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Slu3.0
SLU-PP-332 Research
Mostly mechanism / observational
9 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 medium-quality studies published 2023–2026.
Based on 9 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)
Mostly mechanism / observational4 studies
Metabolic & fat oxidation (preclinical)
Mostly mechanism / observational3 studies
Cardiac & heart failure (preclinical)
Too few graded studies2 studies
Aging & healthspan (preclinical)
Too few graded studies2 studies
Safety profile
Too few graded studies2 studies
Active research area
9 studies in the last 5 years
20232026
1Systematic Review2026
In plain English: Pharmacological activation of ERRα/β/γ is a promising strategy as an exercise mimetic, with potential therapeutic applications in metabolic diseases, aging, and muscle-related conditions.
de Souza-Lima J, Astrosa-Martin BD, Galaz-Rodríguez CA, Silva-Bernal JE, Orellana-Pizarro LI, Mena-Díaz CA. · Revista medica de Chile (2026)
SLU-PP-332 and SLU-PP-915 reduce adiposity, improve glycemic control, and increase basal energy expenditure in obesity models, without evident toxicity.
Additionally, they restore mitochondrial function and reduce inflammation in aging kidneys.
Conclusions Pharmacological activation of ERRα/β/γ is a promising strategy as an exercise mimetic, with potential therapeutic applications in metabolic diseases, aging, and muscle-related conditions.
In plain English: Collectively, the ongoing development of TRβ, ERRα, and LXR modulators exemplifies a new frontier in precision medicine, offering powerful approaches to reprogram dysregulated metabolic pathways with substantial promise for treating metabolic diseases.
Di Giovanni C, Lavecchia A. · Biomolecules (2026)
TRβ agonists, including resmetirom (MGL-3196) and VK2809, have demonstrated compelling efficacy in clinical trials for metabolic dysfunction-associated steatohepatitis (MASH), significantly reducing hepatic steatosis and fibrosis.
Next-generation hepatoselective modulators such as TG68 enhance tissue specificity and potency.
ERRα, a master regulator of mitochondrial biogenesis and energy metabolism, is targeted by inverse agonists (compound 29 , GSK5182) and agonists (JND003, SLU-PP-915), which show promise in ameliorating insulin resistance and promoting lipid oxidation in preclinical obesity models.
In plain English: These findings provide guidance for further study on new ERRγ modulators.
Zheng Y, Du Y, Zhang H, Lv H, Yan Z, Dong N, Li Q, Wang T. · Current medicinal chemistry (2024)
The collision between residue Phe435 and the modulator is a key factor determining the activation or inhibition of ERRγ.
Although more than 20 agonists and inverse agonists of ERRγ have been reported, no clinical studies have been found in the literature.
This review summarizes the important relationship between ERRγ-related signaling pathways and diseases, research progress, and the structure-activity relationship of modulators.
In plain English: This review highlights new findings and provides a path to understanding the current ideas and future studies on ERRγ-mediated cellular activity.
Sadasivam N, Park WR, Choi B, Seok Jung Y, Choi HS, Kim DK. · Steroids (2024)
Moreover, ERRγ has proven crucial in regulating cellular and metabolic activity.
However, many functions mediated via ERRγ remain unknown and require further exploration.
Hence, considering the importance of ERRγ, this review focuses on the critical findings and interactions between ERRγ and co-regulators, agonists, and antagonists alongside its relationship with downstream and upstream signaling pathways and diseases.
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