A practical reference on PPARδ agonist: what it is, how it behaves, what the literature reports, and where the honest uncertainties sit.
This page was last updated on 2026-06-09 and is reviewed periodically as new material appears.
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.
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.
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 |
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.
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.
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.
Dent, London, 1981) ISBN 978-0-460-04535-3 Is Life an Astronomical Phenomenon? (University College Cardiff Press, 1982) ISBN 9780906449493 Why Neo-Darwinism Does Not Work (with Fred Hoyle) (University College Cardiff Press, 1982) ISBN 9780906449509 Proofs that Life is Cosmic (with Fred Hoyle) (Institute of Fundamental Studies, Sri Lanka, Memoirs no.1, 1982) From Grains to Bacteria (with Fred Hoyle) (University College Cardiff Press, 1984) ISBN 9780906449646 Fundamental Studies and the Future of Science (ed.) (University College Cardiff Press, 1984) ISBN 9780906449578 Living Comets (with Fred Hoyle) (University College Cardiff Press, 1985) ISBN 9780906449790 Archaeopteryx, the Primordial Bird: A Case of Fossil Forgery (with Fred Hoyle) (Christopher Davies, Swansea, 1986) ISBN 9780715406656 The Theory of Cosmic Grains (with Fred Hoyle) (Kluwer, Dordrecht, 1991) ISBN 9780792311898 Life on Mars? The Case for a Cosmic Heritage (with Fred Hoyle) (Clinical Press, Bristol, 1997) ISBN 9781854570413 Astronomical Origins of Life: Steps towards Panspermia (with Fred Hoyle) (Kluwer, Dordrecht, 2000) ISBN 9780792360810 Cosmic Dragons: Life and Death on Our Planet (Souvenir Press, London, 2001) ISBN 9780285636064 Fred Hoyle's Universe (ed. with G. Burbidge and J. Narlikar) (Kluwer, Dordrecht, 2003) ISBN 9781402014154 A Journey with Fred Hoyle (World Scientific, Singapore, 2005) ISBN 9789812565792 Comets and the Origin of Life (with J. Wickramasinghe and W.
A group or series of case reports involving patients who were given similar treatment. Reports of case series usually contain detailed information about the individual patients. This includes demographic information (for example, age, gender, ethnic origin) and information on diagnosis, treatment, response to treatment, and follow-up after treatment. (NCI) Case-control study
== History == Factor VIII was first discovered in 1937, but it was not until 1979 that its purification by Edward Tuddenham, Frances Rotblat and coworkers led to the molecular identification of the protein.
Ion exchange can also be used to remove hardness from water by exchanging calcium and magnesium ions for sodium ions in an ion-exchange column. Liquid-phase (aqueous) ion-exchange desalination has been demonstrated. In this technique anions and cations in salt water are exchanged for carbonate anions and calcium cations respectively using electrophoresis. Calcium and carbonate ions then react to form calcium carbonate, which then precipitates, leaving behind fresh water. The desalination occurs at ambient temperature and pressure and requires no membranes or solid ion exchangers. The theoretical energy efficiency of this method is on par with electrodialysis and reverse osmosis.
Sources: en.wikipedia.org
To qualify for protection under the FCA, the whistleblower must demonstrate that they were engaged in FCA-protected activity and that the employer knew their activity was protected under the FCA, which presents a challenge for whistleblowers who merely report regulatory violations. To be protected under the FCA, they must reasonably believe the regulatory noncompliance has or will amount to fraud against the government, and they must put the employer on notice that their protected activity relates to the filing of false or fraudulent claims. Laboratory workers who merely report CLIA violations without tying the issues to Medicare or Medicaid reimbursement are unlikely to receive FCA whistleblower protection. From 2004-2005, approximately 460 patients Maryland General Hospital were tested for Hepatitis C and HIV with invalid controls. Follow-up retesting was not possible as many patients were unreachable due to being homeless. The incident prompted CAP to add whistleblower protections. In September 2015, a Theranos employee emailed a complaint to the Centers for Medicare and Medicaid Services (CMS) outlining regulatory noncompliance, which led to the company's exposure as a fraud and subsequent downfall.
== Automated solid phase polypeptide synthesis == Large scale custom peptide synthesis can be carried out either in a liquid solution or in solid phase. In general, peptides shorter than 8 amino acids are prepared more economically by solution chemistry. Peptides larger than 8 residues are generally assembled by solid phase chemistry. Solid phase peptide synthesis (SPPS) can be carried out either manually or in a fully automated fashion. Manual synthesis for short peptides is advantageous as it allows for more flexibility when scaling up and it permits troubleshooting of unexpected problems with more ease. For example, an operator can wash away piperidine during Fmoc deprotection, in the event of a power failure or instrument failure. Furthermore, thermodynamic mixing can be better controlled with a manual approach. On the other hand, large scale fully automated peptide synthesis instruments have the obvious advantage of unattended operation and extensive documentation of the synthesis run. Therefore, automated peptide synthesis is usually selected as the best choice for the synthesis of longer peptides in the mid-scale range.
SR-17018, also known informally as SR-17 or just SR and as 5,6-dichloro-desmethylchlorphine, is an atypical opioid receptor modulator with unusual actions and effects. It acts as a biased partial agonist of the μ-opioid receptor (MOR), showing strong selectivity for activation of G protein signaling over β-arrestin2 recruitment at this receptor. In addition, the drug appears to also act as a MOR positive allosteric modulator, with this possibly being its primary action. Unlike conventional opioids such as morphine and fentanyl, SR-17018 produces robust analgesic effects in rodents with very little respiratory depression and with much less analgesic tolerance. Moreover, substitution of conventional opioids like morphine with SR-17018 can reverse analgesic tolerance and suppress withdrawal symptoms in rodents. However, conflicting findings exist in terms of analgesic tolerance and respiratory depression. The drug has not been formally studied in humans. SR-17018 was first described in the scientific literature by Laura Bohn and colleagues in 2017. It was encountered online as a novel designer drug by 2023. Subsequently, discussion of SR-17018 on the social media website Reddit dramatically increased in 2024. Although technically a designer opioid, SR-17018 is said to have very different effects from other opioids, for instance producing minimal euphoria. Rather than being used recreationally itself, SR-17018 is typically employed by users to prevent opioid withdrawal symptoms and facilitate opioid discontinuation in the context of opioid dependence.
Sources: en.wikipedia.org
=== 1968–1989: Growth and challenges === Rapid growth began in 1968 and Marriott made optimistic projections. In October 1968, there were reportedly 38 units open and 65 under construction, and by December, 56 opened with 39 under construction. Marriott projected 700 or more Roy Rogers restaurants in four years. By June 1969, 105 units were open with a new projection of 870 in four years. A February 1970 newspaper article reported that over 160 units were in operation. However, growth halted in 1970, when Marriott suspended Roy Rogers franchising, due to financial losses from closing failing locations. The following year, the Texas–based regional franchise, Ram-Hart Systems, filed for Chapter 11 protection, asking to terminate unprofitable leases, which made the entire chain unprofitable. After franchising resumed, only 172 restaurants were open by September 1972, a quarter of the 700 stores projected four years earlier.
Trump names himself as the headliner for the "Great American State Fair" semiquincentennial event, organized by Freedom 250, in Washington D.C., after several artists pull out over concerns that the event became politicized by Trump. Martina McBride, Young MC, Bret Michaels, and the Commodores were among the artists who pulled out. A revised lineup includes artists such as Flo Rida, Milli Vanilli, and Vanilla Ice. May 31 – The National Basketball Association announces that the logo for the Larry O'Brien Championship Trophy will be displayed on the basketball courts of Frost Bank Center in San Antonio, Texas, and Madison Square Garden in New York City for the upcoming NBA Finals between the San Antonio Spurs and New York Knicks, making it the first time the logo decal will be placed on the NBA court during the NBA Finals since 2009.
=== Radiation shielding === 238U is also used as a radiation shield – its alpha radiation is easily stopped by the non-radioactive casing of the shielding and the uranium's high atomic weight and high number of electrons are highly effective in absorbing gamma rays and X-rays. It is not as effective as ordinary water for stopping fast neutrons. Both metallic depleted uranium and depleted uranium dioxide are used for radiation shielding. Uranium is about five times better as a gamma ray shield than lead, so a shield with the same effectiveness can be packed into a thinner layer. DUCRETE, a concrete made with uranium dioxide aggregate instead of gravel, is being investigated as a material for dry cask storage systems to store radioactive waste.
=== Pharmacodynamics === In vitro, cannabidiol has low affinity for, and acts as a negative allosteric modulator of the CB1 cannabinoid receptor Cannabidiol may be an antagonist of GPR55, a G protein-coupled receptor and putative non-homologous CB3 cannabinoid receptor shown by in vitro studies to be widely distributed in the brain. Cannabidiol may interact with various neurotransmitters, such as serotonin, dopamine, and GABA. As of 2024, the cellular effects and mechanisms of cannabidiol in vivo are unknown, as research to date has been inconclusive and based on laboratory studies. The anticonvulsant effects provided by cannabidiol (Epidiolex) in people with certain forms of epilepsy do not appear to involve cannabinoid receptors. A possible mechanism for the effects of cannabidiol on seizures is by affecting the neuronal movement of calcium in brain structures involved in the excessive electrical activity of seizures.
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.