A practical reference on Prohibited list: what it is, how it behaves, what the literature reports, and where the honest uncertainties sit.
This page was last updated on 2026-01-19 and is reviewed periodically as new material appears.
Regulatory treatment varies, but cardarine is not approved as a medicine. Sports authorities list GW501516 as a prohibited substance, and it is banned at all times under the World Anti-Doping Agency code. Many countries restrict sales for human consumption, while online vendors market it as a research chemical. Such products may lack purity data, and their actual contents can differ from the label. Purchasing or possessing cardarine may carry legal consequences depending on jurisdiction. The compound is not a dietary supplement ingredient in regulated markets.
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.
GW501516 acts as an agonist at the peroxisome proliferator-activated receptor delta, a nuclear receptor that regulates gene expression. Activation shifts transcription toward genes involved in fatty acid uptake, oxidation, and energy expenditure. The compound does not bind the androgen receptor and therefore differs from anabolic steroids and SARMs. In rodent models, this metabolic shift has been linked to increased running endurance and reduced fat accumulation. The exact downstream pathways in humans remain incompletely characterized.
Early clinical research explored GW501516 for lipid disorders, obesity, and diabetes. Some short-term human studies reported changes in HDL cholesterol, LDL cholesterol, and triglycerides. The development program was discontinued after rodent studies showed dose-dependent tumor formation in multiple tissues, including liver, bladder, stomach, and skin. These findings raised concerns about long-term cancer risk in humans. Because human exposure data are limited, the clinical significance of the rodent tumors remains uncertain.
Literature on cardarine often separates receptor pharmacology from toxicology. Mechanistic papers describe PPARδ activation and gene expression changes, while safety assessments focus on carcinogenicity and species differences. Questions remain about whether rodent tumors arise through PPARδ-dependent or off-target mechanisms. Another open area is how human metabolism and exposure compare with those in animal studies. Analytical methods such as liquid chromatography–mass spectrometry are used to confirm identity in biological and product samples.
| Property | Value | Notes |
|---|---|---|
| Common synonyms | GW501516; GW-1516; endurobol | GW501516 is the research code |
| Drug class | PPARδ agonist | Not a selective androgen receptor modulator |
| Molecular formula | C21H18F3NO3S2 | Established chemical formula |
| Molar mass | 453.5 g/mol | Calculated from the formula |
| Regulatory status | Prohibited in sport; not approved as medicine | Status varies by country |
Stability of GW501516 depends on form, temperature, light exposure, and moisture. Solid reference material is typically stored frozen or refrigerated in a desiccator and protected from light. Solutions in organic solvents such as dimethyl sulfoxide are often kept frozen in aliquots to reduce freeze-thaw cycling. Aqueous solubility is low, so aqueous stock solutions can be difficult to prepare without cosolvents. Degradation may appear as changes in chromatographic purity or mass spectral signal. Stability studies are needed to establish shelf life for any specific preparation.
Quality assessment for cardarine samples usually combines identity, purity, and impurity testing. Nuclear magnetic resonance spectroscopy and mass spectrometry can confirm molecular structure, while high-performance liquid chromatography estimates purity. Certificates of analysis from testing laboratories may list these results, but they do not establish safety or legality. In the absence of approved manufacturing, products sold online may contain the wrong compound, variable amounts, or unlisted contaminants. Independent verification is therefore central to analytical work and to interpreting any reported biological activity.
Laboratory detection of GW501516 commonly uses liquid chromatography coupled with tandem mass spectrometry. The method can identify the parent compound or its metabolites in urine and blood after sample cleanup. Protein precipitation, solid-phase extraction, or enzymatic hydrolysis may precede analysis, depending on the matrix. Reference standards are required for accurate quantification and confirmation. Because the compound is not approved, testing often occurs in anti-doping, forensic, or research settings rather than routine clinical care. Results are reported with limits of detection and quantification.
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.
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.
=== Plant screening program === In 1955, the NCI in the United States set up the Cancer Chemotherapy National Service Center (CCNSC) to act as a public screening center for anticancer activity in compounds submitted by external institutions and companies. Although the majority of compounds screened were of synthetic origin, one chemist, Jonathan Hartwell, who was employed there from 1958 onwards, had experience with natural product derived compounds, and began a plant screening operation. After some years of informal arrangements, in July 1960, the NCI commissioned the United States Department of Agriculture (USDA) botanists to collect samples from about 1,000 plant species per year. On 21 August 1962, one of those botanists, Arthur S. Barclay, collected bark from a single Pacific yew tree in a forest north of the town of Packwood, Washington, as part of a four-month trip to collect material from over 200 different species. The material was then processed by a number of specialist CCNSC subcontractors, and one of the tree's samples was found to be cytotoxic in a cellular assay on 22 May 1964. Accordingly, in late 1964 or early 1965, the fractionation and isolation laboratory run by Monroe E. Wall in Research Triangle Park, North Carolina, began work on fresh Taxus samples, isolating the active ingredient in September 1966 and announcing their findings at an April 1967 American Chemical Society meeting in Miami Beach. They named the pure compound taxol in June 1967. Wall and his colleague Wani published their results, including the chemical structure, in 1971.
=== Key companies and sectors === The UK is home to several globally significant AI organisations. Google DeepMind, headquartered in London, is one of the world's foremost AI research laboratories and is responsible for landmark achievements including AlphaFold, which computationally solved the protein folding problem. Other prominent UK-headquartered or UK-based AI companies include Darktrace (cybersecurity), Wayve (autonomous vehicles), Synthesia (AI video generation), Tractable (insurance and damage assessment), and Featurespace (fraud detection). The UK is also a significant base for major international AI companies, including OpenAI, Anthropic, Microsoft, and Meta, all of which maintain substantial UK AI operations.
=== Role in wound healing === The role of endothelial progenitor cells in wound healing remains unclear. Blood vessels have been seen entering ischemic tissue in a process driven by mechanically forced ingress of existing capillaries into the avascular region, and importantly, instead of through sprouting angiogenesis. These observations contradict sprouting angiogenesis driven by EPCs. Taken together with the inability to find bone-marrow derived endothelium in new vasculature, there is now little material support for postnatal vasculogenesis. Instead, angiogenesis is likely driven by a process of physical force.
Sources: en.wikipedia.org
=== Autoimmune disorders === People with type 1 diabetes are at an increased risk for developing several autoimmune disorders, particularly thyroid problems – around 20% of people with type 1 diabetes have hypothyroidism or hyperthyroidism, typically caused by Hashimoto thyroiditis or Graves' disease respectively. Celiac disease affects 2–8% of people with type 1 diabetes, and is more common in those who were younger at diabetes diagnosis, and in white people. Type 1 diabetics are also at increased risk of rheumatoid arthritis, lupus, autoimmune gastritis, pernicious anemia, vitiligo, and Addison's disease. Conversely, complex autoimmune syndromes caused by mutations in the immunity-related genes AIRE (causing autoimmune polyglandular syndrome), FoxP3 (causing IPEX syndrome), or STAT3 include type 1 diabetes in their effects.
The discovery of estrogen is usually credited to the American scientists Edgar Allen and Edward A. Doisy. In 1923, they observed that injection of fluid from porcine ovarian follicles produced pubertal- and estrus-type changes (including vaginal, uterine, and mammary gland changes and sexual receptivity) in sexually immature, ovariectomized mice and rats. These findings demonstrated the existence of a hormone which is produced by the ovaries and is involved in sexual maturation and reproduction. At the time of its discovery, Allen and Doisy did not name the hormone, and simply referred to it as an "ovarian hormone" or "follicular hormone"; others referred to it variously as feminin, folliculin, menformon, thelykinin, and emmenin. In 1926, Parkes and Bellerby coined the term estrin to describe the hormone on the basis of it inducing estrus in animals. Estrone was isolated and purified independently by Allen and Doisy and German scientist Adolf Butenandt in 1929, and estriol was isolated and purified by Marrian in 1930; they were the first estrogens to be identified. Estradiol, the most potent of the three major estrogens, was the last of the three to be identified. It was discovered by Schwenk and Hildebrant in 1933, who synthesized it via reduction of estrone. A few milligrams of estradiol was subsequently isolated and purified from 4 tons of sow ovaries by Doisy in 1935, with its chemical structure determined simultaneously, and was referred to variously as dihydrotheelin, dihydrofolliculin, dihydrofollicular hormone, and dihydroxyestrin.
=== Phase 2 === Aildenafil (methisosildenafil) – phosphodiesterase PDE5 inhibitor – erectile dysfunction [10] AN-788 (IP-2018; IP2018; NSD788; NSD-788) – serotonin–dopamine reuptake inhibitor (SDRI) – erectile dysfunction [11] Apomorphine intranasal (AL-101; intranasal apomorphine) – non-selective dopamine receptor agonist, other actions – erectile dysfunction, female sexual dysfunction [12] Autologous mesenchymal stem cell therapy (autologous bone marrow-derived mesenchymal stem cell therapy; Cellgram; Cellgram-ED; Cellgram-LC; Cerecellgram-spine; Hearticellgram-AMI; Immunocellgram; Impocellgram; Livercellgram; Lungcellgram; MSC-1; MSC-2) – cell replacement – erectile dysfunction [13] Botulinum toxin A (AboBoNT-A; AbobotulinumtoxinA; Alluzience; Azzalure; BoNT-A; BTX-A-HAC; BTX-A-HAC NG; Clostridium botulinum toxin type A haemagglutinin complex; Dysport; Dysport NG; Dysport RU; Dysport Solution; Dysport Next Generation; Reloxin) – acetylcholine release inhibitor and neuromuscular blocking agent – vulvodynia [14] Bupropion/trazodone (Lorexys; Orexa; S1P-104; S1P-205; SIP-104; trazodone/bupropion) – combination of bupropion (norepinephrine–dopamine reuptake inhibitor (NDRI), other actions) and trazodone (serotonin antagonist and reuptake inhibitor (SARI), various actions) – erectile dysfunction, female sexual dysfunction, male sexual dysfunction [15] Buspirone/testosterone (Lybridos; testosterone/buspirone) – combination of buspirone (serotonin 5-HT1A receptor agonist, other actions) and testosterone (androgen) – female sexual dysfunction [16] BZ-371A (PnPP-19) – nitric oxide stimulant – erectile dysfunction, female sexual dysfunction [17] Cligosiban (IX-01; PF-3274167) – oxytocin receptor antagonist – premature ejaculation [18] Estetrol (Donesta; E4) – estrogen (estrogen receptor agonist) – atrophic vaginitis, female sexual dysfunction [19] Estriol vaginal ring (VR-102; VR102; long-acting estriol vaginal ring) – estrogen (estrogen receptor agonist) – atrophic vaginitis [20] Fadanafil (XZP-5849) – phosphodiesterase PDE5 inhibitor – erectile dysfunction [21] FKW-00GA (FKW00GA; TGW-00AA; TGW00AA; TGWOOAA; TGW-OOAA) – serotonin 5-HT1A receptor agonist, serotonin 5-HT2A receptor antagonist – sexual function disorders [22] Onabotulinum toxin A (BoNTA; Botox; botulinum toxin A injectable; GSK-1358820; GSK1358820; OnabotA X; OnabotulinumtoxinA X; Vistabel; Vistabex) – acetylcholine release inhibitor and neuromuscular blocking agent – premature ejaculation [23] OPK-88004 (LY-2452473; TT701) – selective androgen receptor modulator (SARM) – erectile dysfunction [24] Pudafensine (IP2015; IP-2015) – serotonin–norepinephrine–dopamine reuptake inhibitor (SNDRI) – erectile dysfunction, vulvodynia, female sexual dysfunction [25] Sildenafil/testosterone (Lybrido; testosterone/sildenafil) – combination of sildenafil (phosphodiesterase PDE5 inhibitor) and testosterone (androgen) – female sexual dysfunction [26] Sildenafil topical – phosphodiesterase PDE5 inhibitor – female sexual dysfunction [27] Testosterone intranasal (low-dose) (MPP-14; Noseafix; TBS-2; Tefina) – androgen (androgen receptor agonist) – anorgasmia, decreased libido [28] TGFK-09SD (TGFK09SD) – serotonin 5-HT1A receptor agonist – female sexual dysfunction [29] Volufralin (LIB-01; LIB01; DIC-2024; DIC2024; Libiguin) – indirect melanocortin MC4 receptor potentiator – erectile dysfunction, premature ejaculation [30]
Coronary artery disease, leading to angina or myocardial infarction ("heart attack") Diabetic myonecrosis ('muscle wasting') Peripheral vascular disease, which contributes to intermittent claudication (exertion-related leg and foot pain) as well as diabetic foot. Stroke (mainly the ischemic type) Carotid artery stenosis does not occur more often in diabetes, and there appears to be a lower prevalence of abdominal aortic aneurysm. However, diabetes does cause higher morbidity, mortality and operative risks with these conditions. Diabetic foot, often due to a combination of sensory neuropathy (numbness or insensitivity) and vascular damage, increases rates of skin ulcers (diabetic foot ulcers) and infection and, in serious cases, necrosis and gangrene. It is why it takes longer for diabetics to heal from leg and foot wounds and why diabetics are prone to leg and foot infections. In the developed world it is the most common cause of non-traumatic adult amputation, usually of toes and/or feet. Female infertility is more common in women with diabetes type 1, despite modern treatment, also delayed puberty and menarche, menstrual irregularities (especially oligomenorrhoea), mild hyperandrogenism, polycystic ovarian syndrome, fewer live born children and possibly earlier menopause. Animal models indicate that on the molecular level diabetes causes defective leptin, insulin and kisspeptin signalling.
Sources: en.wikipedia.org
==== Flashbacks ==== Flashbacks (spontaneous recurrences of a previous psilocybin experience) can occur long after psilocybin use. Hallucinogen persisting perception disorder (HPPD) is characterized by a continual presence of visual disturbances similar to those generated by psychedelic substances. Neither flashbacks nor HPPD are commonly associated with psilocybin usage, and correlations between HPPD and psychedelics are further obscured by polydrug use and other variables.
== External links == The MEROPS online database for peptidases and their inhibitors: S01.233 Archived 2019-09-13 at the Wayback Machine Plasmin at the U.S. National Library of Medicine Medical Subject Headings (MeSH) This article incorporates text from the United States National Library of Medicine, which is in the public domain.
==== Energy policies ==== In his 2006 State of the Union Address, Bush declared, "America is addicted to oil" and launched his Advanced Energy Initiative to increase energy development research. In his 2007 State of the Union Address, Bush renewed his pledge to work toward diminished reliance on foreign oil by reducing fossil fuel consumption and increasing alternative fuel production. Amid high gasoline prices in 2008, Bush lifted a ban on offshore drilling. However, the move was largely symbolic because there was still a federal law banning offshore drilling. Bush said: "This means that the only thing standing between the American people and these vast oil reserves is action from the U.S. Congress." Bush had said in June 2008, "In the long run, the solution is to reduce demand for oil by promoting alternative energy technologies. My administration has worked with Congress to invest in gas-saving technologies like advanced batteries and hydrogen fuel cells ... In the short run, the American economy will continue to rely largely on oil. And that means we need to increase supply, especially here at home.
Sources: en.wikipedia.org
No. Cardarine is GW501516, a PPARδ agonist, while SARMs act on androgen receptors. The two classes are often grouped in informal discussions despite different mechanisms.
No. It has no approved medical indication in any country. Regulatory agencies have not cleared it for treatment or prevention of any condition.
Early clinical work stopped after rodent carcinogenicity findings. Those animal results raised concerns about long-term human risk, although direct human evidence is lacking. The human relevance of the tumors remains an open scientific question.
It targets PPARδ, a nuclear receptor involved in lipid and energy metabolism. It does not act primarily on androgen receptors. This distinction separates it from SARMs.