data are limited to small trials and do not establish long-term safety or efficacy. PPARδ also has roles in cell proliferation, so the relationship between activation and cancer risk remains an open question.
| Property | Value | Notes |
|---|---|---|
| Common name | Cardarine | Common internet and media name. |
| Research code | GW501516 | Also written GW-1516. |
| Drug class | PPARδ agonist | Not a selective androgen receptor modulator. |
| Development status | Discontinued | Clinical development halted after rodent cancer findings. |
| Regulatory status | Prohibited in sport | Listed by WADA; not approved as medicine. |
GW501516 acts as a selective agonist at PPARδ, a nuclear receptor that regulates transcription of genes involved in lipid handling and energy metabolism. Activation of PPARδ in preclinical models increases fatty acid oxidation, mitochondrial biogenesis, and exercise endurance in rodents. These effects have made the compound a subject of metabolic research and also a target for sport anti-doping rules. In humans, however, controlled studies are limited, and whether similar endurance or metabolic changes occur at tolerated exposures remains an open question. The receptor’s broad tissue distribution also means downstream effects may vary by organ and condition.
Detection of GW501516 in biological samples generally relies on liquid chromatography coupled with tandem mass spectrometry. Urine is a common matrix in anti-doping analysis, while blood or plasma may be used in research settings. Sample preparation can involve enzymatic hydrolysis, protein precipitation, or solid-phase extraction before instrumental analysis. Because the compound undergoes metabolism, assays may target the parent molecule, one or more metabolites, or both. Detection windows are not fixed; they depend on factors such as dose, route, individual metabolism, and assay sensitivity. Reference standards are required for accurate identification and quantification.
Stability of GW501516 depends on form, temperature, light exposure, and moisture. Solid reference material is typically stored frozen or refrigerated in a desiccator and protected from light. Solutions in organic solvents such as dimethyl sulfoxide are often kept frozen in aliquots to reduce freeze-thaw cycling. Aqueous solubility is low, so aqueous stock solutions can be difficult to prepare without cosolvents. Degradation may appear as changes in chromatographic purity or mass spectral signal. Stability studies are needed to establish shelf life for any specific preparation.
Quality assessment for cardarine samples usually combines identity, purity, and impurity testing. Nuclear magnetic resonance spectroscopy and mass spectrometry can confirm molecular structure, while high-performance liquid chromatography estimates purity. Certificates of analysis from testing laboratories may list these results, but they do not establish safety or legality. In the absence of approved manufacturing, products sold online may contain the wrong compound, variable amounts, or unlisted contaminants. Independent verification is therefore central to analytical work and to interpreting any reported biological activity.
Weight regain is common upon discontinuation of weight loss medications, and long-term therapy may sometimes be required for sustained weight loss. After stopping treatment with GLP-1 agonists such as semaglutide, liraglutide and tirzepatide, people regain on average more than half (50–70%) of the lost weight within 1 year. People return to their previous weight within a year and a half after stopping anti-obesity medications. Media related to Anti-obesity drugs at Wikimedia Commons Prescription Medications to Treat Overweight & Obesity US National Institute of Diabetes and Digestive and Kidney Diseases
Galega officinalis (French lilac) was used in diabetes treatment for centuries. In the 1920s, guanidine compounds were discovered in Galega extracts. Animal studies showed that these compounds lowered blood glucose levels. Some less toxic derivatives, synthalin A and synthalin B, were used for diabetes treatment, but after the discovery of insulin, their use declined. Biguanides were reintroduced into Type 2 diabetes treatment in the late 1950s. Initially phenformin was widely used, but its potential for sometimes fatal lactic acidosis resulted in its withdrawal from most pharmacopeias (in the U.S. in 1978). Metformin has a much better safety profile, and it is the principal biguanide drug used in pharmacotherapy worldwide.
Angiogenesis, the formation of new blood vessels, is often critical for tumour cells to survive and grow in nutrient-depleted conditions. Akt is activated downstream of vascular endothelial growth factor (VEGF) in endothelial cells in the lining of blood vessels, promoting survival and growth. Akt also contributes to angiogenesis by activating endothelial nitric oxide synthase (eNOS), which increases production of nitric oxide (NO). This stimulates vasodilation and vascular remodelling. Signaling through the PI3K-Akt pathway increases translation of hypoxia-inducible factor α (HIF1α and HIF2α) transcription factors via mTOR. HIF promotes gene expression of VEGF and glycolytic enzymes, allowing metabolism in oxygen-depleted environments.
Sources: en.wikipedia.org
The carbohydrate-insulin model (CIM) posits that obesity is caused by excess consumption of carbohydrate, which then disrupts normal insulin metabolism leading to weight gain and weight-related illnesses. It is contrasted with the mainstream energy balance model (EBM), which holds that obesity is caused by an excess in calorie consumption compared to calorie expenditure. According to the carbohydrate–insulin model, low-carbohydrate diets would be the most effective in causing long-term weight loss. Notable proponents of the carbohydrate–insulin model include Gary Taubes and David Ludwig. The CIM has been tested in mice and humans. Although some experts consider that these studies falsified the CIM, proponents disagree. Available evidence does not support the existence of a long-term advantage in weight loss for low-carbohydrate diets.
Hydrophilic/cytosolic – are soluble in water and are localized at the cytosol, including cAMP, cGMP, IP3, Ca2+, cADPR and S1P. Their main targets are protein kinases as PKA and PKG, being then involved in phosphorylation mediated responses. Hydrophobic/membrane-associated – are insoluble in water and membrane-associated, being localized at intermembrane spaces, where they can bind to membrane-associated effector proteins. Examples: PIP3, DAG, phosphatidic acid, arachidonic acid and ceramide. They are involved in regulation of kinases and phosphatases, G protein associated factors and transcriptional factors. Gaseous – can be widespread through cell membrane and cytosol, including nitric oxide and carbon monoxide. Both of them can activate cGMP and, besides of being capable of mediating independent activities, they also can operate in a coordinated mode.
Adenylyl cyclase is regulated by G proteins, which can be found in the monomeric form or the heterotrimeric form, consisting of three subunits. Adenylyl cyclase activity is controlled by heterotrimeric G proteins. The inactive or inhibitory form exists when the complex consists of alpha, beta, and gamma subunits, with GDP bound to the alpha subunit. In order to become active, a ligand must bind to the receptor and cause a conformational change. This conformational change causes the alpha subunit to dissociate from the complex and become bound to GTP. This G-alpha-GTP complex then binds to adenylyl cyclase and causes activation and the release of cAMP. Since a good signal requires the help of enzymes, which turn on and off signals quickly, there must also be a mechanism in which adenylyl cyclase deactivates and inhibits cAMP. The deactivation of the active G-alpha-GTP complex is accomplished rapidly by GTP hydrolysis due to the reaction being catalyzed by the intrinsic enzymatic activity of GTPase located in the alpha subunit. It is also regulated by forskolin, as well as other isoform-specific effectors:
Sources: en.wikipedia.org
No. Cardarine is a PPARδ agonist, while selective androgen receptor modulators act on androgen receptors. The two classes differ in receptor target and downstream effects.
Preclinical rodent studies reported cancers, including liver and bladder tumors, at tested doses. The human relevance of those findings is uncertain, but development was discontinued. No approved human product resulted.
No. It remains an investigational compound without approved therapeutic labeling. Sports regulators prohibit its use, and health agencies have warned against consuming it.
Cardarine is a common name for the investigational compound GW501516. It acts as a PPARδ agonist and is not approved for human use. It is prohibited in sport.