Cardarine

evidence score

sarm

Research Only

200 studies

GW501516GW1516Endurobol+2 more

Cardarine (GW501516) is a PPARδ agonist (not technically a SARM) that dramatically increases fat oxidation, endurance, and metabolic rate by activating genes involved in fatty acid catabolism. Human clinical development was halted by GlaxoSmithKline in 2007 after accelerated tumor development was observed across multiple organ systems in long-term rodent toxicity studies. Despite this, it remains widely used in athletic communities. The cancer risk in humans is unknown but the animal data is consistent and concerning. This profile is presented for harm reduction purposes only. WARNING: Cardarine caused rapid cancer development in animal studies at doses comparable to human use. The carcinogenic mechanism (PPARδ activation promoting cell survival and proliferation) is not species-specific. Use in humans carries unknown but potentially serious cancer risk.

Evidence

Moderate evidence

Safety

Unknown safety profile

Clinical Status

No formal trials

Research Sync

Feb 19, 2026

Dosing

Typical

10 mg

5 mgRange20 mg

FrequencyOnce daily oral

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Pharmacology

Half-life16–24 hours

OnsetDays for endurance; 2–4 weeks for fat loss

DurationEffects active during dosing period

Routes

oral

Evidence Score

Level B — Moderate

200 studies indexed

Scoring Factors

Volume(40%)~46/100

Quality(30%)~40/100

Sample Size(10%)~100/100

Consistency(10%)~100/100

Replication(5%)~100/100

Recency(5%)~100/100

Scores estimated from study counts. Exact breakdown computed after research sync.

Evidence Levels

AScore ≥75 with at least 1 meta-analysis and 3+ RCTs

BScore ≥50 with at least 1 RCT or meta-analysis

CScore ≥25 — observational or animal evidence only

DScore <25 — very limited or preclinical data

Plain-English Snapshot

Cardarine is currently categorized as a sarm compound.

Evidence is moderate (63/100): promising signal from 200 indexed studies, but context and population still matter.

Safety scoring is incomplete. Start conservatively and monitor carefully.

Core mechanism

PPARδ/β agonist; transcriptionally activates fatty acid oxidation genes (CPT1, ABCA1) in skeletal muscle; dramatically increases mitochondrial biogenesis and fat burning

Practical Context

Strongest current signals

Level C: Distinct Roles of PPARs in Atherosclerosis.
Level D: It is suggested that Pioglitazone reduces PCa cell proliferation and induces metabolic and epithelial changes, highlighting the potential of repurposing metabolic drugs for PCa therapy.
Level D: The results have demonstrated the promise of this combination: an increase in the survival time of combination-treated groups and a reduction of tumor volume and survival studies of the combination immunotherapy in melanoma and breast cancer models, demonstrating the utility of the immunotherapy for other highly metastatic cancers.

Elevated caution signals

1 severe/high side effect flag