SLU-PP-332 Research Guide: ERR Pan-Agonist Exercise Mimetic
SLU-PP-332 is a first-in-class ERR pan-agonist small molecule that reproduces key transcriptional signatures of endurance exercise in animal models.
What is SLU-PP-332?
SLU-PP-332 is a small-molecule ERR pan-agonist developed at Saint Louis University by the Burris lab. It is the first characterized compound to activate all three ERR isoforms in vivo at pharmacologically relevant concentrations.
Mechanism of action
ERRα/β/γ are orphan nuclear receptors that partner with PGC-1α to drive transcription of the mitochondrial biogenesis and fatty-acid oxidation programs. SLU-PP-332 recapitulates this transcriptional signature — the same pattern induced by endurance exercise training.
In published mouse work, SLU-PP-332 doubled running-to-exhaustion time and increased slow-twitch (type I) muscle fiber content without altering body weight or feeding.
Sourcing & purity
Research-grade material should be ≥99% pure by HPLC with peptide content confirmed via mass spectrometry. Redline Bio material ships with batch documentation; independent third-party COAs are published on the lab reports page as testing returns.
Compliance reminder
Sold and distributed for laboratory research use only. Not approved by the FDA for human consumption, diagnosis, treatment, or cure of any disease. Researchers are responsible for compliance with all applicable institutional, state, and federal regulations.
Frequently asked questions
What is SLU-PP-332?
SLU-PP-332 is a small-molecule pan-agonist of the estrogen-related receptors ERRα, ERRβ, and ERRγ — orphan nuclear receptors central to mitochondrial biogenesis and oxidative metabolism.
Mechanism?
ERR activation drives transcription of PGC-1α target genes including those encoding electron transport chain subunits, fatty-acid oxidation enzymes, and slow-twitch (type I) muscle fiber markers — the same program upregulated by endurance exercise.
Published data?
A 2023 Nature Metabolism paper reported that SLU-PP-332 increases running endurance and oxidative capacity in mice without altering body weight, feed intake, or activity level — supporting the 'exercise mimetic' framing.