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SLU-PP-332 research

What published studies found for SLU-PP-332: 6 papers, 1 in humans, with sample sizes and key results.

C
Mostly animal studies
Why: Several mouse studies show more endurance and less fat gain; no human studies of any kind.

SLU-PP-332 is an experimental ERR agonist studied only in mice and cell cultures, where it increased endurance and energy expenditure and reduced fat gain. No human trials exist; a 2026 systematic review states clinical trials are needed.

✓ 5 positive? 1 inconclusive

No human safety data in the published literature; it is studied as a doping target by anti-doping laboratories.

US compounding: Not compoundable. Not an FDA-approved drug and not nominated for FDA's 503A bulks list, so US pharmacies can't legally compound it. Status for every peptide.

Browse and filter these papersSLU-PP-332 prices and vendors

Meta-analyses & systematic reviews

? Inconclusivesystematic reviewRev Med Chil · 2026

[Pharmacological Activation of ERRα/β/γ as an Exercise Mimetic: Potential Therapeutic Applications].

Humans and animalsSystematic review

Systematic review of pan-ERR agonists (2020-2024, animal and cell studies only): exercise-like gene programs, less adiposity and better glucose control in rodents, but efficacy and safety in humans are untested.

Studied
Preclinical animal and cell studies (2020-2024) of pan-ERR agonists, especially SLU-PP-332 and SLU-PP-915
Main outcome
Effects on energy metabolism, muscle function, renal aging and metabolic syndrome
Authors' conclusion
Pharmacological activation of ERR alpha/beta/gamma is a promising exercise-mimetic strategy for metabolic disease, aging and muscle conditions; clinical trials are needed to confirm efficacy and safety in humans.
Limitations
Only preclinical studies; no human data.
PubMed 42024694DOI

Animal & lab studies

✓ PositiveanimalACS Chem Biol · 2023

Synthetic ERRα/β/γ Agonist Induces an ERRα-Dependent Acute Aerobic Exercise Response and Enhances Exercise Capacity.

Humans and animalsIdentification and characterization of SLU-PP-332 in vitro and in vivo

SLU-PP-332 increased mitochondrial respiration in muscle cells and, in mice, increased oxidative type IIa fibres and running endurance via ERRalpha.

Studied
Skeletal muscle cell line and mice
Main outcome
Mitochondrial function, muscle fiber type, exercise endurance, exercise gene program
Authors' conclusion
SLU-PP-332, a pan-ERR agonist most potent at ERR alpha, increased type IIa oxidative fibers and exercise endurance in mice via ERR alpha, supporting the feasibility of ERR alpha-targeted exercise mimetics.
Limitations
Mouse and cell study.
PubMed 36988910DOIFree full text
✓ PositiveanimalJ Pharmacol Exp Ther · 2024

A Synthetic ERR Agonist Alleviates Metabolic Syndrome.

AnimalsSLU-PP-332 administration with metabolic assessments

In diet-induced obese and ob/ob mice, SLU-PP-332 raised energy expenditure and fat oxidation, reduced fat mass and improved insulin sensitivity.

Studied
Diet-induced obese and ob/ob mice
Main outcome
Energy expenditure, fatty acid oxidation, fat mass, insulin sensitivity
Authors' conclusion
SLU-PP-332 mimicked exercise benefits in mice (increased energy expenditure and fatty acid oxidation, decreased fat mass, improved insulin sensitivity); ERR activation may be effective for metabolic syndrome and obesity.
Limitations
Mouse models only.
PubMed 37739806DOIFree full text
✓ PositiveanimalCirculation · 2024

Novel Pan-ERR Agonists Ameliorate Heart Failure Through Enhancing Cardiac Fatty Acid Metabolism and Mitochondrial Function.

AnimalsSLU-PP-332 and SLU-PP-915 treatment with functional, multi-omics and genetic dependency studies6-week pressure overload

In a mouse pressure-overload heart failure model, SLU-PP-332 and SLU-PP-915 improved ejection fraction, reduced fibrosis and increased survival.

Studied
Mice with pressure overload-induced heart failure, plus in vitro cardiomyocyte work
Main outcome
Ejection fraction, fibrosis, survival, cardiac metabolism
Authors' conclusion
Both pan-ERR agonists improved ejection fraction, fibrosis and survival in pressure-overload heart failure without affecting hypertrophy, with ERR gamma the main mediator, supporting further development as heart failure therapeutics.
Limitations
Mouse model; no human data.
PubMed 37961903DOIFree full text
✓ PositiveanimalAm J Pathol · 2023

Estrogen-Related Receptor Agonism Reverses Mitochondrial Dysfunction and Inflammation in the Aging Kidney.

Animals8-week SLU-PP-332 treatment; 3-week STING inhibitor C-176 treatment8 weeks (SLU-PP-332)

8 weeks of SLU-PP-332 in 21-month-old mice reversed age-related albuminuria, kidney mitochondrial dysfunction and inflammation.

Studied
21-month-old mice (and aging human and mouse kidney tissue)
Compared with
Caloric restriction comparison
Main outcome
Albuminuria, podocyte loss, mitochondrial dysfunction, inflammatory cytokines
Authors' conclusion
An 8-week pan-ERR agonist treatment reversed age-related albuminuria, podocyte loss, mitochondrial dysfunction and inflammation in aged mice, similar to caloric restriction, identifying ERRs as calorie-restriction mimetic targets.
Limitations
Mouse study.
PubMed 37717940DOIFree full text
✓ Positivein vitroFront Physiol · 2025

Targeting ERRs to counteract age-related muscle atrophy associated with physical inactivity: a pilot study.

Twenty women (10 active, 10 inactive) undergoing hip arthroplastyPilot study: muscle biopsies plus in vitro SLU-PP-332 treatment of primary myoblastsMyotube differentiation for 15 days

In muscle cells taken from inactive women, SLU-PP-332 lowered oxidative stress and senescence markers and promoted myotube formation; no participants received the drug.

Studied
Women with coxarthrosis (active vs inactive) and myoblasts isolated from inactive women
Compared with
Active vs inactive women; untreated myoblasts
Main outcome
Expression of NOX4, SIRT1, PGC-1alpha, ERR alpha, FNDC5; myoblast differentiation and oxidative stress
Authors' conclusion
SLU-PP-332 down-regulated NOX4, up-regulated SIRT1, PGC-1alpha, ERR alpha and FNDC5 and promoted myotube formation in myoblasts from inactive women; targeting ERRs could be a strategy against muscle atrophy, but mechanisms need clarification.
Limitations
Pilot study; SLU-PP-332 tested only in cultured cells from inactive women.
PubMed 40692696DOIFree full text

Verdicts are judged on each paper's own main outcome; grades run from A (strong human evidence) to D (little or none). Details are read from the abstracts, and figures are reproduced only from openly licensed full texts. Not medical advice.