Cardarine 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 2026-08-01. Where a claim depends on a specific study, the study is described rather than over-claimed.
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 has no approved therapeutic indication and is not marketed as a medicine. The World Anti-Doping Agency lists GW501516 as a prohibited substance at all times, covering both in-competition and out-of-competition periods. National laws vary: some countries treat it as an unapproved drug subject to import controls, while others have specific restrictions on sale for human consumption. It is often sold as a research chemical, a label that does not imply safety or legality. Enforcement actions have targeted online vendors and shipments.
Anti-doping laboratories identify GW501516 and related metabolites using liquid chromatography coupled with tandem mass spectrometry. Urine is the most common matrix, though blood and dried blood spots may also be analyzed. The method targets the parent compound and phase I and phase II metabolites, which extend the detection window. Because the substance is prohibited at all times, athletes can be tested outside competition. Detection limits and windows depend on the assay, sample type, and individual metabolism.
| 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. |
Cardarine is a synthetic compound also known as GW501516, GW-501516, and sometimes endurobol. It was developed as a selective agonist of peroxisome proliferator-activated receptor delta, a nuclear receptor involved in fatty acid oxidation and energy metabolism. The compound was studied in preclinical models for metabolic and cardiovascular conditions, but it did not become a marketed human medicine. In regulatory and anti-doping contexts, it is treated as a prohibited substance rather than a licensed medicine.
The pharmacological interest in cardarine centers on PPARδ activation and its downstream effects on lipid handling and mitochondrial function. In animal studies, PPARδ agonists have been associated with changes in exercise endurance and fatty acid utilization, though results vary by model and protocol. Human data remain sparse, and the absence of large controlled trials limits conclusions about efficacy. Researchers often describe the compound as a tool for probing PPARδ biology rather than a proven therapeutic agent.
GW501516 acts on PPARδ, a nuclear receptor that helps regulate fatty acid oxidation and energy homeostasis. In animal studies, activation of this receptor was associated with increased endurance and changes in lipid metabolism. Human trials examined effects on blood lipids and other metabolic markers, but the compound did not advance to approval. Rodent studies later reported tumors in multiple tissues at doses used in those experiments. Whether those findings translate to human risk remains uncertain, and the clinical relevance of the animal data is still debated.
Regulatory bodies treat GW501516 as a prohibited substance in competitive sport. The World Anti-Doping Agency added it to the prohibited list, and it falls under classes covering metabolic modulators and hormone-related agents. It is not approved by drug regulators for human use, and it is not a lawful dietary supplement. Products sold under the cardarine name may contain unlisted ingredients or different compounds. Because no approved product exists, quality and identity are not guaranteed by pharmaceutical manufacturing standards.
The lawsuit was brought against VPX and its owner for claims of false advertising under the Lanham Act, California laws regarding unfair competition and false advertising, as well as trade libel. The jury issued the verdict on September 29, 2022. Following a trial lasting over a month, the jury awarded Monster Energy $293 million in damages. Among the damages were $272 million awarded for false advertising, $18 million for Bang's interference with contracts, and $3 million for trade secret theft. In October 2023, a judge awarded an additional $43 million dollars to Monster Energy for attorney fees and expenses.
==== 1914–1916: Initial Zionist–British Government discussions ==== In July 1914, war broke out in Europe between the Triple Entente (Britain, France, and the Russian Empire) and the Central Powers (Germany, Austria-Hungary, and, later that year, the Ottoman Empire). The British Cabinet first discussed Palestine at a meeting on 9 November 1914, four days after Britain's declaration of war on the Ottoman Empire, of which the Mutasarrifate of Jerusalem – often referred to as Palestine – was a component. At the meeting David Lloyd George, then Chancellor of the Exchequer, "referred to the ultimate destiny of Palestine". The Chancellor, whose law firm Lloyd George, Roberts and Co had been engaged a decade before by the Zionist Federation of Great Britain and Ireland to work on the Uganda Scheme, was to become prime minister by the time of the declaration, and was ultimately responsible for it.
Cells use glucose for energy. This normally occurs by phosphorylation from the enzyme hexokinase. However, if large amounts of glucose are present (as in diabetes mellitus), hexokinase becomes saturated and the excess glucose enters the polyol pathway when aldose reductase reduces it to sorbitol. This reaction oxidizes NADPH to NADP+. Sorbitol dehydrogenase can then oxidize sorbitol to fructose, which produces NADH from NAD+. Hexokinase can return the molecule to the glycolysis pathway by phosphorylating fructose to form fructose-6-phosphate. However, in uncontrolled diabetics that have high blood glucose - more than the glycolysis pathway can handle - the reactions mass balance ultimately favors the production of sorbitol. Activation of the polyol pathway results in a decrease of reduced NADPH and oxidized NAD+; these are necessary co-factors in redox reactions throughout the body, and under normal conditions they are not interchangeable. The decreased concentration of these NADPH leads to decreased synthesis of reduced glutathione, nitric oxide, myo-inositol, and taurine. Myo-inositol is particularly required for the normal function of nerves. Sorbitol may also glycate nitrogens on proteins, such as collagen, and the products of these glycations are referred-to as AGEs - advanced glycation end-products. AGEs are thought to cause disease in the human body, one effect of which is mediated by RAGE (receptor for advanced glycation end-products) and the ensuing inflammatory responses induced.
Sources: en.wikipedia.org
=== Mechanism of action === Buprenorphine binds strongly to opioid receptors and acts as a pain-reducing medication in the central nervous system (CNS). It binds to the μ-opioid receptor with high affinity, which produces analgesic effects in the CNS. It is a partial μ-opioid receptor agonist and a weak κ-opioid receptor antagonist. As a partial agonist, buprenorphine binds and activates the opioid receptors, but has only partial efficacy at the receptor relative to a full agonist, even at maximal receptor occupancy. It is thus well-suited to treat opioid dependence, as it produces milder effects on the opioid receptor with lower dependence and habit-forming potential. Naloxone is a pure opioid antagonist that competes with opioid molecules in the CNS and prevents them from binding to the opioid receptors. Naloxone's binding affinity is highest for the μ-opioid receptor, then the δ-opioid receptor, and lowest for the κ-opioid receptor. Naloxone has poor bioavailability, and is rapidly inactivated following oral administration. When injected, it exerts its full effects. The principle behind its function as a deterrent is as follows: when taken sublingually as prescribed, buprenorphine's effects at the opioid receptor dominate, while naloxone's effects are negligible due to the low oral absorption. But when someone attempts to misuse the medication via either injection or inhalation, the naloxone is intended to act as an antagonist and either reduce the opioid's euphoric effects or even precipitate withdrawal in those dependent on opioids.
=== Chemistry === Protein hydrolysis is a useful route to the isolation of individual amino acids. Examples include cystine from hydrolysis of hair, tryptophan from casein, histidine from red blood cells, and arginine from gelatin.
=== Psychological and behavioral === Psychological and behavioral therapies are used across all forms of addiction, both alone and together with medication; commonly used approaches include CBT, motivational interviewing, contingency management (which provides tangible rewards for verified abstinence), and twelve-step facilitation. For stimulant use disorder, contingency management (particularly when combined with a community reinforcement approach) has the strongest supporting evidence among psychosocial treatments. For alcohol use disorder, structured twelve-step facilitation programs that encourage participation in Alcoholics Anonymous are at least as effective as other established therapies such as CBT for sustaining abstinence and may lower health-care costs. The creative arts therapies, including art therapy, music therapy, drama and dance, are sometimes offered alongside conventional treatment, and artwork produced during treatment has been used informally to aid assessment and track progress. A 2018 systematic review found insufficient evidence that visual art, drama, or dance and movement therapies reduce substance misuse, though music therapy showed some promise in preparing people to engage with treatment. Proposed benefits include providing a non-verbal outlet for difficult emotions and strengthening engagement in treatment.
Sources: en.wikipedia.org
In transcription, RNA polymerase reads a DNA strand and produces an mRNA strand that can be further translated. In order to initiate transcription, the DNA segment that is to be transcribed must be accessible (i.e. it cannot be tightly packed). Once the DNA segment is accessible, the RNA polymerase can begin to transcribe the coding DNA strand by pairing RNA nucleotides to the template DNA strand. During the initial transcription phase, the RNA polymerase searches for a promoter region on the DNA template strand. Once the RNA polymerase binds to this region, it begins to “read” the template DNA strand in the 3’ to 5’ direction. RNA polymerase attaches RNA bases complementary to the template DNA strand (Uracil will be used instead of Thymine). The new nucleotide bases are bonded to each other covalently. The new bases eventually dissociate from the DNA bases but stay linked to each other, forming a new mRNA strand. This mRNA strand is synthesized in the 5’ to 3’ direction. Once the RNA reaches a terminator sequence, it dissociates from the DNA template strand and terminates the mRNA sequence as well. Transcription is regulated in the cell via transcription factors. Transcription factors are proteins that bind to regulatory sequences in the DNA strand such as promoter regions or operator regions. Proteins bound to these regions can either directly halt or allow RNA polymerase to read the DNA strand or can signal other proteins to halt or allow RNA polymerase reading.
== Testing of individuals == Normal values indicated in the following tables pertain to humans as normal levels vary among species. Measured cortisol levels, and therefore reference ranges, depend on the sample type, the analytical method used, and factors such as age and sex. Test results should, therefore, always be interpreted using the reference range from the laboratory that produced the analysis. An individual's cortisol levels can be measured in blood, serum, urine, saliva, and sweat.
=== Insomnia === Doxepin is used in the treatment of insomnia. In 2016, the American College of Physicians advised that insomnia be treated first by treating comorbid conditions, then with cognitive behavioral therapy and behavioral changes, and then with drugs; doxepin was among those recommended for short-term help maintaining sleep, on the basis of weak evidence. The 2017 American Academy of Sleep Medicine recommendations focused on treatment with drugs were similar. A 2015 Agency for Healthcare Research and Quality review of treatments for insomnia had similar findings. A major systematic review and network meta-analysis of medications for the treatment of insomnia published in 2022 found that doxepin had an effect size (standardized mean difference (SMD)) against placebo for treatment of insomnia at 4 weeks of 0.30 (95% CITooltip confidence interval –0.05 to 0.64). The certainty of evidence was rated as very low, and no data were available for longer-term treatment (3 months). For comparison, the other sedating antihistamines assessed, trimipramine and doxylamine, had effect sizes (SMD) at 4 weeks of 0.55 (95% CI –0.11 to 1.21) (very low certainty evidence) and 0.47 (95% CI 0.06 to 0.89) (moderate certainty evidence), respectively. Benzodiazepines and Z-drugs generally showed larger effect sizes (e.g., SMDs of 0.45 to 0.83) than doxepin, whereas the effect sizes of orexin receptor antagonists, such as suvorexant, were more similar (SMDs of 0.23 to 0.44).
=== Religious concerns === Some brands of the vaccine use gelatin, derived from pigs, as a stabilizer. This has caused reduced take-up among some communities, despite the fact that alternative vaccines without pig derivatives are approved and available.
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.
Legal status varies by country. It is not approved as a medicine, and it is prohibited in sport. Some jurisdictions restrict import, sale, or possession.