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.
Updated 2026-02-16. Numbers and descriptions here follow the published literature rather than marketing material.
Cardarine is a common name for GW501516, a synthetic compound developed in the 1990s through research collaborations involving GlaxoSmithKline. It belongs to a class of molecules known as peroxisome proliferator-activated receptor delta agonists. Early studies explored its effects on lipid metabolism and energy expenditure in animal models. The compound was never approved as a human medicine, and clinical development was discontinued. In the years since, it has appeared in fitness and bodybuilding communities as a performance-enhancing substance. Regulatory agencies classify it as an unapproved drug.
PPARδ is a nuclear receptor that regulates gene expression related to fatty acid oxidation, glucose homeostasis, and mitochondrial function. GW501516 binds to this receptor with high affinity and activates downstream signaling in skeletal muscle and other tissues. Animal studies reported increased endurance and altered fuel preference, but human data remain limited and inconsistent. The precise relationship between receptor activation and observed physiological changes is still an area of active investigation. Researchers have also examined whether the compound affects inflammation or cell proliferation. No approved therapeutic indication exists for cardarine.
In laboratory settings, cardarine is studied as a tool compound for probing PPARδ biology. Published experiments often use cell cultures, rodent models, or isolated tissues. Some investigations focus on metabolic effects, while others assess potential risks such as carcinogenicity observed in long-term animal studies. Because human trials are sparse, most knowledge comes from preclinical work and adverse event reports. Scientific literature frequently notes the gap between animal findings and human outcomes. The compound is not a dietary supplement and is not intended for human consumption.
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.
Regulatory bodies treat GW501516 as a prohibited substance in competitive sport. The World Anti-Doping Agency added it to the prohibited list, and it falls under classes covering metabolic modulators and hormone-related agents. It is not approved by drug regulators for human use, and it is not a lawful dietary supplement. Products sold under the cardarine name may contain unlisted ingredients or different compounds. Because no approved product exists, quality and identity are not guaranteed by pharmaceutical manufacturing standards.
| Property | Value | Notes |
|---|---|---|
| CAS Registry Number | 317318-70-0 | Unique identifier for the compound. |
| Chemical class | PPARδ agonist | Synthetic ligand for peroxisome proliferator-activated receptor delta. |
| Appearance | White to off-white solid | Typical form of research-grade material. |
| Solubility | Soluble in DMSO and ethanol | Poorly soluble in water. |
| Typical storage | -20°C | Recommended for long-term storage of stock solutions. |
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.
Cardarine is prohibited in competitive sport under the World Anti-Doping Agency code, where it is classified as a metabolic modulator. It is not approved as a prescription medicine in the United States, European Union, or other major markets. Regulatory action has focused on its presence in sports and in products marketed as research chemicals. Because it has no accepted medical indication, supply is often unregulated. This status creates legal and safety uncertainties for anyone who encounters the substance.
Anti-doping laboratories detect GW501516 and its metabolites using liquid chromatography-tandem mass spectrometry. Urine is the most common matrix, though blood and dried blood spots may also be used in some programs. Detection depends on factors such as dose, timing, metabolism, and the sensitivity of the assay. Published methods describe limits of detection in the low nanogram per milliliter range for related compounds. Exact detection windows are not fixed for all situations and remain an area of ongoing study.
Enzymatic reporters (e.g., LacZ) encode enzymes that catalyze reactions yielding a visible product. For example, β-galactosidase (encoded by LacZ) cleaves X-gal to produce a blue color, allowing easy identification of successful gene disruption (white colonies) versus intact genes (blue colonies). Bioluminescent reporters (e.g., luciferase) produce light via chemical reactions, enabling live-cell imaging and promoter studies without external light sources. Colorimetric reporters (e.g., CAT) generate detectable color changes when enzymes react with substrates, measurable via spectrophotometry or TLC. Selectable markers (e.g., Neo) confer antibiotic resistance (e.g., to G418), ensuring only transformed cells survive in selective media. In the case of selectable-marker reporters such as CAT, the transfected population can be grown on a chloramphenicol-containing substrate. Only cells with the CAT gene survive, confirming successful transformation.
Using solvent extraction it is possible to extract uranium, plutonium, thorium and many rare earth elements from acid solutions in a selective way by using the right choice of organic extracting solvent and diluent. One solvent used for this purpose is the organophosphate tributyl phosphate (TBP). The PUREX process that is commonly used in nuclear reprocessing uses a mixture of tri-n-butyl phosphate and an inert hydrocarbon (kerosene), the uranium(VI) are extracted from strong nitric acid and are back-extracted (stripped) using weak nitric acid. An organic soluble uranium complex [UO2(TBP)2(NO3)2] is formed, then the organic layer bearing the uranium is brought into contact with a dilute nitric acid solution; the equilibrium is shifted away from the organic soluble uranium complex and towards the free TBP and uranyl nitrate in dilute nitric acid. The plutonium(IV) forms a similar complex to the uranium(VI), but it is possible to strip the plutonium in more than one way; a reducing agent that converts the plutonium to the trivalent oxidation state can be added. This oxidation state does not form a stable complex with TBP and nitrate unless the nitrate concentration is very high (circa 10 mol/L nitrate is required in the aqueous phase). Another method is to simply use dilute nitric acid as a stripping agent for the plutonium. This PUREX chemistry is a classic example of a solvation extraction. In this case, DU = k [TBP]2[NO3−]2.
== Experimental reconstruction == Many research groups are actively attempting experimental reconstruction of the interactions between prebiotic reactions. One major consideration is the ability for these reactions to operate in the same environmental conditions. These one-pot syntheses would likely push the reaction towards specific subgroups of molecules. The key to building proto-metabolic scenarios involves coupling constructive and interconversion reactions. Constructive reactions use autocatalytic prebiotic chemistries to increase the structural complexity of the original molecule, while interconversion reactions connect different prebiotic chemistries by changing the functional groups appended to the original molecule. A functional group is a group of atoms that has similar properties whenever it appears in different molecules. These interconversion reactions and functional group transformations can lead to new prebiotic chemistries and precursor molecules.
Sources: en.wikipedia.org
Symptoms depend on the type and severity of thalassemia. Carriers of thalassemia genes may have no symptoms (thalassemia minor) or very mild symptoms with occasional crisis (thalassemia intermedia); individuals who are homozygous for the mutation have severe and life threatening symptoms (thalassemia major). Alpha thalassemia major is generally fatal to the unborn child, as the absence of alpha globin means that zero functional hemoglobin is produced during gestation. Unmatched gamma globin chains cluster to form hemoglobin Barts, which is ineffective at transporting oxygen. In this situation, a fetus will develop hydrops fetalis, a form of edema, which can be detected on prenatal ultrasound. The child will normally die before or shortly after birth, unless intrauterine blood transfusion is performed. Less severe alpha thalassemia may affect growth and development. Beta thalassemia symptoms typically begin to show during the first six months of life, as the body winds down production of fetal hemoglobin HbF. In a normal individual, this would be replaced by adult hemoglobin HbA. If thalassemia is untreated or undetected in the infant, this can lead to developmental issues such as slowed growth, delayed puberty, bone abnormalities, and intellectual impairment. More generally, impaired production of hemoglobin causes anemia, resulting in tiredness and a general lack of energy, shortness of breath, rapid or irregular heartbeat, dizziness, pale skin, yellowing of the skin and eyes (jaundice). In thalassemia, ineffective erythropoiesis causes the bone marrow to expand.
As a result, bicalutamide appears to not be able to compete with testosterone in this sole part of the body to an extent sufficient to considerably interfere with androgen signaling and function. However, while bicalutamide does not seem to be able to adversely influence testicular spermatogenesis, it may interfere with AR-dependent sperm maturation and transport outside of the testes in the epididymides and vas deferens where androgen levels are far lower, and hence may still be able to impair male fertility. In addition, the combination of bicalutamide with other medications, such as estrogens, progestogens, and GnRH analogues, can compromise spermatogenesis due to their own adverse effects on male fertility. These medications are able to strongly suppress gonadal androgen production, which can severely impair or abolish testicular spermatogenesis, and estrogens also appear to have direct and potentially long-lasting cytotoxic effects in the testes at sufficiently high concentrations.
Acetolactate synthase Acetohydroxy acid isomeroreductase Dihydroxyacid dehydratase α-Isopropylmalate synthase α-Isopropylmalate isomerase Leucine aminotransferase Synthesis of the small, hydrophobic amino acid valine also includes the initial part of this pathway.
Sources: en.wikipedia.org
Cardarine is a common name for GW501516, a synthetic PPARδ agonist developed for research. It has not been approved as a medication in any country. It is classified as an unapproved drug and a prohibited substance in sport.
No. Cardarine is not an anabolic steroid; it belongs to a different chemical class that targets PPARδ. Steroids act primarily through androgen receptors, while cardarine acts through a nuclear receptor involved in metabolism.
Some rodent studies reported increased endurance and changes in fat metabolism after cardarine exposure. Long-term studies in animals also raised concerns about cancer in certain tissues. Human trial data are limited, so these findings cannot be directly translated to people.
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.