Everything below concerns Research chemical. We keep the language plain, cite what the science says, and separate well-supported claims from open questions.
Last reviewed on 2026-03-05. Where a claim depends on a specific study, the study is described rather than over-claimed.
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.
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.
| 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 |
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.
GW501516 acts as a selective agonist at PPARδ, a nuclear receptor that regulates transcription of genes involved in lipid handling and energy metabolism. Activation of PPARδ in preclinical models increases fatty acid oxidation, mitochondrial biogenesis, and exercise endurance in rodents. These effects have made the compound a subject of metabolic research and also a target for sport anti-doping rules. In humans, however, controlled studies are limited, and whether similar endurance or metabolic changes occur at tolerated exposures remains an open question. The receptor’s broad tissue distribution also means downstream effects may vary by organ and condition.
Detection of GW501516 in biological samples generally relies on liquid chromatography coupled with tandem mass spectrometry. Urine is a common matrix in anti-doping analysis, while blood or plasma may be used in research settings. Sample preparation can involve enzymatic hydrolysis, protein precipitation, or solid-phase extraction before instrumental analysis. Because the compound undergoes metabolism, assays may target the parent molecule, one or more metabolites, or both. Detection windows are not fixed; they depend on factors such as dose, route, individual metabolism, and assay sensitivity. Reference standards are required for accurate identification and quantification.
Handling and quality assessment of cardarine reference material follow general laboratory practices for poorly characterized compounds. It typically appears as a white to off-white powder and is sparingly soluble in water but soluble in organic solvents such as dimethyl sulfoxide and ethanol. Storage recommendations usually specify a cool, dry, dark place, with long-term storage at low temperature and desiccation. Purity may be checked by high-performance liquid chromatography with ultraviolet detection, while identity is confirmed by mass spectrometry and nuclear magnetic resonance. No pharmacopeial monograph exists, so reported purity and stability depend on the supplier’s methods.
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.
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.
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.
==== Absorption of HMB-Ca ==== After ingestion, HMB-Ca is converted to β-hydroxy β-methylbutyrate following dissociation in the gut. When the HMB-Ca dosage form is ingested, the magnitude and time at which the peak plasma concentration of HMB occurs depends on the dose and concurrent food intake. Higher HMB-Ca doses increase the rate of absorption, resulting in a peak plasma HMB level (Cmax) that is disproportionately greater than expected of a linear dose-response relationship and which occurs sooner relative to lower doses. Consumption of HMB-Ca with sugary substances slows the rate of HMB absorption, resulting in a lower peak plasma HMB level that occurs later.
Lansoprazole was the second of the PPI drugs to reach the market, being launched in Europe in 1991 and the US in 1995. It has no substitutions at the benzimidazole but two substituents on the pyridine, methyl group at position 3 and a trifluoroethoxy group at position 4. The drug is a 1:1 racemate of the enantiomers dexlansoprazole and levolansoprazole. It is available in gastroresistant capsules and tablets as well as chewable tablets.
Soy sauce (醬油, jiàngyóu) is considered almost as old as soy paste—a type of fermented paste (jiàng, 醬) obtained from soybeans—which had appeared during the Western Han dynasty (206 BC – 220 AD) and was listed in the bamboo slips found in the archaeological site Mawangdui (馬王堆). There are several precursors of soy sauce that are associated products with soy paste. The oldest is qingjiang (清醬), which appeared in AD 40 and was listed in Simin Yueling (四民月令). Others are jiangqing (醬清), chizhi (豉汁) and chiqing (豉清), which were recorded in the Qimin Yaoshu (齊民要術) in AD 540. By the time of the Song dynasty (960–1279 AD), the term jiàng yóu (醬油) had become the accepted name for the liquid condiment, documented in two books: Shanjia Qinggong (山家清供) and Pujiang Wushi Zhongkuilu (浦江吳氏中饋錄) during the Song dynasty (960–1279 AD). Like many salty condiments, soy sauce was originally a way to stretch salt, historically an expensive commodity. During the Zhou dynasty of ancient China, fermented fish with salt was used as a condiment in which soybeans were included during the fermentation process. By the time of the Han dynasty, this had been replaced with the recipe for soy paste and its by-product soy sauce, by using soybeans as the principal ingredient, with fermented fish-based sauces developing separately into fish sauce.
Sources: en.wikipedia.org
It is hypothesized that the various introductions led to multiple genotypes which are adapted to either oaks or conifers. Californian specimens of A. phalloides frequently display yellowish to mustard-yellow caps, a coloration that can closely resemble the edible species Amanita velosa and Amanita calyptroderma, both of which are commonly foraged and consumed in California. This deceptive appearance is the result of environmental homoplasy with Asian cousin Amanita subjunquillea: the fungus expresses a phylogenetically conserved pigment palette (derived from the shikimate pathway) under the particular microclimatic conditions of coastal California oak woodlands. Prolonged high humidity from summer fog drip, followed by intense sunlight and oxidative stress once the fog burns off, upregulates polyphenolic compounds and causes oxidative bleaching of the originally greener or olive tones, producing the characteristic yellowish hues. Such similarity poses a significant risk of fatal misidentification for foragers, as the highly toxic death cap may be mistaken for these otherwise edible look-alikes. A. phalloides were conveyed to new countries across the Southern Hemisphere with the importation of hardwoods and conifers in the late twentieth century. Introduced oaks appear to have been the vector to Australia and South America; populations under oaks have been recorded from Melbourne, Canberra (where two people died in January 2012, of four who were poisoned), Adelaide, and further observed by citizen scientists in Beechworth, Sydney and Albury.
The typical appearance of plantar fibromatosis on magnetic resonance imaging (MRI) is a poorly defined, infiltrative mass in the aponeurosis next to the plantar muscles. Only 25% of patients show symptoms on both feet (bilateral involvement). The disease may also infiltrate the dermis or, very rarely, the flexor tendon sheath.
== Contribution to radioactivity of reprocessed uranium == The half-life of 238U is about 190 times as long as that of 236U; therefore, 236U has about 190 times as much specific activity. Thus, in reprocessed uranium with 0.5% 236U, the 236U and 238U will produce about the same level of radioactivity. (235U contributes only a few percent.) The ratio is less than 190 when the decay products of each are included. The decay chain of uranium-238 to uranium-234 and eventually lead-206 involves emission of eight alpha particles in a time (hundreds of thousands of years) short compared to the half-life of 238U; so a sample of 238U in equilibrium with its decay products (as in natural uranium ore) has eight times the alpha activity of 238U alone. Even purified natural uranium where the post-uranium decay products have been removed, contains an equilibrium quantity of 234U and therefore about twice the alpha activity of pure 238U. Enrichment to increase 235U content will increase 234U to an even greater degree, and roughly half of this 234U will survive in the spent fuel. On the other hand, 236U decays to thorium-232 which has a half-life of 14 billion years, much longer than its own; so its decay chain effectively stops after one step even at long timescales; and the fact that it is an alpha decay means the external exposure hazard is negligible compared to the natural isotopes.
Low-density lipoprotein receptor-related protein 5 is a protein that in humans is encoded by the LRP5 gene. LRP5 is a key component of the LRP5/LRP6/Frizzled co-receptor group that is involved in canonical Wnt pathway. Mutations in LRP5 can lead to considerable changes in bone mass. A loss-of-function mutation causes osteoporosis pseudoglioma syndrome with a decrease in bone mass, while a gain-of-function mutation causes drastic increases in bone mass.
Sources: en.wikipedia.org
== Preparation == Traditionally, stock is made by simmering various ingredients in water. A newer approach is to use a pressure cooker. The ingredients may include some or all of the following: Bones: Beef and chicken bones are most commonly used; fish is also common. The flavor of the stock comes from the bone marrow, cartilage and other connective tissue. Connective tissue contains collagen, which is converted into gelatin that thickens the liquid. Stock made from bones needs to be simmered for long periods; pressure cooking methods shorten the time necessary to extract the flavor from the bones. Meat: Cooked meat still attached to bones is also used as an ingredient, especially with chicken stock. Meat cuts with a large amount of connective tissue, such as shoulder cuts, are also used. Mirepoix: Mirepoix is a combination of onions, carrots, celery, and sometimes other vegetables added to flavor the stock. Sometimes, the less desirable parts of the vegetables that may not otherwise be eaten (such as carrot skins and celery cores and leaves) are used, as the solids are removed from stock. Herbs and spices: The herbs and spices used depend on availability and local traditions. In classical cuisine, the use of a bouquet garni ('bag of herbs') consisting of parsley, bay leaves, a sprig of thyme, and possibly other herbs, is common. This is often placed in a sachet to make it easier to remove once the stock is cooked.
This series of lists omits periods from acronyms and initialisms. It uses periods for certain abbreviations that traditionally often have them (mostly older Latin/Neo-Latin abbreviations). For example, both bid and b.i.d. may be found in the list. It generally uses the singular form of an abbreviation (not the plural) as the headword. This list uses significant capitalization for headwords (the abbreviations) and their expansions.
The two substrates of this enzyme are D-threitol and oxidised nicotinamide adenine dinucleotide phosphate (NADP+). Its products are D-erythrulose, reduced NADPH, and a proton. This enzyme belongs to the family of oxidoreductases, specifically those acting on the CH-OH group of donor with NAD+ or NADP+ as acceptor. The systematic name of this enzyme class is erythritol:NADP+ oxidoreductase. This enzyme is also called D-erythrulose reductase.
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.
Legal status varies by country, but cardarine is not approved as a medicine in major jurisdictions. It is often sold as a research chemical, a category that may not be lawful for human use. Buyers should check local laws and product labels carefully.