SLU-PP-332
A preclinical pan-ERR agonist studied as an exercise-mimetic metabolic tool compound in cells and mice.
What SLU-PP-332 is
SLU-PP-332 is a synthetic agonist of estrogen-related receptors ERRα, ERRβ, and ERRγ. It is not a peptide; it is a small-molecule research tool that activates ERR-driven transcriptional programs linked to mitochondrial function, fatty-acid oxidation, and exercise-responsive gene sets.
Landmark 2023–2024 papers showed acute aerobic-exercise-like gene activation, improved exercise capacity markers in mice, and mitigation of metabolic-syndrome features in obese models. Related work explores cardiac metabolism and aging-tissue mitochondrial readouts. Human clinical dosage trials are not the basis of current knowledge.
Because internet dosage chatter often outruns evidence, this page keeps ranges tethered to published murine IP regimens and clearly labels them preclinical. Research use only.
Nearly all of the published work on SLU-PP-332 is preclinical: animal models and cell studies. Human evidence is thinner than the volume of online discussion suggests.
How it works
ERRs are nuclear receptors that partner with cofactors such as PGC-1α to control oxidative metabolism genes. SLU-PP-332 acts as a pan-ERR agonist with particularly notable ERRα potency in the original characterization. Activation upregulates mitochondrial and fatty-acid oxidation programs in muscle cells and in vivo mouse tissues, producing an exercise-mimetic molecular signature without being a classical adrenergic stimulant.
Who works with it, and what they are measuring
Nuclear-receptor chemists, exercise-physiology molecular labs, and cardiometabolic research groups are the primary investigators. Doping-control analysts have also begun watching ERR agonists as emerging misuse risks, which is another reason precise research framing matters.
What the research examines
Research areas, not results. A topic on this list is being studied, not settled.
How it appears in the literature
Taken from the methods sections of the cited work. Not a recommendation.
| Research context | Reported amount | Frequency | Route |
|---|---|---|---|
| Published mouse efficacy studies (Billon and related metabolic work) | 50 mg | twice daily | intraperitoneal (preclinical) |
| Pharmacokinetic / exposure mouse experiments | 30 mg – 50 mg | single or repeated IP dosing per study arm | intraperitoneal (preclinical) |
Handling & storage
Store solid compound dry, cold, and light-protected per supplier data sheet. Solutions for animal work are typically prepared fresh or aliquoted in validated solvents; this is not a standard bacteriostatic-water peptide workflow.
Notes on combined research
Literature positions SLU-PP-332 against exercise itself and against metabolic disease standards rather than as a partner to common injectable peptides. Mechanistic neighbors include other ERR agonists (for example SLU-PP-915 in cardiac work) and PGC-1α pathway tools. Any multi-agent combination remains experimental.
SLU-PP-332 questions
Published in vivo work centers on mouse doses around 50 mg/kg intraperitoneally twice daily. There is no established human clinical dosage series in that foundational literature.
Bacteriostatic water peptide math usually does not apply. SLU-PP-332 is a small molecule requiring solvent systems specified in methods sections or chemical data sheets.
In mice, 50 mg/kg BID implies a high total daily mg/kg exposure split into two IP injections. That schedule is preclinical only.
A responsible chart lists mouse mg/kg, route (IP), frequency, model (DIO, exercise test, heart-failure), and citation. Human capsule charts without clinical citations are speculative.
Public discussion should stick to study exposure measurements rather than a single consumer half-life claim. It is handled as a repeatedly dosed preclinical agonist, not a weekly peptide.
Researchers compare it with exercise and explore related ERR chemotypes. Validated peptide stacks are not a feature of the core papers.
No. It is a synthetic ERR agonist small molecule sometimes sold adjacent to research peptides because of overlapping metabolic-research demand.
Because it turns on ERR-dependent gene programs that overlap with acute aerobic exercise responses and can increase endurance-related readouts in mouse studies.
Read the research yourself
These references were validated against the NCBI database. No citation appears here unless it resolves to a real paper.
- Synthetic ERRα/β/γ Agonist Induces an ERRα-Dependent Acute Aerobic Exercise Response and Enhances Exercise Capacity.PubMed
- A Synthetic ERR Agonist Alleviates Metabolic Syndrome.PubMed
- Novel Pan-ERR Agonists Ameliorate Heart Failure Through Enhancing Cardiac Fatty Acid Metabolism and Mitochondrial Function.PubMed