Searches for "cardarine", "cardarine UK legal" and "cardarine benefits" tend to come from people who have heard two things about the compound: that it was once studied as an "exercise mimetic", and that it was abandoned because it caused cancer in animals. Both are broadly true, and both need context. This guide explains what GW-501516 is, what the short human trials measured, what the animal studies found, why the pharmaceutical programme was stopped, and where the compound stands under UK, EU and US law and the WADA Prohibited List. It contains no guidance on use. Cardarine is sold on this site for laboratory research only.
What is cardarine?
Cardarine is the market name for GW-501516, also written GW501516 or GW1516 and sometimes called endurobol. It is a synthetic phenoxyacetic acid derivative discovered in a collaboration between Ligand Pharmaceuticals and GlaxoSmithKline in the 1990s. It is a selective agonist of peroxisome proliferator-activated receptor delta (PPAR-delta, also written PPAR-beta/delta), a nuclear receptor that regulates genes involved in fatty acid transport and oxidation, particularly in skeletal muscle.
Cardarine is frequently listed alongside SARMs and searched with them, but it is not a SARM. It does not bind the androgen receptor and has no anabolic mechanism. It is grouped with them commercially because it emerged on the same grey market at the same time. GSK took it through phase 1 and phase 2 trials for dyslipidaemia and metabolic syndrome, then discontinued it in 2007. It has never been approved as a medicine anywhere.
Mechanism of action
PPAR-delta is expressed at high levels in skeletal muscle, where it controls the expression of genes for fatty acid uptake and oxidation, including CPT1 and CD36. Activating it shifts muscle metabolism towards burning fat and, in mice, towards a more oxidative, slow-twitch fibre profile. The widely quoted 2008 paper from the Salk Institute reported that a PPAR-delta agonist combined with treadmill training synergistically increased oxidative muscle fibres and running endurance in adult mice (Narkar et al., 2008). A detail often lost in retelling: the finding that did not require training belonged to a different compound. It was the AMPK activator AICAR that, after four weeks, raised running endurance in sedentary mice by 44 per cent. The "exercise in a pill" label later attached to cardarine rests on a mouse result that was paired with exercise.
In human tissue, GW-501516 increased fatty acid oxidation and upregulated CPT1, CD36 and ABCA1 in cultured skeletal muscle cells (Sprecher et al., 2007). In a human kinetic study it increased the removal of VLDL particles by the liver and lowered the production of apoC-III, a protein that slows the clearance of triglyceride-rich particles (Ooi et al., 2011). These are the mechanisms behind the lipid changes seen in the trials.
What the research reports
Human trials
Three small trials form the entire published human dataset.
- Healthy volunteers, two weeks. Twenty-four hospitalised, sedentary volunteers received placebo or one of two doses of GW-501516 for two weeks (Sprecher et al., 2007). HDL cholesterol rose in both active groups while it fell in the placebo group; triglycerides trended downward and clearance of fat after a test meal improved. The authors called this the first report of a PPAR-delta agonist in man.
- Overweight men, two weeks. Eighteen moderately overweight men were randomised to GW-501516, a PPAR-alpha comparator or placebo for two weeks (Risérus et al., 2008). GW-501516 reduced fasting triglycerides by 30 per cent, apolipoprotein B by 26 per cent, LDL cholesterol by 23 per cent and insulin by 11 per cent, reduced liver fat by 20 per cent and urinary isoprostanes by 30 per cent, and increased skeletal muscle CPT1b expression. HDL was unchanged.
- Dyslipidaemic men, six weeks. Thirteen men with central obesity completed a randomised crossover trial with six-week periods (Ooi et al., 2011). GW-501516 lowered triglycerides, fatty acids and apoB, increased the clearance of VLDL, raised HDL cholesterol and apoA-II, and reduced cholesteryl ester transfer protein activity.
| Study | Participants | Design and length | Main measures |
|---|---|---|---|
| Sprecher et al., 2007 | 24 healthy sedentary volunteers | Placebo-controlled, two weeks in hospital | HDL cholesterol, triglycerides, fat clearance after a test meal |
| Risérus et al., 2008 | 18 moderately overweight men, 6 per group | Double-blind, three parallel groups, two weeks | Fasting lipids, insulin, liver fat, fat oxidation, muscle gene expression |
| Ooi et al., 2011 | 13 dyslipidaemic men with central obesity | Double-blind crossover, two six-week periods | Lipoprotein kinetics, apoC-III, HDL particles |
The limitations are severe. The longest exposure was six weeks, the largest group was 24 people, and none of the trials was designed to detect harm. None measured endurance, body composition or performance in people. The trials measured blood lipids, liver fat and markers of fat oxidation; they say nothing about long-term harm.
Animal carcinogenicity and the end of development
In 2007 GSK discontinued GW-501516. The developer's two-year carcinogenicity studies in rats and mice, later presented at a toxicology conference in 2009, reported tumours in multiple organs. That report exists as a conference abstract rather than a full peer-reviewed paper, so we do not cite it as a reference. A peer-reviewed 2014 review of the PPAR agonist field records that development of GW-501516 "has been abandoned because of safety issues" (Sahebkar et al., 2014). A biological rationale was already in the literature. In 2004, mice genetically predisposed to intestinal polyps that were given GW-501516 developed significantly more and larger polyps than untreated mice, with a fivefold increase in the number of polyps larger than 2 mm (Gupta et al., 2004). The authors concluded that PPAR-delta is involved in regulating intestinal adenoma growth. This is a model with a strong built-in cancer predisposition, so it does not show what happens in normal animals or in people, but it pointed in the same direction as the later toxicology findings. Whether the rodent findings translate to humans is unknown, because no human has been exposed for anything like two years under observation. That absence of data is itself the point.
What is not known
There is no human data on long-term exposure, no data in healthy young adults beyond two weeks, no controlled data on exercise performance, and no information at all about the content of grey-market "cardarine". In a 2017 analysis of 44 products sold online as SARMs, only 23 contained a SARM; 17 more contained another unapproved drug, GW-501516 among them, 4 contained no active compound, and only 18 matched their label for the amount of active ingredient (Van Wagoner et al., 2017). Grey-market labelling cannot be taken on trust. Nothing above is a claim about any product on this site. Products here are for laboratory research only and have not been tested for any effect in people.
Regulatory status
United Kingdom
Cardarine is not a licensed medicine; the MHRA has never granted it a marketing authorisation. It is not an authorised food supplement or novel food and may not be sold or marketed for consumption. It is not controlled under the Misuse of Drugs Act 1971. It is supplied as a research chemical to adults aged 18 and over, which is the only basis on which Free Muscle stocks it. The brands held are compared in the Cardarine collection.
European Union
No EU marketing authorisation or novel food authorisation exists. Buyers in EU countries are responsible for their own national import rules.
United States
The FDA has not approved GW-501516 for any use. It is not a lawful dietary supplement ingredient, and the FDA has issued warning letters to firms marketing products containing it.
WADA and sport
GW-501516 is prohibited at all times under section S4.4 of the WADA Prohibited List, metabolic modulators, which covers PPAR-delta agonists. WADA took the unusual step in 2013 of issuing a specific public warning about GW-501516, citing the developer's cancer findings. Detection is well established: a controlled excretion study found the sulfone metabolite of GW1516 detectable in urine by LC-MS/MS for up to 40 days after a single oral dose, while the parent compound was measurable only briefly (Sobolevsky et al., 2012). That figure comes from a single-dose excretion study; detection windows after other exposure patterns have not been established in the references cited here.
Common questions
Is cardarine legal in the UK?
Cardarine is not a controlled drug under the Misuse of Drugs Act 1971, so possession is not an offence under that Act. It is not a licensed medicine or an authorised food, so it cannot lawfully be sold for human consumption. Free Muscle supplies it for laboratory research only, to adults aged 18 and over. It is prohibited in sport at all times.
Is cardarine a SARM?
No. It is a PPAR-delta agonist. It has no action at the androgen receptor and no anabolic mechanism. It appears in SARM listings for commercial, not pharmacological, reasons.
Is cardarine a peptide?
No. It is a small synthetic molecule. See SARMs vs Peptides for how these categories differ.
Cardarine vs SR9009 (stenabolic)
Both are sold as metabolic research compounds and both are WADA-prohibited under S4.4. SR9009 is a REV-ERB agonist, acting on a different nuclear receptor involved in circadian regulation, and has no human trial data at all. Its very low oral bioavailability in animal studies is a major limitation. Cardarine has short human trials and a rodent cancer signal. See the SR9009 collection.
Cardarine and ostarine
The two are often searched together. Ostarine is an androgen receptor agonist with a substantial clinical programme; cardarine is a PPAR-delta agonist with an abandoned one. We do not publish guidance on combining compounds. See the Ostarine collection.
Cardarine benefits, dosage, results, before and after
We do not publish dosing, cycle or outcome guidance and we make no claims about what cardarine does in people. The three human trials measured lipid changes over two to six weeks in small groups under medical supervision; that is the whole of the evidence, and it sits next to the reason development ended.
Does cardarine cause cancer?
In two-year studies in rats and mice, the developer reported tumours in multiple organs, and development was abandoned on safety grounds. A separate mouse study found accelerated intestinal polyp growth. No long-term human data exist, so the risk in people is unknown rather than disproven.
How to verify a batch
A certificate of analysis for the specific batch should show identity (HPLC or LC-MS against a reference standard, confirming the compound is GW-501516), purity as a percentage, the measured content per unit against the stated strength, a batch number that matches the pack, a test date and the name of an independent laboratory. Purity without identity proves nothing; a generic brand PDF without a batch number is not a batch certificate.
Every Free Muscle-brand batch is assayed by Janoshik Analytical, and the certificate for your batch is sent on request by email. For other brands on Muscle Market, a certificate is shown only where the manufacturer supplies one for the batch held. Read How to Read a Certificate of Analysis, What Is Janoshik Analytical? and the lab tests page.
Related reading
- Cardarine (GW-501516) collection: every brand stocked, compared on strength per capsule and batch testing.
- SR9009 (Stenabolic) collection
- CUT collection and SARMs collection
- Ostarine (MK-2866) and Andarine (S-4) collections.
- What Are SARMs? The 2026 Research Guide
- Price per milligram: comparing listings honestly.
Cardarine is sold for laboratory research use only. It is not a licensed medicine, has not been evaluated by the MHRA, EMA or FDA, is not a food supplement and is not for human consumption. Products are supplied to adults aged 18 and over. Nothing on this page is medical advice or dosing, cycle or usage guidance. Summaries of published studies describe what researchers reported in their study populations and are not claims about any product.
References
- Narkar VA, et al. AMPK and PPARdelta agonists are exercise mimetics. Cell. 2008;134(3):405-415. PMID: 18674809.
- Sprecher DL, et al. Triglyceride:high-density lipoprotein cholesterol effects in healthy subjects administered a peroxisome proliferator activated receptor delta agonist. Arterioscler Thromb Vasc Biol. 2007;27(2):359-365. PMID: 17110604.
- Risérus U, et al. Activation of peroxisome proliferator-activated receptor (PPAR)delta promotes reversal of multiple metabolic abnormalities, reduces oxidative stress, and increases fatty acid oxidation in moderately obese men. Diabetes. 2008;57(2):332-339. PMID: 18024853.
- Ooi EM, et al. Mechanism of action of a peroxisome proliferator-activated receptor (PPAR)-delta agonist on lipoprotein metabolism in dyslipidemic subjects with central obesity. J Clin Endocrinol Metab. 2011;96(10):E1568-E1576. PMID: 21816786.
- Sahebkar A, et al. New peroxisome proliferator-activated receptor agonists: potential treatments for atherogenic dyslipidemia and non-alcoholic fatty liver disease. Expert Opin Pharmacother. 2014;15(4):493-503. PMID: 24428677.
- Sobolevsky T, et al. Detection of PPARδ agonists GW1516 and GW0742 and their metabolites in human urine. Drug Test Anal. 2012;4(10):754-760. PMID: 22977012.
- Van Wagoner RM, et al. Chemical Composition and Labeling of Substances Marketed as Selective Androgen Receptor Modulators and Sold via the Internet. JAMA. 2017;318(20):2004-2010. PMID: 29183075.
- Gupta RA, et al. Activation of nuclear hormone receptor peroxisome proliferator-activated receptor-delta accelerates intestinal adenoma growth. Nat Med. 2004;10(3):245-247. PMID: 14758356.