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.
Last reviewed on 2026-01-08. Where a claim depends on a specific study, the study is described rather than over-claimed.
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.
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.
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.
| 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. |
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.
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.
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.
== Asia == Asian countries are the primary destination for crude oil from the Gulf, with most of it travelling via the Strait of Hormuz. In 2024, around 84 per cent of the crude oil and 83 per cent of LNG passing through the Strait went to Asia; nearly 70 per cent of the oil went to China, India, Japan, and South Korea. Governments and businesses across the region have been imposing measures to reduce the impact of the fuel crisis, and among the worst hit countries in the region include Pakistan, Bangladesh, and Vietnam.
Spontaneous deamination is the hydrolysis reaction of cytosine into uracil, releasing ammonia in the process. This can occur in vitro through the use of bisulfite, which deaminates cytosine, but not 5-methylcytosine. This property has allowed researchers to sequence methylated DNA to distinguish non-methylated cytosine (shown up as uracil) and methylated cytosine (unaltered). In DNA, this spontaneous deamination is corrected for by the removal of uracil (product of cytosine deamination and not part of DNA) by uracil-DNA glycosylase, generating an abasic (AP) site. The resulting abasic site is then recognised by enzymes (AP endonucleases) that break a phosphodiester bond in the DNA, permitting the repair of the resulting lesion by replacement with another cytosine. A DNA polymerase may perform this replacement via nick translation, a terminal excision reaction by its 5'⟶3' exonuclease activity, followed by a fill-in reaction by its polymerase activity. DNA ligase then forms a phosphodiester bond to seal the resulting nicked duplex product, which now includes a new, correct cytosine (Base excision repair).
=== Climate change === Panera Bread includes a "Cool Food" pledge in its campaign to "curb global warming". Panera Bread provides American consumers with dietary guidelines to help them change their eating patterns to help reduce carbon emissions. Through the Cool Foods pledge, the company uses traffic lights for different healthy and unhealthy foods. Foods labeled "green" are branded healthy, while those labeled "yellow" are warned to be consumed in moderation. In 2015, Panera Bread also announced its policy against the use of genetically modified organisms (GMOs), making it the first food chain in the country to question the safety and environmental friendliness of these foods.
Sources: en.wikipedia.org
Current regimens for treatment of thyrotoxicosis (including Graves' disease), when a patient is exposed to additional sources of iodine, commonly include 500 mg potassium perchlorate twice per day for 18–40 days. Prophylaxis with perchlorate-containing water at concentrations of 17 ppm, which corresponds to 0.5 mg/kg-day personal intake, if one is 70 kg and consumes 2 litres of water per day, was found to reduce baseline radioiodine uptake by 67% This is equivalent to ingesting a total of just 35 mg of perchlorate ions per day. In another related study where subjects drank just 1 litre of perchlorate-containing water per day at a concentration of 10 ppm, i.e. daily 10 mg of perchlorate ions were ingested, an average 38% reduction in the uptake of iodine was observed. However, when the average perchlorate absorption in perchlorate plant workers subjected to the highest exposure has been estimated as approximately 0.5 mg/kg-day, as in the above paragraph, a 67% reduction of iodine uptake would be expected. Studies of chronically exposed workers though have thus far failed to detect any abnormalities of thyroid function, including the uptake of iodine. this may well be attributable to sufficient daily exposure or intake of healthy iodine-127 among the workers and the short 8 hr biological half-life of perchlorate in the body.
=== Pharmacokinetics === After oral intake, ertugliflozin is practically completely absorbed from the gut and undergoes no relevant first-pass effect. Highest blood plasma concentrations are reached after one hour. When in circulation, 93.6% of the substance are bound to plasma proteins. Ertugliflocin is metabolised mainly to glucuronides by the enzymes UGT1A9 and UGT2B7. Cytochrome P450 enzymes play only a minor role in its metabolism. The elimination half-life is estimated to be 17 hours. 40.9% are eliminated via the feces (33.8% in unchanged form and 7.1% as metabolites) and 50.2% via the urine (1.5% unchanged and 48.7% as metabolites). The high proportion of unchanged substance in the feces is probably due to hydrolysis of the metabolites back to the parent substance.
This converts IDL into low-density lipoprotein (LDL), which is taken up by cells that require cholesterol for incorporation into their cell membranes or for synthetic purposes (e.g. the formation of the steroid hormones). The remainder of the LDLs is removed by the liver. Adipose tissue and lactating mammary glands also take up glucose from the blood for conversion into triglycerides. This occurs in the same way as in the liver, except that these tissues do not release the triglycerides thus produced as VLDL into the blood. Adipose tissue cells store the triglycerides in their fat droplets, ultimately to release them again as free fatty acids and glycerol into the blood (as described above), when the plasma concentration of insulin is low, and that of glucagon and/or epinephrine is high. Mammary glands discharge the fat (as cream fat droplets) into the milk that they produce under the influence of the anterior pituitary hormone prolactin. All cells in the body need to manufacture and maintain their membranes and the membranes of their organelles. Whether they rely entirely on free fatty acids absorbed from the blood, or are able to synthesize their own fatty acids from blood glucose, is not known. The cells of the central nervous system will almost certainly have the capability of manufacturing their own fatty acids, as these molecules cannot reach them through the blood–brain barrier.
Sources: en.wikipedia.org
genetic information stored in the sequence of DNA molecules a "messenger" RNA molecule to carry the instructions for making one protein to the cytoplasm adaptor molecules ("they might contain nucleotides") to match short sequences of nucleotides in the RNA messenger molecules to specific amino acids ribonucleic-protein complexes that catalyse the assembly of amino acids into proteins according to the messenger RNA The adaptor molecules were eventually shown to be tRNAs and the catalytic "ribonucleic-protein complexes" became known as ribosomes. An important step was the realisation by Crick and Brenner on 15 April 1960 during a conversation with François Jacob that messenger RNA was not the same thing as ribosomal RNA. Later that summer, Brenner, Jacob, and Matthew Meselson conducted an experiment which was the first to prove the existence of messenger RNA. None of this, however, answered the fundamental theoretical question of the exact nature of the genetic code. In his 1958 article, Crick speculated, as had others, that a triplet of nucleotides could code for an amino acid. Such a code might be "degenerate", with 4×4×4=64 possible triplets of the four nucleotide subunits while there were only 20 amino acids. Some amino acids might have multiple triplet codes. Crick also explored other codes in which, for various reasons, only some of the triplets were used, "magically" producing just the 20 needed combinations. Experimental results were needed; theory alone could not decide the nature of the code.
Conditions with normally functioning neutrophils – hereditary neutrophilia, chronic idiopathic neutrophilia Pelger–Huët anomaly Down syndrome Leukocyte adhesion deficiency Familial cold urticaria Leukemia (chronic myelogenous (CML)) and other myeloproliferative disorders Surgical removal of spleen Secondary causes
== Medical uses == In 1970, Eckelman and Richards presented the first "kit" containing all the ingredients required to release the 99mTc, "milked" from the generator, in the chemical form to be administered to the patient. Technetium-99m is used in 20 million diagnostic nuclear medical procedures every year. Approximately 85% of diagnostic imaging procedures in nuclear medicine use this isotope as radioactive tracer. Klaus Schwochau's book Technetium lists 31 radiopharmaceuticals based on 99mTc for imaging and functional studies of the brain, myocardium, thyroid, lungs, liver, gallbladder, kidneys, skeleton, blood, and tumors. A more recent review is also available. Depending on the procedure, the 99mTc is tagged (or bound to) a pharmaceutical that transports it to its required location. For example, when 99mTc is chemically bound to exametazime (HMPAO), the drug is able to cross the blood–brain barrier and flow through the vessels in the brain for cerebral blood-flow imaging. This combination is also used for labeling white blood cells (99mTc labeled WBC) to visualize sites of infection. 99mTc sestamibi is used for myocardial perfusion imaging, which shows how well the blood flows through the heart. Imaging to measure renal function is done by attaching 99mTc to mercaptoacetyl triglycine (MAG3); this procedure is known as a MAG3 scan.
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 GW501516, a PPARδ agonist, while SARMs act on androgen receptors. The two classes are often grouped in informal discussions despite different mechanisms.