All compounds

Cardarine

Also sold as GW-501516, GW1516, GSK-516, Endurobol. PPARδ (peroxisome proliferator-activated receptor delta) agonist.

The evidence says don’t (5 of 5)

GlaxoSmithKline developed cardarine as a metabolic drug and stopped when long-term animal studies produced cancers across multiple organs — and it is still sold to athletes today, on the strength of the endurance results from the same programme.

What it is

Cardarine is GW-501516, a PPARδ agonist developed in the 1990s by GlaxoSmithKline in collaboration with Ligand Pharmaceuticals. It was a serious pharmaceutical programme aimed at a serious market: dyslipidaemia and metabolic disease.

It is not a SARM, despite being sold alongside them and constantly described as one. It does not touch the androgen receptor. It works on an entirely different system, and grouping it with SARMs obscures what it actually does.

GlaxoSmithKline stopped developing it. That single fact does more work than any warning we could write. A company that had spent years and a great deal of money on a compound walked away from it. Drugs are abandoned for many reasons — commercial ones, competitive ones, ordinary disappointing results. This one was not abandoned for a commercial reason.

Anti-doping authorities then did something they very rarely do. Rather than simply adding the compound to the prohibited list, the World Anti-Doping Agency issued a public warning directly to athletes in 2013, citing serious health risks rather than fair play. WADA polices sport; warning people about toxicity is not normally its job.

We should be straight about the status of that last claim, because this site’s rule is that you can check what it says. The 2013 warning is widely reported and is not in dispute, but we have not been able to link a stable, durable copy of the original notice — so treat it as public record rather than as a document we are handing you. Everything else on this page is cited to something you can open.

What it actually does

PPARδ is a receptor that sits inside cells and controls which genes get expressed in fat and muscle metabolism. Activating it shifts muscle towards burning fat for fuel rather than glucose.

The effects are real and, in the right context, impressive. In rodents PPARδ activation produced large increases in running endurance — enough that the compound picked up the nickname “exercise in a pill.” In human trials it improved blood lipid profiles, which was the actual clinical target: it raised HDL and lowered triglycerides.²

For an endurance athlete, what that translates to is a genuine change in how long they can hold an effort. This is not a placebo product, and pretending otherwise would be the fastest way to lose anyone reading this page who has actually taken it and noticed it work.

That is the whole difficulty with cardarine. It does what it says. The problem is not on the day you take it.

What the evidence actually shows

In humans: there were short clinical trials, and they showed the intended metabolic effects on lipids. They were short — weeks, not years — and they were designed to test whether the drug moved lipid numbers, not whether it caused cancer. They are the entire human evidence base, and they cannot answer the question that matters.

In animals: this is where the programme ended. Long-duration carcinogenicity studies — the standard multi-year rodent studies every drug candidate must pass before it can go near a long-term human population — produced tumours across multiple organ systems. Development stopped.²

We want to be precise about the status of that evidence, because being precise is the point of this site. The detailed carcinogenicity findings came out of the developer’s preclinical toxicology package. They were reported into the regulatory and anti-doping world rather than published as a standalone peer-reviewed paper you can pull up and read, which is normal for a programme that is terminated before approval and is also genuinely unsatisfying. What is on the public record is the discontinuation itself and WADA’s unusual decision to warn athletes explicitly about health risk.

What that adds up to: the strongest evidence against cardarine is animal evidence, and animal carcinogenicity does not always translate to humans. We are not going to pretend it is a proven human carcinogen, because it has not been demonstrated to be one.

But consider what is actually being proposed. Multi-year rodent carcinogenicity testing exists precisely to catch drugs that will cause cancer in people, before people take them. Cardarine failed that test, comprehensively enough that its developer wrote off the investment. Taking it anyway is a decision to run the experiment the test was designed to prevent, in yourself, without follow-up.

There is also ongoing laboratory work on how PPARδ activation behaves around tumours — including recent studies on immune escape³ and on invasive bladder cancer cell lines.⁴ That is cell-culture work, not evidence of harm in a person, and we flag it as suggestive rather than conclusive.

The risk profile

The evidence says don’t (5 of 5) — The known downside is severe enough that we will say it plainly rather than hedge.

What going wrong looks like from the inside

Nothing. That is the failure mode.

Every other page on this site can tell you what to watch for — the escalation, the shortening gap between doses, the sleep going wrong, the mole that changed. Cardarine has no such signal. There is no tolerance to notice, no withdrawal to run into, no organ that starts complaining, no bad day that tells you to stop.

What you get instead is a compound that works. Your endurance improves. Your lipid panel, if you check it, looks better than it did. You feel good. Every piece of feedback available to you from inside your own body says this was a good decision, and every one of those signals is telling you about the mechanism, not about the risk.

The risk is a tumour, years later, in an organ you were not thinking about, with nothing linking it back. If it happens, it will not present as a cardarine problem. It will present as cancer, and nobody — including you — will be able to say whether the compound caused it.

That is the specific reason this one sits in our most serious band despite scoring 1 for dependence and 1 for acute toxicity. There is no mechanism by which experience can teach you anything. Feeling fine is not information. It is the expected result either way.

Interactions and combinations

Cardarine is not a central nervous system depressant and does not carry the stacking risk that dominates the phenibut and kratom pages. Combining it with alcohol or sedatives is not how it hurts people.

It is very commonly stacked with SARMs, and it is usually sold by the same vendors, which is worth naming for two reasons. First, it means people taking it are frequently also taking compounds with real liver toxicity, and if something does go wrong the picture is muddied. Second, being sold alongside SARMs has caused cardarine to be discussed as though it were one — so people apply what they have read about androgen-receptor side effects and testosterone suppression, and conclude cardarine is the mild one in the stack. On the dimension that matters, it is not.

If you have taken it and you are having any conversation with a doctor, name it separately from anything else in the stack, and say it is a PPARδ agonist. Almost nobody will recognise the name.

If you’re already using it

There is no withdrawal and no reason to come off it gradually. You can stop today and nothing will happen. If you are going to stop, that is the entire procedure.

If you have already taken it, the honest position is this: nobody can tell you what your risk is. There is no test for “did this compound start something.” There is no screening protocol for a general-population exposure to a discontinued PPARδ agonist, and any clinic offering you one is selling something.

What is worth doing is unglamorous. Tell your doctor, by name, what you took and roughly for how long, and ask for it to go in your record. Do not skip routine cancer screening when you become eligible for it. If a symptom shows up that would warrant investigation in anyone, get it investigated rather than waiting.

And it is worth saying plainly, because people who read a page like this often need to hear it: most people who have taken cardarine will be fine. Elevated risk is not certainty. The reason to stop is that the risk is unquantified, permanent, and buys you an endurance benefit you can get other ways.

This page has not yet been reviewed by a clinician. It was written from the published literature and every claim is cited, but no named medical professional has checked it. We say so here rather than let a missing byline read as an implicit one.

Last reviewed 7 September 2026. Found something wrong? Corrections are published, not silently edited.