metabolite raises a handful of sensible questions. This page answers them in order, starting with the fundamentals and moving to applications.
This page was last updated on 2026-08-01 and is reviewed periodically as new material appears.
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 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 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.
| Property | Value | Notes |
|---|---|---|
| Chemical class | PPARδ agonist | Not an anabolic steroid. |
| Common synonyms | GW501516, GW-1516 | Cardarine is an informal name. |
| Appearance | White to off-white powder | Typical for research-grade solid. |
| Solubility class | Poorly soluble in water; soluble in some organic solvents | Such as DMSO or ethanol in laboratory settings. |
| Typical storage temperature | Cool, dry, protected from light | Specific conditions vary by supplier and form. |
Cardarine is prohibited in competitive sport under the World Anti-Doping Agency code, where it is classified as a metabolic modulator. It is not approved as a prescription medicine in the United States, European Union, or other major markets. Regulatory action has focused on its presence in sports and in products marketed as research chemicals. Because it has no accepted medical indication, supply is often unregulated. This status creates legal and safety uncertainties for anyone who encounters the substance.
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.
Anti-doping laboratories identify GW501516 and related metabolites using liquid chromatography coupled with tandem mass spectrometry. Urine is the most common matrix, though blood and dried blood spots may also be analyzed. The method targets the parent compound and phase I and phase II metabolites, which extend the detection window. Because the substance is prohibited at all times, athletes can be tested outside competition. Detection limits and windows depend on the assay, sample type, and individual metabolism.
Cardarine is frequently described as a fat-burning or endurance-enhancing supplement, but these claims exceed the available evidence. The compound is not a hormone, steroid, or selective androgen receptor modulator. Research articles discuss it as a tool compound for studying PPARδ biology, while anti-doping literature focuses on its abuse and detection. Quality of unapproved products is uncertain, and independent analyses have found impurities or incorrect labeling. Open questions include whether human cancer risk resembles that seen in rodents and how often non-athletes use the substance.
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.
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.
=== Mechanical ventilation === Isolated mechanical forces may not adequately explain ventilator induced lung injury (VILI). The damage is affected by the interaction of these forces and the pre-existing state of the lung tissues, and dynamic changes in alveolar structure may be involved. Factors such as plateau pressure and positive end-expiratory pressure (PEEP) alone do not adequately predict injury. Cyclic deformation of lung tissue may play a large part in the cause of VILI, and contributory factors probably include tidal volume, positive end-expiratory pressure and respiratory rate. There is no protocol guaranteed to avoid all risk in all applications.
==== Enamel hypoplasia ==== Enamel hypoplasia refers to transverse furrows or pits that form in the enamel surface of teeth when the normal process of tooth growth stops, leaving a deficit. Enamel hypoplasias generally form due to disease and/or poor nutrition. Linear furrows are commonly referred to as linear enamel hypoplasias (LEHs); LEHs can range in size from microscopic to visible to the naked eye. By examining the spacing of perikymata grooves (horizontal growth lines), the duration of the stressor can be estimated, although Mays argued that the width of the hypoplasia bears only an indirect relationship to the duration of the stressor. Studies of dental enamel hypoplasia are used to study child health. Unlike bone, teeth are not remodeled, so intact enamel can provide a more reliable indicator of past health events. Dental hypoplasias provide an indicator of health status during the time in childhood when the enamel of the tooth crown is forming. The presence, frequency, and severity of enamel hypoplasia (EH) offer valuable information about general health conditions and the occurrence of disease or malnutrition. Elevated rates of EH are often interpreted as evidence of widespread physiological stress, such as famine, infectious disease outbreaks, or prolonged nutritional deficiencies. By comparing the prevalence of dental stress indicators across various groups such as different social classes, geographic regions, or time periods bioarcheologists can also infer disparities in living conditions, access to resources, and overall health.
was renamed Merck Sharp & Dohme, and Schering-Plough renamed as "Merck & Co., Inc." The maneuver was an attempt to avoid a "change-of-control" in order to preserve Schering-Plough's rights to market Remicade. A settlement with Johnson & Johnson was reached in 2011, in which Merck agreed to pay $500 million. Merck Sharp & Dohme remains a subsidiary of the Merck & Co. parent. Richard Clark retired as CEO and company president in October 2011 and Kenneth Frazier became CEO. In October 2013, Merck announced it would cut 8,500 jobs in an attempt to cut $2.5 billion from its costs by 2015. Combined with 7,500 job cuts announced in 2011 and 2012, the layoffs amounted to 20% of its workforce. By 2014, research performed at Merck has led to U.S. FDA approval of 63 new molecular entities. In August 2014, Merck acquired Idenix Pharmaceuticals for $3.85 billion. In September 2014, the US Food and Drug Administration (FDA) approved Pembrolizumab (MK-3475) as a breakthrough therapy for melanoma treatment. In clinical trials, pembrolizumab provided partial tumor regression in about one quarter of patients, many of whom have not seen further progression of their disease in over 6 months of follow-up. In December 2014, the company acquired Swiss biotechnology company OncoEthix for up to $375 million. Between 2010 and 2015, the company cut around 36,450 jobs. During that time, the company sold its consumer health business to Bayer and narrowed the company's focus to immunology, vaccines, diabetes, emerging markets and medicines used in hospitals, like certain antibiotics.
Sources: en.wikipedia.org
DDP-116 – the first of the Series 16 DDP-124 – part of a trio of 24-bit systems: DDP-24, 124, 224. Honeywell bought the company after the 24 trio, and built the balance of the Series 16. The Honeywell 516 was used in the NPL network for the first implementation of packet switching in early 1969. The 516 and later the 316 were also used as Interface Message Processors (IMP) for the ARPANET. In addition, it was later configured as a Terminal IMP (TIP), which added support for up to 63 teletype machines through a multi-line controller. The H-316 was used by Charles H. Moore to develop the first complete, stand-alone implementation of Forth at NRAO in 1971. The original Prime computers were designed to be compatible with the Series-16 minicomputers. The Honeywell 316 also had industrial applications. A 316 was used at Bradwell nuclear power station in Essex as the primary reactor temperature-monitoring computer until summer 2000, when the internal 160k disk failed. Two PDP-11/70s, which had previously been secondary monitors, were moved to primary.
== Early life and education == Balalaie was born on 26 September 1965 in Rasht, Gilan Province, Iran. He completed his undergraduate studies in Chemistry at the University of Tehran (1984–1989), followed by a Master of Science degree in Organic Chemistry from Shahid Beheshti University (1989–1991). He earned his Ph.D. in Organic Chemistry from Sharif University of Technology (1992–1996), where he worked on "Photooxygenation of organic compounds by singlet oxygen" under the supervision of Professor Mohammad Mahmoudi Hashemi. During his doctoral studies, he spent six months as a visiting researcher in Germany working with Professor Junes Ipaktschi.
=== NSAIDs === Nonsteroidal anti-inflammatory drugs (NSAIDs) and alcohol both increase gastrointestinal events such as gastrointestinal bleeding and peptic ulcers. Taking the two together further increases the risk additively. The risk of stomach bleeding is still increased when aspirin is taken with alcohol or warfarin.
Sources: en.wikipedia.org
An immunogen is any substance that generates B-cell (humoral/antibody) and/or T-cell (cellular) adaptive immune responses upon exposure to a host organism. Immunogens that generate antibodies are called antigens ("antibody-generating"). Immunogens that generate antibodies are directly bound by host antibodies and lead to the selective expansion of antigen-specific B-cells. Immunogens that generate T-cells are indirectly bound by host T-cells after processing and presentation by host antigen-presenting cells. An immunogen can be defined as a complete antigen which is composed of the macromolecular carrier and epitopes (determinants) that can induce immune response. An explicit example is a hapten. Haptens are low-molecular-weight compounds that may be bound by antibodies, but cannot elicit an immune response. Consequently, the haptens themselves are nonimmunogenic and they cannot evoke an immune response until they bind with a larger carrier immunogenic molecule. The hapten-carrier complex, unlike free hapten, can act as an immunogen and can induce an immune response. Until 1959, the terms immunogen and antigen were not distinguished.
Sacrificial bonds are non-covalent interactions such as hydrogen bonds, ionic interactions, and hydrophobic interactions, that can break and reform under mechanical stress. The reforming of these bonds takes time, especially when there are more of them, which leads to an increase in hysteresis. However, there is currently research focused on the development of highly entangled hydrogels, which instead rely on the long chain length of the polymers and their entanglement to limit the deformation of the hydrogel, thereby increasing the toughness without increasing hysteresis as there is no need for the reformation of the bonds.
=== Genetic variations === An epigenetic mechanism (hypermethylation of CpG islands in the NET gene promoter region) that results in reduced expression of the noradrenaline (norepinephrine) transporter and consequently a phenotype of impaired neuronal reuptake of norepinephrine has been implicated in both postural orthostatic tachycardia syndrome and panic disorder. rs5569 is a variant of SLC6A2.
== Effects == CJC-1295 may markedly increase plasma growth hormone (GH) and insulin-like growth factor 1 (IGF-1) levels in animals and humans. With a single injection, in human subjects, CJC-1295 DAC may increase plasma GH levels by 2- to 10-fold for 6 days or longer and plasma IGF-1 levels by 0.5- to 3-fold for 9 to 11 days. With the inclusion of the DAC additive, the drug has an estimated half-life of about 6 to 8 days in humans. With multiple doses of CJC-1295, IGF-1 levels were found to remain elevated in humans for up to 28 days. CJC-1295 has been shown to extend the half-life and bioavailability of growth-hormone-releasing hormone 1-29 and stimulate insulin-like growth factor 1 secretion. It increases the half-life of acting agents by bioconjugation. The extended half-life is achieved through the addition of a drug affinity complex (DAC) that binds to albumin, thus prolonging the peptide's presence in the bloodstream. It is primarily used for its potential to stimulate the release of growth hormone (GH) from the pituitary gland.
Sources: en.wikipedia.org
Cardarine is commonly known as GW501516 or GW-1516. These names refer to the same synthetic compound. It is not a brand-name approved medicine.
No, cardarine is not a steroid. It is classified as a PPARδ agonist. Its structure and receptor target differ from anabolic steroids.
No regulatory agency has approved cardarine as a medicine. It was investigated in early research but development was discontinued. It is not available as a prescription drug.
Cardarine is an investigational synthetic compound that acts as a PPARδ agonist. It is also known as GW501516 and has been studied mainly in preclinical research. It is not an approved medicine.