Cardarine

Dosing from the Literature

Published for fat loss: one 2-week trial at 10 mg a day, in which liver fat fell 20% in six moderately overweight men; GSK’s 12-week body-fat trial of a 10 mg dose (71 men) has no posted results. Not published: the body-fat trial’s results, or any trial of it for weight loss.

The table records doses as published: trial doses from lipid and metabolism studies, one registered trial dose with no posted results, an anti-doping excretion dose, and one misuse pattern that forensic toxicologists describe. None is a recommendation.

Animal doses, for context only: 5 mg/kg a day by mouth in mice for 4 weeks (Narkar et al., 2008); 40 mg per kg of food for 8 weeks in mice (Fan et al., 2017); 0.1 rising to 3.0 mg/kg in obese rhesus monkeys (Oliver et al., 2001); and 3 to 80 mg/kg a day for 104 weeks across GSK’s rat and mouse cancer studies (Geiger et al., 2009; Newsholme et al., 2009).

What It Is

Cardarine is GW501516, “also known as GW-1516 or cardarine and endurobol”: a peroxisome proliferator-activated receptor delta (PPARδ) agonist (Kintz et al., 2020). It is a small molecule, not a peptide, with the formula C21H18F3NO3S2 and a molecular weight of 453.5 g/mol (PubChem). GlaxoSmithKline scientists described it in 2001 as “a potent and subtype-selective PPARdelta agonist,” developed with combinatorial chemistry and structure-based drug design (Oliver et al., 2001).

It came out of a partnership. Ligand Pharmaceuticals’ annual report says Ligand began a research collaboration with Glaxo Wellcome (now GlaxoSmithKline) in 1992 to find drugs for atherosclerosis and other cardiovascular disorders; in 1999 several PPAR leads went into exploratory development, and “GW501516 was selected for clinical development and Phase II trials were initiated for cardiovascular disease and dyslipidemia” (Ligand Pharmaceuticals, 2007). In August 2004 Ligand reported a $1.0 million milestone payment as GSK continued Phase II development of GW501516 “for the treatment of dyslipidemias” (Ligand Pharmaceuticals, 2004).

Then it stopped. The annual report Ligand filed in March 2007 says “GW501516 is currently on hold pending the review of preclinical studies” (Ligand Pharmaceuticals, 2007). In 2009 GSK scientists published abstracts of two-year carcinogenicity studies in rats and mice that found drug-related tumors in multiple tissues (Geiger et al., 2009; Newsholme et al., 2009; details under Side Effects & Risks). A 2013 review states that GSK announced any further research would be discontinued because of rodent studies “which linked this drug to wide spread tumour development” (Mackenzie & Lione, 2013). WADA’s 2013 alert says GW501516 “was withdrawn from research by the pharmaceutical company and terminated when serious toxicities were discovered in pre-clinical studies,” and that “Clinical approval has not, and will not be given for this substance” (WADA, 2013).

It also found a second market. In 2010 the Cologne doping-control laboratory bought GW1516 from internet suppliers (Thevis et al., 2011). WADA’s 2013 alert says it had been “available for some months on the black market, through the Internet and elsewhere,” with “a number of positive cases” among athletes (WADA, 2013). A 2014 review says GW501516 and AICAR are “also called ‘exercise pills’ or ‘exercise mimetics’” (Pokrywka et al., 2014). PubMed lists 346 records that name it in the title or abstract, four of them randomized controlled trials (searched September 29, 2026).

GW-0742 is a different molecule: another PPARβ/δ ligand, tested beside GW501516 in cancer-cell and anti-doping studies (Hollingshead et al., 2007; Sobolevsky et al., 2012). It has its own page: GW-0742.

Mechanism of Action

The mechanism work on GW501516 is in cells, mice and monkeys, plus the measurements taken in the four human trials.

• PPARδ (NR1C2), a nuclear receptor — In a cell assay, GW501516 activated human PPARδ with an EC50 of 1.2 nM and was more than 1,000-fold selective over the other PPAR subtypes; up to 1.0 μM it did not promote fat-cell differentiation or bind RXRα (Oliver et al., 2001).
• Reverse cholesterol transport (ABCA1) — In macrophages, fibroblasts and intestinal cells it increased the cholesterol transporter ABCA1 and apolipoprotein A1-specific cholesterol efflux (Oliver et al., 2001); in human skeletal muscle cells it doubled ABCA1 expression (Sprecher et al., 2007).
• Muscle fatty-acid oxidation (CPT1, CD36, FABP3, PDK4) — In rat muscle cells and mouse muscle it switched on genes for fatty-acid transport, beta-oxidation and mitochondrial respiration (Tanaka et al., 2003). In human muscle cells it raised fatty-acid oxidation and CPT1 and CD36 expression (Sprecher et al., 2007), and FABP3, CPT1 and PDK4 through PPARδ (Krämer et al., 2007). In the 2-week trial in overweight men, more of the exhaled CO2 came from the fat in a meal, and muscle CPT1b expression rose (Risérus et al., 2008).
• AMPK–PPARδ crosstalk — In human muscle cells GW501516 activated AMPK, and its effect on glucose uptake needed AMPK but not PPARδ (Krämer et al., 2007). In cultured cells AMPK bound PPARδ and increased its GW1516-driven activity, and in mouse muscle GW1516 with the AMPK activator AICAR induced several oxidative genes synergistically (Narkar et al., 2008).
• Glucose sparing — In sedentary mice given it for 8 weeks, muscle burned less glucose, blood glucose held up longer during running and low blood sugar came later, “without affecting either muscle fiber type or mitochondrial content” (Fan et al., 2017).
• Lipoprotein handling in men — In 13 men, 2.5 mg a day for 6 weeks increased the liver’s removal of VLDL particles, lowered apoC-III production and raised apoA-II production (Ooi et al., 2011).
• Tumor promotion (the toxicologists’ hypothesis) — GSK’s toxicologists call GW501516 non-genotoxic, and wrote that some tumor types in their rat and mouse studies had not been reported with PPARα or PPARγ agonists and “may reflect tumor promotion mediated through PPARδ agonism” (Geiger et al., 2009; Newsholme et al., 2009).

What the Research Shows

The fat-loss and endurance results are animal results. The human trials are under Human Data.

• Obese monkeys (2001) — Six obese, insulin-resistant, middle-aged male rhesus monkeys got rising doses, 0.1 to 3.0 mg/kg in four-week steps, in food snacks twice a day. At 3.0 mg/kg, HDL cholesterol was 79% above baseline and fasting triglycerides 56% lower; small-dense LDL and fasting insulin fell. No changes in body weight or liver enzymes were seen. One monkey whose triglycerides fell below 20 mg/dl ate less and was removed before the top dose (Oliver et al., 2001).
• Mice on a high-fat diet (2003–2004) — In mice fed a high-fat diet, GW501516 “ameliorated diet-induced obesity and insulin resistance,” with a higher metabolic rate and more fat oxidation; in genetically obese ob/ob mice it improved blood glucose and insulin “despite a modest body weight change” (Tanaka et al., 2003). In another high-fat-diet study, mice given GW501516 for two months gained less weight and fat than vehicle-treated mice, five per group (Wang et al., 2004).
• The engineered running mouse (2004) — The mouse that could run up to twice as far as its littermates carried an activated PPARδ gene in muscle, not the drug. Normal mice given GW501516 for 10 days showed a similar type I muscle-fiber gene pattern (Wang et al., 2004).
• Endurance with training (2008) — Four weeks of GW1516 at 5 mg/kg a day did not change treadmill performance in sedentary mice, and neither did treatment for up to 5 months. With four weeks of exercise training, the same dose raised running time 68% and distance 70% over trained mice given vehicle (Narkar et al., 2008).
• Endurance without training (2017) — Sedentary mice given GW501516 in food, 40 mg per kg of food, for 8 weeks ran about 100 minutes longer than untreated controls; the gain was lost in mice lacking PPARδ in muscle (Fan et al., 2017).

Human Data

PubMed indexes four randomized controlled trials of GW501516, all on blood lipids and metabolism and all 12 weeks or shorter. All four list Dennis Sprecher, whose 2007 paper gives his affiliation as GlaxoSmithKline, as an author, and two come from GSK departments (Sprecher et al., 2007; Olson et al., 2012). Only the abstracts of the four trials could be read for this page.

• First in people (2007) — Healthy volunteers took 2.5 mg (n=9) or 10 mg (n=9) or placebo (n=6) once daily for 2 weeks, hospitalized and sedentary. HDL cholesterol was enhanced at both doses (P=0.004 and P<0.001) against an 11.5% fall on placebo; serum triglycerides trended down at 10 mg (P=0.08), and triglyceride clearance after a fat meal improved (P=0.02) (Sprecher et al., 2007).
• Overweight men, 2 weeks (2008) — A double-blind, randomized, three-group study of six moderately overweight men per group: GW501516 10 mg, a PPARα agonist, or placebo. On GW501516, fasting triglycerides fell 30%, apolipoprotein B 26%, LDL cholesterol 23% and insulin 11%; HDL did not change; liver fat fell 20% (P<0.05) and a urine marker of oxidative stress fell 30% (Risérus et al., 2008).
• Lipoprotein kinetics, 6 weeks (2011) — A randomized, double-blind crossover in 13 dyslipidemic men with central obesity, 2.5 mg a day against placebo (Ooi et al., 2011; registered as NCT00841217 by the University of Western Australia).
• Low HDL, 12 weeks (2012) — 268 people with HDL cholesterol below 1.16 mmol/L took 2.5, 5 or 10 mg or placebo: HDL rose by up to 16.9% (10 mg) and apoA-I by up to 6.6%, while LDL cholesterol fell 7.3%, triglycerides 16.9%, apoB 14.9% and free fatty acids 19.4%. A second study in 37 people measured lipoprotein particles (Olson et al., 2012).
• The body-fat trial (registered, no results posted) — GSK registered “a randomized, double-blind, parallel group study to evaluate the effect of 12-week treatment with GW590735X (20ug) or GW501516X (10mg) relative to placebo on measures of adiposity and inflammation in overweight and obese subjects” (NCT00388180). Its primary outcome is “Body fat levels”; 71 men enrolled at one site in Baton Rouge, Louisiana, from December 2004 to June 2006. Neither ClinicalTrials.gov nor GSK’s register posts results, and the register lists no publication. PubMed links the registration to the Olson 2012 paper, whose abstract reports lipids only.
• GSK’s Phase 2 low-HDL trial (registered, no results posted) — 424 people enrolled at European sites for 12 weeks of 2.5, 5 or 10 mg, from August 2004 to June 2006 (NCT00158899). Its registered secondary outcomes include population pharmacokinetics. GSK’s register says “Study Results yet to be posted.” No human half-life appears in the documents read for this page.

Outside the trials, the human record is anti-doping and case reports:

• Excretion — After a single 15 mg oral dose, GW1516’s sulfone metabolite was detectable in urine for up to 40 days; the unchanged drug was measurable only briefly, at low ng/ml levels (Sobolevsky et al., 2012).
• Doping findings — Anti-doping laboratories had reported 139 adverse analytical findings for GW1516 to WADA since 2009, from 1 a year (2012) to 31 (2016) (Breuer et al., 2024).
• Hair and semen — GW501516 was found in the hair of a male user at 32 and 22 pg/mg in two 2-cm segments (Kintz et al., 2020). Of 361 semen samples from a German university hospital, one held GW1516 at about 48 ng/mL (Breuer et al., 2024).
• Case reports — A sport coach hospitalized with muscle breakdown and raised liver enzymes after taking it with ostarine (Kintz et al., 2021), and a man with breast enlargement and low testosterone after six months of three supplements, one of them matched to cardarine by an online search (Chong et al., 2024); both are under Side Effects & Risks.

None of these outside-trial reports measured fat loss. The evidence meter on the cardarine card counts published human data for fat loss, and the one fat measurement in people in the published abstracts is the 2-week liver-fat result.

Reconstitution & Storage

There is nothing to reconstitute. Cardarine is a small molecule taken by mouth, not a peptide: the trials gave it as once-daily oral doses (Sprecher et al., 2007), registered as “GW501516 oral tablets” (NCT00158899). There is no approved product and so no label.

• Research grade — One laboratory supplier sells GW501516 as a crystalline solid, purity ≥98%, with storage at −20°C and stability of ≥4 years. It dissolves in ethanol, DMSO and dimethyl formamide (about 12, 20 and 25 mg/ml) and is sparingly soluble in water-based buffers; the supplier writes, “We do not recommend storing the aqueous solution for more than one day” (Cayman Chemical product information).
• Products sold online — Capsules and liquid solutions, many labeled “Research use only” or “Not for human consumption” (Van Wagoner et al., 2017); an orange/yellow suspension in water and glycerol (Thevis et al., 2011); “mostly available as liquid solutions and tablets,” with bulk powder “essentially in China” (Kintz et al., 2021).
• Storage of those products — No document read for this page gives storage conditions or shelf life for them.

Side Effects & Risks

No long-term safety study in people appears in the documents read for this page. What the documents show:

• In the human trials — The four published abstracts report lipid and metabolic results and give no adverse-event counts. In the 2-week trial, a urine marker of oxidative stress fell 30% rather than rising (Risérus et al., 2008).
• Muscle breakdown and raised liver enzymes (case report) — A 43-year-old sport coach said he took GW1516 at 20 mg a day for 4 days and ostarine for 1 day, ten days before admission; he had also cycled 120 km the day before. The day after admission his creatine phosphokinase was 86,435 UI/L and AST 2,558 UI/L. His blood held cardarine at 403 ng/mL, and his hair held both drugs, which the authors read as repeated use over about two months. He recovered fully by six weeks. The authors note that liver injury had been described with ostarine, and not until then with cardarine (Kintz et al., 2021).
• Breast enlargement and low testosterone (case report) — A 40-year-old man took three supplements labeled B-140, B-677 and B-GW daily for six months; an online search matched them to RAD-140, MK-677 and cardarine. Lab tests of all three also detected undisclosed testosterone, estradiol and growth hormone. His symptoms resolved after he stopped; the authors believe the undisclosed hormones and MK-677 could have caused them (Chong et al., 2024).
• Muscle lesions in rats — In a 14-day rat study, sanofi-aventis scientists used GW501516 as a “model compound to induce lesions” in type I and type II skeletal muscle (Hemmann et al., 2009).
• Intestinal tumors in mouse models — In Apc(min) mice, which are prone to intestinal polyps, GW501516 increased the number and size of polyps, with five times as many polyps larger than 2 mm (Gupta et al., 2004); in a chemically induced colitis-cancer model it “significantly enhanced” colorectal cancer (Zhou et al., 2019). Other work found that neither GW501516 nor GW0742 increased the growth of human cancer cell lines (Hollingshead et al., 2007), and GSK’s two-year mouse study did “not support a role for PPARδ in colon carcinogenesis” (Newsholme et al., 2009).
• What is in the bottle — In a JAMA study of 44 products sold online as SARMs and bought in 2016, nine listed GW501516 on the label: three matched the label in identity and amount, one matched but also held undeclared tamoxifen, three held a different amount (two held 0.1–1 mg per capsule against 5 or 10 mg claimed), and two held none. Four more held GW501516 their labels did not list (Van Wagoner et al., 2017). GW1516 bought online in 2010 was authentic but “considerably lower than indicated on the label”; the substances bought with it arrived in packaging that said “amino acids” and “green tea extract” (Thevis et al., 2011).
• Positive tests possibly from a partner — In one of two anti-doping cases, a female athlete’s positive test for GW1516 metabolites was plausibly traced to unprotected intercourse: her urine sample held semenogelin, a protein found in seminal fluid, and she was not banned (Breuer et al., 2024).
• WADA prohibited — WADA prohibits PPARδ agonists, naming GW1516 and GW501516, at all times under S4.4.1; substances in S4.4 are non-Specified Substances (Prohibited List 2026).
• Drug interactions — No interaction study appears in the documents read for this page.

Bloodwork & Monitoring

No monitoring guidance for cardarine has been published. These are the measurements the documents report:

• Lipid panel and apolipoproteins — HDL cholesterol and triglycerides were outcomes of all four published trials, and LDL and apolipoproteins of three (Sprecher et al., 2007; Risérus et al., 2008; Ooi et al., 2011; Olson et al., 2012).
• Insulin and liver fat — Measured in the 2-week trial in overweight men (Risérus et al., 2008).
• Creatine phosphokinase, AST and ALT — The tests that showed muscle breakdown and raised liver enzymes in the 2021 case report (Kintz et al., 2021).
• LH, FSH, testosterone and estradiol — The tests that showed low testosterone in the 2024 case report, and its recovery after the supplements stopped (Chong et al., 2024).
• Anti-doping tests — In urine it is best monitored as its sulfone metabolite, detectable for up to 40 days after one 15 mg dose (Sobolevsky et al., 2012); hair tests have found it too (Kintz et al., 2020).
• Which tests fit a given person — A question for a licensed healthcare provider. This page can’t answer it.

Commonly Stacked With

The four published trials gave cardarine alone against placebo, one of them with a separate PPARα-agonist arm (Risérus et al., 2008); none tested it with another drug. These are the combinations a mouse study tested or a case report records.

Legal Status

Related Compounds

People researching cardarine often also look at these:

Next Steps

References

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Related Research

• GW-0742PPARβ/δ Ligand (a different molecule, tested beside GW501516)
• SR9009Rev-erbα Agonist (WADA S4.4.1, with GW501516)
• AICARAMPK Activator (tested with GW1516 in the 2008 mouse paper)
• MOTS-cMitochondrial-Derived Peptide (WADA S4.4.1, AMPK activators)
• SLU-PP-332ERR Agonist (a different receptor family)
• MK-677Ibutamoren (found with GW501516 in products sold as SARMs)