This is a working overview of GW501516, written for readers who want more than a one-paragraph summary but less than a textbook.
Reviewed 2026-05-03. Anything still debated is marked as such rather than presented as settled.
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.
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.
| Property | Value | Notes |
|---|---|---|
| Chemical class | Synthetic PPARδ agonist | Not a steroid or a selective androgen receptor modulator. |
| Common synonyms | Cardarine, GW501516, GW-501516, endurobol | Names vary by supplier and literature source. |
| Appearance | White to off-white powder | Consistent with many small-molecule research chemicals. |
| Solubility | Low in water; soluble in DMSO and ethanol | Often prepared in organic solvent for laboratory work. |
| Primary target | PPARδ (NR1C2) | Nuclear receptor involved in lipid and energy metabolism. |
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.
Stability of GW501516 depends on form, temperature, light exposure, and moisture. Solid reference material is typically stored frozen or refrigerated in a desiccator and protected from light. Solutions in organic solvents such as dimethyl sulfoxide are often kept frozen in aliquots to reduce freeze-thaw cycling. Aqueous solubility is low, so aqueous stock solutions can be difficult to prepare without cosolvents. Degradation may appear as changes in chromatographic purity or mass spectral signal. Stability studies are needed to establish shelf life for any specific preparation.
Quality assessment for cardarine samples usually combines identity, purity, and impurity testing. Nuclear magnetic resonance spectroscopy and mass spectrometry can confirm molecular structure, while high-performance liquid chromatography estimates purity. Certificates of analysis from testing laboratories may list these results, but they do not establish safety or legality. In the absence of approved manufacturing, products sold online may contain the wrong compound, variable amounts, or unlisted contaminants. Independent verification is therefore central to analytical work and to interpreting any reported biological activity.
Laboratory detection of GW501516 commonly uses liquid chromatography coupled with tandem mass spectrometry. The method can identify the parent compound or its metabolites in urine and blood after sample cleanup. Protein precipitation, solid-phase extraction, or enzymatic hydrolysis may precede analysis, depending on the matrix. Reference standards are required for accurate quantification and confirmation. Because the compound is not approved, testing often occurs in anti-doping, forensic, or research settings rather than routine clinical care. Results are reported with limits of detection and quantification.
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.
Laboratory detection of cardarine typically involves sample preparation followed by chromatographic separation and mass spectrometric identification. Urine is the most common matrix for anti-doping tests, though blood and hair have also been explored. Methods can target the parent compound or its metabolites, depending on the expected window of detection. Reference standards are required for accurate quantification. Matrix effects and dilution can influence results, so laboratories use internal standards and validation protocols. The exact detection window varies with dose, route, and individual metabolism.
Cardarine is not approved for human therapeutic use in any major jurisdiction. It appears on the World Anti-Doping Agency Prohibited List as a PPARδ agonist within the hormone and metabolic modulators category. Sports organizations test for it because it has been detected in athlete samples and seized products. Regulatory actions against marketed research chemical versions have occurred in several countries, though enforcement varies. Availability through unregulated channels complicates oversight.
Analytical laboratories typically identify cardarine and its metabolites using liquid chromatography-tandem mass spectrometry. Urine is a common matrix in anti-doping testing, while blood and tissue may be used in research settings. Detection windows depend on the assay, the sample matrix, and the compound's metabolism. Because cardarine is extensively metabolized, laboratories often target specific metabolites to improve sensitivity and confirmation. Reference standards are required for reliable quantification. Method validation includes checks for selectivity, linearity, and carryover.
A persistent misconception is that cardarine is a fat-burning drug or a safe alternative to anabolic steroids. No approved therapeutic product exists, and human safety data are limited. The tumor findings in rodents remain a central concern in scientific reviews. Products sold online may contain inaccurate labels, impurities, or different compounds entirely, which complicates any assessment of effects. Independent testing of such products has reported frequent mislabeling. For these reasons, discussions in the literature emphasize risks and unknowns rather than benefits.
== References == This article was submitted to WikiJournal of Medicine for external academic peer review in 2022 (reviewer reports). The updated content was reintegrated into the Wikipedia page under a CC-BY-SA-3.0 license (2023). The version of record as reviewed is: Maxim Masiutin, Maneesh Yadav, et al. (2023). "Alternative androgen pathways" (PDF). WikiJournal of Medicine. 10 (1): 3. doi:10.15347/wjm/2023.003. Wikidata Q100737840.
In microbiology, colonial morphology refers to the visual appearance of bacterial or fungal colonies on an agar plate. Examining colonial morphology is the first step in the identification of an unknown microbe. The systematic assessment of the colonies' appearance, focusing on aspects like size, shape, colour, opacity, and consistency, provides clues to the identity of the organism, allowing microbiologists to select appropriate tests to provide a definitive identification.
Next, an epimerization domain changes the stereochemistry of L-alanine (L-Ala) into D-alanine (D-Ala). CesB is a 305 kDa heterodimer protein composed of CesB1 and CesB2 modules. CesB1 behaves almost identically to CesA1, where ketoisocaproic acid was added and reduced; however, the substrate α-ketoisovaleric acid is reduced to L- α-hydroxyisovaleric acid (L-HIV). Additionally, a condensation domain at the end of CesA (beyond CesA2) facilitates the ester formation between L-HIV and the D-HIC-D-Ala peptide. Next, CesB2 adds L-valine (L-Val) to the adenylation domain, and the condensation domain facilitates the nucleophilic attack of the amine on L-Val onto the D-HIC-D-Ala-L-HIV thioester, which creates a D-HIC-D-Ala-L-HIV-L-Val tetrapeptide on the thiolation domain of CesB2. Finally, the final thioesterase domain combines three units of the aforementioned tetrapeptide between the α-hydroxyl group of D-HIC and the thioester of a L-Val of another tetrapeptide. Ultimately, three esters are formed during this cyclization of 3 tetrapeptides. The resulting cyclic depsipeptide, which contains alternating units of esters and amides, is cereulide.
=== Calcification and lipids === Calcification forms among vascular smooth muscle cells of the surrounding muscular layer, specifically in the muscle cells adjacent to atheromas and on the surface of atheroma plaques and tissue. In time, as cells die, this leads to extracellular calcium deposits between the muscular wall and outer portion of the atheromatous plaques. With the atheromatous plaque interfering with the regulation of calcium deposition, it accumulates and crystallizes. A similar form of intramural calcification, presenting the picture of an early phase of arteriosclerosis, appears to be induced by many drugs with an antiproliferative mechanism of action (Rainer Liedtke 2008). Cholesterol is delivered into the vessel wall by cholesterol-containing low-density lipoprotein (LDL) particles. To attract and stimulate macrophages, the cholesterol must be released from the LDL particles and oxidized, a key step in the ongoing inflammatory process. The process is worsened if there is insufficient high-density lipoprotein (HDL), the lipoprotein particle that removes cholesterol from tissues and carries it back to the liver. The foam cells and platelets encourage the migration and proliferation of smooth muscle cells, which in turn ingest lipids, become replaced by collagen, and transform into foam cells themselves. A protective fibrous cap normally forms between the fatty deposits and the artery lining (the intima). These capped fatty deposits (now called 'atheromas') produce enzymes that cause the artery to enlarge over time.
== Alternatives == Other authors have created topological skin maps. Kraissl's lines differ from Langer's lines particularly on the face. Also, while Langer's lines were defined in cadavers, Kraissl's lines have been defined in living individuals. The method used to identify Kraissl's lines is not traumatic.
Sources: en.wikipedia.org
== Structure == A triple helix is named such because it is made up of three separate helices. Each of these helices shares the same axis, but they do not take up the same space because each helix is translated angularly around the axis. Generally, the identity of a triple helix depends on the type of helices that make it up. For example: a triple helix made of three strands of collagen protein is a collagen triple helix, and a triple helix made of three strands of DNA is a DNA triple helix. As with other types of helices, triple helices have handedness: right-handed or left-handed. A right-handed helix moves around its axis in a clockwise direction from beginning to end. A left-handed helix is the right-handed helix's mirror image, and it moves around the axis in a counterclockwise direction from beginning to end. The beginning and end of a helical molecule are defined based on certain markers in the molecule that do not change easily. For example: the beginning of a helical protein is its N terminus, and the beginning of a single strand of DNA is its 5' end. The collagen triple helix is made of three collagen peptides, each of which forms its own left-handed polyproline helix. When the three chains combine, the triple helix adopts a right-handed orientation. The collagen peptide is composed of repeats of Gly-X-Y, with the second residue (X) usually being Pro and the third (Y) being hydroxyproline.
These rubidium standards are often used with GNSS to produce a "primary frequency standard" that has greater accuracy and is less expensive than caesium standards. Such rubidium standards are often mass-produced for the telecommunications industry. Other potential or current uses of rubidium include a working fluid in vapor turbines, as a getter in vacuum tubes, and as a photocell component. Rubidium is also used as an ingredient in special types of glass, in the production of superoxide by burning in oxygen, in the study of potassium ion channels in biology, and as the vapor in atomic magnetometers. In particular, 87Rb is used with other alkali metals in the development of spin-exchange relaxation-free (SERF) magnetometers. Rubidium-82 is used for positron emission tomography. Rubidium is very similar to potassium, and tissue with high potassium content will also accumulate the radioactive rubidium. One of the main uses is myocardial perfusion imaging. As a result of changes in the blood–brain barrier in brain tumors, rubidium collects more in brain tumors than normal brain tissue, allowing the use of radioisotope rubidium-82 in nuclear medicine to locate and image brain tumors. Rubidium-82 has a very short half-life of 76 seconds, and the production from decay of strontium-82 must be done close to the patient. Rubidium was tested for the influence on bipolar disorder and depression. Dialysis patients suffering from depression show a depletion in rubidium, and therefore a supplementation may help during depression.
== Reactions == As a lactone, GBL is hydrolyzed under basic conditions, for example in a sodium hydroxide solution into sodium gamma-hydroxybutyrate, the sodium salt of gamma-hydroxybutyric acid. In acidic water, a mixture of the lactone and acid forms exists in an equilibrium. These compounds then may go on to form the polymer poly(4-hydroxybutyrate) as well as the dimer 1,6-Dioxecane-2,7-dione. When treated with a non-nucleophilic base, such as lithium diisopropylamide, GBL undergoes deprotonation of the alpha carbon atom to the carbonyl.
=== REDEFINE 2 === In June 2025, results were published in the New England Journal of Medicine on REDEFINE 2, a 68-week, double-blind, Phase III clinical trial enrolling 1,206 participants. REDEFINE 2 reported that obese or overweight adult patients with type 2 diabetes lost 13.7% of their weight over 68 weeks with Cagrilintide/semaglutide, compared with 3.1% with placebo.
Direct skin contact with nickel-releasing item Prolonged skin contact with nickel-releasing item A sufficient amount of nickel is released and absorbed into the skin to cause a reaction The pathophysiology is divided into induction elicitation phases. Induction is the critical phase (immunological event) when skin contact to nickel results in antigen presentation to the T cells, and T cell duplication (cloning) occurs. The metal cation Ni++ is a low molecular weight hapten that easily penetrates the stratum corneum (top layer of skin). Nickel then binds to skin protein carriers creating an antigenic epitope. The determining factor in sensitization is exposure of significant amounts of "free nickel". This is important because different metal alloys release different amounts of free nickel. The antigenic epitope is collected by dermal dendritic cells and Langerhans cells, the antigen-presenting cells (APC) of the skin, and undergo maturation and migration to regional lymph nodes. The complex is predominantly expressed on major histocompatibility complex (MHC) II, which activates and clonally expands naive CD4+ T cells. Upon re-exposure these now primed T cells will be activated and massively recruited to the skin, resulting in the elicitation phase and the clinical presentation of Ni-ACD. Although ACD has been considered a Th1 predominate process, recent studies highlight a more complex picture. In Ni-ACD other cells are involved including: Th17, Th22, Th1/IFN and the innate immune responses consistent with toll-like receptor 4.
Sources: en.wikipedia.org
The BBC reports that security is to be increased at Champions League games, following threats from a pro-IS media channel. Foreign Secretary David Cameron confirms that the UK will not suspend the sale of arms to Israel. The governor of the Bank of England, Andrew Bailey and chief cashier Sarah John, present King Charles III with his banknotes. 10 April A review into gender services carried out by paediatrician Dr Hilary Cass calls for gender services for young people to match the standards of other NHS care. Five people are arrested after pro-Palestinian protestors spray red paint on the Ministry of Defence building in London. Meta lowers the minimum age for WhatsApp users in the UK and EU from 16 to 13. 11 April The Victoria and Albert Museum and British Museum return a number of artefacts to Ghana on long-term loan, more than 150 years after they were taken. The Metropolitan Police says it will partly reinvestigate its decision to charge television presenter Caroline Flack with assaulting her boyfriend because "new witness evidence may be available". 12 April Data from the Office for National Statistics shows the UK economy grew by 0.1% in February, which is attributed to increases in production and manufacturing. The British government advises against all travel to Israel and Palestinian territories due to the imminent threat of an Iranian attack. 13 April Former subpostmaster Alan Bates says he will consider raising funds to bring a private prosecution against Post Office bosses over the Horizon IT scandal.
=== Pharmacokinetics === After injection into a vein, 14% of the circulating ioxaglic acid is bound to blood plasma proteins, which is unusually high for a water-soluble iodinated contrast agent. The substance is distributed in the body with a half-life of 12 minutes (range 4 to 17 minutes) and eliminated in unmetabolized (unchanged) form via the kidneys with a half-life of 92 minutes (range 61 to 140 minutes). In people with kidney failure, it is eliminated via the bile duct, saliva or sweat.
Misuzu Henderson (観鈴・ヘンダーソン, Misuzu Hendaason) Voiced by: Yoko Hikasa Leader of the "Kasai" Reformist group. She's called "Gozen" and organized the attack on the Town of Winter where Hinagiku was kidnapped. In the past, Misuzu's father was the leader of the Insurgents. Misuzu once had a daughter, but her daughter died, leaving Misuzu traumatized. Feeling powerless, Misuzu decides to kidnap, ransom, and kill agents. She becomes obsessed with Hinagiku, whom she attempts to brainwash into acting as her daughter. After eight years of Misuzu's mental and physical torture, it finally becomes Misuzu's fatal mistake, especially of trying to impregnant Hinagiku with one of her henchmen. Hinagiku finally snaps and destroys the Insurgent base and escapes. Misuzu survives and goes into hiding, attempting to rebuild the organization in the meantime. Misuzu saw Nadeshiko and decided to do same thing she did to Hinagiku. Despite being nearly killed by Hinagiku, Misuzu wanted to recapture her. Mikami (美上, Mikami) Voiced by: Hinata Tadokoro Misuzu's right-hand man. He has strong feelings for Misuzu despite his desire to leave the Reformists and start a new life.
=== Production during the Manhattan Project === During World War II the U.S. government established the Manhattan Project, for developing an atomic bomb. The three primary research and production sites of the project were the plutonium production facility at what is now the Hanford Site, the uranium enrichment facilities at Oak Ridge, Tennessee, and the weapons research and design lab, now known as Los Alamos National Laboratory, LANL.
Sources: en.wikipedia.org
Cardarine is a common name for GW501516, a synthetic PPARδ agonist. It is not a steroid or a selective androgen receptor modulator. It was developed and studied as a research compound for metabolic pathways.
It binds to and activates PPARδ, a nuclear receptor that regulates genes related to fatty acid oxidation and energy use. This activation alters transcription in tissues such as skeletal muscle and liver. The full range of downstream effects in humans is not fully established.
No, cardarine is not known to occur naturally in plants, animals, or humans. It is a synthetic molecule produced for laboratory research. Products labeled as cardarine should therefore be treated as manufactured chemicals with variable purity.
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.