Cardarine comes up often in conversation and rarely with the context attached. Here we lay out the basics in order, then work through the practical considerations.
Last reviewed on 2025-12-22. Where a claim depends on a specific study, the study is described rather than over-claimed.
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.
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.
At the molecular level, GW501516 binds and activates PPARδ, a nuclear receptor that regulates transcription. Activation shifts expression of genes involved in fatty acid oxidation, energy expenditure, and lipid transport in skeletal muscle and liver. Animal studies report increased endurance and altered lipid profiles after exposure. Human data are limited to small trials and do not establish long-term safety or efficacy. PPARδ also has roles in cell proliferation, so the relationship between activation and cancer risk remains an open question.
Published literature on cardarine includes in vitro assays, rodent experiments, and a small number of human studies. Reports describe effects on exercise capacity and lipid metabolism in animals, while human evidence is sparse. Many online descriptions present the compound as a proven endurance aid, a claim not supported by regulatory approval or large clinical trials. Analytical studies focus on identifying the parent compound and its metabolites in biological samples. Important uncertainties include species differences, dose-response relationships, and the relevance of rodent tumor findings to humans.
| Property | Value | Notes |
|---|---|---|
| Chemical class | PPARδ agonist | Not an anabolic steroid. |
| Common synonyms | GW501516, GW-1516 | Cardarine is an informal name. |
| Appearance | White to off-white powder | Typical for research-grade solid. |
| Solubility class | Poorly soluble in water; soluble in some organic solvents | Such as DMSO or ethanol in laboratory settings. |
| Typical storage temperature | Cool, dry, protected from light | Specific conditions vary by supplier and form. |
In laboratory settings, cardarine is studied as a tool compound for probing PPARδ biology. Published experiments often use cell cultures, rodent models, or isolated tissues. Some investigations focus on metabolic effects, while others assess potential risks such as carcinogenicity observed in long-term animal studies. Because human trials are sparse, most knowledge comes from preclinical work and adverse event reports. Scientific literature frequently notes the gap between animal findings and human outcomes. The compound is not a dietary supplement and is not intended for human consumption.
Cardarine is a common name for GW501516, a synthetic compound developed in the 1990s through research collaborations involving GlaxoSmithKline. It belongs to a class of molecules known as peroxisome proliferator-activated receptor delta agonists. Early studies explored its effects on lipid metabolism and energy expenditure in animal models. The compound was never approved as a human medicine, and clinical development was discontinued. In the years since, it has appeared in fitness and bodybuilding communities as a performance-enhancing substance. Regulatory agencies classify it as an unapproved drug.
PPARδ is a nuclear receptor that regulates gene expression related to fatty acid oxidation, glucose homeostasis, and mitochondrial function. GW501516 binds to this receptor with high affinity and activates downstream signaling in skeletal muscle and other tissues. Animal studies reported increased endurance and altered fuel preference, but human data remain limited and inconsistent. The precise relationship between receptor activation and observed physiological changes is still an area of active investigation. Researchers have also examined whether the compound affects inflammation or cell proliferation. No approved therapeutic indication exists for cardarine.
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.
Until January 1918, the Free Cossacks of Ukraine were subordinate to the Ukrainian General Secretariat of Internal Affairs. With the beginning of the Ukrainian-Soviet War, their units were incorporated into the regular army. However, after a number of battles against the Bolsheviks, Free Cossacks were disarmed in compliance with orders of the German command, whose troops had occupied Ukraine in March–April 1918 after the Treaty of Brest-Litovsk. On 29 April 1918 Pavlo Skoropadskyi, the earlier leader of Free Cossacks, was proclaimed Hetman of Ukraine at a congress of the conservative All-Ukrainian Union of Landowners. This coup was backed by generals of German and Austrian armies which were occupying Ukraine at that time. The previously democratic Ukrainian People's Republic was replaced with the Hetmanate, the Central Rada and the Council of Ministers of the Ukrainian People's Republic were abolished, with all their powers, as well as command over the military, being transferred to Skoropadskyi, and private land ownership was reinstated. Local administration was entrusted to commissioners personally appointed by the hetman. To achieve legitimacy among the Ukrainian population, the Skoropadskyi styled his regime as a continuation of Ukrainian Cossack traditions of the 17-18th centuries. The hetman's government included representatives of old Cossack nobility (starshyna), most prominently Fedir Lyzohub (head of the Conucil of Ministers) and Dmytro Doroshenko (Minister of Foreign Affairs).
TCM "holds that the body's vital energy (chi or qi) circulates through channels, called jingluo ("meridians and collaterals"), that have branches connected to bodily organs and functions." Its view of the human body is only marginally concerned with anatomical structures, but focuses primarily on the body's functions (such as digestion, breathing, temperature maintenance, etc.): These functions are aggregated and then associated with a primary functional entity – for instance, nourishment of the tissues and maintenance of their moisture are seen as connected functions, and the entity postulated to be responsible for these functions is xiě (blood). These functional entities thus constitute concepts rather than something with biochemical or anatomical properties. The primary functional entities used by traditional Chinese medicine are qì, xuě, the five zàng organs, the six fǔ organs, and the meridians which extend through the organ systems. These are all theoretically interconnected: each zàng organ is paired with a fǔ organ, which are nourished by the blood and concentrate qi for a particular function, with meridians being extensions of those functional systems throughout the body. Concepts of the body and of disease used in TCM are pseudoscientific, similar to Mediterranean humoral theory. TCM's model of the body is characterized as full of pseudoscience. Some practitioners no longer consider yin and yang and the idea of an energy flow to apply.
The Byzantine Empire, also known as the Eastern Roman Empire, was the continuation of the Roman Empire centred on Constantinople during late antiquity and the Middle Ages. Having survived the fall of the Western Roman Empire in the 5th century AD, it endured until the fall of Constantinople to the Ottoman Empire in 1453. The term 'Byzantine Empire' was coined only after its demise; its citizens used the term 'Roman Empire' and called themselves 'Romans'. During the early centuries of the Roman Empire, the western provinces were Latinised, but the eastern parts kept their Hellenistic culture. Constantine I (r. 324–337) legalised Christianity and moved the capital to Constantinople. Theodosius I (r. 379–395) made Christianity the state religion and Greek gradually replaced Latin for official use. The empire adopted a defensive strategy and, throughout its remaining history, experienced recurring cycles of decline and recovery. The Byzantine Empire reached its greatest extent under the reign of Justinian I (r. 527–565), who briefly reconquered much of Italy and the western Mediterranean coast. A plague began around 541, and a prolonged warfare with Persia placed fiscal and military strain on the empire, contributing to political and strategic challenges in the decades that followed. In the 630s and 640s the Arab conquests defeated Byzantine field armies in Syria and Egypt, resulting in the permanent loss of those provinces to the Rashidun Caliphate. In 698, Africa was lost to the Umayyad Caliphate, but the empire stabilised under the Isaurian dynasty.
=== In the human brain === Iron is vital for function of the human brain. Iron is tightly regulated in the brain, limiting the impact of both iron deficiency and excess. If these systems are overwhelmed by nutritional deficiency, especially in pregnancy and infancy, there can be long-term health consequences but direct connections are difficult to establish because nutritional deficiency is usually linked to other health related problems. Excess iron is correlated with some neurodegenerative conditions but the cause is not known.
Sources: en.wikipedia.org
== Regulation by the photoperiod == The levels of proopiomelanocortin (pomc) are regulated indirectly in some animals by the photoperiod. It is referred to the hours of light during a day and it changes across the seasons. Its regulation depends on the pathway of thyroid hormones that is regulated directly by the photoperiod. An example are the siberian hamsters who experience physiological seasonal changes dependent on the photoperiod. During spring in this species, when there is more than 13 hours of light per day, iodothyronine deiodinase 2 (DIO2) promotes the conversion of the prohormone thyroxine (T4) to the active hormone triiodothyronine (T3) through the removal of an iodine atom on the outer ring. It allows T3 to bind to the thyroid hormone receptor (TR), which then binds to thyroid hormone response elements (TREs) in the DNA sequence. The pomc proximal promoter sequence contains two thyroid-receptor 1b (Thrb) half-sites: TCC-TGG-TGA and TCA-CCT-GGA indicating that T3 may be capable of directly regulating pomc transcription. For this reason during spring and early summer, the level of pomc increases due to the increased level of T3. However, during autumn and winter, when there is less than 13 hours of light per day, iodothyronine desiodinase 3 removes an iodine atom which converts thyroxine to the inactive reverse triiodothyronine (rT3), or which converts the active triiodothyronine to diiodothyronine (T2). Consequently, there is less T3 and it blocks the transcription of pomc, which reduces its levels during these seasons.
==== Fugitive, new sentences, and marriage ==== Olofsson escaped from the Norrköping prison on 20 March 1975. In April that year, he went into a bank in Copenhagen with a gun in each hand, fired a warning shot, and robbed the bank of SEK194,000. One month after the escape, Olofsson was in Marseille on the French Riviera. Together with a companion, he bought the sailboat Saga for 50,000 francs, and for three months they sailed around the Mediterranean. In August, they passed through the Strait of Gibraltar, out onto the Atlantic past the Azores. With the help of Inger and Mikael von Heijne from Djursholm, on their way home from the Caribbean, Olofsson got on the right course and finally reached Ireland. From there, they went to Denmark where Danish police came upon them. Olofsson escaped and it was not until January 1976 that the police caught up with him and managed to track him down at a crossroads outside Brussels. He managed to shoot himself free; on a train in Germany during this escape, he met 19-year-old Marijke Demuynck. On 24 March 1976, Olofsson robbed Handelsbanken on Östra Hamngatan 27 in Gothenburg of SEK 930,000 - at the time the largest robbery in Swedish criminal history. At the same time, he took two people hostage. He was arrested at 22:30, nine hours after the robbery, at hotel Gyllene Kärven in Herrljunga. SEK 230,000 was recovered during Olofsson‘s arrest; the rest was never found.
Gramicidin S or Gramicidin Soviet is an antibiotic that is effective against some gram-positive and gram-negative bacteria as well as some fungi. It is a derivative of gramicidin, produced by the gram-positive bacterium Brevibacillus brevis. Gramicidin S is a cyclodecapeptide, constructed as two identical pentapeptides joined head to tail, formally written as cyclo(-Val-Orn-Leu-D-Phe-Pro-)2. That is to say, it forms a ring structure composed of five different amino acids, each one used twice within the structure. Another interesting point is that it utilizes two amino acids uncommon in peptides: ornithine as well as the atypical stereoisomer of phenylalanine. It is synthesized by gramicidin S synthetase.
=== Controversies === In July 2019, the British company Reckitt Benckiser Group (RB Group) and its current/former affiliated entities (notably Indivior, which split from RB Group in 2014) settled with the US Department of Justice (DOJ) regarding the sale and marketing of brand name Suboxone (buprenorphine/naloxone). The non-prosecution agreement involves RB Group paying up to $1.4 billion, the largest settlement payment in U.S. history involving an opioid-class medication. This record was surpassed in October 2020, when Purdue Pharma reached an $8 billion settlement for claims related to injuries and deaths caused by the opioid epidemic, which includes criminal fines, forfeiture, and civil damages. The 2019 case alleged anti-competitive behavior by RB Group and Indivior surrounding the expiration of their regulatory exclusivity for Suboxone sublingual tablets. The DOJ alleged that RB Group and Indivior employed a product hopping scheme (when a firm ceases production of a product upon expiration of regulatory exclusivity in favor of another product that still has regulatory exclusivity in order to prevent generic manufacturer competition) by misrepresenting that the Suboxone sublingual film formulation was safer than the sublingual tablet formulation because "children are less likely to be accidentally exposed to the film product". There was no scientific evidence for that claim.
Nalmefene, sold under the brand name Revex among others, is a medication that is used in the treatment of opioid overdose and alcohol dependence. Nalmefene belongs to the class of opioid antagonists and can be taken by mouth, administered by injection, or delivered through nasal administration. In terms of its chemical structure and biological activity, nalmefene is similar to another opioid antagonist called naltrexone, as they are both derivatives of opiates. However, nalmefene offers certain advantages over naltrexone. These include a longer elimination half-life, which means it stays in the body for a longer duration, improved absorption when taken by mouth, and no observed liver toxicity that is dependent on the dosage. Nalmefene is available as a generic medication.
Sources: en.wikipedia.org
== Children == Pediatric MASLD was first reported in 1983. It is the most common chronic liver disease among children and adolescents since at least 2007, affecting 10 to 20% of them in the US in 2016. MASLD is associated with metabolic syndrome, which is a cluster of risk factors that contribute to the development of cardiovascular disease and type 2 diabetes mellitus. Studies have demonstrated that abdominal obesity and insulin resistance, in particular, are significant contributors to the development of MASFLD. Coexisting liver diseases, such as hepatitis C and cardiovascular diseases such as atherosclerosis, are also associated with an increased risk of MASFLD. Some children were diagnosed as early as two years old, with a mean age of diagnosis between 11 and 13 years old. The mean age is usually above 10 years, as children can also report non-specific symptoms and are thus difficult to diagnose for MASLD. Boys are more likely to be diagnosed with MASLD than girls. Overweight, or even weight gain, in childhood and adolescence, is associated with an increased risk of MASLD later in life, with adult MASLD predicted in a 31-year follow-up study by risk factors during childhood including BMI, plasma insulin levels, male sex, genetic background (PNPLA3 and TM6SF2 variants) and low birth weight, an emerging risk factor for adulthood MASLD. In a study, simple steatosis was present in up to 45% in children with a clinical suspicion of MASLD.
All LSF reactions are chemoselective but not every chemoselective reaction fulfills the requirements of the definition for LSF. High chemoselectivity is required for a useful LSF with a predictable reaction outcome because complex molecules typically feature several distinct functional groups that need to be tolerated. In this sense, chemoselectivity is sometimes referred to as functional group tolerance. Furthermore, high chemoselectivity avoids often undesired over-functionalization of the valuable substrate, which is used as a limiting reagent in LSF reactions. Every C–H bond functionalization on a complex molecule classifies as LSF, except when a directing or activating group must be installed in a previous step of the synthesis to accomplish the transformation. For functional group manipulations, the distinction between LSF and functional-group-tolerant reactions is more subtle. For example, peptide bioconjugation reactions make use of the native functionality in amino acid side chains, and thus classify as LSF. In contrast, bioorthogonal 1,3-dipolar cycloadditions (see also copper-free click chemistry and Huisgen cycloaddition) generally require prior introduction of azide or cycloalkyne functionalities to biomolecules. Hence, such transformations do not classify as LSF despite their excellent functional group tolerance.
Free fatty acid receptor 2 (FFAR2), also known as G-protein coupled receptor 43 (GPR43), is a rhodopsin-like G-protein coupled receptor (GPCR) encoded by the FFAR2 gene. In humans, the FFAR2 gene is located on the long arm of chromosome 19 at position 13.12 (19q13.12). FFAR2, like other GPCRs, is located on the cell membrane and is activated by binding specific ligands, regulating various cellular functions. FFAR2 is part of the free fatty acid receptor family, which also includes FFAR1 (GPR40), FFAR3 (GPR41), and FFAR4 (GPR120). FFAR2 and FFAR3 are activated by short-chain fatty acids (SCFAs), while FFAR1 and FFAR4 respond to long-chain fatty acids. SCFAs, produced by intestinal bacteria, play a key role in various bodily functions by activating FFAR2. This receptor is implicated in regulating insulin and glucose levels, inflammation, fat tissue development, and certain cancerous and non-cancerous cell growth. Due to its role in these processes, FFAR2 has been studied for its potential involvement in conditions such as diabetes, inflammation, obesity, ketoacidosis, certain types of cancer, neurological diseases, and infections. Therapies targeting FFAR2 are being developed to modulate its activity in these conditions, offering potential new treatments for diseases influenced by SCFAs.
Visceral fat or abdominal fat (also known as organ fat or intra-abdominal fat) is located inside the abdominal cavity, packed between the organs (stomach, liver, intestines, kidneys, etc.). Visceral fat is different from subcutaneous fat underneath the skin, and intramuscular fat interspersed in skeletal muscles. Fat in the lower body, as in thighs and buttocks, is subcutaneous and is not consistently spaced tissue, whereas fat in the abdomen is mostly visceral and semi-fluid. Visceral fat is composed of several adipose depots, including mesenteric, epididymal white adipose tissue (EWAT), and perirenal depots. Visceral fat is often expressed in terms of its area in cm2 (VFA, visceral fat area). An excess of visceral fat is known as abdominal obesity, or "belly fat", in which the abdomen protrudes excessively. New developments such as the Body Volume Index (BVI) are specifically designed to measure abdominal volume and abdominal fat. Excess visceral fat is also linked to type 2 diabetes, insulin resistance, inflammatory diseases, and other obesity-related diseases. Likewise, the accumulation of neck fat (or cervical adipose tissue) has been shown to be associated with mortality. Several studies have suggested that visceral fat can be predicted from simple anthropometric measures, and predicts mortality more accurately than body mass index or waist circumference. Men are more likely to have fat stored in the abdomen due to sex hormone differences. Estrogen (female sex hormone) causes fat to be stored in the buttocks, thighs, and hips in women.
As the membrane potential is increased, sodium ion channels open, allowing the entry of sodium ions into the cell. This is followed by the opening of potassium ion channels that permit the exit of potassium ions from the cell. The inward flow of sodium ions increases the concentration of positively charged cations in the cell and causes depolarization, where the potential of the cell is higher than the cell's resting potential. The sodium channels close at the peak of the action potential, while potassium continues to leave the cell. The efflux of potassium ions decreases the membrane potential or hyperpolarizes the cell. For small voltage increases from rest, the potassium current exceeds the sodium current and the voltage returns to its normal resting value, typically −70 mV. However, if the voltage increases past a critical threshold, typically 15 mV higher than the resting value, the sodium current dominates. This results in a runaway condition whereby the positive feedback from the sodium current activates even more sodium channels. Thus, the cell fires, producing an action potential. The frequency at which a neuron elicits action potentials is often referred to as a firing rate or neural firing rate. Currents produced by the opening of voltage-gated channels in the course of an action potential are typically significantly larger than the initial stimulating current. Thus, the amplitude, duration, and shape of the action potential are determined largely by the properties of the excitable membrane and not the amplitude or duration of the stimulus.
Sources: en.wikipedia.org
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.
No, cardarine is not a steroid. It is classified as a PPARδ agonist. Its structure and receptor target differ from anabolic steroids.
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.
Cardarine is a common name for the investigational compound GW501516. It acts as a PPARδ agonist and is not approved for human use. It is prohibited in sport.