Cardarine

Cardarine (GW501516) is a synthetic agonist of peroxisome proliferator-activated receptor delta, developed at GlaxoSmithKline as a treatment for dyslipidaemia.

Human trialsNon-peptide compound reference

Also known as: GW501516, GW-501516, GW1516, GSK-516, Endurobol, UNII 7I2HA1NU22, CHEBI:73726, DTXSID3041037

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Dosing & scaling, explained

Amounts reported for Cardarine are listed under Reported protocols, each with its source and study kind. No amount ladder is inferred from them. This is educational source context, not a protocol or recommendation.

No source-supported amount ladder is shown

Enter a target amount only from your own reviewed source. The calculator can convert it into concentration, volume and device markings, but it will not infer an amount from product availability or another compound.

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No independently verified schedule

Clinical context

Human study rows are described per source under Reported protocols; they belong to their trial populations and are not a general amount.

Storage, handling and interpretation

Product identity

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Storage & handling

Follow the product label, certificate and validated laboratory SOP; no universal storage assumption is applied here.

Prepared solutions

Label concentration and preparation date, use sterile technique where applicable, and follow a validated stability protocol.

Reported protocols for Cardarine

What published studies and recent community write-ups report about amounts, timing and course length. 3 clinical, 2 preclinical and 1 community-reported rows, each linked to its source. These are descriptions of what others report, not instructions, and nothing here is medical advice.

ContextDoseFrequencyRouteCourseSource
Clinical3 rows
First administration to humans, healthy volunteers24 healthy volunteers, hospitalised and sedentary throughout2.5 mg (n=9) or 10 mg (n=9) against placebo (n=6)Once dailyOral2 weeksNone describedArteriosclerosis, Thrombosis, and Vascular Biology (PubMed)2007
HDL cholesterol rose in both treated groups, against a fall of 11.5% in the placebo group. Serum triglycerides trended down at 10 mg without reaching significance, while triglyceride clearance after a fat-feeding challenge improved on drug. The report is a lipid study: it records no safety analysis, and the total sample is 24 people over 2 weeks.
Metabolic syndrome features, moderately overweight men6 healthy moderately overweight men per group, in a three-group randomised double-blind design10 mgOnce dailyOral2 weeksNone describedDiabetes (PubMed)2008
Fasting triglycerides fell 30%, apolipoprotein B 26%, LDL cholesterol 23% and insulin 11%, with liver fat down 20% and urinary isoprostanes down 30%. HDL cholesterol was unchanged in this trial, a null result where the other three human studies reported increases. A PPAR-alpha comparator moved only triglycerides. Six men per arm is a very small sample.
Largest trial, low HDL cholesterol268 patients with HDL cholesterol below 1.16 mmol/L, plus a second exploratory group of 372.5, 5.0 or 10.0 mgDailyOral12 weeks, the longest human exposure ever publishedNone describedArteriosclerosis, Thrombosis, and Vascular Biology (PubMed)2012
At 10 mg, HDL cholesterol rose up to 16.9% and apoA-I 6.6%, while LDL cholesterol fell 7.3%, triglycerides 16.9%, apoB 14.9% and free fatty acids 19.4%. The exploratory group showed very LDL particles down 19%, intermediate-density lipoprotein down 52% and HDL particle number up 10%. These are lipid endpoints only; no muscle, strength or endurance outcome was measured in any human trial of this compound.
Preclinical2 rows
Exercise-mimetic mouse study, the origin of the endurance claimsMale C57BL/6J mice, 8 weeks old, 9 per cohort with 6 per group run5 mg/kg/dayDailyOral gavage in mice4 weeks, with or without 4 weeks of treadmill trainingNot applicableCell (PubMed Central)2008
In sedentary mice the drug changed oxidative muscle gene expression but did not improve running endurance. Only when the same dose was paired with four weeks of treadmill training did running time rise 68% and distance 70% against trained controls. The widely repeated figure of a 70% endurance gain comes from that trained arm and carries the training requirement with it. A separate 44% figure belongs to AICAR, a different compound tested in parallel at 500 mg/kg/day. Animal milligram-per-kilogram amounts do not translate to human doses.
Two-year rodent carcinogenicity studies that ended the programmeRats and CD1 mice in 104-week bioassays run for the sponsor3-40 mg/kg/day in rats; 10-80 mg/kg/day in miceDailyOral gavage104 weeksNot applicableCommunity resource2026
Tumours considered treatment related were reported across liver, stomach, tongue, skin, bladder, thyroid, testes, ovary and uterus, at all doses tested in rats, with increased female mortality at all doses; the mouse study found liver and stomach tumours with combined squamous cell tumours at all doses and reduced survival from 30 mg/kg/day. Both studies exist only as 2009 Society of Toxicology conference abstracts and were never peer-reviewed or published in full. Neither abstract states a tumour incidence percentage, so figures such as a ninety per cent incidence trace to no source. This ledger retrieved and read both abstracts verbatim.
Community-reported1 row
What is actually in products sold onlineLabel amount matched laboratory analysis in only 18 of 44 productsNot statedProducts bought from internet suppliers and analysed under anti-doping proceduresNot statedJAMA (PubMed)2017
This JAMA analysis bought 44 products marketed as selective androgen receptor modulators and found that 52% contained a SARM, while 39% contained a different unapproved drug, this compound among them. No active compound at all was detected in 9%, substances absent from the label were present in 25%, and the stated amount differed substantially from the measured amount in 59%. A product sold under this name may contain something else, or a different quantity than the label claims.

How a course is commonly described

  1. Published human courses: 2 to 12 weeksClinical

    Every human exposure on record is a lipid trial: 2 weeks at 2.5 or 10 mg in healthy volunteers, 2 weeks at 10 mg in overweight men, 6 weeks at 2.5 mg in a crossover study and 12 weeks at 2.5 to 10 mg in 268 patients. Nothing longer than twelve weeks has ever been given to a person in a published study.

  2. Rodent lifetime exposure: 104 weeksPreclinical

    The studies that decided the compound's fate ran for two years of daily gavage in two species. They are the reason no regulator will see an application for it, and they are the single most important thing to know about the molecule.

  3. What circulates insteadCommunity-reported

    Marketing copy for this compound carries endurance percentages, half-life figures and reassurances about hormonal safety that cannot be traced to any primary source. The endurance numbers belong to a trained-exercise arm or to a different drug, no published human trial reports a pharmacokinetic parameter, and no human study measured testosterone or gonadotropins during administration.

  • This compound is not an approved medicine anywhere. GlaxoSmithKline ended development in 2006 and 2007 on the rodent carcinogenicity findings, and in 2013 the World Anti-Doping Agency took the rare step of publicly warning athletes about it, stating that clinical approval had not been and would not be given.
  • It is prohibited in sport at all times, in and out of competition. The 2026 Prohibited List names it at S4.4.1 among metabolic modulators, alongside AMPK activators and Rev-erb-alpha agonists, and not among anabolic agents.
  • No published human trial of this compound reports a half-life or any other pharmacokinetic parameter, so the 16 to 24 hour figures used to build daily dosing schedules rest on no primary measurement.
  • An absence of reported harm in four short lipid trials is not a finding of safety. None of those reports contains a safety analysis, and none of the four trial registrations has results posted.
Sources for this section (7)
  1. Triglyceride:High-Density Lipoprotein Cholesterol Effects in Healthy Subjects Administered a Peroxisome Proliferator Activated Receptor delta AgonistArteriosclerosis, Thrombosis, and Vascular Biology (PubMed)2007Clinical
  2. 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 menDiabetes (PubMed)2008Clinical
  3. Lipid Effects of Peroxisome Proliferator-Activated Receptor-delta Agonist GW501516 in Subjects With Low High-Density Lipoprotein Cholesterol: Characteristics of Metabolic SyndromeArteriosclerosis, Thrombosis, and Vascular Biology (PubMed)2012Clinical
  4. AMPK and PPARdelta Agonists Are Exercise MimeticsCell (PubMed Central)2008Preclinical
  5. WADA issues alert on GW501516World Anti-Doping Agency2013Clinical
  6. Chemical Composition and Labeling of Substances Marketed as Selective Androgen Receptor Modulators and Sold via the InternetJAMA (PubMed)2017Clinical

Plus 1 community resource (a dosing guide, forum thread or vendor write-up), reported above but not linked.

Overview

Cardarine (GW501516) is a synthetic agonist of peroxisome proliferator-activated receptor delta, developed at GlaxoSmithKline as a treatment for dyslipidaemia and never approved as a medicine in any country. Four human trials were published between 2007 and 2012, all of them measuring lipids and lipoproteins at 2.5 to 10 mg a day, the longest running twelve weeks. Development was terminated after two 104-week rodent carcinogenicity studies linked the compound to tumours in multiple organs at every dose tested, and it has been prohibited in sport at all times since 2009.

What researchers are exploring

These themes describe recurring questions in published research. They are not claims of effectiveness or recommendations for use.

  • 1

    Metabolic research

    Energy balance, body composition and incretin signaling.

  • 2

    Muscle & performance

    Androgen receptor modulators, myostatin pathways and exercise-mimetic research.

  • 3

    First administration to humans, healthy volunteers

    HDL cholesterol rose in both treated groups, against a fall of 11.5% in the placebo group. Serum triglycerides trended down at 10 mg without reaching significance, while triglyceride clearance after a fat-feeding.

  • 4

    Metabolic syndrome features, moderately overweight men

    Fasting triglycerides fell 30%, apolipoprotein B 26%, LDL cholesterol 23% and insulin 11%, with liver fat down 20% and urinary isoprostanes down 30%. HDL cholesterol was unchanged in this trial, a null result where the.

  • 5

    Largest trial, low HDL cholesterol

    At 10 mg, HDL cholesterol rose up to 16.9% and apoA-I 6.6%, while LDL cholesterol fell 7.3%, triglycerides 16.9%, apoB 14.9% and free fatty acids 19.4%. The exploratory group showed very LDL particles down 19%.

  • 6

    Exercise-mimetic mouse study, the origin of the endurance claims

    In sedentary mice the drug changed oxidative muscle gene expression but did not improve running endurance. Only when the same dose was paired with four weeks of treadmill training did running time rise 68% and distance.

What the current evidence can support

Study models remain visible so laboratory and animal findings are not mistaken for established human outcomes.

  • Human

    Human studies and registrations

    3 protocol rows on this page come from human trials, trial registrations, regulator labels or reviews of human data. Approval status and populations are stated per row.

  • Animal

    Preclinical models

    2 protocol rows describe animal, cell or toxicology work. Amounts from these rows do not translate to people.

  • Not graded

    Community-reported use

    1 row record what blogs, vendor write-ups or forums describe for Cardarine. None has been verified against primary literature.

Chemistry identifiers

Sequence, synonyms and registry identifiers as recorded in PubChem, the National Library of Medicine's open chemistry database. Formula, mass and CAS number are summarized at the top of the page.

Also listed as

GW501516, GW-501516, GW1516, GSK-516, Endurobol, UNII 7I2HA1NU22, CHEBI:73726, DTXSID3041037

InChIKey

YDBLKRPLXZNVNB-UHFFFAOYSA-N

IUPAC name

2-[2-methyl-4-[[4-methyl-2-[4-(trifluoromethyl)phenyl]-1,3-thiazol-5-yl]methylsulfanyl]phenoxy]acetic acid

Limitations and unknowns

Important limitations

  • Every amount on this page is a report of what a source describes, not a protocol to follow.
  • Preclinical and community rows do not establish a human amount, schedule or route.
  • Formulation, purity and presentation vary by supplier and are not covered by the dossier.

Sources

7 curated references, each with its journal, year and study model, plus 1 community resource reported but not linked.

  1. GW 501516 (PubChem CID 9803963)PubChem, National Library of Medicine2026Not graded
  2. Triglyceride:High-Density Lipoprotein Cholesterol Effects in Healthy Subjects Administered a Peroxisome Proliferator Activated Receptor delta AgonistArteriosclerosis, Thrombosis, and Vascular Biology (PubMed)2007Human
  3. 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 menDiabetes (PubMed)2008Human
  4. Lipid Effects of Peroxisome Proliferator-Activated Receptor-delta Agonist GW501516 in Subjects With Low High-Density Lipoprotein Cholesterol: Characteristics of Metabolic SyndromeArteriosclerosis, Thrombosis, and Vascular Biology (PubMed)2012Human
  5. AMPK and PPARdelta Agonists Are Exercise MimeticsCell (PubMed Central)2008Animal
  6. WADA issues alert on GW501516World Anti-Doping Agency2013Human
  7. Chemical Composition and Labeling of Substances Marketed as Selective Androgen Receptor Modulators and Sold via the InternetJAMA (PubMed)2017Human