If you have been reading about PPARδ agonist 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.
Last reviewed on 2026-02-13. Where a claim depends on a specific study, the study is described rather than over-claimed.
Laboratory studies have examined GW501516 in cell cultures and rodents for conditions such as dyslipidemia, insulin resistance, and obesity. Some trials in humans were initiated, but development was discontinued after preclinical findings raised concerns about cancer in certain models. Those findings do not prove that the compound causes cancer in people, but they contributed to regulatory caution. Later reviews often describe the evidence as preliminary and insufficient for assessing long-term safety.
In the fitness and bodybuilding literature, cardarine is frequently discussed as an endurance agent or fat-loss compound, although such claims are not supported by robust clinical evidence. Online descriptions often mix animal data, user anecdotes, and marketing language. Researchers who study PPARδ agonists distinguish between receptor activation in controlled experiments and unsupervised use of unverified products. The latter introduces unknown purity, dose, and interactions, making reported experiences difficult to interpret scientifically.
GW501516 acts as an agonist at peroxisome proliferator-activated receptor delta, a nuclear receptor involved in transcription of genes related to lipid handling and energy use. Activation of PPARδ can shift skeletal muscle toward greater fatty acid oxidation in animal models, which is one reason it drew interest for metabolic disease and exercise research. The exact downstream effects depend on tissue, species, dose, and duration. Human data are sparse, so many proposed benefits remain hypotheses rather than established clinical outcomes.
Safety discussions about cardarine frequently cite rodent carcinogenicity findings reported in the 2000s. In those studies, treated animals developed tumors at multiple sites, leading sponsors to discontinue clinical development. The relevance of these findings to humans has not been resolved, but they are a major reason the compound is not approved. Current literature emphasizes uncertainty about long-term effects and the risks of unregulated use. Regulators and health agencies have not established a safe human exposure level.
Cardarine is a synthetic compound also known as GW501516, GW-501516, and sometimes endurobol. It was developed as a selective agonist of peroxisome proliferator-activated receptor delta, a nuclear receptor involved in fatty acid oxidation and energy metabolism. The compound was studied in preclinical models for metabolic and cardiovascular conditions, but it did not become a marketed human medicine. In regulatory and anti-doping contexts, it is treated as a prohibited substance rather than a licensed medicine.
| Property | Value | Notes |
|---|---|---|
| Solubility | Soluble in dimethyl sulfoxide and some organic solvents; practically insoluble in water | Solvent choice affects laboratory handling |
| Typical storage | -20 °C, desiccated, protected from light | Common condition for research samples |
| Analytical method | Liquid chromatography–tandem mass spectrometry (LC-MS/MS) | Used for identification and quantification in biological or product samples |
| Common synonyms | GW501516, GW-501516, GSK-516, Endurobol | Names found in research and anti-doping literature |
| Regulatory status | Unapproved therapeutic; prohibited in competitive sport | Status can vary by country and context |
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.
Sporting authorities added GW501516 to prohibited lists after it appeared in athlete samples and online markets. The World Anti-Doping Agency classifies it as a hormone and metabolic modulator, and its use can lead to an anti-doping rule violation. Some early laboratory work suggested effects on fatty acid oxidation and endurance-related metabolism in animals, but those findings do not establish safe or effective use in people. Reports of adverse events in humans are scarce and often anecdotal, which complicates risk assessment.
Legal status varies by country. In some places, cardarine is controlled under medicines or psychoactive substances laws; in others, it may be sold with minimal oversight as a research chemical. Customs agencies have intercepted shipments, and several national health agencies have issued warnings about products marketed for bodybuilding or performance enhancement. The lack of a standardized pharmaceutical supply means identity, purity, and contamination levels can differ widely between samples. These factors make cardarine a regulatory and public health concern rather than a conventional prescription drug.
Cardarine is a common name for GW501516, a synthetic compound first described in the 1990s as a selective agonist of the peroxisome proliferator-activated receptor delta. It was studied in preclinical models for metabolic and cardiovascular conditions, but it has not been approved as a medicine in the United States, Europe, or other major jurisdictions. Retail products labeled as cardarine are generally research chemicals or supplements, not pharmaceutical formulations. Because human safety and efficacy data remain limited, regulatory agencies treat it as an unapproved substance rather than a therapeutic product.
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.
Cardarine is explicitly prohibited by the World Anti-Doping Agency under the class of PPARδ agonists. Its presence in urine or blood samples can be detected using mass spectrometry-based methods, often liquid chromatography-tandem mass spectrometry. Athletes who test positive may face sanctions, including bans from competition. The compound is also regulated as a prescription-only or unapproved drug in many countries. Enforcement varies by jurisdiction, and some regions treat it as a controlled substance. Online sales may occur despite these restrictions, creating quality and legal risks.
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.
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.
Everyone always asks if that is Demri Parrott on the Dirt Cover. I think Demri's name might have been mentioned as a possible model once or twice, but it was never a serious consideration. In an interview with the Canadian magazine M.E.A.T. in December 1992, Layne Staley said about the cover:
== Production == Phage display libraries of 109 randomized sequences are used to screen for Affimer proteins that exhibit high-specificity binding to the target protein with binding affinities in the nM range. The ability to direct in vitro screening techniques allows the identification of specific, high affinity Affimers. In vitro screening and development also mean that the target space for Affimers is not limited by the animal immune system. Affimers are generated using recombinant systems, so their generation is more rapid and reproducible compared to the production of polyclonal antibodies. Multimeric forms Affimers have been generated and shown to yield titres in the range of 200–400 mg/L under small-scale culture using bacterial host systems. Multimeric forms of Affimers with the same target specificity provide avidity effects in target binding. Many different tags and fusion proteins, such as fluorophores, single-stranded DNA, His, and c-Myc tags can be conjugated to Affimers. Specific cysteine residues can be introduced to the protein to allow thiol chemistry to uniformly orient Affimers on a solid support eg ELISA plates. This flexible functionalisation of the Affimer molecule allows functionality across multiple applications and assay formats.
===== Primary pathogens ===== Primary pathogens cause disease as a result of their presence or activity within the normal, healthy host, and their intrinsic virulence (the severity of the disease they cause) is, in part, a necessary consequence of their need to reproduce and spread. Many of the most common primary pathogens of humans only infect humans, however, many serious diseases are caused by organisms acquired from the environment or that infect non-human hosts.
In Nova Kakhovka, 900 people were evacuated, 600 houses were reported to have been flooded and a state of emergency was declared by Russian authorities as water levels rose to over 11 meters (36 feet). The city's Kazkova Dibrova zoo lost all its 300 animals in the floods, while the town of Oleshky was reported to have been heavily flooded. Seven people were reported missing in Nova Kakhovka, while about 100 residents were reported to have been trapped. Thousands of animals were reported to have been killed in the Nizhnedniprovsky National Nature Park. At least eight people were reported to have died due to the resulting floods, while about 600 square kilometres (230 square miles) of the region was underwater, 68 percent of which was on the Russian-controlled side. Over the following days, the death toll rose to a total of 58.
== History == Heparin was discovered by Jay McLean and William Henry Howell in 1916, although it did not enter clinical trials until 1935. It was originally isolated from dog liver cells, hence its name (ἧπαρ hēpar is Greek for 'liver'; hepar + -in). McLean was a second-year medical student at Johns Hopkins University, and was working under the guidance of Howell investigating pro-coagulant preparations when he isolated a fat-soluble phosphatide anticoagulant in canine liver tissue. In 1918, Howell coined the term 'heparin' for this type of fat-soluble anticoagulant. In the early 1920s, Howell isolated a water-soluble polysaccharide anticoagulant, which he also termed 'heparin', although it was different from the previously discovered phosphatide preparations. McLean's work as a surgeon probably changed the focus of the Howell group to look for anticoagulants, which eventually led to the polysaccharide discovery. It had at first been accepted that it was Howell who discovered heparin. However, in the 1940s, Jay McLean became unhappy that he had not received appropriate recognition for what he saw as his discovery. Though relatively discreet about his claim and not wanting to upset his former chief, he gave lectures and wrote letters claiming that the discovery was his. This gradually became accepted as fact, and indeed after he died in 1959, his obituary credited him as being the true discoverer of heparin.
Sources: en.wikipedia.org
== Novel antidepressant == Arketamine appears to be more effective as a rapid-acting antidepressant than esketamine in preclinical research. In rodent studies, esketamine produced hyperlocomotion, prepulse inhibition deficits, and rewarding effects, while arketamine did not, in accordance with its lower potency as an NMDA receptor antagonist and dopamine reuptake inhibitor. As such, arketamine may have a lower propensity for producing psychotomimetic effects and a lower abuse potential in addition to superior antidepressant efficacy. A study conducted in mice found that ketamine's antidepressant activity is not caused by ketamine inhibiting NMDAR, but rather by sustained activation of a different glutamate receptor, the AMPA receptor, by a metabolite, (2R,6R)-hydroxynorketamine; as of 2017 it was unknown if this was happening in humans. Arketamine is an AMPA receptor agonist. Paradoxically, arketamine shows greater and longer-lasting rapid antidepressant effects in animal models of depression relative to esketamine. It has been suggested that this may be due to the possibility of different activities of arketamine and esketamine and their respective metabolites at the α7-nicotinic receptor, as norketamine and hydroxynorketamine are potent antagonists of this receptor and markers of potential rapid antidepressant effects (specifically, increased mammalian target of rapamycin function) correlate closely with their affinity for it. The picture is unclear however, and other mechanisms have also been implicated.
Selegiline has been limitedly studied in large animals like horses and its dosage in these animals has not been established. In preliminary research, a dose of selegiline of 30 mg orally or intravenously in horses had no observable effects on behavior or locomotor activity. The doses of selegiline used in animals are described as extremely high relative to those used in humans (which are ~0.1 mg/kg body weight).
=== Agronomy study === After the initial sowing into seed beds, seedlings at 3 days old can be transplanted into pots. Seedlings typically reach 20-25 centimetres tall after 20 weeks in the nursery, at which point they can be planted out into the field; direct sowing is possible, but its viability largely depends on soil moisture and the degree of insect/rodent threats. Preliminary ploughing "contributes to proper establishment of seedlings in the field with a success rate of 82% four years" in some cases after planting. Seeds can be treated with concentrated sulphuric acid "in a concentration of 97% for 10 minutes and then immersed in water for 24 hours to break their dormancy period." Seedlings grow comparatively fast – they can reach a height of 1 metre in just 1 year. They will begin to flower at 5–7 years during the dry season in the Sahel (December to April), while occurring slightly earlier in less dry regions. The tree is pollinated primarily by bats, but can also occur by way of "honeybees, flies, wasps, ants, tenebrionid beetles and tettigometid bugs." Fruiting can occur at anywhere from 5–10 years, and they will start to ripen just before the first rains and continue over most of the season. Foliage of locust bean has been found to contribute to soil fertility improvement. In one experiment, the isolated relative effect of locust bean in the third year of the experiment was 86%, compared to 138% for neem, a related tree.
The Amitāyurdhyāna Sūtra mentions that Vaidehi had, on listening to the teaching in this sutra, attained "great awakening with clarity of mind and reached the insight into the non-arising of all dharmas." Similarly, the Vimalakirti sutra mentions various bodhisattvas (including Vimalakirti) that have attained "the forbearance of the nonarising of dharmas." The Lotus Sutra states that when the "thought of the highest path" arises in sentient beings "they will become convinced of the nonarising of all dharmas and reside in the stage of non-retrogression." The Samdhinirmochana Sutra's chapter 7 mentions a teaching which states: "All phenomena are without an essence, unborn, unceasing, primordially in the state of peace, and naturally in the state of nirvāṇa." However, it states that this teaching is that of the "discourses of provisional meaning", and that it should be taught along with the teachings of the third turning of the wheel of Dharma. Similarly, the Lankavatara sutra explains the doctrine of the unborn and unoriginated nature of dharmas through the idealistic philosophy of mind-only. Since all things are illusory manifestations of the mind, they do not really originate or arise.
TGOT, also known as [Thr4,Gly7]-oxytocin, is a synthetic peptide oxytocin receptor agonist which is widely used in scientific research. It is a potent and selective agonist of the oxytocin receptor. The drug has very high affinity and selectivity for the oxytocin receptor in rodents but the same is not true in humans, and hence it shows no advantage over oxytocin in humans. TGOT has been found to partially reverse the adverse behavioral changes caused by social isolation in rodents, for instance social avoidance and aggression. It shows partially dissociable effects from those of oxytocin in rodents, which may be related to comparative selectivity against vasopressin receptors. TGOT was first described in the scientific literature by 1977. TGOT, or [Thr4,Gly7]-oxytocin, should not be confused with triglycyl-oxytocin, which is also known by the acronym TGOT but is a different peptide oxytocin analogue that is far less-known in comparison.
Sources: en.wikipedia.org
It binds and activates PPARδ, a nuclear receptor that influences gene expression related to fatty acid metabolism and energy balance. This mechanism has been studied mainly in animals and cell models, not established as a safe human therapy.
No. It is not an anabolic-androgenic steroid; it is a synthetic PPARδ agonist. Because it is banned in sport, it is sometimes grouped with doping agents even though its chemical class differs from steroids.
Human data are limited and development was discontinued, so major effects and long-term risks are not well characterized. Some early studies examined metabolic markers, but they do not provide a basis for unsupervised use.
Cardarine is an investigational synthetic compound that acts as a PPARδ agonist. It is also known as GW501516 and has been studied mainly in preclinical research. It is not an approved medicine.