Cardarine (GW501516): The Complete Guide

Cardarine’s safety record is dispositive, not theoretical. The entity with the strongest financial incentive to sell GW501516 — GlaxoSmithKline — looked at its own 2-year rodent toxicology data and chose to abandon a billion-dollar Phase 2 program rather than carry the liability into humans.

Any framing of Cardarine as “discontinued for business reasons” or “pulled because of misuse” inverts the actual record. GSK terminated this molecule because it produced cancer in animals at multiple organ sites, in both sexes, in a dose-dependent manner.

The regulatory anchors:

• GSK / Ligand discontinuation, 2007–2008. Around Phase 2, after long-term rodent carcinogenicity studies revealed dose-dependent tumors in multiple organ systems.
• WADA Prohibited List 2009–present. Currently classified under S4.5 Metabolic Modulators, prohibited at all times.
• WADA Public Health Alert, 21 March 2013. A rare, named, compound-specific advisory citing “serious toxicities discovered in pre-clinical studies.”
• USADA / Sport Integrity Australia have issued downstream advisories specifically about GW1516.
• Beyaz et al. Nature 2016 (PMID 26935695) — PPARδ signaling permits Apc-loss tumor formation in intestinal progenitor cells; mechanistic corroboration.
• Qian et al. 2025 (PMID 39993702) — tumor immune escape via CD47 upregulation; further oncology mechanism.

If you decide to use Cardarine anyway, do so with the carcinogenicity record fully visible. This guide does not endorse use.

Cardarine (GW501516, GW1516, Endurobol) is a synthetic small-molecule PPARδ (peroxisome proliferator-activated receptor delta) agonist. It is not a peptide and not a SARM, despite living in peptide-adjacent vendor catalogs and being commonly stacked with SARMs in gray-market practice.

Origin:

• Co-developed by GlaxoSmithKline and Ligand Pharmaceuticals in the late 1990s and early 2000s.
• Original therapeutic rationale: dyslipidemia / metabolic syndrome (raise HDL, lower triglycerides via PPARδ).
• Reached Phase 2 clinical trials.
• Discontinued by GSK around 2007–2008 after long-term rodent carcinogenicity findings.
• No INN was ever assigned (the molecule never advanced far enough).
• Pelton 2006 (Curr Opin Investig Drugs, PMID 16625823) captures the program at peak development just before the carcinogenicity disclosures.

Names you’ll see:

GW501516 and GW1516 are used interchangeably (“GW1516” is preferred by WADA / doping-control literature). Cardarine and Endurobol are trivial / market names.

Regulatory status:

• FDA (US): never approved. No NDA filed.
• EMA (EU): never approved.
• WADA 2026: prohibited at all times under S4.5 Metabolic Modulators. Detection windows: GW1516 and its sulfoxide / sulfone metabolites are routinely detected in human urine for 20–40 days post-administration (Sobolevsky 2012 PMID 22977012; Thevis 2010 PMID 19946680).

The mechanism is real and reproducible:

• PPARδ binding. GW501516 is a high-affinity, selective PPARδ agonist (selective vs PPARα and PPARγ).
• PPARδ activation drives transcription of fatty-acid oxidation genes, mitochondrial biogenesis genes, and a fiber-type shift toward type I (oxidative, slow-twitch) muscle.
• Transgenic muscle-specific activated PPARδ doubled running endurance in mice (Wang 2004, PLoS Biol, PMID 15328533) — a foundational paper.
• GW501516 + AMPK activation acted as a "pharmacological exercise mimetic" in untrained mice (Narkar & Evans 2008, Cell, PMID 18674809).
• Metabolomic confirmation in mice (Chen 2015, PMID 25943561).

The endurance phenotype is biologically real. The problem isn’t the on-target effect; it’s the off-target oncology.

Tumor-mechanism corroboration:

• Beyaz et al. Nature 2016 (PMID 26935695) — PPARδ signaling enables Apc-loss tumor formation in intestinal progenitor cells. Direct mechanistic plausibility for GI tumor risk.
• Qian et al. 2025 (PMID 39993702) — PPARδ-driven CD47 upregulation enables tumor immune escape.

The GSK rodent toxicology dossier itself was never published as a primary research paper (IND-stage tox is rarely published). The publicly available record is captured in WADA’s 2013 advisory and downstream regulatory communications.

A small number of Phase 1 / Phase 2 lipid trials were conducted before the long-term tumor disclosures or were terminated early. All are ≤ 12 weeks; none address the cancer-latency question.

Study	Population	Duration	Result
Sprecher 2007 (PMID 17110604)	Healthy subjects	Short	Lipid effects characterized
Risérus 2008 (PMID 18024853)	Moderately obese men	2 weeks	10 mg/d; HDL effects
Ooi 2011 (PMID 21816786)	Dyslipidemic central obesity	Short	Lipoprotein metabolism mechanism
Olson 2012 (PMID 22814748)	Low-HDL	12 weeks	HDL increase; secondary endpoints

No long-term human safety data exists. The cancer-latency question is unanswered in humans — and given the rodent multi-organ tumor signal at clinically relevant exposures, that gap matters.

Doping detection (proves it’s detectable):

• Routine doping controls since 2009 (Thevis 2010, PMID 19946680).
• Urinary metabolites detectable 20–40 days post-administration (Sobolevsky 2012, PMID 22977012; Ishii 2021, PMID 33319421).
• Hair detection (Kintz 2020, PMID 32298044).
• Combined GW1516 + ostarine cases — not all subjects claimed knowing co-administration (Kintz 2021, PMID 34678947).
• Transmission case report (Breuer 2024, PMID 38704758).

StackTrax does not endorse Cardarine use. The dosing below is community / forum convention.

Parameter	Common Range
Dose	10–20 mg/day oral
Cycle length	4–8 weeks (community); GSK Phase 2 dosed up to 12 weeks
Route	Oral capsule / liquid
Half-life	~24 hr

Harm-reduction rules for users who proceed anyway:

• Shortest possible exposure. Cardarine’s rodent tumors emerged in long-term (2-year) studies. Short cycles plausibly reduce risk; do not normalize chronic use.
• Do not stack with SARMs. The published case literature (Kintz 2021 PMID 34678947) documents combined use; it amplifies hepatic and oncology risk asymmetrically.
• Do not use during cancer screening lapses. If you’re not current on age-appropriate screens (colonoscopy, mammogram, PSA, etc.), get current first.
• Recognize the asymmetry. Short-term feel is benign; long-latency cancer risk is asymmetric in time. Subjective wellness is not safety data.

Acute (community reports):

• Mild GI effects (nausea, occasional).
• Fatigue early in cycle (paradoxical, given the endurance framing).
• Headache.

Lipids:

• HDL increase (the original therapeutic rationale).
• Triglyceride decrease.
• These lipid effects are real but do not offset the cancer concern over time.

The dominant concern: cancer-latency risk

• Multi-organ rodent carcinogenicity at clinically relevant exposures (GSK 2007–2008 disclosures; WADA 2013 advisory).
• Mechanistic corroboration in independent literature (Beyaz 2016 PMID 26935695; Qian 2025 PMID 39993702).
• No long-term human safety data.
• Cancer effects have long latency — the absence of acute symptoms during use is not informative about the actual risk.

• Active or prior cancer of any kind — absolute. Multi-organ rodent carcinogenicity + intestinal Apc-loss tumor mechanism (Beyaz 2016) make this a strong line.
• Family history of cancer (especially GI / colorectal, given the Apc mechanism) — relative caution.
• Lapsed cancer screening — do not start until age-appropriate screens are current.
• Pregnancy / breastfeeding / planning pregnancy — absolute.
• Liver disease — class caution for any small-molecule with hepatic metabolism.
• Concurrent SARM use — documented in case literature; amplifies risk.
• Athletes subject to anti-doping testing — do not use. WADA S4.5; metabolites detectable 20–40 days; hair detectable longer.
• Anyone unwilling to accept long-latency cancer risk for short-term endurance benefit.

• Seladelpar (MBX-8025) — a different PPARδ agonist that DID reach approval (FDA 2024, for primary biliary cholangitis). Seladelpar is not Cardarine and the seladelpar approval does not retroactively rehabilitate GW501516. Different molecule, different exposure profile, different indication.
• PPARγ agonists (TZDs — rosiglitazone, pioglitazone) — different receptor subtype, different metabolic effects.
• Fibrates (PPARα agonists) — different receptor subtype.
• SARMs (RAD-140, LGD-4033, etc.) — androgen receptor modulators, completely different target. Common stacking partners but mechanistically unrelated.
• SR9009 — Rev-erbα agonist, completely different target. Vendor framing of "SR9009 = safer Cardarine" is unsupported.
• SLU-PP-332 — ERRβ/γ agonist; another exercise-mimetic class candidate.
• AICAR — AMPK activator (different mechanism).