If you have been reading about research chemical 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.
Updated 2026-03-06. Numbers and descriptions here follow the published literature rather than marketing material.
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.
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.
Laboratory studies indicate that GW501516 activates PPARδ, a nuclear receptor involved in fatty acid oxidation and energy metabolism. In rodent experiments, treated animals often showed increased endurance and reduced fat mass. These effects were observed under controlled conditions and do not establish safe or effective use in humans. The exact dose-response relationship in humans remains poorly characterized. Species differences in metabolism can affect how results translate across animals and people.
Safety concerns emerged from long-term animal studies. In rodents given the compound for extended periods, researchers found an increased incidence of certain cancers, including liver and bladder tumors. These findings contributed to the discontinuation of clinical development. Whether similar risks apply to short-term or low-level exposure in humans is not established, and controlled human safety data are limited. The relevance of high-dose rodent carcinogenicity findings to human use remains a subject of debate.
| Property | Value | Notes |
|---|---|---|
| Common name | Cardarine | Also called GW501516 and endurobol. |
| Chemical formula | C21H18F3NO3S2 | Molecular weight about 453.5 g/mol. |
| Appearance | White to off-white solid | Form depends on synthesis and purity. |
| Solubility | Soluble in DMSO and ethanol | Low solubility in water. |
| Typical storage | -20 °C, desiccated, protected from light | Common for research chemicals. |
Laboratory studies have examined GW501516 in cell cultures and rodents for conditions such as dyslipidemia, insulin resistance, and obesity. Some trials in humans were initiated, but development was discontinued after preclinical findings raised concerns about cancer in certain models. Those findings do not prove that the compound causes cancer in people, but they contributed to regulatory caution. Later reviews often describe the evidence as preliminary and insufficient for assessing long-term safety.
In the fitness and bodybuilding literature, cardarine is frequently discussed as an endurance agent or fat-loss compound, although such claims are not supported by robust clinical evidence. Online descriptions often mix animal data, user anecdotes, and marketing language. Researchers who study PPARδ agonists distinguish between receptor activation in controlled experiments and unsupervised use of unverified products. The latter introduces unknown purity, dose, and interactions, making reported experiences difficult to interpret scientifically.
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.
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.
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.
== Adverse effects == The most common adverse reactions include upper respiratory tract infections, vomiting, cough, other viral infections, headache, gastroenteritis, and pharyngitis (sore throat). An increased risk of fractures, including serious fractures, was observed in people treated with apitegromab. Apitegromab may cause fetal harm and may affect reproductive function.
=== Breast cancer === Anastrozole is used in the treatment and prevention of breast cancer in women. The Arimidex, Tamoxifen, Alone or in Combination (ATAC) trial was of localized breast cancer and women received either anastrozole, the selective estrogen receptor modulator tamoxifen, or both for five years, followed by five years of follow-up. After more than 5 years the group that received anastrozole had better results than the tamoxifen group. The trial suggested that anastrozole is the preferred medical therapy for postmenopausal women with localized estrogen receptor-positive breast cancer.
== Mechanism of action == The iRGD peptide homes to and penetrates tumors through a 3-step process. First, the RGD sequence motif mediates binding to αVβ3 and αVβ5 integrins that are expressed on tumor endothelial cells. Second, upon αV binding, a protease cleavage event is activated, revealing the C-terminal CendR motif (R/KXXR/K) of the peptide. Third, the CendR motif is now able to bind to neuropilin-1, activating an endocytotic/exocytotic transport pathway. The pathway triggered by iRGD can be used for the enhanced transport of coupled and coadministered anti-cancer drugs into tumors.
Sources: en.wikipedia.org
=== FORTUNE, Modern Healthcare and Press Ganey awards === Southern Ohio Medical Center has been recognized as one of FORTUNE Magazine’s Best Places to Work in America for six straight years. In 2013, it came in 29th on the list with FORTUNE noting: “Employees are proud to work for a medical provider that has won numerous awards for patient care, a fact that's reflected in its average tenure. Nearly 20% of the staff has worked there for more than 20 years.” SOMC was recognized on the FORTUNE list again in 2014 (coming in 18th) and 2015 (coming in 44th). In the 2015 survey, 93% of SOMC employees described their workplace as "a great place to work." Modern Healthcare Magazine also recognized SOMC as one of the nation's best healthcare employers in 2010, 2011 and 2012. In 2012, Southern Ohio Medical Center was one of only 13 Press Ganey clients in the nation to be chosen as a Distinctive Workplace Award winner. The award was given to organizations that reached, and sustained, the 95th percentile in employee satisfaction – SOMC was at the 99th percentile.
=== Early years === Brothers Jim and William Reid formed a band in the early 1980s in response to their distaste of the music at the time, saying, "It was the crap coming out of the radio that made us want to be in a band". This worked in their favour, as William said, "It was perfect timing because there weren't any guitar bands. Everybody was making this electronic pop music." Before forming the band, the brothers had spent five years on the dole, during which they wrote and recorded songs at home and worked out the sound and image of the band. Originally called The Poppy Seeds, and then Death of Joey, they initially told journalists that they had taken their eventual name from a line in a Bing Crosby film, although six months later they admitted that this was not true. Other accounts suggest that the name derived from an offer on a breakfast cereal packet, where customers could send off for a gold Jesus & Mary chain. As neither brother wanted to be the singer, they decided on Jim via coin toss. The brothers started recording and sending demos to record companies in 1983 (using a Portastudio bought with £300 given to them by their father from redundancy pay after he lost his factory job), and by early 1984 they had recruited bass player Douglas Hart and teenage drummer Murray Dalglish. Early influences included the Velvet Underground, the Stooges, New York Dolls, Suicide, the Shangri-Las, and Einstürzende Neubauten.
=== Other uses === Leaves of the palm may be made into hats, mats, baskets, brooms and roof thatch for homes, and trunk wood, resistant to pests, for building construction. Tree trunks may be processed to yield dietary minerals. Comprising 80% of the fruit mass, açaí seeds may be ground for livestock food or as a component of organic soil for plants. Planted seeds are used for new palm tree stock, which, under the right growing conditions, can require months to form seedlings. Seeds may become waste in landfills or used as fuel for producing bricks.
Several trials have attempted dietary interventions with the hope of reducing the autoimmunity that leads to type 1 diabetes. Trials that withheld cow's milk or gave infants formula free of bovine insulin decreased the development of β-cell-targeted antibodies, but did not prevent the development of type 1 diabetes. Similarly, trials that gave high-risk individuals injected insulin, oral insulin, or nicotinamide did not prevent diabetes development. Other strategies under investigation for the prevention of type 1 diabetes include gene therapy, stem cell therapy, and modulation of the gut microbiome. Gene therapy approaches are still in early stages. They aim to alter genetic factors that contribute to beta-cell destruction by editing immune responses. Stem cell therapies are also being researched, with the hope that they can either regenerate insulin-producing beta cells or protect them from immune attack. Trials using stem cells to restore beta cell function or regulate immune responses are ongoing. Modifying the gut microbiota through the use of probiotics, prebiotics, or specific diets has also gained attention. Some evidence suggests that the gut microbiome plays a role in immune regulation, and researchers are investigating whether altering the microbiome could reduce the risk of autoimmunity and, subsequently, type 1 diabetes. Tolerogenic therapies, which seek to induce immune tolerance to beta-cell antigens, are another area of interest.
Sources: en.wikipedia.org
Cardarine is a common name for the investigational compound GW501516. It acts as a PPARδ agonist and is not approved for human use. It is prohibited in sport.
It activates PPARδ, a nuclear receptor that influences gene expression related to lipid and energy metabolism. Animal studies show changes in endurance and lipid levels. Human effects and risks are not well established.
No, cardarine is not a steroid. It belongs to a different chemical class, the PPARδ agonists. It is also not a selective androgen receptor modulator.
Rodent studies reported increased endurance and fat oxidation after GW501516 exposure. Long-term studies also found higher rates of some tumors, which led to halted development.