Cardarine is a common name for GW501516 (also written GW1516). It is an experimental oral drug that activates PPARδ (peroxisome proliferator-activated receptor delta), a nuclear receptor that controls how cells burn fat. GlaxoSmithKline (GSK) first reported it in 2001 and tested it as a possible treatment for low HDL cholesterol and other features of the metabolic syndrome.
Cardarine is often grouped with SARMs, but it does not act on the androgen receptor and is not a hormone. The most important fact about it: development was abandoned because of safety issues, after animal studies showed carcinogenic effects (Sahebkar et al., Expert Opin Pharmacother 2014; Breuer et al., Forensic Toxicol 2024). It was never approved as a medicine, and its “endurance” reputation rests on mouse studies.
This page summarizes what the published human trials, animal studies and anti-doping authorities report. It is for education only and is not medical advice.
| Property | Detail |
|---|---|
| Drug class | Selective PPARδ agonist (not a SARM, not a steroid) |
| Other names | GW501516, GW1516, cardarine |
| Developer | GlaxoSmithKline; development abandoned |
| Route | Oral, once daily in trials |
| Doses studied in humans | 2.5, 5 and 10 mg/day for 2–12 weeks |
| Half-life | No peer-reviewed human value located |
| Detection in urine | Sulfone metabolite detectable up to 40 days after a single 15 mg dose |
| US status | Never approved by FDA or any other regulator |
| WADA status | Prohibited at all times (class S4.4.1, metabolic modulators); non-specified |
What it is
GW501516’s chemical name is 2-[2-methyl-4-[[4-methyl-2-[4-(trifluoromethyl)phenyl]-1,3-thiazol-5-yl]methylsulfanyl]phenoxy]acetic acid: formula C₂₁H₁₈F₃NO₃S₂, molecular weight 453.5 g/mol (PubChem). It has no steroid structure.
PPARs are nuclear receptors that act as sensors of dietary fats and switch on genes for fat and sugar metabolism. There are three subtypes, and two of them are already drug targets (Oliver et al., PNAS 2001):
| Subtype | Existing drugs | Main use |
|---|---|---|
| PPARα | Fibrates | Lowering triglycerides |
| PPARγ | Glitazones | Type 2 diabetes |
| PPARδ | None in 2001; selective ligands were lacking | Experimental |
GSK scientists used combinatorial chemistry and structure-based design to make GW501516 as a potent, subtype-selective PPARδ agonist (Oliver et al., 2001). In cell culture, it raised expression of ABCA1, a transporter that moves cholesterol out of cells toward HDL. In insulin-resistant, obese, middle-aged rhesus monkeys, it caused a dose-dependent rise in HDL cholesterol and lowered small dense LDL, fasting triglycerides and fasting insulin.
In human skeletal muscle cells, GW501516 increased fatty acid oxidation and the expression of fat-handling genes such as CPT1 and CD36 (Sprecher et al., ATVB 2007). Muscle biopsies from treated volunteers also showed higher CPT1b, an enzyme that carries fatty acids into mitochondria to be burned (Risérus et al., Diabetes 2008). This shift toward burning fat in muscle is the proposed basis for both its lipid effects and its endurance reputation.
How it works in the body
Human pharmacokinetic data are not published in any detail. We could not find a peer-reviewed human half-life, so we do not give one. Clinical trials used once-daily dosing.
What is documented comes mostly from anti-doping research:
| Finding | Detail | Source |
|---|---|---|
| Main metabolic route | Oxidation of the sulfur atom to a sulfoxide and then a sulfone (shown with human liver microsomes) | Thevis et al., 2010 |
| Unchanged drug in urine | Measurable only for a short time and at low ng/mL levels | Sobolevsky et al., 2012 |
| Best urine marker | Sulfone metabolite, detectable up to 40 days after a single 15 mg oral dose | Sobolevsky et al., 2012 |
| Seminal fluid | GW1516 and its metabolites were measured in human ejaculate | Breuer et al., 2024 |
Regulatory status
- Never approved. GW501516 reached phase 2 lipid trials, but its development was abandoned because of safety issues (Sahebkar et al., 2014). Clinical trials were discontinued when animal studies showed carcinogenic effects, and it is not available anywhere as an approved drug (Breuer et al., 2024).
- Registered trials. ClinicalTrials.gov lists three completed GW501516 studies, all started in 2003–2004: a GSK trial in people with low HDL, a GSK study of body fat and inflammation, and a University of Western Australia lipoprotein study (ClinicalTrials.gov).
- Sport. WADA first listed GW1516 in 2009 (Pokrywka et al., J Physiol Pharmacol 2014). The 2026 Prohibited List names it as an example of a PPARδ agonist under S4.4.1, metabolic modulators. Class S4 is banned in and out of competition, and S4.4 substances are “non-specified” (WADA 2026 List, official Austrian publication). A 2024 report counted 139 adverse analytical findings (positive tests) involving GW1516 reported to WADA since 2009, with a peak of 31 in 2016 (Breuer et al., 2024).
What the research shows
All controlled human data come from four small, short studies of blood lipids and metabolism. No human trial has tested GW501516 for endurance, athletic performance, muscle or fat loss in healthy, active people.
Blood lipids and metabolism in humans
| Study | Design and participants | Dose and duration | Main results |
|---|---|---|---|
| Sprecher et al., 2007 | Healthy volunteers, hospitalized and sedentary; placebo n=6, 2.5 mg n=9, 10 mg n=9 | 2.5 or 10 mg/day, 2 weeks | HDL rose with both doses vs a fall of 11.5% on placebo (p = 0.004 and p under 0.001). Triglycerides trended down (p = 0.08); triglyceride clearance after a fat meal improved (p = 0.02). |
| Risérus et al., 2008 | Randomized, double-blind, three parallel groups of 6 moderately overweight men (GW501516, a PPARα agonist, placebo) | 10 mg/day, 2 weeks | Triglycerides −30%, apoB −26%, LDL −23%, insulin −11%, liver fat −20%, urinary isoprostanes (an oxidative stress marker) −30%. HDL unchanged. More meal fat burned to CO₂. |
| Ooi et al., 2011 | Randomized, double-blind crossover; 13 dyslipidemic men with central obesity | 2.5 mg/day, 6 weeks per period | Lower triglycerides, apoB-100 and apoB-48; higher HDL. The liver cleared VLDL particles faster. |
| Olson et al., 2012 | 268 patients with HDL under 1.16 mmol/L; placebo-controlled | 2.5, 5 or 10 mg/day, 12 weeks | See table below |
The largest trial, by Olson and colleagues, reported these best changes from baseline across the dose groups (Olson et al., ATVB 2012):
| Measure | Change |
|---|---|
| HDL cholesterol | Up to +16.9% (10 mg) |
| Apolipoprotein A-I | Up to +6.6% |
| LDL cholesterol | −7.3% |
| Triglycerides | −16.9% |
| Apolipoprotein B | −14.9% |
| Free fatty acids | −19.4% |
A second, exploratory study in 37 similar patients found fewer VLDL (−19%), IDL (−52%) and LDL (−14%) particles, and 10% more HDL particles. These are surrogate markers. No trial tested whether GW501516 prevents heart attacks or strokes, and the longest exposure in these published trials was 12 weeks.
A GSK study of adiposity and inflammation in overweight and obese people (10 mg/day for 12 weeks, 71 enrolled) is listed as completed, but no results are posted on the registry (ClinicalTrials.gov NCT00388180).
Endurance (animal studies only)
The endurance reputation comes from mice:
- Genetically engineered mice. Mice built to express a permanently active form of PPARδ in muscle had more type I (slow, fatigue-resistant) fibers and could run up to twice as far as normal littermates. Giving normal mice a PPARδ agonist produced a similar type I fiber gene pattern (Wang et al., PLoS Biol 2004).
- Drug alone did not work. In sedentary mice, GW1516 at 5 mg/kg/day for 4 weeks switched on muscle fat-burning genes but did not change treadmill endurance. Treatment for up to 5 months also had no effect (Narkar et al., Cell 2008).
- Drug plus training did. In mice that also trained on a treadmill for 4 weeks, the same dose increased running time by 68% and running distance by 70% compared with trained mice given vehicle (Narkar et al., 2008).
About “exercise in a pill.” Cardarine is often described as giving endurance without training. In the mouse study behind that idea, GW1516 alone did not improve running at all; the endurance gain appeared only when it was combined with exercise. It was AICAR, a different drug, that improved running in sedentary mice. None of this has been tested in people.
Fat loss
No published human trial has reported a fat-loss result. The human studies measured blood lipids, liver fat and how much dietary fat was burned. The 20% fall in liver fat over 2 weeks in six men is the closest finding (Risérus et al., 2008).
Side effects and risks
Cancer signals in animals
The key safety issue is cancer in animal studies. Reviews state that development was abandoned for safety reasons and that trials stopped when animal studies showed carcinogenic effects (Sahebkar et al., 2014; Breuer et al., 2024). We could not locate a peer-reviewed report of the full rodent carcinogenicity studies, so we do not list the tumor types, doses or rates.
Separate published work shows a related signal. In Apc-min mice, which are genetically prone to intestinal polyps, GW501516 increased the number and size of polyps, with a fivefold rise in polyps larger than 2 mm (Gupta et al., Nat Med 2004). These are animal results. They do not show what happens in people, but no study has followed humans long enough to rule out a cancer risk.
Unknown long-term human safety
The human trials lasted 2–12 weeks and involved a few hundred people in total. The published abstracts focus on lipid outcomes. There are no long-term human safety data at any dose.
Product quality
Because it is not an approved drug, cardarine sold online has no quality control. In a JAMA analysis of 44 products sold online as SARMs, 17 (39%) contained another unapproved drug, including GW501516, ibutamoren or SR9009. Only 41% of products contained the labeled amount of the active compound, and 25% contained substances not on the label (Van Wagoner et al., JAMA 2017).
Athletes
GW1516 is prohibited at all times (WADA 2026 List), and it has no minimum reporting level, so any detected amount counts as a positive test (Breuer et al., 2024). Its sulfone metabolite can be detected for weeks after a single dose (Sobolevsky et al., 2012). In one documented case, a female athlete’s positive test was judged plausibly caused by her partner’s semen after unprotected intercourse (Breuer et al., 2024).
Key takeaways
- A PPARδ agonist, not a SARM. GW501516 switches on fat-burning genes through a nuclear receptor and has no androgen or steroid activity.
- Abandoned for safety reasons. GSK stopped development after animal studies showed carcinogenic effects, and it was never approved anywhere.
- Human data are lipid studies only. Four short trials (2–12 weeks, 2.5–10 mg/day) showed higher HDL and lower triglycerides, LDL and apoB.
- The endurance claim is from mice. The drug alone did not improve running in sedentary mice; it improved endurance only when combined with training, and this has never been tested in people.
- Banned in sport and long detectable. WADA prohibits it at all times, and a metabolite can be found in urine up to 40 days after one 15 mg dose.
- Products are unreliable. Online “research” products are often mislabeled or contain other unapproved drugs.
Sources
- Oliver WR Jr, Shenk JL, Snaith MR, et al. A selective peroxisome proliferator-activated receptor delta agonist promotes reverse cholesterol transport. Proc Natl Acad Sci U S A. 2001;98(9):5306–5311. PubMed.
- Sprecher DL, Massien C, Pearce G, 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. PubMed.
- Risérus U, Sprecher D, Johnson T, 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. PubMed.
- Ooi EM, Watts GF, Sprecher DL, 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. PubMed.
- Olson EJ, Pearce GL, Jones NP, et al. Lipid effects of peroxisome proliferator-activated receptor-δ agonist GW501516 in subjects with low high-density lipoprotein cholesterol: characteristics of metabolic syndrome. Arterioscler Thromb Vasc Biol. 2012;32(9):2289–2294. PubMed.
- Wang YX, Zhang CL, Yu RT, et al. Regulation of muscle fiber type and running endurance by PPARdelta. PLoS Biol. 2004;2(10):e294. PubMed.
- Narkar VA, Downes M, Yu RT, et al. AMPK and PPARdelta agonists are exercise mimetics. Cell. 2008;134(3):405–415. PubMed; PMC.
- Gupta RA, Wang D, Katkuri S, et al. Activation of nuclear hormone receptor peroxisome proliferator-activated receptor-delta accelerates intestinal adenoma growth. Nat Med. 2004;10(3):245–247. PubMed.
- Sahebkar A, Chew GT, Watts GF. 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. PubMed.
- Breuer J, Garzinsky AM, Thomas A, et al. Complementary information concerning the suspected interindividual transmission of GW1516, a substance prohibited in sport, through intimate contact: a case report. Forensic Toxicol. 2024;42(2):248–254. PubMed.
- Thevis M, Möller I, Thomas A, et al. Characterization of two major urinary metabolites of the PPARdelta-agonist GW1516 and implementation of the drug in routine doping controls. Anal Bioanal Chem. 2010;396(7):2479–2491. PubMed.
- Sobolevsky T, Dikunets M, Sukhanova I, et al. Detection of PPARδ agonists GW1516 and GW0742 and their metabolites in human urine. Drug Test Anal. 2012;4(10):754–760. PubMed.
- Pokrywka A, Cholbinski P, Kaliszewski P, et al. Metabolic modulators of the exercise response: doping control analysis of an agonist of the peroxisome proliferator-activated receptor δ (GW501516) and 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR). J Physiol Pharmacol. 2014;65(4):469–476. PubMed.
- Van Wagoner RM, Eichner A, Bhasin S, 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. PubMed.
- National Center for Biotechnology Information. PubChem Compound Summary for CID 9803963, GW501516. PubChem.
- ClinicalTrials.gov. GW501516 in subjects who have low level of high-density lipoprotein cholesterol (NCT00158899); An exploratory study to look at the effect of two investigational drugs on body fat and inflammation (NCT00388180); Regulation of lipoprotein transport in metabolic syndrome (NCT00841217). NCT00158899; NCT00388180; NCT00841217.
- World Anti-Doping Agency. Prohibited List 2026, published as Annex to the Anti-Doping Convention. Bundesgesetzblatt für die Republik Österreich. December 30, 2025;III(219). RIS.