Everything below concerns GW501516. We keep the language plain, cite what the science says, and separate well-supported claims from open questions.
Updated 2025-11-18. Numbers and descriptions here follow the published literature rather than marketing material.
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, 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.
| 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 |
At the molecular level, GW501516 binds and activates PPARδ, a nuclear receptor that regulates transcription. Activation shifts expression of genes involved in fatty acid oxidation, energy expenditure, and lipid transport in skeletal muscle and liver. Animal studies report increased endurance and altered lipid profiles after exposure. Human data are limited to small trials and do not establish long-term safety or efficacy. PPARδ also has roles in cell proliferation, so the relationship between activation and cancer risk remains an open question.
Published literature on cardarine includes in vitro assays, rodent experiments, and a small number of human studies. Reports describe effects on exercise capacity and lipid metabolism in animals, while human evidence is sparse. Many online descriptions present the compound as a proven endurance aid, a claim not supported by regulatory approval or large clinical trials. Analytical studies focus on identifying the parent compound and its metabolites in biological samples. Important uncertainties include species differences, dose-response relationships, and the relevance of rodent tumor findings to humans.
Cardarine is the common name for GW501516, a synthetic compound studied as a peroxisome proliferator-activated receptor delta agonist. Researchers developed it to explore treatments for lipid disorders and metabolic conditions. It is not an approved medicine in any country. Early clinical work examined changes in HDL cholesterol and triglycerides, but development was discontinued after animal studies raised concerns about cancer. The compound remains available as a research chemical and appears in discussions of performance enhancement.
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.
== Vertebrates == Tendon cells, or tenocytes, are elongated fibroblast type cells. The cytoplasm is stretched between the collagen fibres of the tendon. They have a central cell nucleus with a prominent nucleolus. Tendon cells have a well-developed rough endoplasmic reticulum and they are responsible for synthesis and turnover of tendon fibres and ground substance.
=== Successful prevention and identification === The first successful preventive measure against beriberi was discovered by Takaki Kanehiro, a British-trained Japanese medical doctor of the Imperial Japanese Navy, in the mid-1880s. Beriberi was a serious problem in the Japanese navy; sailors fell ill an average of four times a year in the period 1878 to 1881, and 35% were cases of beriberi. In 1882, Takaki learned of a very high incidence of beriberi among cadets on a training mission from Japan to Hawaii, via New Zealand and South America. The voyage lasted more than nine months and resulted in 169 cases of sickness and 25 deaths on a ship of 376 men. Takaki observed that beriberi was common among low-ranking crew who were often provided free rice, thus ate little else, but not among crews of Western navies, nor among Japanese officers who consumed a more varied diet. With the support of the Japanese Navy, he conducted an experiment in which another ship was deployed on the same route, except that its crew was fed a diet of meat, fish, barley, rice, and beans. At the end of the voyage, this crew had only 14 cases of beriberi and no deaths. Takaki's results of his experiment impressed the Japanese Navy, which adopted his proposed solution. By 1887, beriberi had been eliminated on Navy ships. In the same year, Takaki's experiment was described favorably in The Lancet, but his nutritional deficiency etiology was not taken seriously, with Western medicine overwhelmingly favoring miasmatic theories, believing the disease to be caused either by microorganisms or toxins.
Cohen (1952), former co-owner of the Boston Celtics and the Brooklyn Nets; former chairman and CEO of the Madison Square Garden Corporation Lawrence K. Grossman (1952), president of PBS 1976–1984 and NBC News 1985–1988 Richard Wald (1952), former president of NBC News 1973–1977 Robert A. Belfer (1955), oilman and philanthropist, namesake of the Belfer Center for Science and International Affairs at Harvard University Thomas Ludlow Chrystie II (1955), first chief financial officer of Merrill Lynch & Company and creator of the Cash Management Account Alfred Lerner (1955), chairman of MBNA Bank and ex-owner of the Cleveland Browns Richard Ravitch (1955), chairman of the Metropolitan Transportation Authority and the Bowery Savings Bank Sid Sheinberg (1955), head of Universal Pictures Barry F. Sullivan (1955), chairman and CEO of First Chicago Bank, deputy mayor of New York City under David Dinkins Edward Botwinick (1956), IT entrepreneur and inventor, co-founder of Timeplex Franklin A. Thomas (1956), former president of The Ford Foundation James R. Barker (1957), chairman of Interlake Steamship Company, former chairman and CEO of Moore-McCormack Peter L.
Sources: en.wikipedia.org
During development of amphibians and fish, the notochord induces development of the hypochord through secretion of vascular endothelial growth factor. The hypochord is a transient structure ventral to the notochord, and is primarily responsible for correct development of the dorsal aorta. Notochord flexion, when the notochord bends to form a part of the developing caudal fin, is a hallmark of an early growth stage of some fish.
Serum haptocorrin binds 80-90% of circulating B12, rendering it unavailable for cellular delivery by transcobalamin II. This is conjectured to be a circulating storage function. Several serious, even life-threatening diseases cause elevated serum haptocorrin, measured as abnormally high serum vitamin B12, while potentially manifesting as a symptomatic vitamin deficiency because of insufficient vitamin bound to transcobalamin II which transfers the vitamin to cells.
In contrast, it declined by approximately 2.2 percent in the placebo group (P=0.006). There is an emerging recognition of the role that diet and exercise can play in functionally limiting symptom progression. This is an area for further study, as there is no clear consensus guideline, but rather a body of case study work that suggests that appropriate physical activity can be an effective tool in managing disease progression. In one such study, side-alternating vibration training was used 3 times weekly for 15 weeks. The results showed that, at 15 weeks, the patient had a 116-meter (70%) improvement to their 6MWT, which is significant compared with the results from the aforementioned LOTS study.
=== Low-intensity conflict (8 April – 24 May) === On 8 April, the Taliban-run Afghan foreign ministry stated that talks with Pakistani officials in China had concluded and described the discussions as constructive. Chinese officials said that representatives of Pakistan and the Taliban had agreed to work toward an early easing of tensions and to avoid actions that could escalate the situation. Pakistani officials did not comment on the outcome of talks. On the same day, Amir Khan Muttaqi, the Taliban's foreign minister, said while meeting with diplomats from Central Asian states that the group would not permit Afghan territory to be used by any group to threaten neighboring states. Although he did not name any organisation, he said the presence of such elements anywhere was unacceptable and that the Taliban intended to deal with the matter. He also stated that the Taliban were committed to easing tensions with Pakistan through dialogue and said he hoped the talks would produce positive outcomes. However, on 9 April, Mohammad Naeem Wardak, the Taliban's deputy foreign minister, said that talks between Pakistani and Taliban officials in China had ended without agreement and attributed their failure to Pakistani officials. On 10 April, local elders in Kunar and Nuristan said that Taliban border forces had withdrawn from several border posts in Bari Kot in Nari district, Kunar, and in Kamdesh district, Nuristan, and had taken shelter in village mosques.
Sources: en.wikipedia.org
== Function == CART is a neuropeptide that produces similar behavior in animals as cocaine and amphetamine, but conversely blocks the effects of cocaine when they are co-administered. The peptide is found in several areas, among them the ventral tegmental area (VTA) of the brain. When CART was injected into rat VTA, increased locomotor activity was seen, which is one of the signs of "central stimulation" caused by psychostimulants, such as cocaine and amphetamine. The same rats also tended to return to the place where they were injected. This is called conditioned place preference and is also seen after injection of cocaine. CART peptides, in particular, CART(55–102), seem to have an important function in the regulation of energy homeostasis and interact with several hypothalamic appetite circuits. CART expression is regulated by several peripheral peptide hormones involved in appetite regulation, including leptin, cholecystokinin and ghrelin, with CART and cholecystokinin having synergistic effects on appetite regulation. CART is released in response to repeated dopamine release in the nucleus accumbens, and may regulate the activity of neurons in this area. CART production is upregulated by CREB, a protein thought to be involved with the development of drug addiction, and CART may be an important therapeutic target in the treatment of stimulant abuse.
Smoking earlier in life and smoking cigarettes with higher tar content increases the risk of these diseases. Additionally, other forms of environmental tobacco smoke exposure, known as passive smoke and third-hand smoke, have manifested harmful health effects in people of all ages. Tobacco use is also a significant risk factor in miscarriages among pregnant women who smoke. It contributes to several other health problems for the fetus, such as premature birth and low birth weight, and increases the chance of sudden infant death syndrome (SIDS) by 1.4 to 3 times. The incidence of erectile dysfunction is approximately 85 percent higher in men who smoke compared to men who do not smoke. Many countries have taken measures to control tobacco consumption by restricting its usage and sales. They have printed warning messages on packaging. Moreover, smoking bans in public places like workplaces, theaters, bars, and restaurants have been enacted to reduce exposure to passive smoke. Tobacco taxation inflating the price of tobacco products, have also been imposed. In the late 1700s and the 1800s, the idea that tobacco use caused certain diseases, including mouth cancers, was initially accepted by the medical community. In the 1880s, automation dramatically reduced the cost of cigarettes, cigarette companies greatly increased their marketing, and use expanded. From the 1890s onwards, associations of tobacco use with cancers and vascular disease were regularly reported.
=== Lipids === The lipids found in green coffee include: linoleic acid, palmitic acid, oleic acid, stearic acid, arachidic acid, diterpenes, triglycerides, unsaturated long-chain fatty acids, esters, and amides. The total content of lipids in dried green coffee is 11.7–14 g/100 g. Lipids are present on the surface and in the interior matrix of green coffee beans. On the surface, they include derivatives of carboxylic acid-5-hydroxytryptamides with an amide bond to fatty acids (unsaturated C6 to C24) making up to 3% of total lipid content or 1200 to 1400 microgram/g dried green coffee bean. Such compounds form a wax-like cover on the surface of the coffee bean (200–300 mg lipids/100 g dried green coffee bean) protecting the interior matrix against oxidation and insects. Further, such molecules have antioxidative activity due to their chemical structure. Lipids of the interior tissue are triglycerides, linoleic acid (46% of total free lipids), palmitic acid (30% to 35% of total free lipids), and esters. Arabica beans have a higher content of lipids (13.5–17.4 g lipids/100 g dried green coffee beans) than robustas (9.8–10.7 g lipids/100 g dried green coffee beans). The content of diterpenes is about 20% of the lipid fraction. The diterpenes found in green coffee include cafestol, kahweol and 16-O-methylcafestol. Some of these diterpenes have been shown in in vitro experiments to protect liver tissue against chemical oxidation. In coffee oil from green coffee beans the diterpenes are esterified with saturated long chain fatty acids.
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.
Cardarine is a common name for GW501516, a synthetic PPARδ agonist developed for research. It has not been approved as a medication in any country. It is classified as an unapproved drug and a prohibited substance in sport.