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Identity And Pharmacological Classification — Evidence Review

By Editorial Desk · published 2026-07-15 · last reviewed 2026-08-01 · Topic

PPARδ 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.

Identity and Pharmacological Classification

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.

Detection, Regulation, and Quality Context

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.

Cardarine at a glance

PropertyValueNotes
Chemical classPPARδ agonistNot an anabolic steroid.
Common synonymsGW501516, GW-1516Cardarine is an informal name.
AppearanceWhite to off-white powderTypical for research-grade solid.
Solubility classPoorly soluble in water; soluble in some organic solventsSuch as DMSO or ethanol in laboratory settings.
Typical storage temperatureCool, dry, protected from lightSpecific conditions vary by supplier and form.

Mechanism and Detection Methods

GW501516 acts as a selective agonist at PPARδ, a nuclear receptor that regulates transcription of genes involved in lipid handling and energy metabolism. Activation of PPARδ in preclinical models increases fatty acid oxidation, mitochondrial biogenesis, and exercise endurance in rodents. These effects have made the compound a subject of metabolic research and also a target for sport anti-doping rules. In humans, however, controlled studies are limited, and whether similar endurance or metabolic changes occur at tolerated exposures remains an open question. The receptor’s broad tissue distribution also means downstream effects may vary by organ and condition.

Detection of GW501516 in biological samples generally relies on liquid chromatography coupled with tandem mass spectrometry. Urine is a common matrix in anti-doping analysis, while blood or plasma may be used in research settings. Sample preparation can involve enzymatic hydrolysis, protein precipitation, or solid-phase extraction before instrumental analysis. Because the compound undergoes metabolism, assays may target the parent molecule, one or more metabolites, or both. Detection windows are not fixed; they depend on factors such as dose, route, individual metabolism, and assay sensitivity. Reference standards are required for accurate identification and quantification.

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Identity and Pharmacological Mechanism

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.

Regulation and Analytical Detection

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.

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.

Identity and Regulatory Status

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.

Supporting material

=== Neonicotinoids === Neonicotinoids are a class of neuro-active insecticides chemically similar to nicotine, with much lower acute mammalian toxicity and greater field persistence. These chemicals are acetylcholine receptor agonists. They are broad-spectrum systemic insecticides, with rapid action (measured in minutes or hours). They are applied as sprays, drenches, seed and soil treatments. Treated insects exhibit leg tremors, rapid wing motion, stylet withdrawal (aphids), disoriented movement, paralysis and death. Imidacloprid, of the neonicotinoid family, is the most widely used insecticide in the world. In the late 1990s neonicotinoids came under increasing scrutiny over their environmental impact and were linked in a range of studies to adverse ecological effects, including honey-bee colony collapse disorder (CCD) and loss of birds due to a reduction in insect populations. In 2013, the European Union and a few non EU countries restricted the use of certain neonicotinoids. and its potential to increase the susceptibility of rice to planthopper attacks.

Whitefish or white fish is a fisheries term for several species of demersal fish with fins, particularly Atlantic cod (Gadus morhua), whiting (Merluccius bilinearis), haddock (Melanogrammus aeglefinus), hake (Urophycis), and pollock (Pollachius), among others. Whitefish live on or near the seafloor, and can be contrasted with the oily or blue fish (also known as fatty fish), including pelagic fish, which live away from the seafloor. Whitefish do not have much oil in their tissue, and have flakier white or light-coloured flesh. Most of the oil found in their bodies is concentrated in the organs, e.g. cod liver oil. Whitefish can be divided into benthopelagic fish (round fish that live near the sea bed, such as cod and coley) and benthic fish (which live on the sea bed, such as flatfish like plaice). Whitefish is sometimes eaten straight but is often used reconstituted for fishsticks, gefilte fish, lutefisk, surimi (imitation crab meat), etc. Because of their lower oil and fat content, whitefish are particularly suitable for preservation by salting and drying. For centuries it was preserved by drying as stockfish and clipfish and traded as a world commodity. It is commonly used as the fish in the classic British dish of fish and chips.

γ-L-Glutamyl-L-cysteine, also known as γ-glutamylcysteine (GGC), is a dipeptide found in animals, plants, fungi, some bacteria, and archaea. It has a relatively unusual γ-bond between the constituent amino acids, L-glutamic acid and L-cysteine and is a key intermediate in the γ-glutamyl cycle first described by Meister in the 1970s. It is the most immediate precursor to the antioxidant glutathione.

Sources: en.wikipedia.org

Notes from published material

Historic center of Sanlúcar de Barrameda Castle of Santiago, from the 15th century Palace of the Infantes of Orleans and Borbón, which is now used as the City Hall Palace of the Dukes of Medina Sidonia; it includes the house of Medina Sidonia, which now houses the municipal archives Palace of Arizón, which now houses the General catalogue of historic heritage of Andalusia; part of the house is now a hotel Church of Nuestra Señora de la O church of Santo Domingo, a 16th-century building Church of Merced Convent of San Francisco Las Covachas Ébora Bastion of San Salvador Fortifications of Sanlúcar de Barrameda

== History == The first Mel's Drive-In was founded in 1947 by Mel Weiss and Harold Dobbs in San Francisco, California. It later expanded to several other locations. After the last of the original restaurants closed in the 1970s, Weiss's son Steven Weiss and partner Donald Wagstaff opened the first of a new generation of Mel's Drive-In restaurants in 1985. A family rift between father and son caused them to part ways and form two chains, with Steven retaining the "Mel's Drive-In" name and Mel calling his restaurants "Original Mels". The elder Weiss then sold his company in 1994. The Original Mels locations are not listed on the official Mel's Drive-In website, and vice versa.

In that war, British submarines sank 2 million tons of enemy shipping and 57 major warships, the latter including 35 submarines. Among these is the only documented instance of a submarine sinking another submarine while both were submerged. This occurred when HMS Venturer engaged U-864; the Venturer crew manually computed a successful firing solution against a three-dimensionally maneuvering target using techniques which became the basis of modern torpedo computer targeting systems. Seventy-four British submarines were lost, the majority, forty-two, in the Mediterranean.

Sources: en.wikipedia.org

Further detail

=== Thyroid storm === Thyroid storm presents with extreme symptoms of hyperthyroidism. It is treated aggressively with resuscitation measures along with a combination of the above modalities including: intravenous beta blockers such as propranolol, followed by a thioamide such as methimazole, an iodinated radiocontrast agent or an iodine solution if the radiocontrast agent is not available, and an intravenous steroid such as hydrocortisone. Propylthiouracil is the preferred thioamide in thyroid storm as it can prevent the conversion of T4 to the more active T3 in the peripheral tissues in addition to inhibiting thyroid hormone production.

== Technique == The technique for dry needling depends on which tissue is being targeted and the overall objective of the treatment. For example, one of the most common treatment objectives for dry needling, myofascial trigger points (TrPs), differs physiologically from treatments for scar tissue, connective tissue problems, and other medical issues. In the treatment of trigger points for persons with myofascial pain syndrome, dry needling is an invasive procedure in which a filiform needle is inserted into the skin and muscle directly at a myofascial trigger point. A myofascial trigger point consists of multiple, hyperirritable contraction knots related to the production and maintenance of the pain cycle; essentially, myofascial trigger points will generate much local pain upon stimulation or irritation. Deep dry needling for treating trigger points was first introduced by the Czech neurologist Karel Lewit in 1979. Lewit had noticed that the success of injections into trigger points in relieving pain was apparently unconnected to the analgesic used. Dry needling can be divided into categories in terms of depth of penetration: deep and superficial dry needling. Deep dry needling will inactivate myofascial trigger points by provoking a local twitch response (LTR), which is an involuntary spinal cord reflex in which the muscle fibers in the taut band of muscle contract. The LTR indicates the proper placement of the needle in a trigger point. Dry needling that elicits LTRs improves treatment outcomes, and may work by activating endogenous opioids.

== Recommended daily intake == Many countries and health organizations have published recommendations for healthy levels of daily intake of food energy. For example, the United States government estimates 8,400 and 10,900 kJ (2,000 and 2,600 kcal) needed for women and men, respectively, between ages 26 and 45, whose total physical activity is equivalent to walking around 2.5 to 5 km (1+1⁄2 to 3 mi) per day in addition to the activities of sedentary living. These estimates are for a "reference woman" who is 1.63 m (5 ft 4 in) tall and weighs 57 kg (126 lb) and a "reference man" who is 1.78 m (5 ft 10 in) tall and weighs 70 kg (154 lb). Because caloric requirements vary by height, activity, age, pregnancy status, and other factors, the USDA created the DRI Calculator for Healthcare Professionals in order to determine individual caloric needs. According to the Food and Agriculture Organization of the United Nations, the average minimum energy requirement per person per day is about 7,500 kJ (1,800 kcal). Although the U.S. has changed over time with a growth in population and processed foods or food in general, Americans today have available roughly the same level of calories as the older generation. [1] Older people and those with sedentary lifestyles require less energy; children and physically active people require more. Recognizing these factors, Australia's National Health and Medical Research Council recommends different daily energy intakes for each age and gender group.

This resulted in the creation of the NOD-scid mice which lacked T cells, B cells, and NK cells. This mouse model permitted for a slightly higher level of human cell reconstitution. Nevertheless, a major breakthrough in this field came with the introduction of the mutant IL-2 receptor (IL2rg) gene in the NOD-scid model. This accounted for the creation of the NOD-scid-γcnull mice (NCG, NSG or NOG) models which were found to have defective signaling of interleukins IL-2, IL-4, IL-7, IL-9, IL-15 and IL-21. Researchers evolved this NSG model by knocking out the RAG1 and RAG2 genes (recombination activation genes), resulting into the RAGnull version of the NSG model that was devoid of major cells of the immune system including the natural killer cells, B lymphocytes and T lymphocytes, macrophages and dendritic cells, causing the greatest immunodeficiency in mice models so far. The limitation with this model was that it lacked the human leukocyte antigen. In accordance to this limitation, the human T cells when engrafted in the mice, failed to recognize human antigen-presenting cells, which consequated in defective immunoglobulin class switching and improper organization of the secondary lymphoid tissue. To circumvent this limitation, the next development came with the introduction of transgenes encoding for HLA I and HLA II in the NSG RAGnull model that enabled buildout of human T-lymphocyte repertoires as well as the respective immune responses. Mice with such human genes are technically human-animal hybrids.

Sources: en.wikipedia.org

Frequently asked questions

What is cardarine also known as?

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.

Is cardarine a steroid?

No, cardarine is not a steroid. It is classified as a PPARδ agonist. Its structure and receptor target differ from anabolic steroids.

Has cardarine been approved for human use?

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.

How is cardarine detected in anti-doping tests?

Anti-doping laboratories typically use LC-MS/MS to detect GW501516 and its metabolites in urine. The method is sensitive and can identify the compound at low concentrations. Detection depends on sample timing, metabolism, and the specific assay.

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