Everything below concerns Investigational drug. We keep the language plain, cite what the science says, and separate well-supported claims from open questions.
Updated 2026-06-06. Numbers and descriptions here follow the published literature rather than marketing material.
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.
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.
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.
Safety discussions about cardarine frequently cite rodent carcinogenicity findings reported in the 2000s. In those studies, treated animals developed tumors at multiple sites, leading sponsors to discontinue clinical development. The relevance of these findings to humans has not been resolved, but they are a major reason the compound is not approved. Current literature emphasizes uncertainty about long-term effects and the risks of unregulated use. Regulators and health agencies have not established a safe human exposure level.
| 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. |
Products sold as cardarine have been found to contain incorrect compounds, variable amounts, or no active ingredient at all. Independent testing is required to verify identity and purity. Common analytical approaches include high-performance liquid chromatography, mass spectrometry, and nuclear magnetic resonance for structural confirmation. These methods can distinguish GW501516 from related PPAR agonists and from unrelated steroids. For regulators and researchers, such verification is central to interpreting both biological results and adverse event reports.
Cardarine is prohibited in competitive sport under the World Anti-Doping Agency code, where it is classified as a metabolic modulator. It is not approved as a prescription medicine in the United States, European Union, or other major markets. Regulatory action has focused on its presence in sports and in products marketed as research chemicals. Because it has no accepted medical indication, supply is often unregulated. This status creates legal and safety uncertainties for anyone who encounters the substance.
Anti-doping laboratories detect GW501516 and its metabolites using liquid chromatography-tandem mass spectrometry. Urine is the most common matrix, though blood and dried blood spots may also be used in some programs. Detection depends on factors such as dose, timing, metabolism, and the sensitivity of the assay. Published methods describe limits of detection in the low nanogram per milliliter range for related compounds. Exact detection windows are not fixed for all situations and remain an area of ongoing study.
Cardarine is frequently described as a fat-burning or endurance-enhancing supplement, but these claims exceed the available evidence. The compound is not a hormone, steroid, or selective androgen receptor modulator. Research articles discuss it as a tool compound for studying PPARδ biology, while anti-doping literature focuses on its abuse and detection. Quality of unapproved products is uncertain, and independent analyses have found impurities or incorrect labeling. Open questions include whether human cancer risk resembles that seen in rodents and how often non-athletes use the substance.
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.
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.
Cardarine is a common name for the investigational chemical GW501516, also written GW-1516. It was developed as a peroxisome proliferator-activated receptor delta agonist for metabolic conditions such as dyslipidemia. Early research focused on lipid handling and energy use in skeletal muscle and other tissues. The compound was never approved as a medicine. In public discussion, it is often grouped with performance-enhancing substances, although its receptor target differs from that of anabolic steroids or selective androgen receptor modulators. Regulatory and health authorities have issued warnings about its use.
Writing for The Guardian, Seumas Milne stated the result of the post–Cold War narrative that Stalin and Hitler were twin evils, therefore communism is as monstrous as Nazism, "has been to relativise the unique crimes of Nazism, bury those of colonialism and feed the idea that any attempt at radical social change will always lead to suffering, killing and failure." Other leftists, including some Marxist–Leninists, apply self-criticism, and have at times criticised Marxist–Leninist praxis and some actions by Marxist–Leninist governments, while acknowledging its advancements, emancipatory acts such as their support of labour rights, women's rights, anti-imperialism, democratic efforts, egalitarian achievements, modernisation, and the creation of mass social programs for education, health, housing, and jobs as well as the increase of living standards.
== Function == Renin activates the renin–angiotensin system by using its endopeptidase activity to cleave the peptide bonds between leucine and valine residues in angiotensinogen, produced by the liver, to yield angiotensin I, which is further converted into angiotensin II by ACE, the angiotensin–converting enzyme primarily within the capillaries of the lungs. Angiotensin II then constricts blood vessels, increases the secretion of ADH and aldosterone, and stimulates the hypothalamus to activate the thirst reflex, each leading to an increase in blood pressure. Renin's primary function is therefore to eventually cause an increase in blood pressure, leading to restoration of perfusion pressure in the kidneys. Renin is secreted from juxtaglomerular kidney cells, which sense changes in renal perfusion pressure, via stretch receptors in the vascular walls. The juxtaglomerular cells are also stimulated to release renin by signaling from the macula densa. The macula densa senses changes in sodium delivery to the distal tubule, and responds to a drop in tubular sodium load by stimulating renin release in the juxtaglomerular cells. Together, the macula densa and juxtaglomerular cells comprise the juxtaglomerular complex. Renin secretion is also stimulated by sympathetic nervous stimulation, mainly through β1 adrenoreceptor activation.
=== Other uses === Prostanoids, including alprostadil, do not reduce the risk of limb amputation but may offer a slight improvement in rest-pain and leg ulcer healing in persons with critical limb ischemia. Preventative administration of alprostadil may reduce the risk of kidney injury (specifically contrast-induced nephropathy) in persons having cardiac angiography or percutaneous coronary intervention. Lubiprostone is a PGE1 derivative used to treat chronic constipation. It is taken orally. Common side effects include diarrhea, vomiting, and abdominal pain.
nirantarāndhakārita-digantara-kandaladamanda-sudhārasa-bindu-sāndratara-ghanāghana-vṛnda-sandehakara-syandamāna-makaranda-bindu-bandhuratara-mākanda-taru-kula-talpa-kalpa-mṛdul̥a-sikatā-jāla-jaṭila-mūla-tala-maruvaka-miladalaghu-laghu-laya-kalita-ramaṇīya-pānīya-śālikā-bālikā-karāra-vinda-galantikā-galadelā-lavaṅga-pāṭala-ghanasāra-kastūrikātisaurabha-medura-laghutara-madhura-śītalatara-saliladhārā-nirākariṣṇu-tadīya-vimala-vilocana-mayūkha-rekhāpasārita-pipāsāyāsa-pathika-lokān from the Varadāmbikā Pariṇaya Campū by Tirumalāmbā, composed of 195 Sanskrit letters (428 letters in the roman transliteration, dashes excluded), thus making it the longest word ever to appear in worldwide literature. Each hyphen separates every individual word this word is composed of. The approximate meaning of this word is:
Sources: en.wikipedia.org
Eventually, explanation what implies "the balance of power favoring freedom" was dropped by "US National Security and Defense Strategies" of 2018: The Pentagon will ensure that the United States remain the "preeminent military power in the world," and the regional "balances of power remain in our favor." [Emphasis added] The "balance of power favoring freedom" appeared identical with the balance of power favoring "us." Russian President Vladimir Putin complained: "Instead of establishing a new balance of power … they [the United States] took steps that threw the [international] system into sharp and deep imbalance." In 1826, George Canning "called the new world into existence to redress the balance of the old". In 1898, Theodore Roosevelt found that the United States had become "more and more the balance of power of the whole globe." In 1941, a New Deal Economist with the National Resources Planning Board, Otto T. Mallery, averred that "destiny offers to the United States the ultimate balance of power and of resources in the world after the war." Colin Gray titled his 2005 chapter by question, "Where Is the Balance of Power?" The chapter opens: "The short answer is that the United States is the balance of power."
After the state election in September 2017, Stephan Weil remained Minister-President, with the SDP in coalition with the CDU. After the 2022 Election, Weil was once again elected as Minister-President with an SDP-Greens coalition.
The Rumack–Matthew nomogram, also known as the acetaminophen nomogram, is an acetaminophen toxicity nomogram. It plots serum concentration of acetaminophen against the time since ingestion, in order to predict possible liver toxicity and allow a clinician to decide whether to proceed with N-Acetylcysteine (NAC) treatment. It is a logarithmic graph starting 4 hours after ingestion; at this time the absorption of acetaminophen is considered likely to be complete. This nomogram allows for timely management of an acetaminophen overdose. Generally, a serum plasma concentration (APAP) of 140–150 μg/mL (or mg/L) at 4 hours post-ingestion indicates the need for NAC treatment. This nomogram is not used alone if the patient has altered mental status or if the history is not reliable; rather, an additional line should be drawn and plotted to see if the slope of the line remains at or above the nomogram. Additionally, a formal half-life may also be determined, by measuring concentration first upon admission of the patient and again 4 hours later; from these measurements, half-life can be calculated. If half-life is more than 4 hours, then treatment is necessary to prevent hepatotoxicity and liver failure. The original line, sometimes referred to as the Rumack–Matthew line, starts at 200 μg/mL at 4 hours and was published in 1975 by Barry H. Rumack and Henry Matthew. When the NAC study began in 1976, the U.S. Food and Drug Administration (FDA) required a line that was 25% below the original. This line is referred to as the treatment line and starts at 150 μg/mL at 4 hours.
=== Pharmacokinetics === A single 40-mg oral dose of relugolix has been found to result in peak levels of relugolix of 29 ng/mL (47 nmol/L) after 1.5 hours. Steady-state levels are reached within 7 days with 40 mg/day relugolix administration. There is an approximate 2-fold accumulation of relugolix by 2 weeks of continuous administration. Food diminishes the oral bioavailability of relugolix by about 50%. Relugolix is a substrate for P-glycoprotein, which may have a limiting effect on its absorption and distribution. The plasma protein binding of relugolix is approximately 68 to 71% over a concentration range of 0.05 to 5 μg/mL. Relugolix is not a substrate for CYP3A4. The elimination half-life of relugolix is 36 to 65 hours across a dosage range of 20 to 180 mg/day. There is moderate to high interindividual variability in systemic exposure to relugolix. Relugolix is excreted mainly in feces (83%) and to a small degree in urine (4%). Only about 6% of a dose of relugolix is excreted unchanged.
== Mistaken portrait == For two centuries, until the discovery of the error in 2005, books, paintings and articles had incorrectly shown a profile portrait of the obscure French politician Louis Legendre (1752–1797) as a portrait of the mathematician. The error arose from the fact that the sketch was labelled simply "Legendre" and appeared in a book along with contemporary mathematicians such as Lagrange. One of only two known portraits of Legendre, rediscovered in 2008, is found in the 1820 book Album de 73 portraits-charge aquarellés des membres de I'Institut, a book of caricatures of seventy-three members of the Institut de France in Paris by the French artist Julien-Léopold Boilly as shown below. The other portrait is from the book Le Panthéon scientifique de la tour Eiffel.
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.
Cardarine is an investigational synthetic compound that acts as a PPARδ agonist. It is also known as GW501516 and has been studied mainly in preclinical research. It is not an approved medicine.