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SS-LUP-332 ERRα/γ Agonism: Mechanism Comparison
The table below contrasts SS-LUP-332 ERRα/γ agonism against alternative metabolic pathways across key research endpoints: mitochondrial biogenesis, substrate flexibility, tissue specificity, and functional performance outcomes. | Mechanism | Primary Target | M
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- The table below contrasts SS-LUP-332 ERRα/γ agonism against alternative metabolic pathways across key research endpoints: mitochondrial biogenesis, substrate flexibility, tissue specificity, and functional performance outcomes.
- | Mechanism | Primary Target | Mitochondrial Biogenesis | Substrate Flexibility | Tissue Specificity | Functional Outcome | Professional Assessment ||—|—|—|—|—|—|| SS-LUP-332 ERRα/γ agonism | ERRα/γ nuclear receptors | 40–60% increase in mitochondrial density (citrate synthase activity) within 28 days | Dual enhancement: fat oxidation +50%, preserves glycolytic capacity | Skeletal muscle, heart, BAT, liver. Highest in oxidative tissues | VO2max +34%, endurance +89%, RER shift to 0.78 (fat-dominant) | Gold standard for coordinated metabolic remodeling. Synergistic dual-receptor activation produces outcomes single-pathway modulators cannot replicate || PPAR-δ agonism (GW501516) | Peroxisome proliferator-activated receptor delta | Minimal direct effect. Upregulates FAO enzymes but not mitochondrial content | Increases fat oxidation but impairs high-intensity glycolytic output | Skeletal muscle, liver | Endurance +18%, fat oxidation +30%, no VO2max improvement | Strong for fat metabolism b