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Identity And Pharmacological Mechanism — Reference Sheet

By Editorial Desk · published 2025-08-11 · last reviewed 2025-08-30 · Guide

If you have been reading about PPARδ and want a single page that covers the useful parts, this is it: definitions, context, how it is studied, and the questions that come up repeatedly.

Updated 2025-08-30. Numbers and descriptions here follow the published literature rather than marketing material.

Identity and Pharmacological Mechanism

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.

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.

Mechanism and Detection

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.

Cardarine at a glance

PropertyValueNotes
Chemical classSynthetic PPARδ agonistNot a steroid or a selective androgen receptor modulator.
Common synonymsCardarine, GW501516, GW-501516, endurobolNames vary by supplier and literature source.
AppearanceWhite to off-white powderConsistent with many small-molecule research chemicals.
SolubilityLow in water; soluble in DMSO and ethanolOften prepared in organic solvent for laboratory work.
Primary targetPPARδ (NR1C2)Nuclear receptor involved in lipid and energy metabolism.

Identity and Regulatory Status

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.

Regulatory treatment varies, but cardarine is not approved as a medicine. Sports authorities list GW501516 as a prohibited substance, and it is banned at all times under the World Anti-Doping Agency code. Many countries restrict sales for human consumption, while online vendors market it as a research chemical. Such products may lack purity data, and their actual contents can differ from the label. Purchasing or possessing cardarine may carry legal consequences depending on jurisdiction. The compound is not a dietary supplement ingredient in regulated markets.

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.

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Regulation and Detection

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.

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.

Mechanism and Safety Research

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.

Literature on cardarine often separates receptor pharmacology from toxicology. Mechanistic papers describe PPARδ activation and gene expression changes, while safety assessments focus on carcinogenicity and species differences. Questions remain about whether rodent tumors arise through PPARδ-dependent or off-target mechanisms. Another open area is how human metabolism and exposure compare with those in animal studies. Analytical methods such as liquid chromatography–mass spectrometry are used to confirm identity in biological and product samples.

Notes from published material

== Uses == Acetamide is used as a plasticizer and an industrial solvent. Molten acetamide is good solvent with a broad range of applicability. Notably, its dielectric constant is higher than most organic solvents, allowing it to dissolve inorganic compounds with solubilities closely analogous to that of water. Acetamide has uses in electrochemistry and the organic synthesis of pharmaceuticals, pesticides, and antioxidants for plastics. It is a precursor to thioacetamide.

In the northern Appalachians and at higher elevations of the central and southern Appalachians these diverse mesic forests give way to less diverse northern hardwood forests with canopies dominated only by American beech, sugar maple, American basswood (Tilia americana) and yellow birch and with far fewer species of shrubs and herbs. Drier and rockier uplands and ridges are occupied by oak–chestnut forests dominated by a variety of oaks (Quercus spp.), hickories (Carya spp.) and, in the past, by the American chestnut (Castanea dentata). The American chestnut was virtually eliminated as a canopy species by the introduced fungal chestnut blight (Cryphonectaria parasitica), but lives on as sapling-sized sprouts that originate from roots, which are not killed by the fungus. In present-day forest canopies, chestnut has been largely replaced by oaks. The oak forests of the southern and central Appalachians consist largely of black, northern red, white, chestnut and scarlet oaks (Quercus velutina, Q. rubra, Q. alba, Q. prinus and Q. coccinea) and hickories, such as the pignut (Carya glabra) in particular. The richest forests, which grade into mesic types, usually in coves and on gentle slopes, have predominantly white and northern red oaks, while the driest sites are dominated by chestnut oak, or sometimes by scarlet or northern red oaks. In the northern Appalachians the oaks, except for white and northern red, drop out, while the latter extends farthest north. The oak forests generally lack the diverse small tree, shrub and herb layers of mesic forests.

== Marine plastic waste == Thailand was ranked sixth of 20 nations (1=biggest contributor; 20=lowest contributor) for its contribution to marine plastic waste in 2010. Other ASEAN nations were ranked: Indonesia, 2; Philippines, 3; Vietnam, 4; Malaysia, 8; Myanmar, 17. Thailand's contribution to sea debris has reportedly risen from 400,000 tonnes in 1967 to one million tonnes in 2019.

=== Distillation === Distilled water is produced by a process of distillation. Distillation involves boiling the water and then condensing the vapor into a clean container, leaving solid contaminants behind. Distillation produces very pure water. A white or yellowish mineral scale is left in the distillation apparatus, which requires regular cleaning. Distilled water, like all purified water, must be stored in a sterilized container to guarantee the absence of bacteria. For many procedures, more economical alternatives are available, such as deionized water, and are used in place of distilled water.

Sources: en.wikipedia.org

Further detail

== Medical uses == Sertraline has been approved for major depressive disorder, obsessive–compulsive disorder (OCD), post-traumatic stress disorder (PTSD), premenstrual dysphoric disorder, panic disorder, social anxiety disorder (SAD), and generalized anxiety disorder (GAD). Sertraline is approved for use in children with OCD.

== Medical use == According to phase III randomized trials, a cangrelor–clopidogrel combination is safe and has been found to be more effective than standard clopidogrel treatment at reducing ischemic events in the heart, without increasing major bleeding in the treatment of stenotic coronary arteries. The advantages of this drug combination are most prominent in patients with myocardial infarction. Available antiplatelet drugs have delayed onset and offset of action. Since cangrelor's effects are immediate and quickly reversed, it is a more desirable drug for elective treatment of stenotic coronary arteries, high risk acute coronary syndromes treated with immediate coronary stenting, and for bridging those surgery patients who require P2Y12 inhibition. Evidence regarding cangrelor therapy is limited by the lack studies assessing cangrelor administration in conjunction with either prasugrel or ticagrelor. Cangrelor been approved for adults undergoing percutaneous coronary intervention (PCI).

In addition, the HTR of 5-HTP is abolished by indolethylamine N-methyltransferase (INMT) inhibitors, which block conversion of serotonin and other endogenous tryptamines into N-methylated tryptamines, such as N-methylserotonin (NMS; norbufotenin), bufotenin (5-hydroxy-N,N-dimethyltryptamine; 5-HO-DMT), and N,N-dimethyltryptamine (DMT). These N-methylated tryptamines are well-known for their psychedelic effects, whereas serotonin itself, without biotransformation, does not seem to produce psychedelic effects. 5-HTP has not been found to produce psychedelic effects in humans, which has been attributed to the high doses required to produce such effects. The 5-HTP doses that produce the HTR in rodents are orders of magnitude higher than the doses of 5-HTP that have been used safely and therapeutically in humans. It remains unknown whether 5-HTP can produce psychedelic effects in humans. The highest dosage of 5-HTP that is known to have been evaluated in humans is about 3,000 mg per day. Serotonin syndrome and associated hallucinations have been reported with overdose of serotonin-elevating drugs, but psychedelic-like effects have not been reported. The lack of the HTR and psychedelic effects with serotonin itself has been attributed to the fact that these effects appear to be dependent on activation of a population of intracellular 5-HT2A receptors expressed in cortical neurons in the medial prefrontal cortex (mPFC) that lack the serotonin transporter (SERT) and are inaccessible to serotonin.

Sources: en.wikipedia.org

Frequently asked questions

What is cardarine?

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.

How does cardarine interact with the body?

It binds to and activates PPARδ, a nuclear receptor that regulates genes related to fatty acid oxidation and energy use. This activation alters transcription in tissues such as skeletal muscle and liver. The full range of downstream effects in humans is not fully established.

Is cardarine found naturally?

No, cardarine is not known to occur naturally in plants, animals, or humans. It is a synthetic molecule produced for laboratory research. Products labeled as cardarine should therefore be treated as manufactured chemicals with variable purity.

How does cardarine work in the body?

It binds to and activates PPAR delta, a nuclear receptor that controls expression of genes related to fatty acid oxidation. This mechanism can alter energy metabolism in animal models. It is not a direct stimulant or fat-burning enzyme.

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