The short version of GW501516 fits in a sentence. The long version — which is the one that helps — is below.
This page was last updated on 2025-12-02 and is reviewed periodically as new material appears.
Regulatory treatment varies, but cardarine is not approved as a medicine. Sports authorities list GW501516 as a prohibited substance, and it is banned at all times under the World Anti-Doping Agency code. Many countries restrict sales for human consumption, while online vendors market it as a research chemical. Such products may lack purity data, and their actual contents can differ from the label. Purchasing or possessing cardarine may carry legal consequences depending on jurisdiction. The compound is not a dietary supplement ingredient in regulated markets.
Clinical development stopped after rodent studies showed tumors at multiple sites. Whether those findings predict human cancer risk remains an open question, but they led sponsors to discontinue programs. Human safety data are limited to small, short-term studies that were not designed to assess cancer risk. Reported effects in those studies included changes in blood lipids, but the evidence is insufficient for medical use. Long-term consequences of nonmedical use are not well characterized. Questions about dose, duration, and individual susceptibility remain unresolved.
Cardarine is a common name for GW501516, an investigational compound developed in the 1990s for metabolic conditions. It acts as an agonist at peroxisome proliferator-activated receptor delta, a nuclear receptor involved in lipid and energy metabolism. The compound is frequently mislabeled as a selective androgen receptor modulator, or SARM, but its molecular target is different. GW501516 reached early clinical testing before development was discontinued. It has no approved therapeutic use in any country. The name cardarine is not a formal international nonproprietary name.
A common misconception is that cardarine has been proven safe for human use. In reality, human clinical data are limited, and long-term animal studies have raised concerns about cancer. Another misconception is that it is a supplement or vitamin-like compound. It is a synthetic research chemical with no approved medical indication. Scientific discussion often focuses on its mechanism and detection rather than therapeutic use. Regulatory and anti-doping literature treats it primarily as a prohibited substance.
Cardarine is explicitly prohibited by the World Anti-Doping Agency under the class of PPARδ agonists. Its presence in urine or blood samples can be detected using mass spectrometry-based methods, often liquid chromatography-tandem mass spectrometry. Athletes who test positive may face sanctions, including bans from competition. The compound is also regulated as a prescription-only or unapproved drug in many countries. Enforcement varies by jurisdiction, and some regions treat it as a controlled substance. Online sales may occur despite these restrictions, creating quality and legal risks.
| Property | Value | Notes |
|---|---|---|
| Common synonyms | GW501516; GW-1516; endurobol | GW501516 is the research code |
| Drug class | PPARδ agonist | Not a selective androgen receptor modulator |
| Molecular formula | C21H18F3NO3S2 | Established chemical formula |
| Molar mass | 453.5 g/mol | Calculated from the formula |
| Regulatory status | Prohibited in sport; not approved as medicine | Status varies by country |
Human trials of GW501516 were small and short in duration. They examined lipid levels, glucose handling, and other metabolic markers, but the programs were halted after the animal cancer findings. No approved therapeutic product exists, and published human data are insufficient for establishing long-term safety. Reports of use for athletic performance come mainly from non-clinical settings and cannot be verified through controlled trials. Independent testing of products sold as cardarine has found inconsistent purity and labeling.
Laboratory studies indicate that GW501516 activates PPARδ, a nuclear receptor involved in fatty acid oxidation and energy metabolism. In rodent experiments, treated animals often showed increased endurance and reduced fat mass. These effects were observed under controlled conditions and do not establish safe or effective use in humans. The exact dose-response relationship in humans remains poorly characterized. Species differences in metabolism can affect how results translate across animals and people.
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.
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.
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.
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 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.
=== Inhibition === NADPH oxidase can be inhibited by apocynin, nitric oxide (NO), and diphenylene iodonium. Apocynin acts by preventing the assembly of the NADPH oxidase subunits. Apocynin decreases influenza-induced lung inflammation in mice in vivo and so may have clinical benefits in the treatment of influenza. Inhibition of NADPH oxidase by NO blocks the source of oxidative stress in the vasculature. NO donor drugs (nitrovasodilators) have therefore been used for more than a century to treat coronary artery disease, hypertension, and heart failure by preventing excess superoxide from deteriorating healthy vascular cells. More advanced NADPH oxidase inhibitors include GKT-831 (Formerly GKT137831), a dual Inhibitor of isoforms NOX4 and NOX1 which was patented in 2007. The compound was initially developed for Idiopathic pulmonary fibrosis and obtained orphan drug designation by the FDA and EMA at end of 2010.
The origin of the hydrophobic effect is not fully understood. Some argue that the hydrophobic interaction is mostly an entropic effect originating from the disruption of highly dynamic hydrogen bonds between molecules of liquid water by the nonpolar solute. A hydrocarbon chain or a similar nonpolar region of a large molecule is incapable of forming hydrogen bonds with water. Introduction of such a non-hydrogen bonding surface into water causes disruption of the hydrogen bonding network between water molecules. The hydrogen bonds are reoriented tangentially to such surface to minimize disruption of the hydrogen bonded 3D network of water molecules, and this leads to a structured water "cage" around the nonpolar surface. The water molecules that form the "cage" (or clathrate) have restricted mobility. In the solvation shell of small nonpolar particles, the restriction amounts to some 10%. For example, in the case of dissolved xenon at room temperature a mobility restriction of 30% has been found. In the case of larger nonpolar molecules, the reorientational and translational motion of the water molecules in the solvation shell may be restricted by a factor of two to four; thus, at 25 °C the reorientational correlation time of water increases from 2 to 4-8 picoseconds. Generally, this leads to significant losses in translational and rotational entropy of water molecules and makes the process unfavorable in terms of the free energy in the system. By aggregating together, nonpolar molecules reduce the surface area exposed to water and minimize their disruptive effect.
== Sources == L. S. Ettre (2004) American Laboratory, May 2004, pages 4-6 In memoriam: Csaba Horváth A. Guttman (2000) American Laboratory, June 2000, pages 6-10 Archived 2022-05-20 at the Wayback Machine Happy Birthday Csaba Horváth The Hungary Page Nobel Prize Winners and Famous Hungarians: Science, Mathematics & Technology Yale news of his death at the Wayback Machine (archived June 17, 2004) "Speeches at his remembrance Service". Archived from the original on June 18, 2004. Retrieved September 13, 2007. Claudia Flavell-White The Chemical Engineer October 2010 pp 54–55 "Degrees of Separation: Chemical Engineers who Changed the World - Csaba Horváth" An Introduction to Separation Science, (1973) B.L. Karger, Cs. Horváth and L.R. Snyder, Wiley
== Biosynthesis == Pancreatic elastase is formed by activation of proelastase from mammalian pancreas by trypsin. After processing to proelastase, it is stored in the zymogen granules and then activated to elastase in the duodenum by the tryptic cleavage of a peptide bond in the inactive form of the precursor molecule. This process results in the removal of an activation peptide from the N-terminal, that enables the enzyme to adopt its native conformation.
== See also == Substituted methylenedioxyphenethylamine List of investigational hallucinogens and entactogens List of investigational autism and pervasive developmental disorder drugs List of investigational social anxiety disorder drugs
Sources: en.wikipedia.org
Genetic engineering and cloning – Different monoclonal antibodies or antibody fragments are fused. Recombinant DNA technology is applied to generate one single, bispecific antibody. Preparation of expression system – An expression system is chosen and prepared for antibody expression. Frequently used expression systems for therapeutic bispecific antibodies are mammalian cells, such as CHO cells, as they are effective in performing complex post-translational modifications. Transfection and protein production – Either via stable or transient transfection, genetic information of the desired bispecific antibodies is inserted into the expression system, which consequently expresses the proteins accordingly. Protein purification – Steps to isolate and enrich bispecific antibodies are taken. This can include several purification processes, such as protein A affinity chromatography or peptide tagging. Antibody characterization – Characterization and quality control conclude the production process. Effector functions, stability and binding specificity are examined at this stage.
Lectins fractionate cells to avoid graft-versus-host disease in hematopoietic stem cell transplantation. Activation and expansion of cytolytic CD8 T cells in cancer treatment. Glycomics is particularly important in microbiology because glycans play diverse roles in bacterial physiology. Research in bacterial glycomics could lead to the development of:
== Substrate recognition == Ubiquitin ligases are the final, and potentially the most important determinant of substrate specificity in ubiquitination of proteins. The ligases must simultaneously distinguish their protein substrate from thousands of other proteins in the cell, and from other (ubiquitination-inactive) forms of the same protein. This can be achieved by different mechanisms, most of which involve recognition of degrons: specific short amino acid sequences or chemical motifs on the substrate.
== Non-inertial frame of reference == The rotating frame of reference introduces some interesting pseudo-forces into the equations through the material derivative term. Consider a stationary inertial frame of reference
==== Hair clippers ==== Sharp hair clippers are used to shave the animal and expose its bare skin. Close contact between brand and bare skin is much more important in freeze branding than in hot branding. This is due to hair's excellent heat insulation, which can drastically reduce heat flux during cryogenic branding. An animal not being shaved closely enough is the main cause of failed brands.
Sources: en.wikipedia.org
No. Cardarine is GW501516, a PPARδ agonist, while SARMs act on androgen receptors. The two classes are often grouped in informal discussions despite different mechanisms.
No. It has no approved medical indication in any country. Regulatory agencies have not cleared it for treatment or prevention of any condition.
Early clinical work stopped after rodent carcinogenicity findings. Those animal results raised concerns about long-term human risk, although direct human evidence is lacking. The human relevance of the tumors remains an open scientific question.
Yes, WADA prohibits cardarine as a PPARδ agonist. It appears on the prohibited list and can be detected in urine or blood. Athletes using it risk sanctions.