This is a working overview of PPARδ agonist, written for readers who want more than a one-paragraph summary but less than a textbook.
Reviewed 2025-10-10. Anything still debated is marked as such rather than presented as settled.
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.
GW501516 acts on PPARδ, a nuclear receptor that helps regulate fatty acid oxidation and energy homeostasis. In animal studies, activation of this receptor was associated with increased endurance and changes in lipid metabolism. Human trials examined effects on blood lipids and other metabolic markers, but the compound did not advance to approval. Rodent studies later reported tumors in multiple tissues at doses used in those experiments. Whether those findings translate to human risk remains uncertain, and the clinical relevance of the animal data is still debated.
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.
| 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. |
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.
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.
GW501516 acts as a ligand for PPAR delta, a nuclear receptor that regulates transcription of genes involved in fatty acid oxidation and energy use. Activation of this receptor in skeletal muscle shifts metabolism toward fat burning in animal models. The compound does not burn fat directly; it changes gene expression over hours to days. Researchers study it to understand metabolic flexibility and exercise adaptation. Effects observed in rodents are not automatically expected in humans.
Preclinical research reported that GW501516 increased running endurance in mice and improved lipid profiles in some animal species. Early human trials explored effects on high-density lipoprotein cholesterol, triglycerides, and glucose handling, but the program was discontinued. Published human data are sparse and do not establish efficacy for any condition. Studies also examined PPAR delta in cancer biology, with conflicting findings across models. The relationship between receptor activation, tissue context, and disease risk remains an active area of investigation.
Anti-doping laboratories identify GW501516 and its metabolites using liquid chromatography-tandem mass spectrometry. Urine is the usual matrix, and detection can occur after the parent compound has cleared from blood. The exact detection window depends on dose, formulation, individual metabolism, and assay sensitivity. Because the compound is prohibited at all times, athletes are subject to testing in and out of competition. Analytical methods continue to improve as new metabolites and designer analogs are characterized.
GW501516 acts as an agonist at the peroxisome proliferator-activated receptor delta, a nuclear receptor that regulates gene expression. Activation shifts transcription toward genes involved in fatty acid uptake, oxidation, and energy expenditure. The compound does not bind the androgen receptor and therefore differs from anabolic steroids and SARMs. In rodent models, this metabolic shift has been linked to increased running endurance and reduced fat accumulation. The exact downstream pathways in humans remain incompletely characterized.
Early clinical research explored GW501516 for lipid disorders, obesity, and diabetes. Some short-term human studies reported changes in HDL cholesterol, LDL cholesterol, and triglycerides. The development program was discontinued after rodent studies showed dose-dependent tumor formation in multiple tissues, including liver, bladder, stomach, and skin. These findings raised concerns about long-term cancer risk in humans. Because human exposure data are limited, the clinical significance of the rodent tumors remains uncertain.
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.
=== Pharmacogenetics === Since doxepin is mainly metabolized by CYP2D6, CYP2C9, and CYP2C19, genetic variations within the genes coding for these enzymes can affect its metabolism, leading to changes in the concentrations of the drug in the body. Increased concentrations of doxepin may increase the risk for side effects, including anticholinergic and nervous system adverse effects, while decreased concentrations may reduce the drug's efficacy. Individuals can be categorized into different types of cytochrome P450 metabolizers depending on which genetic variations they carry. These metabolizer types include poor, intermediate, extensive, and ultrarapid metabolizers. Most people are extensive metabolizers, and have "normal" metabolism of doxepin. Poor and intermediate metabolizers have reduced metabolism of the drug as compared to extensive metabolizers; patients with these metabolizer types may have an increased probability of experiencing side effects. Ultrarapid metabolizers break down doxepin much faster than extensive metabolizers; patients with this metabolizer type may have a greater chance of experiencing pharmacological failure. A study assessed the metabolism of a single 75 mg oral dose of doxepin in healthy volunteers with genetic polymorphisms in CYP2D6, CYP2C9, and CYP2C19 enzymes. In CYP2D6 extensive, intermediate, and poor metabolizers, the mean clearance rates of (E)-doxepin were 406, 247, and 127 L/hour, respectively (~3-fold difference between extensive and poor).
Pregnancy: MMR vaccine and its components should not be given to pregnant women. Women of childbearing age should check with their doctor about getting vaccinated prior to getting pregnant. HIV-infected children, who may receive measles vaccines if their CD4+ lymphocyte count is greater than 15%. Weakened immune system due to HIV/AIDS or certain medical treatments Having a parent or sibling with a history of immune problems Condition that makes a patient bruise or bleed easily Recent transfusion of blood or blood products Tuberculosis Receiving other vaccines in the past 4 weeks Moderate or severe illness. However, mild illness (e.g., common cold) is usually not contraindicated.
[H3SO4]+[HSO4]− = 2.7 × 10−4 The corresponding equilibrium constant for water, Kw is 10−14, a factor of 1010 (10 billion) smaller. In spite of the viscosity of the acid, the effective molar conductivities of the H3SO+4 and HSO−4 ions are high due to an intramolecular proton-switch mechanism (analogous to the Grotthuss mechanism in water), making sulfuric acid a good conductor of electricity.
=== Accusations of falsification and manipulation === According to Minakowski, pro-Polish activists decided to boycott the preparations for electoral commissions before the plebiscite to protest the unequal treatment of the Polish and German side and pro-German terror, which allowed German officials to falsify lists with eligible voters by adding names of dead or ineligible people. During the plebiscite, Germans transported pro-German voters to numerous locations, which allowed them to cast multiple votes. In Allenstein (Olsztyn), cards with pro-Polish votes were simply taken away by a German official, who declared that they were "invalid" and presented voters with pro-German cards. Voters were observed by the German police in polling stations. Pro-Polish voting cards were often hidden or taken away, and Polish controllers were removed from polling stations. A large number of Poles feared reprisals and did not turn out for the plebiscite.
Sources: en.wikipedia.org
== Higher education == In 1928 at age 18 Hodgkin entered Somerville College, Oxford, where she studied chemistry. She graduated in 1932 with a first-class honours degree, the third woman at this institution to achieve this distinction.
== Research and partnerships == Mondobiotech investigated whether information already published about naturally occurring human substances could suggest new uses in rare diseases. A 2010 case study by researchers at the University of St. Gallen described its use of scientific literature, external researchers and laboratories, and licensing partners instead of maintaining a conventional in-house laboratory operation. Financial news reporting also described the company's approach as searching medical databases for drug candidates and licensing rights to other companies. In 2002, Mondobiotech and InterMune agreed to collaborate on interferon gamma-1b research for pulmonary diseases, including asthma; the arrangement also covered specified patent rights relating to idiopathic pulmonary fibrosis. In 2006, Biogen Idec licensed rights to develop aviptadil for pulmonary arterial hypertension. The agreement included a US$7.5 million upfront payment and up to US$30 million in possible development and commercialization milestones; the milestone amount was conditional, not a payment already received. Biogen stated in a later regulatory filing that it ended its participation in the aviptadil development program in December 2009. In February 2010, Mondobiotech entered a partnership with Lung Rx, a subsidiary of United Therapeutics, for further development of aviptadil. The company also agreed in 2009 to have Bachem develop and manufacture peptides for its research programs.
== Role of macrophages == The primary role of macrophages in peripheral regeneration is demylenation during Wallerian degeneration. Immunohistochemical analysis showed that in tellurium demylenated, crushed, and cut nerves, expression of lysozyme, which is a marker for myelin phagocytosis, and of ED1, which is a marker for macrophages, occurred in the same region. Lysozyme was also investigated with respect to the temporal progression of myelin phagocytosis by macrophages in nerve injury. Northern blotting showed that peak lysozyme mRNA expression occurred at an appropriate time with respect to temporal models of myelin phagocytosis. Macrophages do not phagocytose all cellular debris at the nerve injury site; they are selective and will salvage certain factors. Macrophages produce apolipoprotein E which is involved in rescuing cholesterol in damaged nerves. In the same investigation, temporal levels of apolipoprotein E mRNA expression in the three models for demylenation and nerve damage were consistent with respect to models for cholesterol salvage in nerve injury. Macrophages play a role in salvaging cholesterol during nerve injury. Macrophages also play a role in inducing the proliferation of Schwann cells that occurs during Wallerian degeneration. Supernatant has been collected from medium in which macrophages are active in myelin phagocytosis where lysosomal processing of the myelin occurs within the macrophage.
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.
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.