This is a working overview of Research chemical, written for readers who want more than a one-paragraph summary but less than a textbook.
This page was last updated on 2025-11-28 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.
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.
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.
| 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. |
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.
Cardarine has no approved therapeutic indication and is not marketed as a medicine. The World Anti-Doping Agency lists GW501516 as a prohibited substance at all times, covering both in-competition and out-of-competition periods. National laws vary: some countries treat it as an unapproved drug subject to import controls, while others have specific restrictions on sale for human consumption. It is often sold as a research chemical, a label that does not imply safety or legality. Enforcement actions have targeted online vendors and shipments.
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.
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.
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.
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.
==== Other actions ==== Tianeptine modestly enhances the mesolimbic release of dopamine and potentiates CNS D2 and D3 receptors. Tianeptine has no affinity for the dopamine transporter or the dopamine receptors. CREB-TF (CREB, cAMP response element-binding protein) is a cellular transcription factor. It binds to certain DNA sequences called cAMP response elements (CRE), thereby increasing or decreasing the transcription of the genes. CREB has a well-documented role in neuronal plasticity and long-term memory formation in the brain. Cocaine- and amphetamine-regulated transcript, also known as CART, is a neuropeptide protein that in humans is encoded by the CARTPT gene. CART appears to have roles in reward, feeding, stress, and it has the functional properties of an endogenous psychostimulant. Taking into account that CART production is upregulated by CREB, it could be hypothesized that due to tianeptine's central role in BDNF and neuronal plasticity, this CREB may be the transcription cascade through which this drug enhances mesolimbic release of dopamine. Research indicates possible anticonvulsant (anti-seizure) and analgesic (painkilling) activity of tianeptine via downstream modulation of adenosine A1 receptors (as the effects could be experimentally blocked by antagonists of this receptor). Tianpetine is also weak histone deacetylase (HDAC) inhibitor, specifically of HDAC1 and HDAC2 but not of HDAC3, and analogues with greatly increased potency such as tianeptinaline have been developed.
On Truth Social, Trump expressed his anger that the press pool had "refused to cover one of the Biggest and Most Beautiful Events to take place in many years". The press pool resumed its coverage of Trump on September 25 after the administration reinstated the news outlets.
== Corporate history == KCI was founded in 1976 in San Antonio, Texas, by James R. Leininger, then an emergency room physician who wanted to help prevent the pulmonary complications associated with immobility. Over time, the company developed or acquired a line of therapeutic specialty beds, introducing a specialty bed for acute care patients with pulmonary complications. Initially KCI's product development focused on therapeutic beds and surfaces then expanded to introduce the first commercial negative pressure wound therapy products in the mid-1990s. KCI acquired regenerative medicine company, LifeCell, in 2008 in a non-hostile transaction for US$1.7 billion. In January 2012, LifeCell was made a sister company to KCI. In 2013, LifeCell and KCI recombined into one company.
=== Other inventions === Jones also developed a portable x-ray machine. He also developed an early prototype of a snowmobile called a "snow machine" that attached skis to the undercarriage of an airplane fuselage and attached a propeller, and a sound track synchroniser (later selling the patent to RCA). An early radio service for local doctors were also counted among his inventions.
Sources: en.wikipedia.org
=== EC 2.7.8: Transferases for other substituted phosphate groups === EC 2.7.8.1: diacylglycerol ethanolaminephosphotransferase EC 2.7.8.2: diacylglycerol cholinephosphotransferase EC 2.7.8.3: ceramide cholinephosphotransferase EC 2.7.8.4: serine ethanolaminephosphotransferase EC 2.7.8.5: CDP-diacylglycerol—glycerol-3-phosphate 1-phosphatidyltransferase EC 2.7.8.6: undecaprenyl-phosphate galactose phosphotransferase EC 2.7.8.7: holo-[acyl-carrier-protein] synthase EC 2.7.8.8: CDP-diacylglycerol—serine O-phosphatidyltransferase EC 2.7.8.9: phosphomannan mannosephosphotransferase EC 2.7.8.10: sphingosine cholinephosphotransferase EC 2.7.8.11: CDP-diacylglycerol—inositol 3-phosphatidyltransferase EC 2.7.8.12: CDP-glycerol glycerophosphotransferase EC 2.7.8.13: phospho-N-acetylmuramoyl-pentapeptide-transferase EC 2.7.8.14: CDP-ribitol ribitolphosphotransferase EC 2.7.8.15: UDP-N-acetylglucosamine—dolichyl-phosphate N-acetylglucosaminephosphotransferase EC 2.7.8.16: deleted, now included with EC 2.7.8.2 diacylglycerol cholinephosphotransferase EC 2.7.8.17: UDP-N-acetylglucosamine—lysosomal-enzyme N-acetylglucosaminephosphotransferase EC 2.7.8.18: UDP-galactose—UDP-N-acetylglucosamine galactose phosphotransferase EC 2.7.8.19: UDP-glucose—glycoprotein glucose phosphotransferase EC 2.7.8.20: phosphatidylglycerol—membrane-oligosaccharide glycerophosphotransferase EC 2.7.8.21: membrane-oligosaccharide glycerophosphotransferase EC 2.7.8.22: 1-alkenyl-2-acylglycerol choline phosphotransferase EC 2.7.8.23: carboxyvinyl-carboxyphosphonate phosphorylmutase EC 2.7.8.24: CDP-diacylglycerol—choline O-phosphatidyltransferase EC 2.7.8.25: Now EC 2.4.2.52, triphosphoribosyl-dephospho-CoA synthase EC 2.7.8.26: adenosylcobinamide-GDP ribazoletransferase EC 2.7.8.27: sphingomyelin synthase EC 2.7.8.28: 2-phospho-L-lactate transferase EC 2.7.8.29: L-serine-phosphatidylethanolamine phosphatidyltransferase EC 2.7.8.30: Now EC 2.4.2.53, undecaprenyl-phosphate 4-deoxy-4-formamido-L-arabinose transferase EC 2.7.8.31: undecaprenyl-phosphate glucose phosphotransferase EC 2.7.8.32: 3-O-α-D-mannopyranosyl-α-D-mannopyranose xylosylphosphotransferase EC 2.7.8.33: UDP-N-acetylglucosamine—undecaprenyl-phosphate N-acetylglucosaminephosphotransferase EC 2.7.8.34: CDP-L-myo-inositol myo-inositolphosphotransferase EC 2.7.8.35: UDP-N-acetylglucosamine—decaprenyl-phosphate N-acetylglucosaminephosphotransferase EC 2.7.8.36: undecaprenyl phosphate N,N′-diacetylbacillosamine 1-phosphate transferase EC 2.7.8.37: α-D-ribose 1-methylphosphonate 5-triphosphate synthase EC 2.7.8.38: archaetidylserine synthase EC 2.7.8.39: archaetidylinositol phosphate synthase EC 2.7.8.40: UDP-N-acetylgalactosamine-undecaprenyl-phosphate N-acetylgalactosaminephosphotransferase EC 2.7.8.41: cardiolipin synthase (CMP-forming) EC 2.7.8.42: Kdo2-lipid A phosphoethanolamine 7′′-transferase EC 2.7.8.43: lipid A phosphoethanolamine transferase EC 2.7.8.44: teichoic acid glycerol-phosphate primase EC 2.7.8.45: teichoic acid glycerol-phosphate transferase EC 2.7.8.46: teichoic acid ribitol-phosphate primase EC 2.7.8.47: teichoic acid ribitol-phosphate polymerase
== Data collection == Protein NMR utilizes multidimensional nuclear magnetic resonance experiments to obtain information about the protein. Ideally, each distinct nucleus in the molecule experiences a distinct electronic environment and thus has a distinct chemical shift by which it can be recognized. However, in large molecules such as proteins the number of resonances can typically be several thousand and a one-dimensional spectrum inevitably has incidental overlaps. Therefore, multidimensional experiments that correlate the frequencies of distinct nuclei are performed. The additional dimensions decrease the chance of overlap and have a larger information content, since they correlate signals from nuclei within a specific part of the molecule. Magnetization is transferred into the sample using pulses of electromagnetic (radiofrequency) energy and between nuclei using delays; the process is described with so-called pulse sequences. Pulse sequences allow the experimenter to investigate and select specific types of connections between nuclei. The array of nuclear magnetic resonance experiments used on proteins fall in two main categories — one where magnetization is transferred through the chemical bonds, and one where the transfer is through space, irrespective of the bonding structure. The first category is used to assign the different chemical shifts to a specific nucleus, and the second is primarily used to generate the distance restraints used in the structure calculation, and in the assignment with unlabelled protein.
"There's no way Rush will ever exist again because Neil's not here to be a part of it... that's not to say that we can't do other things and we can't do things that benefit our communities and all of that. I have lots of plans for that sort of thing that don't necessarily include Geddy. I get asked this all the time—are we gonna do this, or are we gonna do that? Who knows? All I know is we still love each other and we're still very, very good friends, and we always will be."
The exact nature of cortisone's anti-inflammatory action remained a mystery for years after, however, until the leukocyte adhesion cascade and the role of phospholipase A2 in the production of prostaglandins and leukotrienes was fully understood in the early 1980s. Corticosteroids were voted Allergen of the Year in 2005 by the American Contact Dermatitis Society.
Jane Shelby Richardson (born January 25, 1941) is an American biophysicist best known for developing the Richardson diagram, or ribbon diagram, a method of representing the 3D structure of proteins. Ribbon diagrams have become a standard representation of protein structures that has facilitated further investigation of protein structure and function globally. With interests in astronomy, math, physics, botany, and philosophy, Richardson took an unconventional route to establishing a science career. Richardson is a professor in biochemistry at Duke University.
Sources: en.wikipedia.org
=== Dosages === For prostate cancer, the dosage of buserelin by subcutaneous injection is 500 μg three times per day (once every 8 hours, 1,500 μg/day total) for one week and then 200 μg once daily thereafter. If buserelin is used as a nasal spray, the dosage for prostate cancer is 800 μg sprayed into the nostrils three times per day (once every 8 hours, 2,400 μg/day total) for one week followed by 400 μg sprayed into the nostrils three times per day (once every 8 hours, 1,200 μg/day total) thereafter. For endometriosis, buserelin is used specifically as a nasal spray and the dosage is the same as that used for prostate cancer. These dosages of buserelin for both subcutaneous injection and nasal spray have been found to decrease testosterone levels to near-castrate levels in men with prostate cancer, although suppression was more complete with subcutaneous injection presumably due to suboptimal absorption with intranasal administration.
A normal eosinophil count is considered to be less than 0.65×109/L. Eosinophil counts are higher in newborns and vary with age, time (lower in the morning and higher at night), exercise, environment, and exposure to allergens. Eosinophilia is never a normal lab finding. Efforts should always be made to discover the underlying cause, though the cause may not always be found.
Technetium-99m (Tc-99m) can be readily detected in the body by medical equipment because it emits 140.5 keV gamma rays (these are about the same wavelength as emitted by conventional X-ray diagnostic equipment), and its half-life for gamma emission is six hours (meaning 94% of it decays to 99Tc in 24 hours). Besides, it emits virtually no beta radiation, thus keeping radiation dosage low. Its decay product, 99Tc, has a relatively long half-life (211,000 years) and emits little radiation. The short physical half-life of 99mTc and its biological half-life of 1 day with its other favourable properties allows scanning procedures to collect data rapidly and keep total patient radiation exposure low. Chemically, technetium-99m is selectively concentrated in the stomach, thyroid, and salivary glands, and excluded from cerebrospinal fluid; combining it with perchlorate abolishes its selectiveness.
=== Intranasal === Insulin can be delivered to the central nervous system via the intranasal (IN) route with little to no systemic uptake or associated peripheral side effects. It has been demonstrated that intranasally delivered insulin rapidly accumulates in CSF fluid, indicating effective transport to the brain. This accumulation is thought to occur along olfactory and nearby routes. Although numerous studies have published encouraging results, further study is still being conducted to comprehend its long-term impacts in order to begin the successful clinical application.
Levothyroxine In rats given only 10 μg of D, L-thyroxine daily for 15 days, liver cysteine desulfhydrase activity disappears and serine and threonine dehydrase and alanine glutamate transaminase activities decrease about 40%. Either in vivo feeding of pyridoxal-5-phosphate or in vitro addition of the coenzyme to the liver preparations restores full activity to all these enzymes, and the slight in vitro inhibition in the presence of 10−5 M thyroxine is also reversed by pyridoxal-5-phosphate. The inactive form pyridoxine competitively inhibits the active pyridoxal-5'-phosphate. Consequently, symptoms of vitamin B6 supplementation in the pyridoxine form can mimic those of vitamin B6 deficiency; an effect which perhaps might be avoided by supplementing with P5P instead. AlaP (alanine phosphonate) inhibits alanine racemases, but its lack of specificity has prompted further designs of ALR inhibitors. Gabaculine and Vigabatrin inhibit GABA aminotransferase Canaline and 5-fluoromethylornithine inhibit ornithine aminotransferase Amino-oxy SAM inhibits ACC synthase
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.
Legal status varies by country, but cardarine is not approved as a medicine in major jurisdictions. It is often sold as a research chemical, a category that may not be lawful for human use. Buyers should check local laws and product labels carefully.