SLU-PP-332 is a synthetic benzohydrazide-class compound developed at Saint Louis University as a pan-agonist of the estrogen-related receptors (ERRα, ERRβ, ERRγ). Its primary research interest lies in its ability to pharmacologically replicate the transcriptional effects of aerobic exercise at the cellular level — a property that has made it a leading candidate in the field of exercise mimetics. All available data are preclinical (animal models); no human clinical trials have been completed as of mid-2026.
Chemical class: benzohydrazide derivative. Primary target: ERRα (EC50 ≈ 98 nM); ERRβ (EC50 ≈ 230 nM); ERRγ (EC50 ≈ 430 nM). Classification: synthetic pan-ERR nuclear receptor agonist.
Important classification note: SLU-PP-332 is a small molecule, not a peptide in the chemical sense. It is listed alongside research peptides because it is widely researched in metabolic-disease contexts adjacent to peptide-based metabolic research.
The estrogen-related receptors (ERRs) are nuclear receptors that regulate genes governing mitochondrial biogenesis, fatty acid oxidation, and oxidative phosphorylation. They are primarily co-activated by PGC-1α — the master regulator of mitochondrial biogenesis and the key mediator of exercise adaptation.
SLU-PP-332 binds the ligand-binding domain of ERRα/β/γ, stabilizing an active receptor conformation and enhancing PGC-1α recruitment. The downstream transcriptional output is an aerobic-exercise-like gene program: upregulation of CPT1B, COX4I1, and dozens of genes governing mitochondrial respiration and oxidative capacity.
In skeletal muscle, this effect is primarily ERRα-dependent for the acute exercise gene signature. ERRγ activity appears more prominent in cardiac tissue. The net effect: enhanced cellular energy expenditure, increased fat oxidation, and metabolic adaptation that mirrors the molecular response to sustained aerobic exercise — without the physical stimulus.
Foundational Skeletal Muscle Study (Billon et al., 2023, PMID: 36988910): SLU-PP-332 induces an ERRα-dependent aerobic exercise gene program in skeletal muscle cells (C2C12 myocytes), increases mitochondrial respiration, and extends running endurance in mice.
Metabolic Syndrome Model (Billon et al., 2024, PMC10801787): In diet-induced obese mouse models, SLU-PP-332 produced significant increases in whole-body energy expenditure and fatty acid oxidation, reduced fat mass accumulation, improved insulin sensitivity, and normalized glucose homeostasis — without altering food intake.
Cardiovascular Research (AHA Circulation, 2024): Pan-ERR agonism demonstrated cardioprotective effects in models of metabolic cardiomyopathy, primarily through enhanced myocardial fatty acid metabolism and mitochondrial efficiency.
SLU-PP-332 is studied in: metabolic disease pharmacology, exercise physiology and mimetics, mitochondrial biogenesis research, obesity and fat oxidation models, and nuclear receptor pharmacology.
Additional emerging research contexts include cardiometabolic disease modeling, aging-associated mitochondrial dysfunction, sarcopenia and muscle-atrophy investigation, and comparative pharmacology against other nuclear-receptor modulators. The compound is also used as a chemical probe to dissect PGC-1-alpha-dependent and independent ERR signaling, providing a valuable tool for basic transcriptional biology research beyond its exercise-mimetic profile.
Form: lyophilized powder or solution. Purity: ≥98% HPLC verified. Storage: −20°C, desiccated.
For research use only. Not for human consumption. No human clinical trials completed.
No. Despite being marketed alongside peptides, SLU-PP-332 is a synthetic small molecule (benzohydrazide class). It is not a peptide in the chemical sense.
An exercise mimetic is a compound that pharmacologically replicates cellular adaptations induced by physical exercise — such as mitochondrial biogenesis and fat oxidation — without requiring physical exertion.
As of mid-2026, all SLU-PP-332 data are preclinical. No human clinical trials have been completed or registered.
SLU-PP-332 is a pan-ERR agonist with highest potency at ERRα (EC50 ≈98 nM), followed by ERRβ (≈230 nM) and ERRγ (≈430 nM).