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.
Updated 2026-05-21. Numbers and descriptions here follow the published literature rather than marketing material.
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.
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.
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.
| Property | Value | Notes |
|---|---|---|
| Chemical class | PPARδ agonist | Not an anabolic steroid. |
| Common synonyms | GW501516, GW-1516 | Cardarine is an informal name. |
| Appearance | White to off-white powder | Typical for research-grade solid. |
| Solubility class | Poorly soluble in water; soluble in some organic solvents | Such as DMSO or ethanol in laboratory settings. |
| Typical storage temperature | Cool, dry, protected from light | Specific conditions vary by supplier and form. |
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 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.
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.
=== Federal politics (2011–2025) === She was named the Conservative Party's candidate for Delta—Richmond East in March 2011, and won the seat in that year's federal election. During the 41st Parliament, she served as member of the House of Commons Standing Committee on Justice and Human Rights, and sat on a selection panel to help choose a replacement for Marie Deschamps of Quebec, who retired as puisne justice of the Supreme Court of Canada. She was named Parliamentary Secretary to the Minister of Justice in May 2011, and as Associate Minister of National Defence on February 22, 2013. She then served as the Minister of National Revenue from July 15, 2013, until November 4, 2015.
aminoglycosides (gentamicin, amikacin, tobramycin, but not kanamycin) quinolones (ciprofloxacin, levofloxacin, but not moxifloxacin) cephalosporins (ceftazidime, cefepime, cefoperazone, cefpirome, ceftobiprole, but not cefuroxime, cefotaxime, or ceftriaxone) antipseudomonal penicillins: carboxypenicillins (carbenicillin and ticarcillin), and ureidopenicillins (mezlocillin, azlocillin, and piperacillin). P. aeruginosa is intrinsically resistant to all other penicillins. carbapenems (meropenem, imipenem, doripenem, but not ertapenem) polymyxins (polymyxin B and colistin) monobactams (aztreonam) As fluoroquinolones are one of the few antibiotic classes widely effective against P. aeruginosa, in some hospitals, their use is severely restricted to avoid the development of resistant strains. On the rare occasions where infection is superficial and limited (for example, ear infections or nail infections), topical gentamicin or colistin may be used. For pseudomonal wound infections, acetic acid with concentrations from 0.5% to 5% can be an effective bacteriostatic agent in eliminating the bacteria from the wound. Usually a sterile gauze soaked with acetic acid is placed on the wound after irrigation with normal saline. Dressing would be done once per day. Pseudomonas is usually eliminated in 90% of the cases after 10 to 14 days of treatment.
An overview of the diversity and evolution of snake fangs. Snake VenomsUMich Orientation of Proteins in Membranes families/superfamily-55 - Calculated orientations of snake venom phospholipases A2 and myotoxins in the lipid bilayer. An untapped biochemical archive in natural history collections, study of venom components for new drugs. BioRxiv, May 22, 2026. doi: https://doi.org/10.64898/2026.05.22.727068 LD50's for most toxic venoms. Australian Venom Research Unit Archived 24 February 2015 at the Wayback Machine – a general source of information for venomous creatures in Australia. biomedcentral.com – Medicinal and ethnoveterinary remedies of hunters in Trinidad. reptilis.net – How venom works. snakevenom.net – Drying and storage of snake venom.
== History == In 1902, William Bayliss and Ernest Starling were studying how the nervous system controls the process of digestion. It was known that the pancreas secreted digestive juices in response to the passage of food (chyme) through the pyloric sphincter into the duodenum. They discovered (by cutting all the nerves to the pancreas in their experimental animals) that this process was not, in fact, governed by the nervous system. They determined that a substance secreted by the intestinal lining stimulates the pancreas after being transported via the bloodstream. They named this intestinal secretion secretin. This type of 'chemical messenger' substance is now called a hormone, a term coined by Starling in 1905. Secretin is frequently erroneously stated to have been the first hormone identified. However, British researchers George Oliver and Edward Albert Schäfer had already published their findings of an adrenal extract increasing blood pressure and heart rate in brief reports in 1894 and a full publication in 1895, making adrenaline the first discovered hormone.
Sources: en.wikipedia.org
The Census Bureau's 2006–2010 American Community Survey showed that (in 2010 inflation-adjusted dollars) median household income was $105,625 (with a margin of error of +/− $14,945) and the median family income was $128,382 (+/− $16,732). Males had a median income of $95,795 (+/− $24,665) versus $72,188 (+/− $16,155) for females. The per capita income for the borough was $56,485 (+/− $6,202). About 2.4% of families and 4.0% of the population were below the poverty line, including 1.8% of those under age 18 and 9.4% of those age 65 or over.
Instead, they reduce the release of excitatory neurotransmitters including glutamate, monoamine neurotransmitters and Substance P. Although not thought to be a major site of action, gabapentinoids such as gabapentin, but not pregabalin, have been found to activate Kv voltage-gated potassium channels (KCNQ). The endogenous α-amino acids L-leucine and L-isoleucine, which resemble the gabapentinoids in chemical structure (see figure) are ligands of the α2δ VDCC subunit with similar affinity as gabapentin and pregabalin (e.g., IC50 = 71 nM for L-isoleucine), and are present in human cerebrospinal fluid at micromolar concentrations (e.g., 12.9 μM for L-leucine, 4.8 μM for L-isoleucine). It has been hypothesized that they may be endogenous ligands of the subunit and that they may competitively antagonize the effects of gabapentinoids in brain tissues. In accordance, while gabapentin and pregabalin have nanomolar binding affinities for the α2δ subunit, their potencies in vivo are in the low micromolar range, and competition for binding by endogenous L-amino acids is likely responsible for this discrepancy. In one study, the affinity (Ki) values of gabapentinoids for the α2δ subunit expressed in rat brain were found to be 0.05 μM for gabapentin, 23 μM for (R)-phenibut, 39 μM for (S)-phenibut, and 156 μM for baclofen. Their affinities (Ki) for the GABAB receptor were >1 mM for gabapentin, 92 μM for (R)-phenibut, >1 mM for (S)-phenibut, 6 μM for Baclofen.
== Metabolism == The enzyme taxifolin 8-monooxygenase uses taxifolin, NADH, NADPH, H+, and O2 to produce 2,3-dihydrogossypetin, NAD+, NADP+, and H2O. The enzyme leucocyanidin oxygenase uses leucocyanidin, alpha-ketoglutarate, and O2 to produce cis-dihydroquercetin, taxifolin, succinate, CO2, and H2O.
With use, muscles consume energy derived from both fat and glycogen. Due to the large size of leg muscles, walking, running and cycling are the most effective means of exercise to reduce body fat. Exercise affects macronutrient balance. During moderate exercise, equivalent to a brisk walk, there is a shift to greater use of fat as a fuel. To maintain health, the American Heart Association recommends a minimum of 30 minutes of moderate exercise at least 5 days a week. The Cochrane Collaboration found that exercising alone led to limited weight loss. In combination with diet, however, it resulted in a 1 kilogram weight loss over dieting alone. A 1.5 kilograms (3.3 pounds) loss was observed with a greater degree of exercise. Even though exercise as carried out in the general population has only modest effects, a dose response curve is found and very intense exercise can lead to substantial weight loss. During 20 weeks of basic military training with no dietary restriction, obese military recruits lost 12.5 kg (28 lb). High levels of physical activity seem to be necessary to maintain weight loss. A pedometer appears useful for motivation. Over an average of 18-weeks of use, physical activity increased by 27% resulting in a 0.38 decrease in BMI. Signs that encourage the use of stairs as well as community campaigns have been shown to be effective in increasing exercise in a population. The city of Bogotá, Colombia, for example, blocks off 113 kilometers (70 mi) of roads every Sunday and on holidays to make it easier for its citizens to get exercise.
Cobalt (Co) is a rare, essential trace element needed by adults at the level of 0.1 μg per day as part of vitamin B12. Levels above 10 mg per day can cause severe cardiomyopathies. Copper (Cu) is essential for human health and copper toxicity is rare and occurs primarily in inherited diseases of the liver. Iron (Fe) is required for hemoglobin in red blood cells. Large excesses of iron from dietary supplements, on the order of 0.5 g, can cause acute iron poisoning. Magnesium (Mg), important for many types of reactions in cells, rarely poses a hazard unless ingested by people with severe renal failure or as metal fume fever from magnesium oxide. Manganese (Mn) inhalation during mining causes manganese poisoning. Molybdenum (Mo) is an essential element with low toxicity. Its toxicity resembles copper deficiency and treatment with copper reduces the toxic effects of molybdenum. Selenium (Se) is a required nutrient to form selenoproteins; inadequate amounts lead to Keshan disease. Excess selenium causes Selenosis. However the element itself has low solubility and the biologically active forms are ions +6, +4, and +2. Zinc (Zn) has a Recommended dietary allowance of 15 mg and is only toxic at ten times that amount. Zinc toxicity is rare. Free zinc ion in solution is highly toxic to bacteria, plants, invertebrates, and fish. Metal fume fever occurs when zinc oxide (ZnO) is inhaled by welders working on galvanized steel or brass. Dietary deficits of some metals, including calcium (Ca), zinc, iron, selenium, copper, chromium and manganese increase toxic effects of metals.
Sources: en.wikipedia.org
Cardarine is commonly known as GW501516 or GW-1516. These names refer to the same synthetic compound. It is not a brand-name approved medicine.
No, cardarine is not a steroid. It is classified as a PPARδ agonist. Its structure and receptor target differ from anabolic steroids.
No regulatory agency has approved cardarine as a medicine. It was investigated in early research but development was discontinued. It is not available as a prescription drug.
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.