A practical reference on GW501516: what it is, how it behaves, what the literature reports, and where the honest uncertainties sit.
This page was last updated on 2026-06-16 and is reviewed periodically as new material appears.
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 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.
Safety discussions about cardarine frequently cite rodent carcinogenicity findings reported in the 2000s. In those studies, treated animals developed tumors at multiple sites, leading sponsors to discontinue clinical development. The relevance of these findings to humans has not been resolved, but they are a major reason the compound is not approved. Current literature emphasizes uncertainty about long-term effects and the risks of unregulated use. Regulators and health agencies have not established a safe human exposure level.
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.
| 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. |
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.
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.
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.
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.
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.
Cardarine is a common name for GW501516, a synthetic compound studied for its effects on lipid and glucose metabolism. It functions as an agonist at peroxisome proliferator-activated receptor delta, or PPARδ, a nuclear receptor that influences gene expression. The molecule is not a steroid, nor is it a selective androgen receptor modulator. It is also known in research and sports literature as GW-501516 and endurobol. Early laboratory work examined its metabolic activity in cell cultures and animal models.
PPARδ is a nuclear receptor that influences transcription of genes involved in fatty acid oxidation, lipid transport, and energy homeostasis. GW501516 binds and activates this receptor with high selectivity relative to PPARα and PPARγ in laboratory assays. Activation alters expression of target genes in skeletal muscle, liver, and adipose tissue in animal models. The exact clinical consequences of these changes in humans remain incompletely characterized, and observed effects in animals do not establish therapeutic benefit or safety.
Published studies have examined GW501516 in animal models of obesity, insulin resistance, and exercise endurance. Early human trials reportedly ended, and development was discontinued after preclinical findings raised concerns about cancer in some rodent studies. Regulatory agencies have not approved cardarine for any medical use. Its availability through non-pharmaceutical channels raises questions about identity, purity, and legal status that are separate from its laboratory pharmacology. Those questions are often addressed through analytical testing rather than assumptions about product labels.
phosphorylation The attachment of a phosphate ion, PO3−4, to another molecule or ion or to a protein by covalent bonding. Phosphorylation and the inverse reaction, dephosphorylation, are essential steps in numerous biochemical pathways, including in the production of adenosine triphosphate (ATP) (as in oxidative phosphorylation); in the metabolism of glucose and the synthesis of glycogen; and in the post-translational modification of amino acid residues in many proteins. Enzymes which catalyze phosphorylation reactions are known as kinases; those that catalyze dephosphorylation are known as phosphatases.
=== Lobbying the FDA === In 2011, the FDA made it a priority to clarify the requirements for approval for such a closed-loop monitoring and drug delivery device for T1D, and announced it was preparing draft guidelines. Breakthrough T1D launched a campaign to influence those guidelines to be lenient. After the first closed-loop device was approved in 2016, Breakthrough T1D lobbied insurance companies to cover it. The campaign also put resources into educating people with diabetes on how to navigate health insurance in the United States, and into lobbying Congress to continue funding diabetes research through the NIH. The FDA lobbying campaign was part of a gradual realignment of the organization to focus on issues other than helping find a cure for type 1 diabetes, but to help treat and manage the disease. This broadened scope meant that the organization increasingly directed its funds to education and advocacy, along with research funding. This included lobbying insurance companies to pay for CGM devices, educating patients on how to advocate for themselves, and lobbying Congress for more NIH funding.
During the Perestroika era of the Soviet Union of the late 1980s, many descendants of the Cossacks became enthusiastic about reviving their national traditions. In 1988, the Soviet Union passed a law allowing the reestablishment of former hosts and creation of new ones. The ataman of the largest, the Almighty Don Host, was granted Marshal rank and the right to form a new host. Simultaneously, many attempts were made to increase Cossack's impact on Russian society, and throughout the 1990s many regional authorities agreed to hand over some local administration and policing duties to the Cossacks. According to the 2002 Russian Census, 140,028 people self-identified as ethnic Cossacks. Between 3.5 and 5 million people associate themselves with the Cossack identity in post-Soviet Russia and around the world.
Oxidation response is stimulated by a disturbance in the balance between the production of reactive oxygen species and antioxidant responses, known as oxidative stress. Active species of oxygen naturally occur in aerobic cells and have both intracellular and extracellular sources. These species, if not controlled, damage all components of the cell, including proteins, lipids and DNA. Hence cells need to maintain a strong defense against the damage. The following table gives an idea of the antioxidant defense system in bacterial system.
The metabolism of drugs is often divided into the following three phases. Phase I: modification, phase II: conjugation, and phase III: excretion. These phases act in concert to detoxify drugs and remove them from cells and eventually from the body. The purpose of phase I is to introduce polar groups that either themselves directly facilitate excretion or to create reactive functional groups. These reactive groups can be conjugated in a phase II reaction with molecules that are recognized by transport proteins. In the last step, transport proteins eliminate the drug conjugate from the body. In phase I, enzymes such as Cytochrome P450 oxidases introduce reactive or polar groups into xenobiotics. These modified compounds are then conjugated to polar compounds in phase II reactions. These reactions are catalyzed by transferase enzymes such as glutathione S-transferases. Finally, in phase III, the conjugated xenobiotics may be further processed, before being recognized by efflux transporters and pumped out of cells. Drug metabolism often converts lipophilic compounds into hydrophilic products that are more readily excreted.
Sources: en.wikipedia.org
In metallocenes of the type (C5R5)2M, the cyclopentadienyl rings rotate with very low barriers. Single crystal X-ray diffraction studies reveal both eclipsed or staggered rotamers. For non-substituted metallocenes the energy difference between the staggered and eclipsed conformations is only a few kJ/mol. Crystals of ferrocene and osmocene exhibit eclipsed conformations at low temperatures, whereas in the related bis(pentamethylcyclopentadienyl) complexes the rings usually crystallize in a staggered conformation, apparently to minimize steric hindrance between the methyl groups.
Ishibashi T, Yokoi N, Kinoshita S (2003). "Comparison of the effects of topical levobunolol and timolol solution on the human ocular surface". Cornea. 22 (8): 709–15. doi:10.1097/00003226-200311000-00001. PMID 14576520. S2CID 25444383. Ogasawara H, Yoshida A, Fujio N, Konno S, Ishiko S (1999). "[Effect of topical levobunolol on retinal, optic nerve head, and choroidal circulation in normal volunteers]". Nippon Ganka Gakkai Zasshi. 103 (7): 544–50. PMID 10443129. Leung M, Grunwald J (1997). "Short-term effects of topical levobunolol on the human retinal circulation". Eye. 11 (3): 371–6. doi:10.1038/eye.1997.78. PMID 9373479.
Ronke Mojoyinola Olabisi (born 26 June 1976) is an associate professor of biomedical engineering at University of California, Irvine. She works on speciality of bone and human tissue. She is working with Mae Jemison on 100 Year Starship, an interdisciplinary initiative that is exploring the possibility of human interstellar travel.
The expression of aflatoxin-related diseases is influenced by factors such as species, age, nutrition, sex, and the possibility of concurrent exposure to other toxins. The main target organ in mammals is the liver, so aflatoxicosis is primarily a hepatic disease. Conditions increasing the likelihood of aflatoxicosis in humans include limited availability of food, environmental conditions that favor mold growth on foodstuffs, and lack of regulatory systems for aflatoxin monitoring and control. A regular diet including apiaceous vegetables, such as carrots, parsnips, celery, and parsley may reduce the carcinogenic effects of aflatoxin. There is no specific antidote for aflatoxicosis. Symptomatic and supportive care tailored to the severity of the liver disease may include intravenous fluids with dextrose, active vitamin K, B vitamins, and a restricted, but high-quality protein diet with adequate carbohydrate content.
=== Elimination === Alcohol is removed from the bloodstream by a combination of metabolism, excretion, and evaporation. 90-98% of ingested ethanol is metabolized into carbon dioxide and water. Around 5 to 10% of ethanol that is ingested is excreted unchanged in urine, breath, and sweat. Transdermal alcohol that diffuses through the skin as insensible perspiration or is exuded as sweat (sensible perspiration) can be detected using wearable sensor technology such as SCRAM ankle bracelet or the more discreet ION Wearable. Ethanol or its metabolites may be detectable in urine for up to 96 hours (3–5 days) after ingestion. Unlike most physiologically active materials, in typical recreational use, ethanol is removed from the bloodstream at an approximately constant rate (linear decay or zero-order kinetics), rather than at a rate proportional to the current concentration (exponential decay with a characteristic elimination half-life). This is because typical doses of alcohol saturate the enzymes' capacity. In Widmark's model, the elimination rate from the blood, β, contributes 60% of the uncertainty. Similarly to ρ, its value depends on the units used for blood. β varies 58% by occasion and 42% between subjects; it is thus difficult to determine β precisely, and more practical to use a mean and a range of values. Typical elimination rates range from 10 to 34 mg/dL per hour, with Jones recommending the range 0.10 - 0.25 g/L/h for forensic purposes, for all subjects.
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.