If you have been reading about PPARδ agonist and want a single page that covers the useful parts, this is it: definitions, context, how it is studied, and the questions that come up repeatedly.
Last reviewed on 2026-05-26. Where a claim depends on a specific study, the study is described rather than over-claimed.
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.
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.
GW501516 binds and activates PPARδ, a nuclear receptor that influences transcription of genes involved in fatty acid oxidation and energy use. Activation shifts some metabolic pathways in preclinical models, which is why the compound has been studied for lipid disorders and exercise-related endpoints. The exact downstream effects in humans are incompletely mapped. PPARδ is expressed in many tissues, including skeletal muscle, liver, and adipose tissue, so broad activation may have varied consequences. Researchers continue to examine how selective or partial activation might alter the balance between benefits and risks.
Published human data are sparse and mostly come from early-phase trials. Those studies examined short-term changes in lipids, glucose, and exercise capacity, but they were not large enough to establish efficacy or long-term safety. Some animal experiments reported increased running endurance, yet such findings do not prove a performance benefit in people. Anti-doping laboratories detect GW501516 and its metabolites in urine or blood using liquid chromatography-tandem mass spectrometry. Detection windows depend on dose, sample type, and individual metabolism. The method is sensitive enough to identify trace residues in tested samples.
Laboratory handling focuses on identity, purity, and stability. Reference standards are typically stored cold and dry, protected from light, because solutions can degrade over time. Analytical checks may use high-performance liquid chromatography with ultraviolet detection or mass spectrometry. Impurities and related substances can be separated chromatographically and compared with a known standard. Because cardarine is not an approved drug, compendial monographs are absent, and laboratories often rely on in-house methods. Reported purity varies among unregulated products and should not be assumed from a label.
| 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 |
Early clinical research explored GW501516 for lipid disorders, obesity, and diabetes. Some short-term human studies reported changes in HDL cholesterol, LDL cholesterol, and triglycerides. The development program was discontinued after rodent studies showed dose-dependent tumor formation in multiple tissues, including liver, bladder, stomach, and skin. These findings raised concerns about long-term cancer risk in humans. Because human exposure data are limited, the clinical significance of the rodent tumors remains uncertain.
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.
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.
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.
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 a common name for GW501516, a synthetic compound developed in the 1990s through research collaborations involving GlaxoSmithKline. It belongs to a class of molecules known as peroxisome proliferator-activated receptor delta agonists. Early studies explored its effects on lipid metabolism and energy expenditure in animal models. The compound was never approved as a human medicine, and clinical development was discontinued. In the years since, it has appeared in fitness and bodybuilding communities as a performance-enhancing substance. Regulatory agencies classify it as an unapproved drug.
PPARδ is a nuclear receptor that regulates gene expression related to fatty acid oxidation, glucose homeostasis, and mitochondrial function. GW501516 binds to this receptor with high affinity and activates downstream signaling in skeletal muscle and other tissues. Animal studies reported increased endurance and altered fuel preference, but human data remain limited and inconsistent. The precise relationship between receptor activation and observed physiological changes is still an area of active investigation. Researchers have also examined whether the compound affects inflammation or cell proliferation. No approved therapeutic indication exists for cardarine.
In laboratory settings, cardarine is studied as a tool compound for probing PPARδ biology. Published experiments often use cell cultures, rodent models, or isolated tissues. Some investigations focus on metabolic effects, while others assess potential risks such as carcinogenicity observed in long-term animal studies. Because human trials are sparse, most knowledge comes from preclinical work and adverse event reports. Scientific literature frequently notes the gap between animal findings and human outcomes. The compound is not a dietary supplement and is not intended for human consumption.
== See also == Sodium hyaluronate, the sodium salt of hyaluronic acid, a glycosaminoglycan found in various human connective tissue. Microbial hyaluronic acid production, the process by which microorganisms are utilized in fermentation to synthesize hyaluronic acid. Alguronic acid, trade name for a mix of polysaccharides produced by microalgae. Inhibits production of hyaluronic-acid-degrading enzymes. Bloomage, a biomaterial company based in China, primarily specialized in hyaluronic acid and other bioactive substance products.
Erythromycin, ketoconazole and cyclosporine are CYP3A4 inhibitors and therefore inhibit the metabolic pathway of docetaxel. When used with anticonvulsants, which induce CYP3A4, an increased dose of docetaxel may be required. Pre-treatment with corticosteroids has been used to decrease hypersensitivity reactions and oedema in response to docetaxel and has shown no effect on the pharmacokinetics of docetaxel. The efficacy of docetaxel was improved by treatment with oral capecitabine, and after more than 27 months follow-up the survival benefit has been confirmed. Doxorubicin was combined with docetaxel in one study of 24 patients and resulted in an increased AUC of docetaxel by 50 to 70%, indicating doxorubicin may affect the disposition of docetaxel. Etoposide has also been shown to decrease docetaxel clearance, though patient numbers for this observation have been low. Prednisone given with docetaxel led to improved survival, quality of life and pain management in patients with hormone-refractory prostate cancer.
Corticotropin-releasing hormone (CRH) (also known as corticotropin-releasing factor (CRF) or corticoliberin; corticotropin may also be spelled corticotrophin) is a peptide hormone involved in stress responses. It is a releasing hormone that belongs to corticotropin-releasing factor family. In humans, it is encoded by the CRH gene. Its main function is the stimulation of the pituitary synthesis of adrenocorticotropic hormone (ACTH), as part of the hypothalamic–pituitary–adrenal axis (HPA axis). Corticotropin-releasing hormone (CRH) is a 41-amino acid peptide derived from a 196-amino acid preprohormone. CRH is secreted by the paraventricular nucleus (PVN) of the hypothalamus in response to stress. Increased CRH production has been observed to be associated with Alzheimer's disease and major depression, and autosomal recessive hypothalamic corticotropin deficiency has multiple and potentially fatal metabolic consequences including hypoglycemia. In addition to the hypothalamus, CRH is produced by neurons in other brain regions, including the neocortex, limbic system and brainstem. In the olivocerebellar tract, CRH is expressed in neurons that send their axons from the inferior olivary complex to the cerebellar cortex. CRH is also synthesized in peripheral tissues, such as T lymphocytes, and it is highly expressed in the placenta, where it regulates the length of gestation and the timing of parturition and delivery.
Sources: en.wikipedia.org
The isotopes of nickel range in mass number from 48 (48Ni) to 82 (82Ni). Natural nickel is composed of five stable isotopes, 58Ni, 60Ni, 61Ni, 62Ni and 64Ni, of which 58Ni is the most abundant (68.077% natural abundance). Nickel-62 has the highest binding energy per nucleon of any nuclide: 8.7946 MeV/nucleon. Its binding energy is greater than both 56Fe and 58Fe, more abundant nuclides often incorrectly cited as having the highest binding energy. Though this would seem to predict nickel as the most abundant heavy element in the universe, the high rate of photodisintegration of nickel in stellar interiors causes iron to be by far the most abundant. Nickel-60 is the daughter product of the extinct radionuclide 60Fe (half-life 2.6 million years). Due to the long half-life of 60Fe, its persistence in materials in the Solar System may generate observable variations in the isotopic composition of 60Ni. Therefore, the abundance of 60Ni in extraterrestrial material may give insight into the origin of the Solar System and its early history. At least 26 nickel radioisotopes have been characterized; the most stable are 59Ni with half-life 76,000 years, 63Ni (100 years), and 56Ni (6 days). All other radioisotopes have half-lives less than 60 hours and most these have half-lives less than 30 seconds. This element also has one meta state. Radioactive nickel-56 is produced by the silicon burning process and later set free in large amounts in Type Ia supernovae.
== Molecular action of rennet enzymes == One of the main actions of rennet is its protease chymosin cleaving the kappa casein chain. Casein is the main protein of milk. Cleavage removes the slightly negatively charged glycomacropeptide (GMP) from the surface of the casein micelle. Because negative charges repel other negative charges, the GMP prevents casein micelles from adhering to each other. With the GMP removed, the casein micelles can begin to cluster and lose their polar charge, causing them to rise out of the polar water molecules and join non-polar milk fat as a portion of the cheese curd. This action is enhanced in the presence of strong ions like those formed from calcium and phosphate. As such, those chemicals are occasionally added to supplement pre-existing quantities in the cheese making process, especially in calcium phosphate-poor goat milk. The solid truncated casein protein network traps other components of milk, such as fats and minerals, to create cheese.
=== Blood, lymph and nerve supply === The tissues of the vulva are highly vascularised and blood supply is provided by the three pudendal arteries. Venous return is via the external and internal pudendal veins. The organs and tissues of the vulva are drained by a chain of superficial inguinal lymph nodes located along the blood vessels. The ilioinguinal nerve originates from the first lumbar nerve and gives branches that include the anterior labial nerves, which supply the skin of the mons pubis and the labia majora. The perineal nerve is one of the terminal branches of the pudendal nerve and this branches into the posterior labial nerves to supply the labia. The pudendal nerve branches include the dorsal nerve, which gives sensation to the clitoris. The clitoral glans is seen to be populated by a large number of small nerves, a number that decreases as the tissue changes towards the urethra. The density of nerves at the glans indicates that it is the center of heightened sensation. Cavernous nerves from the uterovaginal plexus supply the erectile tissue of the clitoris. These are joined underneath the pubic arch by the dorsal nerve of the clitoris. The pudendal nerve enters the pelvis through the lesser sciatic foramen and continues medial to the internal pudendal artery. The point where the nerve circles the ischial spine is the location where a pudendal block of local anesthetic can be administered to inhibit sensation to the vulva. A number of smaller nerves split off from the pudendal nerve.
The Green Mountain Boys were a militia organization established in 1770 in the territory between the British provinces of New York and New Hampshire, known as the New Hampshire Grants and later in 1777 as the Vermont Republic (which later became the state of Vermont). Headed by Ethan Allen and members of his extended family, it was instrumental in resisting New York's attempts to control the territory, over which it had won de jure control in a territorial dispute with New Hampshire. Some companies served in the American Revolutionary War, including notably when the Green Mountain Boys, led under the command of Ethan Allen while being assisted by Benedict Arnold, captured Fort Ticonderoga on Lake Champlain on May 10, 1775, and invaded Canada later in 1775. In early June 1775, Ethan Allen and his then subordinate, Seth Warner, induced the Continental Congress at Philadelphia to create a Continental Army ranger regiment from the then New Hampshire Grants. Having no treasury, the Congress directed that New York's revolutionary Congress pay for the newly authorized regiment. In July 1775, Allen's militia was granted support from the New York revolutionary Congress. The Green Mountain Boys disbanded more than a year before Vermont declared its independence in 1777 from Great Britain "as a separate, free and independent jurisdiction or state". The Vermont Republic operated for 14 years, before being admitted in 1791 to the United States as the 14th state. The remnants of the Green Mountain Boys militia were largely reconstituted as the Green Mountain Continental Rangers.
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.
Anti-doping and clinical laboratories commonly use liquid chromatography-tandem mass spectrometry. The method can identify GW501516 and its metabolites in urine or blood. Detection depends on sample timing and the amount present.