The short version of GW501516 fits in a sentence. The long version — which is the one that helps — is below.
This page was last updated on 2025-09-28 and is reviewed periodically as new material appears.
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.
Activation of PPARδ changes transcription of genes involved in fatty acid transport, mitochondrial function, and skeletal muscle fuel preference. In rodent studies, pharmacological PPARδ activation was associated with increased endurance and altered body composition. These findings generated interest in performance enhancement, but species differences and study designs limit direct extrapolation to humans. Small human trials were conducted in the 2000s and later discontinued. The extent to which cardarine produces similar metabolic or performance effects in people remains an open question.
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.
| Property | Value | Notes |
|---|---|---|
| Common synonyms | GW501516, GW-501516, GW 501516, endurobol | Names vary in research and anti-doping documents. |
| Chemical class | Synthetic PPARδ agonist | Small-molecule nuclear receptor ligand. |
| CAS Registry Number | 317318-70-0 | Identifier commonly associated with GW501516. |
| Appearance | White to off-white powder | Typical for purified research material. |
| Solubility | Low in water; soluble in DMSO and ethanol | Organic solvents are common for laboratory stock solutions. |
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 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.
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.
== International law == Trump's proposal for Gaza is against international law; the forcible transfer of populations is prohibited. Members of Trump's administration have walked back on elements of the plan on a few occasions, although in one subsequent statement, Trump held firm to his original plan. On 21 February 2025, after opposition from Arab states, Trump said he would "recommend" but not enforce his plan for the American takeover of Gaza and the re-settlement of the Palestinian population. Arab League leaders met in March to create a counter proposal to Trump's plan, which was rejected by the US and Israel due to concerns about the proposed governance of postwar Gaza and other issues. The White House released a statement that Trump stood by his vision of Gaza without Hamas and welcomed additional talks. In July, Netanyahu met with Trump and reiterated support for the plan of relocating Palestinians, saying it was "free choice" if Palestinians wanted to stay or leave. The US and Israel were working to identify cooperating countries for the plan.
Vasoactive intestinal polypeptide receptor 1 also known as VPAC1, is a protein, that in humans is encoded by the VIPR1 gene. VPAC1 is expressed in the brain (cerebral cortex, hippocampus, amygdala), lung, prostate, peripheral blood leukocytes, liver, small intestine, heart, spleen, placenta, kidney, thymus and testis.
Serine proteases (or serine endopeptidases) are enzymes that cleave peptide bonds in proteins. Serine serves as the nucleophilic amino acid at the enzyme's active site. They are found ubiquitously in both eukaryotes and prokaryotes. Serine proteases fall into two broad categories based on their structure: chymotrypsin-like (trypsin-like) or subtilisin-like.
== Signs and symptoms == MODY accounts for at least 1-5% of all diagnoses of diabetes mellitus, though 50-90% of cases are estimated to be misdiagnosed as type 1, or type 2 diabetes. Estimated prevalence rates indicate 1 per 10,000 in adults, and 1 per 23,000 in children. 50% of first-degree relatives will inherit the same mutation, giving them a greater than 95% lifetime risk of developing MODY themselves. For this reason, correct diagnosis of this condition is important. Typically patients present with a strong family history of diabetes (i.e.: presence of diabetes before the age of 25 in two consecutive generations). There are two general types of clinical presentation.
Sources: en.wikipedia.org
== Age and breed prevalence == PPID has been diagnosed in horses as young as 7 years old, although most horses are first diagnosed at ages 19 to 20. An estimated 21% of horses older than 15 years have PPID. All breeds may develop PPID, but pony breeds and Morgans seem to be more commonly affected.
=== Programmed cell death === Dysregulation of apoptosis (programmed cell death) is believed to play a role in the pathogenesis of a variety of autoimmune diseases, though its role in Sjögren's disease is controversial. Both the Fas and Fas ligand proteins are overexpressed in primary Sjögren's patients. Expression of BCL-1, which is known to downregulate apoptosis, was found significantly reduced in acinar and ductal epithelial cells of Sjögren's patients compared to healthy people. In situ studies did not show increased apoptosis among glandular epithelial cells but did show reduced apoptosis among infiltrating mononuclear cells. Reduced apoptosis was also implicated in the accumulation of autoreactive B-cells found in the glands. The relationship between autoantibodies expressed in Sjögren's disease and apoptosis remains an area of active research.
== Side effects == The most common adverse effects are blurred vision, tearing and other kinds of eye discomfort. Eye pain, eye oedema, headache, increased intraocular pressure and other side effects are seen in less than 1% of patients.
Each neurotransmitter has very specific degradation pathways at regulatory points, which may be targeted by the body's regulatory system or medication. Cocaine blocks a dopamine transporter responsible for the reuptake of dopamine. Without the transporter, dopamine diffuses much more slowly from the synaptic cleft and continues to activate the dopamine receptors on the target cell.
== Discovery == The protein was first isolated in 1987 by Thomas J. Martin's team at the University of Melbourne. Miao et al. showed that disruption of the PTHrP gene in mice caused a lethal phenotype and distinct bone abnormalities, suggesting that PTHrP has a physiological function.
Sources: en.wikipedia.org
The officer commanding the Army of India was the Commander-in-Chief, India who reported to the civilian Governor-General of India. The title was used before the creation of a unified British Indian Army; the first reported holder was then-Major Stringer Lawrence in 1748. Lawrence went to India with no larger command than a "small undisciplined garrison of two or three hundred men" facing a significant French presence. In 1903, Lord Kitchener became the Commander-in-Chief of the Indian Army. He instituted large-scale reforms, the greatest of which was the merger of the three armies of the Presidencies into a unified force. He formed higher level formations, eight army divisions, and brigaded Indian and British units. He left his command in 1909. Following Kitchener's reforms, the terminology used for the forces in India was altered. The Indian Army referred from that time to "the force recruited locally and permanently based in India, together with its expatriate British officers;" the British Army in India referred to the British Army units posted to India for a tour of duty, and which would then be posted to other parts of the Empire or back to the UK. The Army of India was used to describe the combined forces of both the Indian Army and the British Army in India. By the early 1900s the three previous separate army staffs had been amalgamated into Headquarters, India (see 1906 Birthday Honours) which by 1922 had become GHQ India (see 1922 New Year Honours).
=== Antiplatelet treatment of STEMI === In patients undergoing primary percutaneous coronary intervention (PCI) for an ST-segment elevation myocardial infarction (STEMI), US, European, and Canadian guidelines recommend that a P2Y12 inhibitor should be administered as soon as possible, although it is unclear whether administration of these medications before the patient arrives at the hospital confers additional benefits compared with in-hospital administration. On the other hand, P2Y12 inhibitors do not change the risk of death when given as a pretreatment prior to routine PCI in people who have had a non-ST-elevation myocardial infarction (NSTEMI). Though, a P2Y12 inhibitor in addition to aspirin should be administered for up to 12 months to most patients with non-ST-elevation acute coronary syndrome. They do however increase the risk of bleeding and decrease the risk of further cardiovascular problems. Thus their routine use in this context is of questionable value. A network meta-analysis of 37 studies involving 88,402 STEMI patients and 5,077 major adverse cardiac events (MACE) patients found that use of prasugrel was associated with lower mortality and MACE than other drugs in this class (clopidogrel and ticagrelor).
=== Dental appliances === Mandibular advancement splints (mandibular advancement devices) are designed to hold the lower jaw slightly down and forward relative to the natural, relaxed position. This position keeps the tongue farther away from the back of the airway and may be enough to relieve apnea or improve breathing. This device is a mouthguard similar to those used in sports to protect the teeth. Mandibular advancement splints are used for snoring and for mild to moderate obstructive sleep apnea. They are most suitable for people with AHI < 25, BMI < 30, and good dentition. Where appropriate, they are considered a good therapy choice as they are non-invasive, easily reversible, and quiet. They are generally well-tolerated because they are less uncomfortable. However, they may not be as effective as CPAP. Oral devices have been shown to treat OSA successfully. These include the polysomnographic indexes of OSA, subjective and objective measures of sleepiness, blood pressure, aspects of neuropsychological functioning, and quality of life. The focus of improvement in appliance design is in reducing bulk, permitting free jaw movement (i.e., yawning, speaking, and drinking), and allowing the user to breathe through their mouth (early "welded gum shield"-type devices prevented oral breathing). Tongue repositioning (retaining) devices are made of soft acrylic and cover the upper and lower teeth, creating a seal with the lips. They have a "bulb" or "bubble" which sticks out of the front of the mouth.
== Principle == Delayed neutrons are associated with the beta decay of the fission products. After prompt fission neutron emission the residual fragments are still neutron rich and undergo a beta decay chain. The more neutron rich the fragment, the more energetic and faster the beta decay. In some cases the available energy in the beta decay is high enough to leave the residual nucleus in such a highly excited state that neutron emission instead of gamma emission occurs. Using U-235 as an example, this nucleus absorbs thermal neutrons, and the immediate mass products of a fission event are two large fission fragments, which are remnants of the formed U-236 nucleus. These fragments emit two to three free neutrons (2.43 on average), called "prompt" neutrons. A subsequent fission fragment occasionally undergoes a stage of radioactive decay (which is a beta minus decay) that yields a new nucleus (the emitter nucleus) in an excited state that emits an additional neutron, called a "delayed" neutron, to get to ground state. These neutron-emitting fission fragments are called delayed neutron precursor atoms. The longest-lived groups can be traced to specific decay chains. In about 70% of 87Br beta decays (half-life 55 s), the 87Kr daughter is left in a nuclear state above the 5.4 MeV needed to eject its last neutron; it promptly releases a neutron, ending as stable 86Kr. The neutron emission rate is set by the rate of formation of 87Kr, so the group carries the 55 s half-life of the precursor.
Hepcidin is a protein that in humans is encoded by the HAMP gene. Hepcidin is a key regulator of the entry of iron into the circulation in mammals. During conditions in which the hepcidin level is abnormally high, such as inflammation, serum iron falls due to iron trapping within macrophages and liver cells and decreased gut iron absorption. This typically leads to anemia due to an inadequate amount of blood serum iron being available for developing red blood cells. When the hepcidin level is abnormally low, such as in hemochromatosis, iron overload occurs due to increased ferroportin mediated iron efflux from storage and increased gut iron absorption.
Sources: en.wikipedia.org
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.
No. Cardarine is not a steroid hormone; it targets the nuclear receptor PPARδ. Its classification in anti-doping rules differs from anabolic steroids, though it remains prohibited in sport.
Early rodent studies reported tumor formation at multiple sites, which raised safety concerns. Sponsors stopped clinical development, and no approved human product exists.
Cardarine is a common name for GW501516, a synthetic PPARδ agonist. It is not a steroid or a selective androgen receptor modulator. It was developed and studied as a research compound for metabolic pathways.