GW501516 comes up often in conversation and rarely with the context attached. Here we lay out the basics in order, then work through the practical considerations.
Updated 2026-03-02. Numbers and descriptions here follow the published literature rather than marketing material.
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.
In the fitness and bodybuilding literature, cardarine is frequently discussed as an endurance agent or fat-loss compound, although such claims are not supported by robust clinical evidence. Online descriptions often mix animal data, user anecdotes, and marketing language. Researchers who study PPARδ agonists distinguish between receptor activation in controlled experiments and unsupervised use of unverified products. The latter introduces unknown purity, dose, and interactions, making reported experiences difficult to interpret scientifically.
GW501516 acts as an agonist at peroxisome proliferator-activated receptor delta, a nuclear receptor involved in transcription of genes related to lipid handling and energy use. Activation of PPARδ can shift skeletal muscle toward greater fatty acid oxidation in animal models, which is one reason it drew interest for metabolic disease and exercise research. The exact downstream effects depend on tissue, species, dose, and duration. Human data are sparse, so many proposed benefits remain hypotheses rather than established clinical outcomes.
Laboratory studies have examined GW501516 in cell cultures and rodents for conditions such as dyslipidemia, insulin resistance, and obesity. Some trials in humans were initiated, but development was discontinued after preclinical findings raised concerns about cancer in certain models. Those findings do not prove that the compound causes cancer in people, but they contributed to regulatory caution. Later reviews often describe the evidence as preliminary and insufficient for assessing long-term safety.
| 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 |
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.
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.
Literature on cardarine often separates receptor pharmacology from toxicology. Mechanistic papers describe PPARδ activation and gene expression changes, while safety assessments focus on carcinogenicity and species differences. Questions remain about whether rodent tumors arise through PPARδ-dependent or off-target mechanisms. Another open area is how human metabolism and exposure compare with those in animal studies. Analytical methods such as liquid chromatography–mass spectrometry are used to confirm identity in biological and product samples.
GW501516 acts as an agonist at the peroxisome proliferator-activated receptor delta, a nuclear receptor that regulates gene expression. Activation shifts transcription toward genes involved in fatty acid uptake, oxidation, and energy expenditure. The compound does not bind the androgen receptor and therefore differs from anabolic steroids and SARMs. In rodent models, this metabolic shift has been linked to increased running endurance and reduced fat accumulation. The exact downstream pathways in humans remain incompletely characterized.
Early clinical research explored GW501516 for lipid disorders, obesity, and diabetes. Some short-term human studies reported changes in HDL cholesterol, LDL cholesterol, and triglycerides. The development program was discontinued after rodent studies showed dose-dependent tumor formation in multiple tissues, including liver, bladder, stomach, and skin. These findings raised concerns about long-term cancer risk in humans. Because human exposure data are limited, the clinical significance of the rodent tumors remains uncertain.
Regulatory treatment of cardarine differs by context and jurisdiction. In competitive sport, the World Anti-Doping Agency lists PPARδ agonists, including GW501516, as prohibited at all times. Outside sport, it lacks approval as a prescription medicine in major drug markets, and products sold for human consumption may be treated as unapproved drugs. Some countries also restrict importation or sale through general consumer protection and medicines laws. These classifications affect availability, testing, and legal risk without establishing therapeutic value.
Because cardarine is not an approved medicine, no pharmacopeial monograph defines its identity, purity, or storage requirements. Laboratories typically rely on in-house methods and reference standards when testing materials labeled as GW501516. Certificates of analysis may report purity and identity for a specific batch, but their scope varies and they do not guarantee safety or legal status. Independent verification can include high-performance liquid chromatography, mass spectrometry, nuclear magnetic resonance, and elemental analysis. The distinction between research chemical labeling and human use is significant because quality standards and oversight differ.
Cardarine can be detected in biological samples and product materials using liquid chromatography coupled to tandem mass spectrometry (LC-MS/MS). The method separates compounds by chromatography and identifies them by mass-to-charge transitions, allowing low-level detection in urine or blood. Sample preparation often involves enzymatic hydrolysis, solid-phase extraction, or protein precipitation. Certified reference materials and isotope-labeled internal standards improve quantification. Detection windows depend on metabolism, matrix, and assay sensitivity, so no single universal window applies.
The valence of an element can be defined either as the number of hydrogen atoms that can combine with it to form a simple binary hydride, or as twice the number of oxygen atoms that can combine with it to form a simple binary oxide (that is, not a peroxide or a superoxide). The valences of the main-group elements are directly related to the group number: the hydrides in the main groups 1–2 and 13–17 follow the formulae MH, MH2, MH3, MH4, MH3, MH2, and finally MH. The highest oxides instead increase in valence, following the formulae M2O, MO, M2O3, MO2, M2O5, MO3, M2O7. Today the notion of valence has been extended by that of the oxidation state, which is the formal charge left on an element when all other elements in a compound have been removed as their ions. The electron configuration suggests a ready explanation from the number of electrons available for bonding; indeed, the number of valence electrons starts at 1 in group 1, and then increases towards the right side of the periodic table, only resetting at 3 whenever each new block starts. Thus in period 6, Cs–Ba have 1–2 valence electrons; La–Yb have 3–16; Lu–Hg have 3–12; and Tl–Rn have 3–8. However, towards the right side of the d- and f-blocks, the theoretical maximum corresponding to using all valence electrons is not achievable at all; the same situation affects oxygen, fluorine, and the light noble gases up to krypton.
The frog's brands were healed and readable within 24 hours of application, making this method nearly immediately effective as a tracking system. The branded area gradually loses its pigmentation such that older brands become almost completely transparent, increasing their legibility over time.
== Pathology == Abnormally elevated levels of glucagon may be caused by pancreatic tumors, such as glucagonoma, symptoms of which include necrolytic migratory erythema, reduced amino acids, and hyperglycemia. It may occur alone or in the context of multiple endocrine neoplasia type 1. Elevated glucagon is the main contributor to hyperglycemic ketoacidosis in undiagnosed or poorly treated type 1 diabetes. As the beta cells cease to function, insulin and pancreatic GABA are no longer present to suppress the freerunning output of glucagon. As a result, glucagon is released from the alpha cells at a maximum, causing a rapid breakdown of glycogen to glucose and fast ketogenesis. It was found that a subset of adults with type 1 diabetes took 8 hours longer on average (18 hours vs 10 hours) to approach ketoacidosis when given somatostatin (inhibits glucagon production) with no insulin. Inhibiting glucagon has been a popular idea of diabetes treatment, however, some have warned that doing so will give rise to brittle diabetes in patients with adequately stable blood glucose. The absence of alpha cells (and hence glucagon) is thought to be one of the main influences in the extreme volatility of blood glucose in the setting of a total pancreatectomy.
== In medicine == Prolactin is available commercially for use in other animals, but not in humans. It is used to stimulate lactation in animals. The biological half-life of prolactin in humans is around 15–20 minutes. The D2 receptor is involved in the regulation of prolactin secretion, and agonists of the receptor such as bromocriptine and cabergoline decrease prolactin levels while antagonists of the receptor such as domperidone, metoclopramide, haloperidol, risperidone, and sulpiride increase prolactin levels. D2 receptor antagonists like domperidone, metoclopramide, and sulpiride are used as galactogogues to increase prolactin secretion in the pituitary gland and induce lactation in humans.
== History == Sildenafil (compound UK-92,480) was synthesized in 1989 by a group of pharmaceutical chemists led by Simon Campbell working at Pfizer's Sandwich, Kent, research facility in England. It was initially studied for use in hypertension (high blood pressure) and angina pectoris (a symptom of ischaemic heart disease). The first clinical trials were conducted in Morriston Hospital in Swansea. Phase I clinical trials under the direction of Ian Osterloh suggested the drug had little effect on angina, but it could induce marked penile erections. Pfizer therefore decided to market it for erectile dysfunction, rather than for angina; this decision became an often-cited example of drug repositioning. The drug was patented in 1996, approved for use in erectile dysfunction by the FDA on 27 March 1998, becoming the first oral treatment approved to treat erectile dysfunction in the United States, and offered for sale in the United States later that year. It soon became a great success: annual sales of Viagra peaked in 2008 at US$1.934 billion.
Sources: en.wikipedia.org
=== ZMapp === A 2014 paper described how Mapp and its collaborators, including investigators at Public Health Agency of Canada, Kentucky BioProcessing, and the National Institute of Allergy and Infectious Diseases, first chimerized the three antibodies comprising ZMAb, then tested combinations of MB-003 and the chimeric ZMAb antibodies in guinea pigs and then primates to determine the best combination, which turned out to be c13C6 from MB-003 and two chimeric mAbs from ZMAb, c2G4 and c4G7. This is ZMapp. In an experiment also published in the 2014 paper, 21 rhesus macaque primates were infected with the Kikwit Congolese variant of EBOV. Three primates in the control arm were given a non-functional antibody, and the 18 in the treatment arm were divided into three groups of six. All primates in the treatment arm received three doses of ZMapp, spaced 3 days apart. The first treatment group received its first dose on 3rd day after being infected; the second group on the 4th day after being infected, and the third group, on the 5th day after being infected. All three primates in the control group died; all 18 primates in the treatment arm survived. Mapp then went on to show that ZMapp inhibits replication of a Guinean strain of EBOV in cell cultures. Mapp remains involved in the production of the drug through its contracts with Kentucky BioProcessing, a subsidiary of Reynolds American.
=== Laser === In 2014, a CO2 infrared laser was used to produce patterned porous three-dimensional laser-induced graphene (LIG) film networks from commercial polymer films. The resulting material exhibits high electrical conductivity and surface area. The laser induction process is compatible with roll-to-roll manufacturing processes. A similar material, laser-induced graphene fibers (LIGF), was reported in 2018.
== Sources == Furlow, John J. (1997). "Betula". In Flora of North America Editorial Committee (ed.). Flora of North America North of Mexico (FNA). Vol. 3. New York and Oxford: Oxford University Press – via eFloras.org, Missouri Botanical Garden, St. Louis, Missouri and Harvard University Herbaria, Cambridge, Massachusetts. Li, Pei-chun; Skvortsov, Alexei K. "Betula". Flora of China. Vol. 4 – via eFloras.org, Missouri Botanical Garden, St. Louis, Missouri and Harvard University Herbaria, Cambridge, Massachusetts. Grimshaw, John (2009). New Trees, Recent introductions to cultivation. Kew Publishing, RBG Kew. pp. 163–174. Chisholm, Hugh, ed. (1911). "Birch" . Encyclopædia Britannica. Vol. 3 (11th ed.). Cambridge University Press. Jonczak, Jerzy; Jankiewicz, Urszula; Kondras, Marek; Kruczkowska, Bogusława; Oktaba, Lidia; Oktaba, Jarosław; Olejniczak, Izabella; Pawłowicz, Edyta; Polláková, Nora; Raab, Thomas; Regulska, Edyta; Słowińska, Sandra; Sut-Lohmann, Magdalena (December 2020). "The influence of birch trees (Betula spp.) on soil environment – A review". Forest Ecology and Management. 477 118486. Bibcode:2020ForEM.47718486J. doi:10.1016/j.foreco.2020.118486.
In animals, fatty acids are formed from carbohydrates predominantly in the liver, adipose tissue, and the mammary glands during lactation. Carbohydrates are converted into pyruvate by glycolysis as the first important step in the conversion of carbohydrates into fatty acids. Pyruvate is then decarboxylated to form acetyl-CoA in the mitochondrion. However, this acetyl CoA needs to be transported into cytosol where the synthesis of fatty acids occurs. This cannot occur directly. To obtain cytosolic acetyl-CoA, citrate (produced by the condensation of acetyl-CoA with oxaloacetate) is removed from the citric acid cycle and carried across the inner mitochondrial membrane into the cytosol. There it is cleaved by ATP citrate lyase into acetyl-CoA and oxaloacetate. The oxaloacetate is returned to the mitochondrion as malate. The cytosolic acetyl-CoA is carboxylated by acetyl-CoA carboxylase into malonyl-CoA, the first committed step in the synthesis of fatty acids. Malonyl-CoA is then involved in a repeating series of reactions that lengthens the growing fatty acid chain by two carbons at a time. Almost all natural fatty acids, therefore, have even numbers of carbon atoms. When synthesis is complete the free fatty acids are nearly always combined with glycerol (three fatty acids to one glycerol molecule) to form triglycerides, the main storage form of fatty acids, and thus of energy in animals.
That the centrifugal force and the frictional force between the wall of the rotating flask and the liquid sample result in the formation of a thin film of warm solvent being spread over a large surface. The forces created by the rotation suppress bumping. The combination of these characteristics and the conveniences built into modern rotary evaporators allow for quick, gentle evaporation of solvents from most samples, even in the hands of relatively inexperienced users. Solvent remaining after rotary evaporation can be removed by exposing the sample to even deeper vacuum, on a more tightly sealed vacuum system, at ambient or higher temperature (e.g., on a Schlenk line or in a vacuum oven). A key disadvantage in rotary evaporations, besides its single sample nature, is the potential of some sample types to bump, e.g. ethanol and water, which can result in loss of a portion of the material intended to be retained. Even professionals experience periodic mishaps during evaporation, especially bumping, though experienced users become aware of the propensity of some mixtures to bump or foam, and apply precautions that help to avoid most such events. In particular, bumping can often be prevented by taking homogeneous phases into the evaporation, by carefully regulating the strength of the vacuum (or the bath temperature) to provide for an even rate of evaporation, or, in rare cases, through use of added agents such as boiling chips (to make the nucleation step of evaporation more uniform).
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.
It binds and activates PPARδ, a nuclear receptor that influences gene expression related to fatty acid metabolism and energy balance. This mechanism has been studied mainly in animals and cell models, not established as a safe human therapy.