The short version of PPARδ agonist fits in a sentence. The long version — which is the one that helps — is below.
This page was last updated on 2026-05-14 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, 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.
| 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 |
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.
Cardarine is a common name for GW501516, also GW-1516, a synthetic compound developed as a peroxisome proliferator-activated receptor delta (PPARδ) agonist. It belongs to a class of agents that modulate gene transcription related to lipid and energy metabolism. The compound was studied in preclinical and early clinical research for metabolic and cardiovascular conditions, but it did not progress to approved therapeutic use. Its name appears in fitness and sports contexts despite not being approved as a drug.
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.
However, estimates vary and the effective dose to the lungs ranges between 0.3 mSv/year to 20 mSv/year. Some of the mineral apatite in Florida used to produce phosphate for US tobacco crops contains uranium, radium, lead-210 and polonium-210 and radon. The radioactive smoke from tobacco fertilized this way is deposited in lungs and releases radiation even if a smoker quits the habit. The combination of carcinogenic tar and radiation in a sensitive organ such as lungs increases the risk of cancer. In contrast, a 1999 review of tobacco smoke carcinogens published in the Journal of the National Cancer Institute states that "levels of polonium-210 in tobacco smoke are not believed to be great enough to significantly impact lung cancer in smokers." In 2011 Hecht has also stated that the "levels of 210Po in cigarette smoke are probably too low to be involved in lung cancer induction".
=== Transportation and detoxification === This could happen in two different ways: ammonia itself might simply diffuse (as NH3) or be transported (as NH4+) across the cell membranes in and out of the extracellular space, or a shuttle system involving carrier molecules (amino acids) might be employed. Certainly, ammonia can diffuse across lipid membranes, and it has been shown that ammonia can be transported by K+/Cl− co-transporters.
The regulation of genetic engineering concerns approaches taken by governments to assess and manage the risks associated with the use of genetic engineering technology, and the development and release of genetically modified organisms (GMO), including genetically modified crops and genetically modified fish. There are differences in the regulation of GMOs between countries, with some of the most marked differences occurring between the US and Europe. Regulation varies in a given country depending on the intended use of the products of the genetic engineering. For example, a crop not intended for food use is generally not reviewed by authorities responsible for food safety. The European Union differentiates between approval for cultivation within the EU and approval for import and processing. While only a few GMOs have been approved for cultivation in the EU a number of GMOs have been approved for import and processing. The cultivation of GMOs has triggered a debate about the coexistence of GM and non-GM crops. Depending on the coexistence regulations, incentives for the cultivation of GM crops differ.
Sources: en.wikipedia.org
=== Active site === Histidinol is held inside the active site thanks to a zinc ion, but the zinc ion does not participate in the catalysis otherwise. The zinc ion is held in place by His262, Gln259, Asp360 and His419 (which, in homodimeric histidinol dehydrogenases, comes from the other monomer). Histidinol itself is held in place by His327 and His367 from one moment unit and Glu414 from the other monomer unit. A Cys residue has been implicated in the catalytic mechanism of the second oxidative step. However, according to newer studies with histidinol dehydrogenase from E. coli, the mechanism is catalyzed by four bases, B1-B4. His327 acts as the first base, deprotonating histidinol's hydroxyl group. Concomitantly, hydride is abstracted from histidinol by NAD+, which is then exchanged for a second NAD+ molecule. Glu325 acts as the second base, deprotonating a molecule of water, which then attacks histidinol. At the same time, His327 (now protonated) donates a proton to the aldehydic oxygen, which results in a gem-diol. After then, His327 again deprotonates one of the hydroxyl groups and NAD+ abstracts a proton from the reactive carbon atom. This series of steps oxidizes the hydroxyl group to a carboxylic acid.
When using different buffers in the gel (discontinuous gel electrophoresis), the gels are made up to one day prior to electrophoresis, so that the diffusion does not lead to a mixing of the buffers. The gel is produced by free radical polymerization in a mold consisting of two sealed glass plates with spacers between the glass plates. In a typical mini-gel setting, the spacers have a thickness of 0.75 mm or 1.5 mm, which determines the loading capacity of the gel. For pouring the gel solution, the plates are usually clamped in a stand which temporarily seals the otherwise open underside of the glass plates with the two spacers. For the gel solution, acrylamide is mixed as gel-former (usually 4% V/V in the stacking gel and 10-12 % in the separating gel), methylenebisacrylamide as a cross-linker, stacking or separating gel buffer, water and SDS. By adding the catalyst TEMED and the radical initiator ammonium persulfate (APS) the polymerisation is started. The solution is then poured between the glass plates without creating bubbles. Depending on the amount of catalyst and radical starter and depending on the temperature, the polymerisation lasts between a quarter of an hour and several hours. The lower gel (separating gel) is poured first and covered with a few drops of a barely water-soluble alcohol (usually buffer-saturated butanol or isopropanol), which eliminates bubbles from the meniscus and protects the gel solution of the radical scavenger oxygen.
== Site-directed mutagenesis == This method use DNA recombinant technology and it gives an actual measurement of protein stability. In his detailed site-directed mutagenesis studies, Utani and his coworkers substituted 19 amino acids at Trp49 of the tryptophan synthase and he measured the free energy of unfolding. They found that the increased stability is directly proportional to increase in hydrophobicity up to a certain size limit. The main disadvantage of site-directed mutagenesis method is that not all the 20 naturally occurring amino acids can substitute a single residue in a protein. Moreover, these methods have cost problems and is useful only for measuring protein stability.
The initial development of the cell marked the passage from prebiotic chemistry to partitioned units resembling modern cells. The final transition to living entities that fulfill all the definitions of modern cells depended on the ability to evolve effectively by natural selection. This transition has been called the Darwinian transition. If life is viewed from the point of view of replicator molecules, cells satisfy two fundamental conditions: protection from the outside environment and confinement of biochemical activity. The former condition is needed to keep complex molecules stable in a varying and sometimes reactive environment; the latter is fundamental for the evolution of biocomplexity. If freely floating molecules that code for enzymes are not enclosed in cells, the enzymes will automatically benefit neighboring replicator molecules as well. Thus, the consequences of diffusion in non-partitioned lifeforms would result in "parasitism by default." Therefore, the selection pressure on replicator molecules will be lower, as the 'lucky' molecule that produces the better enzyme does not fully leverage its advantage over its close neighbors. In contrast, if the molecule is enclosed in a cell membrane, the enzymes coded will be available only to itself. That molecule will uniquely benefit from the enzymes it codes for, increasing individuality and thus accelerating natural selection. Partitioning may have begun from cell-like spheroids formed by proteinoids, which are observed by heating amino acids with phosphoric acid as a catalyst.
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.
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.