Description
SLU-PP-332
Mechanism of action and evidence snapshot with PubMed links. For research and educational purposes only—no medical advice or therapeutic claims.
What is SLUPP-332 for sale?
SLU-PP-332 is a synthetic pan-agonist of the estrogen-related receptors (ERRα/β/γ), nuclear receptors that control programs for oxidative metabolism, mitochondrial function, and energy homeostasis. Published work characterizes SLU-PP-332 as a chemical tool with in vivo activity suitable for modeling exercise-responsive transcriptional programs in preclinical systems.
Mechanism of Action (scientific detail)
1) Direct activation of ERRs (α/β/γ)
SLU-PP-332 binds ERR ligand-binding domains and activates ERR-dependent transcription, with highest potency toward ERRα. This receptor family coordinates genes for mitochondrial respiration, lipid handling, and oxidative muscle phenotypes. In cells, SLU-PP-332 increases markers of mitochondrial function and cellular respiration (e.g., Seahorse assays measuring OXPHOS capacity).1
2) Exercise-like acute gene program
In mouse skeletal muscle, short-term dosing induces an acute aerobic exercise gene signature (RNA-seq), including transient up-regulation of DDIT4 and other ERR targets. This transcriptional response overlaps with gene sets observed after acute endurance exercise in rodents and humans, mapping SLU-PP-332 to an exercise-mimetic transcriptional space (mechanistic context, not a clinical claim).1
3) Mitochondrial & substrate-use remodeling
Preclinical data show increased oxidative enzyme content (OXPHOS complexes), higher mitochondrial markers (e.g., cytochrome c), and a shift toward oxidative type IIa fibers in skeletal muscle after dosing. ERR activation is a known upstream driver of fatty-acid oxidation, mitochondrial biogenesis (PGC-1α–linked coactivation), and improved oxidative capacity at the tissue level.1
4) Whole-body metabolic programming (preclinical)
In diet-induced obesity and metabolic-syndrome models, pharmacologic ERR activation by SLU-PP-332 has been reported to remodel metabolic gene networks in multiple tissues (e.g., muscle, liver) and align physiological readouts with increased energy expenditure and lipid utilization—findings specific to the research setting.2
Evidence Snapshot (preclinical)
- ERR-dependent exercise program & performance (mice): SLU-PP-332 increased mitochondrial function in myocytes, shifted muscle toward oxidative type IIa fibers, and enhanced running endurance; ERRα dependence was demonstrated via genetic models.1
- Metabolic-syndrome context (mice): ERR agonism with SLU-PP-332 aligned with improved oxidative metabolism and transcriptomic remodeling in metabolic tissues in vivo (mechanistic endpoints, not clinical outcomes).2
PubMed References (1–2)
- Billon C, et al. Synthetic ERRα/β/γ Agonist Induces an ERRα-Dependent Acute Aerobic Exercise Response and Enhances Exercise Capacity.
PubMed 36988910 - Billon C, et al. A Synthetic ERR Agonist Alleviates Metabolic Syndrome.
PubMed 37739806
