COMPOUND

Compounds / SARMs

Cardarine

GW-501516 (Endurobol)

SARMs Oral Restricted (FDA Cat. 2)

PPARδ agonist developed by GlaxoSmithKline and Ligand Pharmaceuticals in the late 1990s. GSK abandoned development in 2007 after a 2-year rat carcinogenicity study (Geiger 2009 SOT abstract) showed multi-organ tumor formation including liver, stomach, tongue, skin, bladder, ovaries, uterus, and testes at doses ≥3 mg/kg/day. WADA banned 2009; formal WADA public warning issued 2013 stating clinical approval has not and will not be given. NO SAFE CYCLE EXISTS: the chronic PPARδ activation mechanism is concerning at any duration. Despite this, used in endurance athlete and biohacker communities for reported endurance gains.

At a glance

Half-life
~24 h Community/secondary sources cite 12-24h half-life supporting QD or BID dosing. No published human PK study with formal half-life determination.
Routes
Oral
Evidence base
2 studies 1 human · 1 preclinical

Mechanism

Selective PPARδ (peroxisome proliferator-activated receptor delta) agonist. PPARδ activation in skeletal muscle increases fatty acid oxidation, shifts fuel preference from glucose to lipids, and increases mitochondrial biogenesis. Multi-organ tumor formation (liver, stomach, tongue, skin, bladder, ovaries, uterus, testes) at doses ≥3 mg/kg/day in chronic animal studies: basis for GSK discontinuation and WADA ban. Short-term human phase 2 showed improved HDL and reduced TG in metabolic syndrome patients. The cancer-promoting mechanism is hypothesized to involve chronic PPARδ activation driving cell proliferation in tissues with high baseline PPARδ expression, making any chronic dose mechanistically concerning regardless of cycle length.

Dosing

Any amounts shown here are reported from published studies only. 1 of 2 catalogued studies involved human subjects. COMPOUND does not publish its own dosing guidance.

Published evidence

  1. Human RCT 2012

    Lipid effects of PPAR-δ agonist GW501516 in subjects with low HDL: characteristics of metabolic syndrome

    Olson EJ, Pearce GL, Jones NP, Sprecher DL Arterioscler Thromb Vasc Biol

    Phase 2 clinical trial in metabolic syndrome: improved HDL, reduced TG, modest LDL reduction. Short-term tolerability good. Highest-quality human safety study; sponsored before carcinogenicity findings emerged.

    PMID 22814748

  2. Animal in vivo 2009

    Mouse carcinogenicity study with GW501516, a PPAR delta agonist

    Geiger LI, Dunsford WR, Lewis DH, Brennan C, Liu K, Newsholme S, et al. Toxicologist (SOT 48th Annual Meeting Abstract)

    Sponsor-presented (GSK) abstract, never full-text published. Reported multi-organ tumor formation in chronic dosing studies. Used by WADA as basis for formal warning. Specific dose-response data not publicly accessible.

Reported side effects

Multi-organ tumors at biohacker-equivalent doses (rat carcinogenicity, GSK-discontinued 2007)
Unknown Serious · Geiger 2009 (SOT abstract) reported tumors in liver, stomach, tongue, skin, bladder, ovaries, uterus, testes at doses ≥3 mg/kg/day. Liver tumor incidence approached 90% in high-dose groups at 104 weeks. Rat-to-human BSA conversion places biohacker doses (10-20 mg/day) within the carcinogenic range. Mechanism (chronic PPARδ activation) is biologically plausible at any chronic dose. WADA issued formal warning in 2013 citing cancer risks.
Hepatic effects
Unknown Moderate · Rat liver was a primary tumor site. No formal hepatotoxicity case reports in humans yet, but liver should be monitored. Annual LFTs recommended if used despite warnings.
No HPTA suppression
Rare Mild · PPARδ agonist: no AR or HPG axis activity. Does not require PCT.

Interactions

  • Ostarine Synergy

    'Recomp stack' for cutting. The cardarine carcinogenicity warning overrides any synergy benefit.

  • MK-677 Caution

    GH/IGF-1 elevation may compound proliferative signal of PPARδ agonism. IGF-1 is mitogenic; combined with PPARδ chronic activation, may amplify cancer risk.

Storage

Capsules room temp; liquid PEG/ethanol vehicle, refrigerate after opening.