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Background And Regulatory History — Complete Guide

By Editorial Desk · published 2026-03-03 · last reviewed 2026-03-17 · News

A practical reference on fatty acid oxidation: what it is, how it behaves, what the literature reports, and where the honest uncertainties sit.

This page was last updated on 2026-03-17 and is reviewed periodically as new material appears.

Background and Regulatory History

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.

Mechanism and Detection

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.

Cardarine at a glance

PropertyValueNotes
Common nameCardarineCommon internet and media name.
Research codeGW501516Also written GW-1516.
Drug classPPARδ agonistNot a selective androgen receptor modulator.
Development statusDiscontinuedClinical development halted after rodent cancer findings.
Regulatory statusProhibited in sportListed by WADA; not approved as medicine.

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.

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Mechanism and Laboratory Detection

Published human data are sparse and mostly come from early-phase trials. Those studies examined short-term changes in lipids, glucose, and exercise capacity, but they were not large enough to establish efficacy or long-term safety. Some animal experiments reported increased running endurance, yet such findings do not prove a performance benefit in people. Anti-doping laboratories detect GW501516 and its metabolites in urine or blood using liquid chromatography-tandem mass spectrometry. Detection windows depend on dose, sample type, and individual metabolism. The method is sensitive enough to identify trace residues in tested samples.

Laboratory handling focuses on identity, purity, and stability. Reference standards are typically stored cold and dry, protected from light, because solutions can degrade over time. Analytical checks may use high-performance liquid chromatography with ultraviolet detection or mass spectrometry. Impurities and related substances can be separated chromatographically and compared with a known standard. Because cardarine is not an approved drug, compendial monographs are absent, and laboratories often rely on in-house methods. Reported purity varies among unregulated products and should not be assumed from a label.

Background from the literature

== Pharmacology == Dantrolene depresses excitation-contraction coupling in skeletal muscle by acting as a receptor antagonist to the ryanodine receptor, and decreasing free intracellular calcium concentration.

== Genomics == The human OTC gene is located on the short arm of chromosome X (Xp21.1). The gene is located in the Watson (plus) strand and is 73 kbases in length. The open reading frame of 1,062 nucleotides is disbursed between 10 exons and nine introns. The encoded protein is 354 amino acids long with a predicted molecular weight of 39.935 kD. Postranscriptional modification leaves the mature peptide with 322 amino acids and a weight of 36.1 kD. The protein is located in the mitochondrial matrix. In mammals, OTC is expressed in the liver and small intestinal mucosa.

Kimon Georgiev became prime minister on 19 May 1934, after the coup d'état. He served as Minister of Foreign Affairs and Religious Affairs (19-23 May 1934) and Minister of Justice (23 May 1934 – 22 January 1935) and temporarily served as Minister of War on 19 May 1934. Kimon Georgiev led the new Cabinet, which was primarily made up of Zveno and Military League representatives. Although they denounced the coup, the other bourgeois parties and the non-fascist bourgeois parties accepted it. The BCP called it a fascist coup, but they were unable to put up a united front to fight it due to mistakes in secretarian doctrine. The coup's perpetrators said in their manifesto that a "national supra-party power" would be established. They abolished the Parliament, dissolved the IMRO, and restructured the governmental apparatus on a fascist basis.

Sources: en.wikipedia.org

Reference notes

Adenosine monophosphate deaminase deficiency type 1 or AMPD1, is a human metabolic disorder in which the body consistently lacks the enzyme AMP deaminase, in sufficient quantities. This may result in exercise intolerance, muscle pain and muscle cramping. The disease was formerly known as myoadenylate deaminase deficiency (MADD). In virtually all cases, the deficiency has been caused by an SNP mutation, known as rs17602729 or C34T. While it was initially regarded as a recessive (or purely homozygous) disorder, some researchers have reported the existence of similarly deleterious effects from the heterozygous form of the SNP. In the homozygous form of the mutation, a single genetic base (character) has been changed from cytosine ("C") to thymine ("T") on both strands of Chromosome 1 – in other words, "C;C" has been replaced by "T;T". A rarer but analogous condition, in which two guanine bases ("G;G") bases (in the unmutated form) have been changed to adenine ("A;A") has also been identified. While there has been no consensus on the effects of the heterozygous form – either "C;T" or "A;G" – some evidence has been found that it too has caused AMPD1 deficiency. In addition, some sources have suggested the existence of a rare, acquired form of AMPD1 deficiency. AMPD1 deficiency is caused by a defect in the mechanism for production of AMP deaminase – an enzyme that converts adenosine monophosphate (AMP) to inosine monophosphate (IMP).

Boletus edulis fruit bodies contain diverse phytochemicals, including 500 mg of ergosterol per 100 g of dried mushroom, and ergothioneine. The fruit bodies contain numerous polyphenols, especially a high content of rosmarinic acid, and organic acids (such as oxalic, citric, malic, succinic and fumaric acids), and alkaloids.

==== Quantum dot only solar cells ==== Aromatic self-assembled monolayers (SAMs) (such as 4-nitrobenzoic acid) can be used to improve the band alignment at electrodes for better efficiencies. This technique has provided a record power conversion efficiency (PCE) of 10.7%. The SAM is positioned between ZnO–PbS colloidal quantum dot (CQD) film junction to modify band alignment via the dipole moment of the constituent SAM molecule, and the band tuning may be modified via the density, dipole and the orientation of the SAM molecule.

Sources: en.wikipedia.org

Frequently asked questions

Is cardarine a selective androgen receptor modulator?

No. Cardarine is a PPARδ agonist, while selective androgen receptor modulators act on androgen receptors. The two classes differ in receptor target and downstream effects.

Why did clinical development stop?

Preclinical rodent studies reported cancers, including liver and bladder tumors, at tested doses. The human relevance of those findings is uncertain, but development was discontinued. No approved human product resulted.

Is cardarine approved for medical use?

No. It remains an investigational compound without approved therapeutic labeling. Sports regulators prohibit its use, and health agencies have warned against consuming it.

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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