Everything below concerns prohibited list. We keep the language plain, cite what the science says, and separate well-supported claims from open questions.
Last reviewed on 2025-11-18. Where a claim depends on a specific study, the study is described rather than over-claimed.
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.
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.
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.
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.
| 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.
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.
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.
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.
Horsepox is extinct in the wild, and the only known sample was collected in 1976. Because the sample was collected at the end of the smallpox eradication campaign, scientists considered the possibility that horsepox is a strain of vaccinia that had escaped into the wild. However, as more smallpox vaccines were sequenced, older vaccines were found to be more similar to horsepox than modern vaccinia strains. A smallpox vaccine manufactured by Mulford in 1902 is 99.7% similar to horsepox, closer than any previously known strain of vaccinia. Modern Brazilian vaccines with a documented introduction date of 1887, made from material collected in an 1866 outbreak of "cowpox" in France, are more similar to horsepox than other strains of vaccinia. Five smallpox vaccines manufactured in the United States in 1859–1873 are most similar to each other and horsepox, as well as the 1902 Mulford vaccine. One of the 1859–1873 vaccines was identified as a novel strain of horsepox, containing a complete gene from the 1976 horsepox sample that has deletions in vaccinia.
== Pharmacology == It enhances the binding activity of the GABA_A receptor. Specifically, at a concentration of 0.1 micromolar, (+)-methysticin increases the binding of the receptor ligand [3H]bicuculline methochloride by approximately 18% to 28%, indicating it acts as a positive modulator of the GABAA receptor. This modulatory effect is similar in strength to related kavapyrones such as (+)-kavain and (+)-dihydromethysticin. Importantly, methysticin's effect is not due to interaction with the benzodiazepine receptor, as it does not influence the binding of [3H]flunitrazepam, which is a benzodiazepine receptor ligand. Structural features, such as the angular lactone ring present in methysticin and other enolides, are crucial for this activity. Overall, methysticin enhances GABA_A receptor function through a mechanism distinct from that of benzodiazepines, contributing to the neuroactive properties of kava. Methysticin induces the function of the hepatic enzyme CYP1A1. This enzyme is involved in the toxification of benzo[a]pyrene into (+)-benzo[a]pyrene-7,8-dihydrodiol-9,10-epoxide, a highly carcinogenic substance. Another related compound is dihydromethysticin, which also induces the function of CYP1A1. No report so far has described enhancement of CYP1A1 expression in animals or humans in vivo from any constituent of kava. It was studied for its effects on cytochrome P450 enzymes. It was found to strongly and irreversibly inhibit CYP2C9 in a time-, concentration-, and NADPH-dependent manner, with ~85% inhibition at 50 μM.
The bodies of vascular plants including clubmosses, ferns and seed plants (gymnosperms and angiosperms) generally have aerial and subterranean subsystems. The shoots consist of stems bearing green photosynthesising leaves and reproductive structures. The underground vascularised roots bear root hairs at their tips and generally lack chlorophyll. Non-vascular plants, the liverworts, hornworts and mosses do not produce ground-penetrating vascular roots and most of the plant participates in photosynthesis. The sporophyte generation is nonphotosynthetic in liverworts but may be able to contribute part of its energy needs by photosynthesis in mosses and hornworts. The root system and the shoot system are interdependent – the usually nonphotosynthetic root system depends on the shoot system for food, and the usually photosynthetic shoot system depends on water and minerals from the root system. Cells in each system are capable of creating cells of the other and producing adventitious shoots or roots. Stolons and tubers are examples of shoots that can grow roots. Roots that spread out close to the surface, such as those of willows, can produce shoots and ultimately new plants. In the event that one of the systems is lost, the other can often regrow it. In fact it is possible to grow an entire plant from a single leaf, as is the case with plants in Streptocarpus sect. Saintpaulia, or even a single cell – which can dedifferentiate into a callus (a mass of unspecialised cells) that can grow into a new plant.
Sources: en.wikipedia.org
Ion-exchange resins are widely used in different separation, purification, and decontamination processes. The most common examples are water softening and water purification. In many cases, ion-exchange resins were introduced in such processes as a more flexible alternative to the use of natural or artificial zeolites.
== Career == Somogyi was born on March 7, 1883, in the village of Zsámánd in Hungary (today Reinersdorf, part of Heiligenbrunn, Austria). He graduated in chemical engineering from the University of Budapest in 1905. After an additional year as an assistant in biochemistry, Somogyi went to the United States, where he eventually found a position as an assistant in biochemistry at Cornell University (1906–1908). He returned to Budapest where he worked at the Municipal Laboratory for the next decade. In 1914, he received his Ph.D. from the University of Budapest, submitting a dissertation on catalytic hydrogenation. During World War I he was in charge of providing food to the destitute. Somogyi was invited to return to the United States by Philip A. Shaffer, whom he had known at Cornell. In 1922 Somogyi became an instructor in biochemistry at Washington University School of Medicine. There Somogyi worked with Shaffer and Edward Adelbert Doisy on insulin preparation and insulin's use in the treatment of diabetes. In 1926, Somogyi became the first biochemist on the staff of the new Jewish Hospital of St. Louis where he worked closely with physicians. He directed the hospital's clinical laboratory until he retired in 1957.
The 1st Brigade was among the federal forces that left Baltimore by midnight the same day and three days later, the 2nd Brigade went into an assembly area at Bolling Air Force Base, where they eventually departed back to Fort Bragg sometime later.
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.