PPARδ agonist 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 2026-03-15. Where a claim depends on a specific study, the study is described rather than over-claimed.
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.
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.
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.
| 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 |
Cardarine is not approved for human therapeutic use in any major jurisdiction. It appears on the World Anti-Doping Agency Prohibited List as a PPARδ agonist within the hormone and metabolic modulators category. Sports organizations test for it because it has been detected in athlete samples and seized products. Regulatory actions against marketed research chemical versions have occurred in several countries, though enforcement varies. Availability through unregulated channels complicates oversight.
Analytical laboratories typically identify cardarine and its metabolites using liquid chromatography-tandem mass spectrometry. Urine is a common matrix in anti-doping testing, while blood and tissue may be used in research settings. Detection windows depend on the assay, the sample matrix, and the compound's metabolism. Because cardarine is extensively metabolized, laboratories often target specific metabolites to improve sensitivity and confirmation. Reference standards are required for reliable quantification. Method validation includes checks for selectivity, linearity, and carryover.
A persistent misconception is that cardarine is a fat-burning drug or a safe alternative to anabolic steroids. No approved therapeutic product exists, and human safety data are limited. The tumor findings in rodents remain a central concern in scientific reviews. Products sold online may contain inaccurate labels, impurities, or different compounds entirely, which complicates any assessment of effects. Independent testing of such products has reported frequent mislabeling. For these reasons, discussions in the literature emphasize risks and unknowns rather than benefits.
Safety concerns emerged from long-term animal studies. In rodents given the compound for extended periods, researchers found an increased incidence of certain cancers, including liver and bladder tumors. These findings contributed to the discontinuation of clinical development. Whether similar risks apply to short-term or low-level exposure in humans is not established, and controlled human safety data are limited. The relevance of high-dose rodent carcinogenicity findings to human use remains a subject of debate.
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.
=== Bond strain === This is the principal effect of induced fit binding, where the affinity of the enzyme to the transition state is greater than to the substrate itself. This induces structural rearrangements which strain substrate bonds into a position closer to the conformation of the transition state, so lowering the energy difference between the substrate and transition state and helping catalyze the reaction. However, the strain effect is, in fact, a ground state destabilization effect, rather than transition state stabilization effect. Furthermore, enzymes are very flexible and they cannot apply large strain effect. In addition to bond strain in the substrate, bond strain may also be induced within the enzyme itself to activate residues in the active site.
Nor-LSD, or norLSD, also known as N,N-diethyl-6-norlysergamide or as N-desmethyllysergic acid diethylamide (N-desmethyl-LSD), is a serotonin receptor modulator and putative psychedelic of the lysergamide family related to lysergic acid diethylamide (LSD). It is the analogue of LSD in which the methyl group at the 6 position of the ergoline ring system has been removed.
==== Cross-linking ==== Cross-linkage: another irreversible method that does not require a support material for the attachment of enzyme molecules. In this technique, the molecules of enzymes are covalently bonded to each other to create a matrix consisting of almost only enzyme. The reaction ensures that the binding site does not cover the enzyme's active site, the activity of the enzyme is only affected by immobility. However, the inflexibility of the covalent bonds precludes the self-healing properties exhibited by chemo-adsorbed self-assembled monolayers. Use of a spacer molecule like poly(ethylene glycol) helps in the reduction of steric hindrance by the substrate in this case.
As of 2018, the treaty has been signed by 166 countries, by signing states agreed to take steps to the maximum of their available resources to achieve the right to adequate food. However, after the 1966 International Covenant the global concern for the access to sufficient food only became more present, leading to the first ever World Food Conference that was held in 1974 in Rome, Italy. The Universal Declaration on the Eradication of Hunger and Malnutrition was a UN resolution adopted November 16, 1974, by all 135 countries that attended the 1974 World Food Conference. This non-legally binding document set forth certain aspirations for countries to follow to sufficiently take action on the global food problem. Ultimately this document outline and provided guidance as to how the international community as one could work towards fighting and solving the growing global issue of malnutrition and hunger. Adoption of the right to food was included in the Additional Protocol to the American Convention on Human Rights in the area of Economic, Social, and Cultural Rights, this 1978 document was adopted by many countries in the Americas, the purpose of the document is, "to consolidate in this hemisphere, within the framework of democratic institutions, a system of personal liberty and social justice based on respect for the essential rights of man." A later document in the timeline of global initiatives for malnutrition was the 1996 Rome Declaration on World Food Security, organized by the Food and Agriculture Organization.
Sources: en.wikipedia.org
Open aortic surgery with replacement of the damaged section of the aorta with a tube graft (often made of Dacron) when no damage to the aortic valve is seen Bentall procedure – replacement of the damaged section of the aorta and replacement of the aortic valve David procedure – replacement of the damaged section of the aorta and reimplantation of the aortic valve Thoracic endovascular aortic repair, a minimally invasive surgical procedure usually combined with ongoing medical management Frozen elephant trunk procedure (FET) is one-stage procedure for the repair of acute aortic dissection that permits concurrent total aortic arch replacement with antegrade delivery of a descending aortic stent-graft which itself functions as a proximal landing zone to facilitate prospective endovascular intervention (TEVAR) to treat residual or de novo disease in the more distal aorta. A number of comorbid conditions increase the surgical risk of repair of an aortic dissection. These conditions include the following:
=== As a supplement === A series of studies showed that a combination of betaine and glycocyamine improves the symptoms of patients with chronic illness, including heart disease, without toxicity. Betaine can provide a methyl group to glycocyamine, via methionine, for the formation of creatine. In overall, such treatment led to less fatigue, greater strength and endurance, and an improved sense of well-being. The patients with cardiac decompensation (arteriosclerosis or rheumatic disease) and congestive heart failure had improved cardiac function. The patients gained weight (improved nitrogen balance) and saw lessened symptoms of arthritis and asthma and increased libido, and those people suffering from hypertension experienced transient reduced blood pressure. Also the studies shows the increase of glucose tolerance in both diabetic subjects and subjects without diabetes.
SISCAPA’s use of proteolytic digestion as a first step eliminates the protein:protein complexes (including complexes of a target protein with auto-antibodies) that cause “interferences” in protein capture assays, including conventional immunoassays (e.g., ELISA assays). Elimination of such autoantibody interferences drove the adoption of SISCAPA as an alternative to immunoassays for clinical measurement of thyroglobulin as a marker of thyroid cancer recurrence in patients who exhibit anti-thyroglobulin autoantibodies. A limitation of the specific peptide capture approach is the requirement for a specially developed antibody against the selected peptide. To date several hundred anti-peptide antibody reagents have been developed for enrichment of tryptic peptides from sample digests, mainly for established clinical biomarkers (,) and cancer research targets, but these do not yet cover a majority of protein targets of interest in non-cancer research or clinical contexts. A variety of MS instrument types have been used for quantitation of the enriched peptides, including most frequently triple quadrupole mass spectrometers implementing the “multiple reaction monitoring” (MRM) method (a format sometimes referred to as “immuno-MRM”), and MALDI-ToF (a format sometimes referred to as iMALDI).
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.
LC-MS/MS is common, often after sample cleanup. The assay targets GW501516 or its metabolites.