A practical reference on GW501516: what it is, how it behaves, what the literature reports, and where the honest uncertainties sit.
Reviewed 2026-08-01. Anything still debated is marked as such rather than presented as settled.
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.
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.
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.
| Property | Value | Notes |
|---|---|---|
| Common name | Cardarine | Common internet and media name. |
| Research code | GW501516 | Also written GW-1516. |
| Drug class | PPARδ agonist | Not a selective androgen receptor modulator. |
| Development status | Discontinued | Clinical development halted after rodent cancer findings. |
| Regulatory status | Prohibited in sport | Listed by WADA; not approved as medicine. |
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.
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.
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.
The pharmacological interest in cardarine centers on PPARδ activation and its downstream effects on lipid handling and mitochondrial function. In animal studies, PPARδ agonists have been associated with changes in exercise endurance and fatty acid utilization, though results vary by model and protocol. Human data remain sparse, and the absence of large controlled trials limits conclusions about efficacy. Researchers often describe the compound as a tool for probing PPARδ biology rather than a proven therapeutic agent.
Safety discussions about cardarine frequently cite rodent carcinogenicity findings reported in the 2000s. In those studies, treated animals developed tumors at multiple sites, leading sponsors to discontinue clinical development. The relevance of these findings to humans has not been resolved, but they are a major reason the compound is not approved. Current literature emphasizes uncertainty about long-term effects and the risks of unregulated use. Regulators and health agencies have not established a safe human exposure level.
Cardarine is a synthetic compound also known as GW501516, GW-501516, and sometimes endurobol. It was developed as a selective agonist of peroxisome proliferator-activated receptor delta, a nuclear receptor involved in fatty acid oxidation and energy metabolism. The compound was studied in preclinical models for metabolic and cardiovascular conditions, but it did not become a marketed human medicine. In regulatory and anti-doping contexts, it is treated as a prohibited substance rather than a licensed medicine.
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.
Cardarine is a common name for GW501516, a synthetic compound studied for its effects on lipid and glucose metabolism. It functions as an agonist at peroxisome proliferator-activated receptor delta, or PPARδ, a nuclear receptor that influences gene expression. The molecule is not a steroid, nor is it a selective androgen receptor modulator. It is also known in research and sports literature as GW-501516 and endurobol. Early laboratory work examined its metabolic activity in cell cultures and animal models.
In most eukaryotes, GSA is synthesised from the amino acid glutamate by the bifunctional enzyme 1-pyrroline-5-carboxylate synthase (P5CS). The human P5CS is encoded by the ALDH18A1 gene. The enzyme pyrroline-5-carboxylate reductase converts L-P5C into proline.
=== Prize money === In April 2026, FIFA confirmed the prizes for all participating nations. The total distribution of prize money for the expanded tournament was $871 million, nearly double the amount from the 2022 World Cup. Of this total, $671 million was allocated for performance-based prizes, with the remaining $200 million paid out among teams regardless of performance. Each qualified team received preparation money in the amount of $2.5 million; a team that was eliminated in the group stage would receive a minimum total amount $12.5 million at the tournament, with the winner receiving a total of $52.5 million.
== Later life and death == Schoenheimer had married Salome Glucksohn, a noted zoologist and geneticist, in 1937. They emigrated to the United States together, and they had no children. They later divorced. Schoenheimer was invited to conduct lectures detailing his scientific work and findings. In 1937, he conducted his Harvey Lecture and in 1941 his Dunham Lecture was conducted by his colleagues in his behalf. At the height of his career he committed suicide by ingesting potassium cyanide at his home in Yonkers, having struggled with depression for multiple years.
== See also == List of antidepressants Serotonin modulator and stimulator (SMS) Noradrenergic and specific serotonergic antidepressant (NaSSA) Norepinephrine-dopamine disinhibitor (NDDI) Selective serotonin reuptake inhibitor (SSRI) DSP-6745
Sources: en.wikipedia.org
== Dissolution and successor organisations == In December 1998, Democratic Left in England and Wales was formally dissolved and reconstituted as the New Times Network, which adopted a more inclusive membership policy that welcomed members of the Labour Party and other political organisations. The new body published a monthly magazine, New Times, and worked with the Fabian Society to organise the 'Getting Real' conference in June 1999. The New Times Network was subsequently renamed the New Politics Network in December 1999. In Scotland, the organisation evolved separately into Democratic Left Scotland, which was established in May 1998.
=== Administrative history === Wilmslow was an ancient parish in the Macclesfield Hundred of Cheshire. The parish was subdivided into four townships, called Bollin Fee, Chorley, Fulshaw, and Pownall Fee. The town centre and the parish church of St Bartholomew's lay in the Bollin Fee township. From the 17th century onwards, parishes were gradually given various civil functions under the poor laws, in addition to their original ecclesiastical functions. In some cases, including Wilmslow, the civil functions were exercised by each township separately rather than the parish as a whole. In 1866, the legal definition of 'parish' was changed to be the areas used for administering the poor laws, and so the townships each became separate civil parishes, which therefore diverged from the ecclesiastical parish. In 1862, a Chorley local government district was created, governed by an elected local board. The district covered the eastern part of the Chorley township, plus small adjoining parts of the Bollin Fee and Fulshaw townships. The Chorley district was renamed Alderley Edge in 1894. In 1878, a separate Wilmslow local government district was created covering the remainder of Bollin Fee and Fulshaw, plus Pownall Fee apart from the area north of the River Bollin and River Dean; the excluded area north of the rivers contained the hamlet of Styal. Local government districts were reconstituted as urban districts under the Local Government Act 1894.
It is thought that the symptom of obstruction is caused by the infolding of the circumference of the rectal wall, which "drops down" during defecation and takes up the available space in the anal canal and/or rectum, thereby occluding the lumen. Therefore, the patient may feel like they have feces in their rectum or anal canal, but straining does not relieve the sensation. There is no correlation between the severity of constipation and the degree of internal rectal prolapse as shown on defecography. Furthermore, since a significant amount of people without symptoms have some degree of IRP detectable on defecography, it is debated whether IRP is a cause or effect of obstructed defecation. The fecal incontinence symptom is associated with IRP that has been present for a long time. It has been demonstrated that the severity of internal rectal prolapse, as determined by defecography, has positive correlation with the severity of the fecal incontinence symptom. Fecal incontinence is thought to develop because of occult (undetected) defects of the external anal sphincter, traction induced pudendal neuropathy (nerve damage) caused by stretching of the nerve secondary to chronic straining. The pudendal nerve may undergo irreversible damage if it is stretched by more than 12%. Stretch induced pudendal neuropathy most often results from childbirth (prolonged second stage of labor) and chronic straining (e.g. constipation). There may be widening of the anal canal and reduced sensation. As a result, people with severe IRP may not feel any urge to defecate.
As of 2026, there is no cure or effective treatment for CJD. Some of the symptoms, like twitching, can be managed, but otherwise treatment is palliative care. Psychiatric symptoms like anxiety and depression can be treated with sedatives and antidepressants. Myoclonic jerks can be handled with clonazepam or sodium valproate. Opiates can help with pain. Seizures are very uncommon but can nevertheless be treated with antiepileptic drugs. In 2022, results of an early-stage trial of PRN100, a monoclonal antibody against PrP, were reported: the drug appeared safe and reached the brain, but treated patients did not show clearly improved survival compared to historical controls. While not curative, this trial demonstrated the feasibility of immunotherapy for prion disease. In 2025, preclinical research demonstrated that oral, low-dose treatment with the antiretroviral medication efavirenz extended survival and slowed disease progression in a humanized mouse model of sporadic CJD (sCJD). The drug acts as an allosteric activator of the brain-specific cholesterol-metabolizing enzyme CYP46A1. This mechanism promotes brain cholesterol turnover, reduces the neurotoxic accumulation of pathological prion proteins (PrPSc), and alleviates metabolic lipid alterations in the brain.
2023 Analytical Scientist the Power List - Leaders and Advocates 2020 Society for Glycobiology Molecular and Cellular Proteomics (MCP) / American Society for Biochemistry and Molecular Biology (ASBMB) Lectureship Award 2019 inaugural winner of the US Human Proteome Organization Lifetime Achievement in Proteomics Award 2019 Analytical Scientist the Power List 2017 American Society for Mass Spectrometry John B. Fenn Award for a Distinguished Contribution in Mass Spectrometry 2016 American Association for the Advancement of Science Fellow 2015 Human Proteome Organization Distinguished Service Award 2015 German Mass Spectrometry Society (Deutsche Gesellschaft für Massenspektrometrie, DGMS) Wolfgang Paul Lecture 2013 Boston University The William Fairfield Warren Distinguished Professorship 2011 American Chemical Society Fellow 2010 American Chemical Society Frank H. Field and Joe L. Franklin Award for Outstanding Achievement in Mass Spectrometry 2009 International Mass Spectrometry Foundation Thomson Medal 2008 Human Proteome Organization Discovery in Proteomic Sciences Award
Sources: en.wikipedia.org
== Mathematical analysis of the FcRn mechanism == Antibody binding, salvage and recycling by FcRn is an important part of modelling antibody pharmacokinetics. In fact, besides target-mediated drug dispostiion (TMDD), it is one of the most important factors mediating (non-specific) antibody elimination. Such a mechanism lies at the core of most physiology-based pharmacokinetic (PBPK) models of antibodies, see e.g. Garg and Balthasar, 2007; Shah and Betts, 2012; Niederal et al., 2018; Glassman and Balthasar, 2019; de Witte et al., 2023; De Sutter et al. (2024). Some of first steps towards understanding and gaining mathematical insight into the FcRn mechanism was taken by Patsatzis et al. (2022), using the computational singular perturbation (CSP) approach to analyse a minimal FcRn model. This preliminary work was extended and deepend by Katai et al. (2024) using the method of matched asymptotic expansions. This latter work constituted an asymptotic analysis of the mechanism in the high binding affinity limit, i.e. where binding was assumed to be an order of magnitude faster than all other processes. This resulted in a three-tiered scaling framework for non-saturating doses, with binding on the fastest time scale (typically over seconds or minutes), all other cellular process on an intermediate time scale (hours) and a long 'effective' elimination time scale (days, weeks).
== Drug development risks == Risks that could affect the further development of tecemotide published in the annual reports of Oncothyreon (grantor of the license) and Merck KGaA (license holder; responsible for clinical development, marketing and manufacturing) are listed in the following sections.
Helena was an art installation by Marco Evaristti originally at the Trapholt museum in 2000. The art consisted of a room with 10 blenders, each of which contained a green swordtail (often misreported as goldfish). The fish were vulnerable to any visitor to the exhibit who chose to turn on a blender and kill them. During the exhibition two fish were killed in this way. Persons present at the initial exhibition of the installation noted that "numerous media representatives who were present... virtually encouraged the visitors to press the button in order to initiate a scandal". Legal complaints resulted in the blenders being unplugged, though the installation remained on display.
In 1927, fossils of an ancient wild species of cow, Hanaizumi Moriushi (Leptobison hanaizumiensis), dating from the Paleolithic period about 20,000 years ago, were discovered at the Hanaizumi Site in Ichinoseki City, Iwate Prefecture. The Hanaizumi Moriushi is a species similar to the bison and is said to be close to the steppe bison (Bison priscus) lineage. Fossil bones of Aurochs (Bos primigenius) have also been found in Ichinoseki City. Since Hokkaido and Honshu were land-locked with the Eurasian continent during the Ice Age, these animals came from the continent via Hokkaido. In addition, projectile points made from polished wild cattle bones have been found at the same site, although in small quantities, suggesting that humans existed during this period and that Hanaizumi Moriushi and aurochs were hunted. At the Ohama Site in Goto City, Nagasaki Prefecture, cattle teeth dating to the middle Yayoi period were excavated. Among them were also processed cattle molars. However, this excavation was controversial because it contradicted the statement in Chen Shou's Records of the Three Kingdoms (Wajinden) that there were no cattle or horses in Japan. Later, radiocarbon dating of the excavated cattle molars yielded a date of around 40 AD (±90 years).
== Human proteins == The table below shows the 11 known human OATPs. Note: Human OATPs are designated with capital letters, animal Oatps are designated with lower case letters. The 'SLCO' stands for their gene name; 'solute carrier organic anion.' Previous nomenclature using letters and numbers (e.g. OATP-A, OATP-8 is no longer used. The most well characterised human OATPs are OATP1A2, OATP1B1, OATP1B3 and OATP2B1. Very little is known about the function and characteristics of OATP5A1 and OATP6A1.
Sources: en.wikipedia.org
No. Cardarine is a PPARδ agonist, while selective androgen receptor modulators act on androgen receptors. The two classes differ in receptor target and downstream effects.
Preclinical rodent studies reported cancers, including liver and bladder tumors, at tested doses. The human relevance of those findings is uncertain, but development was discontinued. No approved human product resulted.
No. It remains an investigational compound without approved therapeutic labeling. Sports regulators prohibit its use, and health agencies have warned against consuming it.
It binds and activates PPARδ, a nuclear receptor that influences gene expression related to fatty acid metabolism and energy balance. This mechanism has been studied mainly in animals and cell models, not established as a safe human therapy.