PPAR delta is one of those subjects where the details matter more than the headlines. This page pulls together the background, the mechanisms, and the practical points readers ask about most.
Last reviewed on 2026-04-21. 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.
Laboratory studies indicate that GW501516 activates PPARδ, a nuclear receptor involved in fatty acid oxidation and energy metabolism. In rodent experiments, treated animals often showed increased endurance and reduced fat mass. These effects were observed under controlled conditions and do not establish safe or effective use in humans. The exact dose-response relationship in humans remains poorly characterized. Species differences in metabolism can affect how results translate across animals and people.
Safety concerns emerged from long-term animal studies. In rodents given the compound for extended periods, researchers found an increased incidence of certain cancers, including liver and bladder tumors. These findings contributed to the discontinuation of clinical development. Whether similar risks apply to short-term or low-level exposure in humans is not established, and controlled human safety data are limited. The relevance of high-dose rodent carcinogenicity findings to human use remains a subject of debate.
Human trials of GW501516 were small and short in duration. They examined lipid levels, glucose handling, and other metabolic markers, but the programs were halted after the animal cancer findings. No approved therapeutic product exists, and published human data are insufficient for establishing long-term safety. Reports of use for athletic performance come mainly from non-clinical settings and cannot be verified through controlled trials. Independent testing of products sold as cardarine has found inconsistent purity and labeling.
| 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. |
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.
Laboratory detection of cardarine typically involves sample preparation followed by chromatographic separation and mass spectrometric identification. Urine is the most common matrix for anti-doping tests, though blood and hair have also been explored. Methods can target the parent compound or its metabolites, depending on the expected window of detection. Reference standards are required for accurate quantification. Matrix effects and dilution can influence results, so laboratories use internal standards and validation protocols. The exact detection window varies with dose, route, and individual metabolism.
A common misconception is that cardarine has been proven safe for human use. In reality, human clinical data are limited, and long-term animal studies have raised concerns about cancer. Another misconception is that it is a supplement or vitamin-like compound. It is a synthetic research chemical with no approved medical indication. Scientific discussion often focuses on its mechanism and detection rather than therapeutic use. Regulatory and anti-doping literature treats it primarily as a prohibited substance.
=== Styrene-butane co-polymers === Styrene-butane co-polymers can be produced with a low butene content. Styrene-butane co-polymers include PS-I and SBC (see below), both co-polymers are impact resistant. PS-I is prepared by graft co-polymerization, SBC by anionic block co-polymerization, which makes it transparent in case of appropriate block size. If styrene-butane co-polymer has a high butylene content, styrene-butadiene rubber (SBR) is formed. The impact strength of styrene-butadiene co-polymers is based on phase separation, polystyrene and poly-butane are not soluble in each other (see Flory–Huggins solution theory). Co-polymerization creates a boundary layer without complete mixing. The butadiene fractions (the "rubber phase") assemble to form particles embedded in a polystyrene matrix. A decisive factor for the improved impact strength of styrene-butadiene copolymers is their higher absorption capacity for deformation work. Without applied force, the rubber phase initially behaves like a filler. Under tensile stress, crazes (microcracks) are formed, which spread to the rubber particles. The energy of the propagating crack is then transferred to the rubber particles along its path. A large number of cracks give the originally rigid material a laminated structure. The formation of each lamella contributes to the consumption of energy and thus to an increase in elongation at break. Polystyrene homo-polymers deform when a force is applied until they break.
==== Elimination ==== Pregabalin is eliminated by the kidneys in the urine, mainly in its unchanged form. It has a relatively short elimination half-life, with a reported value of 6.3 hours. Because of its short elimination half-life, pregabalin is administered 2 to 3 times per day to maintain therapeutic levels. The kidney clearance of pregabalin is 73 mL/minute. As pregabalin clearance is directly proportional to creatinine clearance, renal impairment leads to drug accumulation and elevated plasma concentrations. Dose adjustment is therefore required in patients with a creatinine clearance below 60 mL/min, with progressively greater reductions recommended as renal function declines. Patients undergoing hemodialysis require supplemental dosing following each session, as a standard four-hour treatment reduces plasma pregabalin concentrations by approximately 50%.
In June 2020, HHS announced an unusual agreement with Gilead in which HHS agreed to Gilead's wholesale acquisition price, HHS would continue to work together with state governments and drug wholesaler AmerisourceBergen to allocate shipments of remdesivir vials to American hospitals through the end of September 2020, and in exchange, during that three-month timeframe (July, August, and September), American patients would be allocated over 90% of Gilead's projected remdesivir output of more than 500,000 treatment courses. Absent from these announcements was any discussion of allocation of remdesivir production to the approximately 70 countries omitted from Gilead's generic drug licensing agreements—including much of Europe and countries as populous as Brazil, China, and Mexico—or the 127 countries listed on those agreements (during the time it will take for Gilead's generic licensees to ramp up their own production). As the implications of this began to sink in, several countries publicly confirmed the next day that they already had adequate supplies of remdesivir to cover current needs, including Australia, Germany, and the United Kingdom. In August 2020, the FDA broadened the Emergency Use Authorization (EUA) for remdesivir to include all hospitalized patients with suspected or laboratory-confirmed COVID‑19, irrespective of the severity of their disease. The Fact Sheet was updated to reflect the new guidance.
Sources: en.wikipedia.org
Several methods have been used to determine the mechanisms of antimicrobial peptide activity. In particular, solid-state NMR studies have provided an atomic-level resolution explanation of membrane disruption by antimicrobial peptides. In more recent years, X-ray crystallography has been used to delineate in atomic detail how the family of plant defensins rupture membranes by identifying key phospholipids in the cell membranes of the pathogen. Human defensins have been thought to act through a similar mechanism, targeting cell membrane lipids as part of their function. In fact human beta-defensin 2 have now been shown to kill the pathogenic fungi Candida albicans through interactions with specific phospholipids. From the computational point of view, Molecular Dynamics simulations can provide detailed information about the structure and dynamics of the peptide-membrane interactions, including the orientation, conformation, and insertion of the peptide in the membrane, as well as specific peptide interactions with lipids, ions and solvent.
== Overdose == Acute overdosage is often manifested by emesis, lethargy, ataxia, tachycardia and seizures. Plasma, serum or blood concentrations of sertraline and norsertraline, its major active metabolite, may be measured to confirm a diagnosis of poisoning in hospitalized patients or to aid in the medicolegal investigation of fatalities. As with most other SSRIs its toxicity in overdose is considered relatively low.
=== United Kingdom === From 2013, the UK National Health Service (NHS) started offering shingles vaccination to elderly people. People aged either 70 or 79 on 1 September 2013, were offered the vaccine. People aged 71 to 78 on that date would only have an opportunity to have the shingles vaccine after reaching the age of 79. The original intention was for people aged between 70 and 79 to be vaccinated, but the NHS later said that the vaccination program was being staggered as it would be impractical to vaccinate everyone in their 70s in a single year. In 2021, vaccination against shingles is available on the NHS to people aged 70 to 79. Vaccination is with single-dose Zostavax, except for people for whom Zostavax is deemed unsuitable, for example, with a condition that affects the immune system, for whom two-dose Shingrix vaccine is recommended. The NHS stated "The shingles vaccine is not available on the NHS to anyone aged 80 or over because it seems to be less effective in this age group". Since 2023, the shingles vaccines is being offered to healthy people turning 65.
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.
Rodent studies reported increased endurance and fat oxidation after GW501516 exposure. Long-term studies also found higher rates of some tumors, which led to halted development.