GW501516 is one of those subjects where the details matter more than the headlines. This page pulls together the background, the mechanisms, and the practical points readers ask about most.
Last reviewed on 2026-01-23. Where a claim depends on a specific study, the study is described rather than over-claimed.
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.
Published literature on cardarine includes in vitro assays, rodent experiments, and a small number of human studies. Reports describe effects on exercise capacity and lipid metabolism in animals, while human evidence is sparse. Many online descriptions present the compound as a proven endurance aid, a claim not supported by regulatory approval or large clinical trials. Analytical studies focus on identifying the parent compound and its metabolites in biological samples. Important uncertainties include species differences, dose-response relationships, and the relevance of rodent tumor findings to humans.
Cardarine is a synthetic compound also known as GW501516, GW-501516, and sometimes endurobol. It was developed as a selective agonist of peroxisome proliferator-activated receptor delta, a nuclear receptor involved in fatty acid oxidation and energy metabolism. The compound was studied in preclinical models for metabolic and cardiovascular conditions, but it did not become a marketed human medicine. In regulatory and anti-doping contexts, it is treated as a prohibited substance rather than a licensed medicine.
The pharmacological interest in cardarine centers on PPARδ activation and its downstream effects on lipid handling and mitochondrial function. In animal studies, PPARδ agonists have been associated with changes in exercise endurance and fatty acid utilization, though results vary by model and protocol. Human data remain sparse, and the absence of large controlled trials limits conclusions about efficacy. Researchers often describe the compound as a tool for probing PPARδ biology rather than a proven therapeutic agent.
| Property | Value | Notes |
|---|---|---|
| Common name | Cardarine | Also called GW501516 and endurobol. |
| Chemical formula | C21H18F3NO3S2 | Molecular weight about 453.5 g/mol. |
| Appearance | White to off-white solid | Form depends on synthesis and purity. |
| Solubility | Soluble in DMSO and ethanol | Low solubility in water. |
| Typical storage | -20 °C, desiccated, protected from light | Common for research chemicals. |
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.
Laboratory detection of GW501516 commonly uses liquid chromatography coupled with tandem mass spectrometry. The method can identify the parent compound or its metabolites in urine and blood after sample cleanup. Protein precipitation, solid-phase extraction, or enzymatic hydrolysis may precede analysis, depending on the matrix. Reference standards are required for accurate quantification and confirmation. Because the compound is not approved, testing often occurs in anti-doping, forensic, or research settings rather than routine clinical care. Results are reported with limits of detection and quantification.
Laboratory handling focuses on identity, purity, and stability. Reference standards are typically stored cold and dry, protected from light, because solutions can degrade over time. Analytical checks may use high-performance liquid chromatography with ultraviolet detection or mass spectrometry. Impurities and related substances can be separated chromatographically and compared with a known standard. Because cardarine is not an approved drug, compendial monographs are absent, and laboratories often rely on in-house methods. Reported purity varies among unregulated products and should not be assumed from a label.
GW501516 binds and activates PPARδ, a nuclear receptor that influences transcription of genes involved in fatty acid oxidation and energy use. Activation shifts some metabolic pathways in preclinical models, which is why the compound has been studied for lipid disorders and exercise-related endpoints. The exact downstream effects in humans are incompletely mapped. PPARδ is expressed in many tissues, including skeletal muscle, liver, and adipose tissue, so broad activation may have varied consequences. Researchers continue to examine how selective or partial activation might alter the balance between benefits and risks.
Published human data are sparse and mostly come from early-phase trials. Those studies examined short-term changes in lipids, glucose, and exercise capacity, but they were not large enough to establish efficacy or long-term safety. Some animal experiments reported increased running endurance, yet such findings do not prove a performance benefit in people. Anti-doping laboratories detect GW501516 and its metabolites in urine or blood using liquid chromatography-tandem mass spectrometry. Detection windows depend on dose, sample type, and individual metabolism. The method is sensitive enough to identify trace residues in tested samples.
Activation of PPARδ changes transcription of genes involved in fatty acid transport, mitochondrial function, and skeletal muscle fuel preference. In rodent studies, pharmacological PPARδ activation was associated with increased endurance and altered body composition. These findings generated interest in performance enhancement, but species differences and study designs limit direct extrapolation to humans. Small human trials were conducted in the 2000s and later discontinued. The extent to which cardarine produces similar metabolic or performance effects in people remains an open question.
The compound is typically described as a laboratory compound rather than a therapeutic product. Published reports have explored its role in lipid disorders, insulin sensitivity, and exercise metabolism, yet no major drug regulator has approved it for medical use. Commercial samples sold under the cardarine name may vary in purity and identity. Analytical confirmation is therefore necessary when the material is discussed in scientific or regulatory contexts. Its classification as a prohibited substance in sport further shapes how it is studied and reported.
== Career and research == Barrios started her career as an undergraduate researcher in the Department of Radiobiology under Professor Scott C. Miller at the University of Utah. In this lab, she researched radiation poisoning toward the development of an oral medication that could bind to radioactive molecules to take out of the body. She continued her research career during her Ph.D. under Professor Stephen J. Lippard, in the Department of Chemistry at MIT. At MIT, she worked on the metalloenzyme urease and created a compound to understand how the di-nickel center in urease hydrolyzes urea since the mechanism of action had not yet been discovered. While the synthetic compound allowed Barrios to determine the mechanism of action, this mechanism turned out to be similar to, but not the same, as the mechanism that urease uses. She worked on additional metalloenzymes that used iron and nickel during her graduate work. During her postdoctoral fellowship at the University of California under Professor Charles S. Craik, she developed a method to assay the substrate specificity of proteolytic enzymes using lanthanide ion fluorescence. This method was used to develop peptide libraries to determine substrate specificity for proteolytic enzymes. While at the University of Southern California as a Gabilan Assistant Professor of Chemistry, Barrios worked on a tool that allows the visualization of tyrosine phosphatase activity in cells in real-time using protein tyrosine phosphatases (PTPs).
=== Greg Grayson === Greg Grayson (Ben Lloyd-Hughes) is a VP on Pierpoint's CPS desk. He is initially romantically interested in Harper; she rejects his advances, but the two remain friends afterwards. Greg copes with Pierpoint's ruthless culture using drugs, and also explores writing in his spare time, which Eric publicly mocks him for. During an office Christmas party, Harper tells Robert to look after Greg and make sure he stays sober, but Robert and Greg end up indulging in heavy drug use with a client, culminating in Greg running headfirst into a window and injuring himself. Greg leaves Pierpoint after the incident. In series 2 it is revealed that Greg has had a book published. Greg briefly reappears at the end of series 3, now working as a venture capital investor in California. He listens to a sales pitch from Robert for Little Labs, a startup producing medicinal psilocybin.
=== Use in traditional medicine === In modern South Korea, S. mutilans and other Scolopendra species are used in Korean traditional medicine. The centipedes are used whole to treat various medical issues, including joint problems (which is its major use), alopecia areata, stroke, convulsions, lymphangitis, lumps or masses, neoplasm, poisonous tumours, carbuncles, and snake bites. These centipedes were considered one of the most prescribed, medically important, and expensive insect/arthropod drugs in Korean traditional medicine. They are frequently prescribed alone, despite arthropod drugs are usually prescribed with a mix of other medicinal materials for desired effects. In China, S. mutilans is the only centipede species registered for clinical application by the Pharmacopeia of the People's Republic of China. Despite being the only species listed, other species of centipedes, including S. mojiangica, S. multidens, and S. negrocapitis, were also regularly used as substitutes in clinical practice.
Sources: en.wikipedia.org
== Pathophysiology == Organizing pneumonia is usually preceded by some type of lung injury that causes a localized denudation or disruption in continuity of the epithelial basal laminae of the type 1 alveolar pneumocytes that line the alveoli. This injury to the epithelial basal lamina results in inflammatory cells and plasma proteins leaking into the alveolar space and forming fibrin, resulting in an initial fibroblast driven intra-alveolar fibroproliferation. The fibroblasts differentiate into myofibroblasts and continue to form fibrosis resulting in intra-alveolar fibroinflammatory buds (Masson's Bodies) that are characteristic of organizing pneumonia. These Masson's bodies consist of inflammatory cells contained in an extracellular matrix consisting of type I collagen, fibronectin, procollagen type III, tenascin C and proteoglycans. Angiogenesis , or the formation of blood vessels, occurs in the Masson's bodies and this is driven by vascular endothelial growth factor. Remodeling occurs, resulting in the intra-alveolar fibroinflammatory buds (Masson's Bodies) moving into the interstitial space and forming collagen globules that are then covered by type 1 alveolar epithelial cells with well developed basement membranes. These type 1 alveolar epithelial cells (pneumocytes) then proliferate, restoring the continuity and function of the alveolar unit.
We thus come to the remarkable conclusion that, beyond doubt, Van Leeuwenhoek in his experiment with the fully closed tube had cultivated and seen genuine anaerobic bacteria, which would happen again only after 200 years, namely about 1862 by Pasteur. That Leeuwenhoek, one hundred years before the discovery of oxygen and the composition of air, was not aware of the meaning of his observations is understandable. But the fact that in the closed tube he observed an increased gas pressure caused by fermentative bacteria and, in addition, saw the bacteria, prove, in any case, that he not only was a good observer but also was able to design an experiment from which a conclusion could be drawn.
== Medical uses == Hydroxychloroquine treats rheumatic disorders such as systemic lupus erythematosus, rheumatoid arthritis, and porphyria cutanea tarda, and certain infections such as Q fever and certain types of malaria. It is considered the first-line treatment for systemic lupus erythematosus. Certain types of malaria, resistant strains, and complicated cases require different or additional medication. Hydroxychloroquine blocks the effects of some chemicals released in autoimmune diseases, and is used to treat inflammatory conditions. It is widely used to treat primary Sjögren syndrome but does not appear to be effective. Hydroxychloroquine is widely used in the treatment of post-Lyme arthritis. It may have both an anti-spirochete activity and an anti-inflammatory activity, similar to the treatment of rheumatoid arthritis.
Nerve entrapment involves a cascade of physiological changes caused by compression and tension. Some of these changes are irreversible. The magnitude and duration of the forces determines the extent of injury. In the acute form, mechanical injury and metabolic blocks impede nerve function. In the chronic form, there is a sequence of changes starting with a breakdown of the blood-nerve-barrier, followed by edema with connective tissue changes, followed by diffuse demyelination, and finally followed by axonmetesis. The injury will often be a mixed lesion where mild/moderate compression is a combination of a metabolic block and neuropraxia, while severe compression combines elements of neuropraxia and axonmetesis.
Sources: en.wikipedia.org
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.
It activates PPARδ, a nuclear receptor that influences gene expression related to lipid and energy metabolism. Animal studies show changes in endurance and lipid levels. Human effects and risks are not well established.
No, cardarine is not a steroid. It belongs to a different chemical class, the PPARδ agonists. It is also not a selective androgen receptor modulator.
Cardarine is an investigational synthetic compound that acts as a PPARδ agonist. It is also known as GW501516 and has been studied mainly in preclinical research. It is not an approved medicine.