GW501516 raises a handful of sensible questions. This page answers them in order, starting with the fundamentals and moving to applications.
Reviewed 2025-12-13. Anything still debated is marked as such rather than presented as settled.
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.
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.
A common misconception is that cardarine has been proven safe for human use. In reality, human clinical data are limited, and long-term animal studies have raised concerns about cancer. Another misconception is that it is a supplement or vitamin-like compound. It is a synthetic research chemical with no approved medical indication. Scientific discussion often focuses on its mechanism and detection rather than therapeutic use. Regulatory and anti-doping literature treats it primarily as a prohibited substance.
Cardarine is explicitly prohibited by the World Anti-Doping Agency under the class of PPARδ agonists. Its presence in urine or blood samples can be detected using mass spectrometry-based methods, often liquid chromatography-tandem mass spectrometry. Athletes who test positive may face sanctions, including bans from competition. The compound is also regulated as a prescription-only or unapproved drug in many countries. Enforcement varies by jurisdiction, and some regions treat it as a controlled substance. Online sales may occur despite these restrictions, creating quality and legal risks.
| Property | Value | Notes |
|---|---|---|
| Common name | Cardarine | Also called GW501516 and endurobol. |
| Chemical formula | C21H18F3NO3S2 | Molecular weight about 453.5 g/mol. |
| Appearance | White to off-white solid | Form depends on synthesis and purity. |
| Solubility | Soluble in DMSO and ethanol | Low solubility in water. |
| Typical storage | -20 °C, desiccated, protected from light | Common for research chemicals. |
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.
Activation of PPARδ changes transcription of genes involved in fatty acid transport, mitochondrial function, and skeletal muscle fuel preference. In rodent studies, pharmacological PPARδ activation was associated with increased endurance and altered body composition. These findings generated interest in performance enhancement, but species differences and study designs limit direct extrapolation to humans. Small human trials were conducted in the 2000s and later discontinued. The extent to which cardarine produces similar metabolic or performance effects in people remains an open question.
The compound is typically described as a laboratory compound rather than a therapeutic product. Published reports have explored its role in lipid disorders, insulin sensitivity, and exercise metabolism, yet no major drug regulator has approved it for medical use. Commercial samples sold under the cardarine name may vary in purity and identity. Analytical confirmation is therefore necessary when the material is discussed in scientific or regulatory contexts. Its classification as a prohibited substance in sport further shapes how it is studied and reported.
Cardarine is a common name for GW501516, a synthetic compound studied for its effects on lipid and glucose metabolism. It functions as an agonist at peroxisome proliferator-activated receptor delta, or PPARδ, a nuclear receptor that influences gene expression. The molecule is not a steroid, nor is it a selective androgen receptor modulator. It is also known in research and sports literature as GW-501516 and endurobol. Early laboratory work examined its metabolic activity in cell cultures and animal models.
=== Other methods === Of academic interest, palladium acetate, iodine, and oxygen can be used to couple cyclohexyl amine and cyclohexyl isocyanide. Yields of up to 67% have been achieved using this route:
=== As a neurotransmitter === Glycine is a neurotransmitter in the central nervous system with both inhibitory and excitatory roles. Specifically, it is an agonist at the inhibitory glycine receptor, and a co-agonist along with glutamate at the excitatory NMDA receptor. The glycine receptor is expressed throughout the CNS, but especially in the spinal cord, brainstem, and retina. When glycine receptors are activated, chloride enters the neuron via the receptor, causing an inhibitory postsynaptic potential (IPSP). Strychnine is a strong antagonist at ionotropic glycine receptors, whereas bicuculline is a weak one. Removal of glycine from inhibitory glycinergic synapses is hypothesized to be primarily mediated by glycine transporter 2. This glycine transporter protein is predominantly expressed in neurons, and occurs in the hindbrain and spinal cord. Glycine is a required co-agonist along with glutamate at the excitatory NMDA receptors. That is, these receptors only open their ion channels to let cations into the cell, when both glycine and glutamate are present, while the neuron is already somewhat depolarized. Removal of glycine from NMDA receptor-associated synapses is facilitated by glycine transporter 1, which is hypothesized to co-localize with NMDA receptors in the brain. This glycine transporter protein is predominantly expressed in glial cells, and occurs throughout the brain and spinal cord. The LD50 of glycine is 7930 mg/kg in rats (oral), high concentrations are known to cause marked hyperexcitability and neurotoxicity via the activation of NMDA receptors.
Vortioxetine was invented by scientists at Lundbeck who reported the rationale and synthesis for the drug (then called Lu AA21004) in a 2011 paper. In 2007, the compound was in Phase II clinical trials, and Lundbeck and Takeda entered into a partnership in which Takeda paid Lundbeck $40 million up-front, with promises of up to $345 million in milestone payments, and Takeda agreed to pay most of the remaining cost of developing the drug. The companies agreed to co-promote the drug in the US and Japan, and that Lundbeck would receive a royalty on all such sales. The deal included another drug candidate, tedatioxetine (Lu AA24530), and could be expanded to include two other Lundbeck compounds. Vortioxetine was approved by the US Food and Drug Administration (FDA) for the treatment of major depressive disorder (MDD) in adults in September 2013, and it was approved in the European Union in December 2013.
Reform UK removes Ian Cooper, leader of Staffordshire County Council, from the party following an investigation into online racist comments. 6 December – It is announced that transgender women will not be allowed to take part in the main event of the 2026 Labour Women's Conference. Former Conservative minister and peer Malcolm Offord defects to Reform UK, and says he will stand down from the House of Lords to campaign in the 2026 Scottish Parliament election. 7 December – Prime Minister Keir Starmer says that Angela Rayner will return to the cabinet, describing her as "hugely talented". 8 December – Essex Police are investigating allegations made by a former Reform UK councillor that the party overspent while campaigning in the Clacton constituency during the 2024 general election. Reform UK selects Addy Mo Asaduzzaman, a Bangladeshi with indefinite leave to remain in the UK, to stand in Central Southsea at local elections in May 2026. The announcement leads to criticism of the party. 9 December – Home Secretary Shabana Mahmood announces that former Children's Commissioner Baroness Anne Longfield will lead the inquiry into grooming gangs. Thirteen Labour MPs back a Liberal Democrat bill requiring the government to begin negotiations on joining a bespoke customs union with the EU, leading to a tied vote of 100–100. In her capacity as holder of the deciding vote Deputy Speaker Caroline Noakes gives her backing to the bill, allowing for it to have further debate. Ian Cooper resigns as leader of Staffordshire County Council after he was expelled by Reform UK.
== Structure == OcDH is a monomer with a molecular weight of 38kD made of two functionally distinct subunits. The first, Domain I, is composed of 199 amino acids and contains a Rossmann fold. Domain II is composed of 204 amino acids and is connected to the Rossmann fold of Domain I via its N-terminus.
Sources: en.wikipedia.org
An almost immediate move to challenge Gaddis' framework came from Melvyn P. Leffler, who "demonstrated that it was not so much the actions of the Kremlin as it was fears about socioeconomic dislocation, revolutionary nationalism, British weakness, and Eurasian vacuums of power that triggered US initiatives to mold an international system to comport with its concept of security". That provoked "strong rebuttals" from Gaddis and his followers, but Leffler deemed their objections inaccurate and unsubstantiated. However, Leffler himself still falls within the overall post-revisionist camp. Out of the "post-revisionist" literature emerged a new area of inquiry that was more sensitive to nuance and interested less in the question of who started the conflict than in offering insight into United States and Soviet actions and perspectives. From that perspective, the Cold War was not so much the responsibility of either side, but rather the result of predictable tensions between two world powers that had been suspicious of one another for nearly a century. For example, Ernest May wrote in a 1984 essay:
=== Entry into the cytoplasm === Ricin B chain binds complex carbohydrates on the surface of eukaryotic cells containing either terminal N-acetylgalactosamine or beta-1,4-linked galactose residues. In addition, the mannose-type glycans of ricin are able to bind to cells that express mannose receptors. RTB has been shown to bind to the cell surface on the order of 106–108 ricin molecules per cell surface. The profuse binding of ricin to surface membranes allows internalization with all types of membrane invaginations. The holotoxin can be taken up by clathrin-coated pits, as well as by clathrin-independent pathways including caveolae and macropinocytosis. Intracellular vesicles shuttle ricin to endosomes that are delivered to the Golgi apparatus. The active acidification of endosomes is thought to have little effect on the functional properties of ricin. Because ricin is stable over a wide pH range, degradation in endosomes or lysosomes offers little or no protection against ricin. Ricin molecules are thought to follow retrograde transport via early endosomes, the trans-Golgi network, and the Golgi to enter the lumen of the endoplasmic reticulum (ER). For ricin to function cytotoxically, RTA must be reductively cleaved from RTB to release a steric block of the RTA active site. This process is catalysed by the protein PDI (protein disulphide isomerase) that resides in the lumen of the ER. Free RTA in the ER lumen then partially unfolds and partially buries into the ER membrane, where it is thought to mimic a misfolded membrane-associated protein.
Behavioral endocrinology is a branch of endocrinology that studies the Neuroendocrine system and its effects on behavior. Behavioral endocrinology studies the biological mechanisms that produce behaviors, this gives insight into the evolutionary past. The field has roots in ethology, endocrinology and psychology.
=== Sources === Print Bosco, David (2009). Five to Rule Them All: The UN Security Council and the Making of the Modern World. Oxford University Press. ISBN 978-0-19-532876-9. Dallek, Robert (1995). Franklin D. Roosevelt and American Foreign Policy, 1932–1945: With a New Afterword. Oxford University Press. ISBN 978-0-19-982666-7. Gaddis, John Lewis (1972). The United States and the Origins of the Cold War, 1941–1947. Columbia University Press. ISBN 978-0-231-12239-9. Hoopes, Townsend; Brinkley, Douglas (1997). FDR and the Creation of the U.N.. Yale University Press. ISBN 978-0-300-08553-2. Kimball, Warren F. (1991). The Juggler: Franklin Roosevelt as Wartime Statesman. Princeton University Press. ISBN 0-691-03730-2. Ma, Xiaohua (2003). The Sino-American alliance during World War II and the lifting of the Chinese exclusion acts. New York: Routledge. pp. 203–204. ISBN 0-415-94028-1. United States Department of State (1942). "Union of Soviet Socialist Republics". Foreign relations of the United States diplomatic papers, 1942. Europe Volume III. U.S. Government Printing Office. pp. 406–771. Welles, Sumner (January 1951). "Two Roosevelt Decisions: One Debit, One Credit". Foreign Affairs. Vol. 29, no. 2. pp. 182–204. Online "1942: Declaration of The United Nations". United Nations. Archived from the original on May 13, 2016. Retrieved April 21, 2016. "1945: The San Francisco Conference". United Nations. 1945. Archived from the original on October 30, 2015. Retrieved May 16, 2015. Urquhart, Brian (July 16, 1998). "Looking for the Sheriff". New York Review of Books.
For example, visual information like face recognition is normally processed by the right hemisphere which tends to integrate all information from an incoming sensory signal, whereas an ASD brain preferentially processes visual information in the left hemisphere where information tends to be processed for local details of the face rather than the overall configuration of the face. This left lateralization negatively impacts both facial recognition and spatial skills. Increased functional connectivity within the left hemisphere which directly correlates with severity of autism. This observation also supports preferential processing of details of individual components of sensory information over global processing of sensory information in an ASD brain. Prominent abnormal connectivity in the frontal and occipital regions. In autistic individuals low connectivity in the frontal cortex was observed from infancy through adulthood. This is in contrast to long-range connectivity which is high in infancy and low in adulthood in ASD. Abnormal neural organization is also observed in the Broca's area which is important for speech production.
Sources: en.wikipedia.org
Cardarine is a common name for the investigational compound GW501516. It acts as a PPARδ agonist and is not approved for human use. It is prohibited in sport.
It activates PPARδ, a nuclear receptor that influences gene expression related to lipid and energy metabolism. Animal studies show changes in endurance and lipid levels. Human effects and risks are not well established.
No, cardarine is not a steroid. It belongs to a different chemical class, the PPARδ agonists. It is also not a selective androgen receptor modulator.
Yes, WADA prohibits cardarine as a PPARδ agonist. It appears on the prohibited list and can be detected in urine or blood. Athletes using it risk sanctions.