At a glance

Endurance / aerobic capacity (preclinical)
Fat mass reduction (preclinical)
Insulin sensitivity / metabolic health (preclinical)
Mitochondrial biogenesis
Cardiovascular / cardiac safety unknown
No human safety data — unvalidated experimentation
Off-target ERR tissue effects
Oncological risk signal (ERRα–cancer pathways)
BenefitSide effectHealth risk· more & brighter bars = stronger

Effects

  • Endurance / exercise capacity: Mouse models treated with SLU-PP-332 showed 20–30% improvements in running distance and time vs. controls, alongside increased oxidative type IIa muscle fibres [2][4].
  • Fat mass reduction: Preclinical studies in obese mouse models demonstrated significantly decreased fat mass accumulation and enhanced fatty acid oxidation [5][7].
  • Improved insulin sensitivity: ERR agonism reduced obesity and improved insulin sensitivity in diet-induced obese and ob/ob mouse models [5][7].
  • Increased energy expenditure: Whole-body metabolic studies in mice showed increased resting energy expenditure without changes in food intake [7].
  • Mitochondrial biogenesis: Enhances mitochondrial function and cellular respiration in skeletal muscle, recapitulating key adaptations of endurance training [4][5].
  • Potential cardiac protection: ERR agonism has shown cardioprotective effects in pressure-overload heart failure models in preclinical research, linked to maintained oxidative metabolism in cardiomyocytes [8].
Classification

Pan-ERR (ERRα/β/γ) agonist · Exercise mimetic · Research compound only

Active half-life

Not established in humans; rodent estimate ~8–10 h (preclinical only) [14]

Route

Intraperitoneal injection in all published studies; human route unvalidated. Oral bioavailability reportedly poor or absent [13]

Regulatory status

No FDA approval · No IND · No registered human clinical trials · Research use only [9]

EC50 (ERRα)

98 nM (in vitro) [3]