If you have been reading about Prohibited list 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 2025-08-22. Numbers and descriptions here follow the published literature rather than marketing material.
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.
Human trials of GW501516 were small and short in duration. They examined lipid levels, glucose handling, and other metabolic markers, but the programs were halted after the animal cancer findings. No approved therapeutic product exists, and published human data are insufficient for establishing long-term safety. Reports of use for athletic performance come mainly from non-clinical settings and cannot be verified through controlled trials. Independent testing of products sold as cardarine has found inconsistent purity and labeling.
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.
| Property | Value | Notes |
|---|---|---|
| CAS Registry Number | 317318-70-0 | Unique identifier for the compound. |
| Chemical class | PPARδ agonist | Synthetic ligand for peroxisome proliferator-activated receptor delta. |
| Appearance | White to off-white solid | Typical form of research-grade material. |
| Solubility | Soluble in DMSO and ethanol | Poorly soluble in water. |
| Typical storage | -20°C | Recommended for long-term storage of stock solutions. |
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.
Products sold as cardarine have been found to contain incorrect compounds, variable amounts, or no active ingredient at all. Independent testing is required to verify identity and purity. Common analytical approaches include high-performance liquid chromatography, mass spectrometry, and nuclear magnetic resonance for structural confirmation. These methods can distinguish GW501516 from related PPAR agonists and from unrelated steroids. For regulators and researchers, such verification is central to interpreting both biological results and adverse event reports.
A common misconception is that cardarine has been proven safe for human use. In reality, human clinical data are limited, and long-term animal studies have raised concerns about cancer. Another misconception is that it is a supplement or vitamin-like compound. It is a synthetic research chemical with no approved medical indication. Scientific discussion often focuses on its mechanism and detection rather than therapeutic use. Regulatory and anti-doping literature treats it primarily as a prohibited substance.
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.
Legal status varies by country. In some places, cardarine is controlled under medicines or psychoactive substances laws; in others, it may be sold with minimal oversight as a research chemical. Customs agencies have intercepted shipments, and several national health agencies have issued warnings about products marketed for bodybuilding or performance enhancement. The lack of a standardized pharmaceutical supply means identity, purity, and contamination levels can differ widely between samples. These factors make cardarine a regulatory and public health concern rather than a conventional prescription drug.
Cardarine is a common name for GW501516, a synthetic compound first described in the 1990s as a selective agonist of the peroxisome proliferator-activated receptor delta. It was studied in preclinical models for metabolic and cardiovascular conditions, but it has not been approved as a medicine in the United States, Europe, or other major jurisdictions. Retail products labeled as cardarine are generally research chemicals or supplements, not pharmaceutical formulations. Because human safety and efficacy data remain limited, regulatory agencies treat it as an unapproved substance rather than a therapeutic product.
The APA, which published the DSM-5, acknowledged that there was sufficient evidence in order to create a diagnostic model of caffeine dependence for the DSM-5, but they noted that the clinical significance of the disorder is unclear. Due to this inconclusive evidence on clinical significance, the DSM-5 classifies caffeine-use disorder as a "condition for further study". Tolerance to the effects of caffeine occurs for caffeine-induced elevations in blood pressure and the subjective feelings of nervousness though the effects are not drastic. Sensitization, the process whereby effects become more prominent with use, may occur for positive effects such as feelings of alertness and wellbeing. Tolerance varies for daily, regular caffeine users and high caffeine users. High doses of caffeine (750 to 1200 mg/day spread throughout the day) have been shown to produce complete tolerance to some, but not all of the effects of caffeine. Doses as low as 100 mg/day, such as a 6 oz (170 g) cup of coffee or two to three 12 oz (340 g) servings of caffeinated soft-drink, may continue to cause sleep disruption, among other intolerances. Non-regular caffeine users have the least caffeine tolerance for sleep disruption. Some coffee drinkers develop tolerance to its undesired sleep-disrupting effects, but others apparently do not.
Benzodiazepines are usually administered orally; however, very occasionally lorazepam or diazepam may be given intravenously for the treatment of panic attacks. Because of their effectiveness, tolerability, and rapid onset of anxiolytic action, benzodiazepines are frequently used for the treatment of anxiety associated with panic disorder. However, there is disagreement among expert bodies regarding the long-term use of benzodiazepines for panic disorder. The views range from those holding benzodiazepines are not effective long-term and should be reserved for treatment-resistant cases to those holding they are as effective in the long term as selective serotonin reuptake inhibitors (SSRIs). American Psychiatric Association (APA) guidelines, published in January 2009, note that, in general, benzodiazepines are well tolerated, and their use for the initial treatment for panic disorder is strongly supported by numerous controlled trials. APA states that there is insufficient evidence to recommend any of the established panic disorder treatments over another. The choice of treatment between benzodiazepines, SSRIs, serotonin–norepinephrine reuptake inhibitors (SNRIs), tricyclic antidepressants, and psychotherapy should be based on the patient's history, preference, and other individual characteristics. Selective serotonin reuptake inhibitors are likely to be the best choice of pharmacotherapy for many patients with panic disorder, but benzodiazepines are also often used, and some studies suggest that these medications are still used with greater frequency than the SSRIs.
== External links == Clinical trial number NCT00001262 for "Copper Histidine Therapy for Menkes Diseases" at ClinicalTrials.gov Clinical trial number NCT00811785 for "Molecular Bases of Response to Copper Treatment in Menkes Disease, Related Phenotypes, and Unexplained Copper Deficiency" at ClinicalTrials.gov
"(...) Chile's position towards the Peru-Bolivian Confederation is untenable. It cannot be tolerated either by the people or by the Government because it is tantamount to their suicide. We cannot look without concern and the greatest alarm, the existence of two peoples, and that, in the long run, due to the community of origin, language, habits, religion, ideas, customs, will form, as is natural, a single nucleus. United these two States, even if it is only momentarily, will always be more than Chile in every order of issues and circumstances (...) The confederation must disappear forever and ever from the American scene due to its geographical extension; for its larger white population; for the joint riches of Peru and Bolivia, scarcely exploited now; for the dominance that the new organization would try to exercise in the Pacific by taking it away from us; by the greater number of enlightened white people, closely linked to the families of Spanish influence that are in Lima; for the greater intelligence of its public men, although of less character than the Chileans; For all these reasons, the Confederation would drown Chile before very soon (...) The naval forces must operate before the military, delivering decisive blows. We must dominate forever in the Pacific: this must be their maxim now, and hopefully it would be Chile's forever (...)”.
In 2014, Emerald Therapeutics spun out the Emerald Cloud Lab to fully replace the need for a traditional lab environment, enabling scientists from around the world to perform all necessary activities, from experimental design to data acquisition and analysis. Carnegie Mellon University's Mellon College of Science is building the world's first academic cloud laboratory on their campus. The 20,000 square foot laboratory will be completed in 2023 and offer access to CMU researchers and eventually to other schools and life-sciences startups in Pittsburgh.
Sources: en.wikipedia.org
Klaus H. Hofmann (February 21, 1911 – December 25, 1995) was an American biological chemist and medical researcher. The New York Times called Hofmann an "expert on synthesis of body compounds". His career was highlighted by synthesis of a prototype birth control pill, isolation and structural characterization of biotin (vitamin H), determination of the lysine specificity of the pancreatic protease trypsin (an attribute that made it the enzyme of first choice in protein sequence determinations), the first chemical synthesis of a fully biologically-active portion of the peptide hormone (adrenocorticotopic hormone - ACTH), and structure-function studies on ribonuclease (RNase).
== Gene regulation == MMP3 itself can enter in nuclei of cells and regulate target gene such as CTGF/CCN2 gene. Expression of MMP3 is primarily regulated at the level of transcription, where the promoter of the gene responds to various stimuli, including growth factors, cytokines, tumor promoters, and oncogene products. A polymorphism in the promoter of the MMP3 gene was first reported in 1995. The polymorphism is caused by a variation in the number of adenosines located at position -1171 relative to the transcription start site, resulting in one allele having five adenosines (5A) and the other allele having six adenosines (6A). In vitro promoter functional analyses showed that the 5A allele had greater promoter activities as compared with the 6A allele. It has been shown in different studies that individuals carrying the 5A allele have increased susceptibility to diseases attributed to increased MMP expression, such as acute myocardial infarction and abdominal aortic aneurysm. On the other hand, the 6A allele has been found to be associated with diseases characterized by insufficient MMP-3 expression due to a lower promoter activity of the 6A allele, such as progressive coronary atherosclerosis. The -1171 5A/6A variant has also been associated with congenital anomalies such as cleft lip and palate, where individuals with cleft lip/palate presented significantly more 6A/6A genotypes than controls.
Most animals and plants can synthesize vitamin C through a sequence of enzyme-driven steps, which convert monosaccharides to vitamin C. However, some mammals have lost the ability to synthesize vitamin C, notably simians and tarsiers. These make up one of two major primate suborders, haplorrhini, and this group includes humans. The strepsirrhini (non-tarsier prosimians) can make their vitamin C, and these include lemurs, lorises, pottos, and galagos. Ascorbic acid is also not synthesized by at least two species of caviidae, the capybara and the guinea pig. Certain birds and fish do not synthesize their vitamin C. All species that do not synthesize ascorbate require it in the diet. Deficiency causes scurvy in humans, and somewhat similar symptoms in other animals. Animals that can contract scurvy all lack the L-gulonolactone oxidase (GULO) enzyme, which is required in the last step of vitamin C synthesis. The genomes of these species contain GULO as pseudogenes, which serve as insight into the evolutionary past of the species.
==== Structural problems ==== Structurally, changes within the musculature in the intestine, such as increased elastin, can lead to increased frequency of herniation. Laxity of the phreno-esophageal and gastro-hepatic ligaments can lead to hiatal hernia, which in turn can lead to commonly reported symptoms such as acid reflux, abdominal pain, early satiety, and bloating. Internal organ prolapses and intestinal intussusceptions occur with greater frequency in patients with weakened connective tissues.
Sources: en.wikipedia.org
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.
No. Cardarine is not an anabolic steroid; it belongs to a different chemical class that targets PPARδ. Steroids act primarily through androgen receptors, while cardarine acts through a nuclear receptor involved in metabolism.
Some rodent studies reported increased endurance and changes in fat metabolism after cardarine exposure. Long-term studies in animals also raised concerns about cancer in certain tissues. Human trial data are limited, so these findings cannot be directly translated to people.
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.