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Slu3.0
SLU-PP-332 Research
Mostly mechanism / observational
5 peer-reviewed studies
What the evidence says
Mostly mechanism / observational
Most SLU-PP-332 studies are mechanism or observational rather than RCTs that measure a clinical effect — keep findings provisional.
Most evidence is from mixed-quality studies published 2023–2025.
Based on 5 studies
Confidence
Low confidence
By outcome
Endurance & exercise capacity (preclinical)Increased endurance and fat oxidation in mice as a pan-ERR "exercise mimetic"; no human data of any kind. · Not established (no human data)
Too few graded studies2 studies
Metabolic & fat oxidation (preclinical)
Too few graded studies1 study
Cardiac & heart failure (preclinical)
Too few graded studies1 study
Aging & healthspan (preclinical)
Too few graded studies1 study
Safety profile
Too few graded studies1 study
Active research area
5 studies in the last 5 years
1Animal2023
In plain English: An 8-week treatment with a pan-ERR agonist (SLU-PP-332) reversed the age-related increases in albuminuria, podocyte loss, mitochondrial dysfunction, and inflammatory cytokines in aged mice.
Wang XX, Myakala K, Libby AE, Krawczyk E, Panov J, Jones BA, et al. · Am J Pathol (2023)
Treated 21-month-old mice with the pan-ERR agonist SLU-PP-332 for 8 weeks
Reversed age-related albuminuria, podocyte loss, mitochondrial dysfunction, and inflammation — similar to lifelong caloric restriction
Acts via cGAS-STING and STAT3 signaling; ERR expression was lower in aging human and mouse kidneys
In plain English: Both SLU-PP-332 and SLU-PP-915 significantly improved ejection fraction, ameliorated fibrosis, and increased survival associated with pressure overload-induced heart failure.
Xu W, Billon C, Li H, Wilderman A, Qi L, Graves A, et al. · Circulation (2024)
Tested SLU-PP-332 and the sibling pan-ERR agonist SLU-PP-915 in a mouse pressure-overload heart-failure model
Both improved ejection fraction, reduced fibrosis, and increased survival without affecting cardiac hypertrophy
Mechanism via transcriptional activation of fatty-acid-metabolism and mitochondrial genes, increasing cardiac oxidative capacity and fatty-acid use in vivo and in vitro
In plain English: Pharmacological exercise mimetics may be effective in the treatment of obesity and metabolic syndrome; SLU-PP-332, an ERR agonist, alleviated metabolic syndrome in mice.
Billon C, Schoepke E, Avdagic A, Chatterjee A, Butler AA, Elgendy B, et al. · J Pharmacol Exp Ther (2024)
Direct follow-up testing SLU-PP-332 as a pharmacological exercise mimetic in a mouse metabolic-disease model
Enhanced fatty-acid/fat oxidation and alleviated features of diet-induced obesity and metabolic syndrome
Frames ERR agonism as a candidate approach for obesity and metabolic syndrome
In plain English: A synthetic pan-ERR agonist (SLU-PP-332) induced an ERRα-dependent acute aerobic exercise response in skeletal muscle and enhanced exercise capacity.
Foundational paper introducing SLU-PP-332 — the first synthetic compound with meaningful ERRα agonist activity (ERRβ/γ agonists existed before; ERRα had been hard to drug)
In mice, the compound induced the same acute aerobic-exercise transcriptional program in skeletal muscle that physical exercise triggers, and the response was ERRα-dependent
Enhanced exercise capacity (running performance) — the central 'exercise mimetic' result
In plain English: Primary cultures of myoblasts from inactive women were treated with the ERRs agonist SLU-PP-332 to assess metabolic and expression changes associated with ERR activation.
Bonanni R, Falvino A, Matticari A, Rinaldi AM, D'Arcangelo G, Cifelli P, et al. · Front Physiol (2025)
Applied SLU-PP-332 to myoblasts cultured from muscle biopsies of physically inactive women — an ex-vivo human-cell pilot, NOT a human clinical trial
Inactive women's muscle showed reduced SIRT1, PGC-1α, ERRα, and FNDC5 (and elevated NOX4) versus active women
Probes the PGC-1α/ERRα 'exercise' axis the compound is proposed to activate, in human-derived cells