Cardarine (GW-501516)
GW-501516 / Endurobol
Cardarine (GW-501516) (GW-501516 / Endurobol) is a metabolic & fat loss research compound. PPARδ agonist — shifts fuel use toward fat oxidation and boosts endurance. Important: rodent studies showed cancer at high chronic doses.
Cardarine (GW-501516) quick facts
| Reported research dose (Oral) | 2.5mg-20mg |
| Route | Oral |
| Frequency | 1x Daily AM · 5 On 2 Off or Daily |
| Half-life | ~20–24 hrs |
| Forms | Oral, Injectable |
| Evidence level | Animal (efficacy) + safety flag |
| Other forms available | Injectable — dosed differently |
Endurance is real, but the carcinogenicity signal in rodents is why I keep people cautious and cycled. Don't ignore it.
How Cardarine (GW-501516) works
PPARδ agonist — shifts fuel use toward fat oxidation and boosts endurance. Important: rodent studies showed cancer at high chronic doses.
Proposed benefits
Endurance and fat oxidation (note the rodent carcinogenicity flag).
Where to get Cardarine (GW-501516)
Cardarine (GW-501516) is sold in 2 forms. They are not interchangeable — the dose and the route differ, so pick the one this page describes unless you know why you want another.
Bacteriostatic water is the diluent — sterile water with 0.9% benzyl alcohol, which is what lets a vial be drawn from more than once. It does not come with the vial, and unlike the compound it is bought again every time.
Need bacteriostatic water? Get it at AminoWell USA (my company) → Code CAMERON.
The evidence for Cardarine (GW-501516)
Graded by what exists behind each claim.
✅ Clinically validated
- It reached human trials and was abandoned, and why matters. GlaxoSmithKline took it into phase 2 for dyslipidemia, where it did what it was designed to do — raised HDL and lowered triglycerides.
- Development stopped after long-term rodent carcinogenicity studies showed tumors across multiple organs — liver, bladder, stomach, thyroid, skin — at a range of doses. That is not a failed efficacy endpoint; it is a toxicology finding, which is a different and more serious category.
- The honest counter-argument, stated fairly: the rodent studies used high doses over a full lifespan, and rodent PPAR findings do not always translate to humans. That argument is real. It is also unresolved, because nobody ran the study that would resolve it.
📊 Correlative data
- Extensive real-world use in endurance sport despite the WADA ban, and consistently reported endurance and fat-loss effects. There is no long-term human safety follow-up of that population, which is the specific data that would answer the cancer question and does not exist.
🧪 Theoretical / extrapolated
- A PPARδ agonist. PPARδ is a nuclear receptor that shifts skeletal muscle toward fatty acid oxidation and type I fiber characteristics — sparing glycogen, which is a coherent mechanism for the endurance effect.
- PPARδ is expressed nearly everywhere, and that ubiquity is the mechanistic basis of the carcinogenicity concern: a transcription factor driving proliferation and metabolism in every tissue has every tissue available to it.
- Cam's ruling on the Vault is that this stays listed because people are using it regardless and deserve the full picture — including the part the sellers leave out.
How to read these tiers: they say how much human evidence exists, not how well something works — and ✗ flags harm, never a disappointing trial. How the evidence tiers work →
What Cardarine (GW-501516) actually does
GW501516 is a selective agonist at PPAR-delta, and PPAR-delta is not a switch. It is a ligand-activated transcription factor, and what it transcribes depends entirely on which cell it is sitting in. On binding its ligand it heterodimerizes with the retinoid X receptor, the pair occupies peroxisome proliferator response elements in target promoters, corepressors are exchanged for coactivators, and a gene program runs. In skeletal muscle that program is the fatty-acid oxidation program: CPT1B, the fatty acid transport proteins, PDK4, and the mitochondrial biogenesis machinery, with PDK4 in particular suppressing pyruvate dehydrogenase so the fiber burns fat and spares glucose Crossland 2021.
That fuel switch is the whole appeal and it is also the whole problem, because it is one output of a receptor with many. PPAR-delta is expressed in muscle, but also in liver, gut epithelium, keratinocytes, macrophages and vascular endothelium. The same ligand reaches all of them at the same plasma concentration. There is no tissue-selective dosing of a nuclear receptor taken by mouth.
The famous experiment is more careful than the way it is quoted. The 2008 Cell paper that made this molecule notorious tested both an AMPK activator and a PPAR-delta agonist as exercise mimetics. AICAR alone, in sedentary mice, raised running endurance by 44%. The PPAR-delta agonist's endurance effect in that paper came in combination with exercise training, not instead of it Narkar 2008. Cardarine is quoted everywhere as the drug that gave untrained mice endurance. In the paper it is the drug that amplified training. That distinction changes what the compound is for and it is the single most misreported fact about it.
And the same receptor family runs a growth program in epithelium. PPAR-delta dysregulation drives the CCL20/CCR6 axis in gastric adenocarcinoma and remodels the tumor microenvironment Liu 2023. That is a mechanism paper, in a cancer model, about the receptor this compound is designed to activate. It is not proof that this compound causes cancer in a person. It is the reason the question is not paranoid.
Cell, rodent, human — and where it stops
Step one, cells and rodents, where the case is strong. The PPAR-delta fuel-metabolism program is reproducible across muscle models and is reviewed with its contraction and disease context intact Crossland 2021. The exercise-mimetic result is real Narkar 2008. Rodent work also shows a systemic dimension nobody prices in: PPAR-beta/delta agonism alters immune parameters, and exercise training partly masks the change in blood samples Sibille 2021. So even in rodents this is not a muscle-only drug.
Step two, humans — and here the page has to be blunt. There is no completed randomized human efficacy trial of GW501516 in any indication. Development was abandoned. The published human record is not a trial literature at all; it is a forensic literature, written by doping-control and clinical-toxicology laboratories, and it is the only human data that exists.
What that forensic record actually contains. A 43-year-old man taking GW1516 with the SARM ostarine presented with ALT up to 922 U/L, AST up to 2558 U/L, and massive rhabdomyolysis with CPK up to 86,435 U/L; blood analysis confirmed cardarine at 403 ng/mL and ostarine at 1 ng/mL, and he recovered fully over six weeks Kintz 2021. That is one case, with a second drug on board, and it cannot be attributed to cardarine alone — but it is the closest thing to human safety data in existence, the numbers are enormous, and it deserves to be on the page rather than in a footnote.
Step three, the obstacle, stated exactly. The rodent carcinogenicity finding that everyone cites as the reason GlaxoSmithKline stopped — tumors across multiple organs on long-term dosing — has never been published as a paper you can open. It reaches the public through anti-doping communications and secondary accounts of a sponsor's own toxicology. This page will not pretend otherwise. What IS checkable is that PPAR-delta drives a pro-tumorigenic program in a specific epithelial cancer model Liu 2023, that development stopped, and that the compound is prohibited in sport at all times. Those three facts point the same way. None of them is a two-year bioassay you can read.
Cardarine (GW-501516) pharmacokinetics — how much of it actually gets in
The card says ~20–24 hours. No human pharmacokinetic study of GW501516 has been published to support that or any other number, so here is what can be reasoned and where it stops.
What degrades it. GW501516 is a small, lipophilic thiazole-containing carboxylic acid. Its metabolic fate has been worked out in detail, but in the horse, by a doping-control laboratory characterizing the parent and its metabolites for detection purposes Trevisiol 2021 — the relevant routes are oxidative metabolism by cytochrome P450 followed by phase II glucuronidation of the carboxylic acid, with the sulfoxide as a characteristic metabolite. Detection windows in doping control run to days after a single dose, which is a lower bound on total body exposure and is a far more reliable statement than the plasma half-life printed on the card.
The oral barrier. A carboxylic acid of this size and lipophilicity is well absorbed and subject to significant first-pass metabolism in the liver — which is also the tissue with high PPAR-delta expression, so hepatic exposure exceeds systemic exposure. That is a mechanistically important asymmetry: the organ that sees the highest concentration is not the muscle the user is dosing for.
Numbers, from the only human sample sets that exist. Whole blood in a heavy user reached 403 ng/mL Kintz 2021. In an entirely separate line of work, GW1516 and its metabolites were quantified in human seminal fluid, in a case where intimate contact was the confirmed route of an adverse analytical finding Breuer 2024. Read that as a distribution fact: this molecule reaches compartments most people never consider, and it is detectable there at concentrations that can produce a positive test in someone who never took it.
The injectable form the card lists is the least characterized of all. An injected dose skips first-pass metabolism entirely, which raises systemic exposure per milligram relative to the oral route and lowers the liver-to-muscle concentration ratio. Whether that is better or worse depends on which tissue's PPAR-delta program you are worried about, and nobody has measured either version in a person.
What would have to be true, and how you would know it was not
Three predictions. The first two are the reason to draw blood at all; the third is the one that argues against the compound.
1. The lipid panel should improve, and specifically HDL should rise more than LDL falls. PPAR-delta agonism upregulates reverse cholesterol transport genes, and the fuel switch reduces hepatic lipogenesis. Draw a lipid panel and ApoB at baseline and at 8 weeks. Prediction: HDL up, triglycerides down, ApoB roughly unchanged, because ApoB counts particles and this mechanism changes their cargo more than their number. If ApoB falls substantially, something other than PPAR-delta is happening.
2. Fasting insulin should fall while HbA1c stays flat, and the gap between them is the mechanism's fingerprint. PDK4 induction makes muscle burn fat and spare glucose, which raises glucose availability rather than disposal. Draw fasting insulin and HbA1c together at baseline and 12 weeks. A falling insulin with an unchanged HbA1c is what a fuel switch looks like. A falling HbA1c would suggest genuine improvement in glucose disposal, which is a different and more valuable claim, and nobody has demonstrated it for this molecule in a person.
3. The prediction that cuts against it, and it is the one to run first: liver enzymes and CK. The only detailed human case recorded ALT at 922 U/L and CPK at 86,435 U/L Kintz 2021. Order GGT alongside a CMP at baseline, week 4 and week 8 — GGT because it is the enzyme least confounded by training, and the CMP because it carries ALT and AST. Prediction from the mechanism: a modest rise in transaminases in a meaningful minority. There is no marker at all for the carcinogenicity question, and that is the point: the risk everyone is worried about is the one no blood test can see, which is why the mechanistic literature Liu 2023 matters more here than a lab panel.
What nobody has tested yet
Four things that have never been tested and could be.
Nobody has published a human pharmacokinetic curve for GW501516. Not one. Every half-life quoted for it, on this site and everywhere else, is inferred from detection windows and from equine metabolism work Trevisiol 2021. Six timed plasma samples after one oral dose would be the first human PK data this compound has ever had.
Nobody has measured whether the immune signature seen in rodents appears in people. PPAR-beta/delta agonism altered immunity in a rodent gene-doping model, and exercise training partly masked the change in blood Sibille 2021. A lymphocyte subset panel before and after is an ordinary, orderable test, and it would be the first look at whether that finding transfers.
Nobody has separated the training effect from the drug effect in a human. The founding paper's own design says the two interact Narkar 2008. A crossover in trained versus untrained people, with VO2 and a fat-oxidation measurement, is a normal exercise-physiology study. It has never been run, because the compound has no sponsor.
Nobody has quantified secondary exposure, and one case says it is real. GW1516 and its metabolites were measured in human seminal fluid, and intimate contact was confirmed as the source of a positive test in a partner Breuer 2024. That single case implies an entire unexamined question — how long, at what concentration, in which fluids — that matters to any tested athlete with a partner who uses this compound.
Cardarine (GW-501516) — its own safety story, not its class's
This compound's risk story has three parts, and only one of them is the one people argue about.
The cancer question, stated as precisely as the evidence allows. The reason to be cautious is not a paper — it is the combination of an abandoned development program, a prohibition in sport at all times, and a published mechanism by which PPAR-delta activation remodels a tumor microenvironment and drives a chemokine axis in gastric adenocarcinoma Liu 2023. What does NOT exist in the open literature is the long-term rodent carcinogenicity dataset itself. Anyone who tells you they have read it is describing a summary of a summary. The honest position is that the biological plausibility is high, the primary evidence is not public, and no human outcome data exists in either direction.
The liver and muscle question, which is the one with numbers. In the single detailed human toxicology case, transaminases and creatine kinase reached values compatible with hepatitis and severe rhabdomyolysis, and the subject recovered over six weeks Kintz 2021. He was taking a SARM as well, so causation is unattributable — but rhabdomyolysis on a drug whose entire mechanism is a forced change in muscle fuel handling is not a coincidence anyone should dismiss, and it is the risk a stack makes worse rather than better.
The testing question, which is specific to this compound and almost never mentioned. GW1516 is prohibited in sport at all times and is detectable for days by routine methods Trevisiol 2021. Beyond the user, one published case documents transfer to a partner through intimate contact producing an adverse analytical finding Breuer 2024. If anyone in the household is drug-tested, that is a consequence of using this compound that has nothing to do with the person taking it.
What reduces risk here, mechanistically rather than generically. Not injection technique — this is usually oral. The mechanism-linked measures are: run GGT and a CMP before starting rather than after symptoms, because transaminase rise is silent; do not stack it with a 17-alpha-alkylated oral or a SARM, because the documented human case is a combination case; and treat duration rather than dose as the variable that matters, since every concern above is about chronic transcriptional activation rather than an acute peak.
Sources read for this page
- Kintz P, et al. Peroxisome Proliferator-Activated Receptor Delta Agonist (PPAR-delta) and Selective Androgen Receptor Modulator (SARM) Abuse: Clinical, Analytical and Biological Data in a Case Involving a Poisonous Combination of GW1516 (Cardarine) and MK2866 (Ostarine). Toxics 2021 · PMID 34678947
- Trevisiol S, et al. Comprehensive characterization of the peroxisome proliferator activated receptor-delta agonist GW501516 for horse doping control analysis. Drug Testing and Analysis 2021 · PMID 33547737
- Breuer J, et al. Complementary information concerning the suspected interindividual transmission of GW1516, a substance prohibited in sport, through intimate contact: a case report. Forensic Toxicology 2024 · PMID 38704758
- Liu Y, et al. PPARdelta dysregulation of CCL20/CCR6 axis promotes gastric adenocarcinoma carcinogenesis by remodeling gastric tumor microenvironment. Gastric Cancer 2023 · PMID 37572185
- Sibille B, et al. Gene Doping with Peroxisome-Proliferator-Activated Receptor Beta/Delta Agonists Alters Immunity but Exercise Training Mitigates the Detection of Effects in Blood Samples. International Journal of Molecular Sciences 2021 · PMID 34768927
- Crossland H, et al. The Regulatory Roles of PPARs in Skeletal Muscle Fuel Metabolism and Inflammation: Impact of PPAR Agonism on Muscle in Chronic Disease, Contraction and Sepsis. International Journal of Molecular Sciences 2021 · PMID 34575939
Cardarine (GW-501516) — safety, predicted from mechanism
Predicted from mechanism, not from a human safety trial. How that reasoning works →
What the mechanism predicts
Derived from the molecule, not a trial.
- Beta-2 agonists (clenbuterol, albuterol) and central stimulants (tesofensine) share one predicted problem: cardiac load. Raised heart rate, palpitations, tremor and insomnia are the mechanism showing up, not an idiosyncratic reaction.
- Beta-2 agonists drive potassium into cells, so hypokalemia is predicted — and low potassium is itself arrhythmogenic, which is how a stimulant side effect becomes a cardiac one.
- Clenbuterol's half-life is long (well over a day in humans), so it accumulates across daily dosing. The dose that felt fine on day one is not the exposure you have on day five.
- Beta-2 receptors downregulate within around two weeks — the thermogenic effect fades while the cardiac effect persists longer. That is the worst possible combination and it is why escalating the dose to chase the original effect is the dangerous move.
What has actually been reported
- Cardiac hypertrophy is documented in animal models at sustained high doses. Human data comes largely from poisoning case reports — tachycardia, tremor, hypokalemia, and arrhythmia.
- Tesofensine raised blood pressure and heart rate in trials, which is part of why its development for obesity stalled.
How to reduce the risk
Same mechanism as the prediction.
- Take a resting heart rate every morning. It moves before anything else does and it is a better early signal than any quarterly panel.
- Potassium and magnesium intake matter here specifically because of the intracellular shift — this is one of the few places a supplement addresses the actual mechanism rather than a vague deficiency.
- Do not escalate to recover a faded effect. The fade is receptor downregulation, and the answer is a break, not more.
What it does to your bloodwork
A fact about the assay.
- Potassium and magnesium (a CMP covers potassium). Blood pressure and resting heart rate are the real monitoring and they are free.
Don't run this if
- You have any arrhythmia, structural heart disease, or uncontrolled hypertension.
- You are already taking another stimulant, including high-dose caffeine — the cardiac effects are additive and people do not count coffee.
The honest unknown
- Whether the cardiac hypertrophy seen in animals occurs at the doses and durations used in humans is not established, and it would be difficult to study ethically.
Not medical advice. If you take prescription medication or have a diagnosed condition, check this with a pharmacist or doctor.
Cardarine (GW-501516) — interference & stacking
Predicted from mechanism, not from an interaction study. How mechanism-predicted claims are made →
What Cardarine (GW-501516) moves on your bloodwork
Expected direction, not a measured one.
- hs-CRP (High-Sensitivity C-Reactive Protein) — ↓ expected to fall
Where these work, systemic inflammation is the plausible readout.
What to do: hs-CRP is cheap and moves. Baseline and 12 weeks. - HbA1c (Hemoglobin A1c) — ↓ expected to fall
Improved mitochondrial and metabolic function should show here if the effect is real at all.
What to do: The honest use of these markers is as a falsification test: if nothing moves in 12 weeks, the compound is not doing much for you. - Comprehensive Metabolic Panel (CMP) — ◆ worth watching
Liver and kidney function — the standard baseline for anything run long term.
What to do: Twice a year is enough on a stable protocol.
This class is where honest expectation-setting matters most: the markers above are how you find out whether anything happened, and for most of these compounds that question is genuinely open.
- How to work up to it, and when not to
- When to take it, and why that window
- Cycle length
- Time off between cycles
- Fasted or fed, and when in the day
- How the forms differ in dose
- Coach Cam's personal notes
- Which compounds push the same lever, and why the dose adds up faster than people count
- What blunts it — the stacks that waste your money
- What compounds the risk, so a side effect arrives sooner than any one of them suggests
- Coach Cam's read on running it alongside the rest of your protocol
Everything above is free and stays free. Skool is where it becomes a plan — Cardarine (GW-501516) in an order, with the rest of what you're running.
Unlock in Skool — $10/mo →Bloodwork to run alongside Cardarine (GW-501516)
Baseline first, then again at 8–12 weeks.
| Marker | What it’s watching for |
|---|---|
| Comprehensive Metabolic Panel (CMP) | Liver and kidney baseline before a compound abandoned for cancer signals |
| Lipid Panel (Cholesterol, HDL, LDL, Triglycerides) | The HDL and triglyceride effect people take it for |
| Complete Blood Count (CBC) with Differential | Broad screen — human safety data here is essentially absent |
The Fatty Liver & Liver Health panel covers these in one order — 8 markers, $291.15 with the discount applied.
Check results you already have → · All 103 markers A–Z
Cardarine (GW-501516) — frequently asked questions
What is Cardarine (GW-501516)?
Cardarine (GW-501516) (GW-501516 / Endurobol) is a metabolic & fat loss research compound. PPARδ agonist — shifts fuel use toward fat oxidation and boosts endurance. Important: rodent studies showed cancer at high chronic doses.
Is the full Cardarine (GW-501516) protocol on this page?
The reported research dose is on this page, along with how Cardarine (GW-501516) works and the evidence behind it. The protocol — how to work up to it, frequency, cycle length, time off, what not to stack it with and Coach Cam's notes — is inside Skool.
What is the half-life of Cardarine (GW-501516)?
Cardarine (GW-501516) has an approximate half-life of ~20–24 hrs, which is part of what determines how often it's dosed.
What forms does Cardarine (GW-501516) come in?
Cardarine (GW-501516) is available as: Oral, Injectable.
What's the evidence behind Cardarine (GW-501516)?
Current evidence level: Animal (efficacy) + safety flag. Cardarine (GW-501516) is offered for research purposes only and is not an approved medicine.
Cardarine (GW-501516) inside a finished plan
One arm of 1 Protocol Blueprint, free to read in full.
What Cardarine (GW-501516) is used for
Cardarine (GW-501516) appears under 2 goals in the goal router.
Related Metabolic & Fat Loss compounds
Where this goes next
Cardarine (GW-501516) is the mitochondrial arm of this plan. The page above is the free breakdown of one compound; the plan it belongs to — the dosing, the order to correct things in, the week-by-week schedule and what to retest — is a lesson inside Skool.