SLU-PP-332: ERR Agonist Research Data

What Is SLU-PP-332?

SLU-PP-332 is a small synthetic molecule — an acyl hydrazone — with no amino acids and no peptide bonds. PubChem lists it as C₁₈H₁₄N₂O₂, with a molecular weight of about 290.3 g/mol, CAS number 303760-60-3, and PubChem CID 5338394; ChEMBL classifies it as a small molecule.^[6][7] Descriptions of it as a "research peptide" are simply incorrect.

It activates all three estrogen-related receptors — ERRα, ERRβ and ERRγ — nuclear receptors that regulate mitochondrial and oxidative-metabolism genes and that, despite the name, do not bind the body's own estrogens. In cell assays its potency is highest at ERRα (EC₅₀ 98 nM, against 230 nM at ERRβ and 430 nM at ERRγ), a real but modest preference.^[1][3]

Origin: the Burris Group

SLU-PP-332 comes from Thomas Burris's group, with medicinal chemists Bahaa Elgendy and John Walker; the chemical series was first published in 2020 and the compound was characterised in detail in 2023.^[8][1] The series is named for Saint Louis University, which holds related intellectual property. The "exercise pill" framing came from a 2023 University of Florida news release about the mouse metabolic studies, not from any clinical result.^[9]

Proposed Mechanisms and the Evidence Behind Each

Which receptor matters depends on the tissue: the muscle effects required ERRα, while in the heart-failure model the protection ran mainly through ERRγ.^[1][10] The developers state that the compound is not selective enough to separate the three receptors' roles.^[1]

The Animal Evidence, Study by Study

1. Endurance and Muscle (Billon et al. 2023)

In male mice, treated animals ran about 70% longer and 45% further than controls, with more oxidative muscle. On the marker gene most tied to acute exercise, the compound alone produced about a three-fold response against six-fold for treadmill running, and the two were additive — so it did not substitute for exercise.^[1]

2. Metabolic Syndrome (Billon et al. 2024)

In diet-induced obese and leptin-deficient male mice, fatty-acid oxidation rose about 25%, fat mass fell and glucose tolerance improved, with no change in food intake; groups had seven or eight animals each.^[2]

3. Heart Failure (Xu et al. 2024)

In a pressure-overload model, SLU-PP-332 and a related compound improved ejection fraction, reduced fibrosis and increased survival, without affecting cardiac hypertrophy; the paper does not state the sex of the animals in the main experiments.^[10]

4. Kidney Ageing (Wang et al. 2023)

In 21-month-old male mice, treatment reversed age-related increases in albuminuria, mitochondrial dysfunction and inflammatory markers.^[11]

Almost all of this work is in male mice, in groups of roughly four to ten, and every in-vivo study includes the developer group. No independent laboratory has reproduced the endurance effect.^[12]

Human Data: None

No human has received SLU-PP-332 in any published study. ClinicalTrials.gov and the EU Clinical Trials Register list no trials, and none of the 10 indexed PubMed records is a clinical trial.^[4][13][14]

The closest thing to human work is an independent Italian pilot study that applied the compound to cultured muscle cells taken from 20 elderly women — human cells in a dish, not people. It reported lower oxidative stress and senescence markers in cells from inactive women.^[15] Two anti-doping laboratories have mapped its metabolites in human liver fractions to build detection methods; those are laboratory studies too.^[16][17] An independent 2026 systematic review concluded that clinical studies are needed to establish efficacy, safety and bioavailability in humans.^[12]

Known Limitations as a Compound

• No oral bioavailability. Its developers report that it lacks oral bioavailability; all in-vivo efficacy data come from injection, and they built a separate orally active successor, SLU-PP-915.^[18]
• Poor solubility and conflicting stability data. A 2026 paper measured extremely low solubility and a moderate microsomal half-life, conflicting with an earlier report of good stability from the same group.^[19][20]
• A flagged chemical linkage. The developers' own 2026 review calls it metabolically unstable and notes that its hydrazone linkage is considered problematic in medicinal chemistry because of rapid metabolism and possible toxicity.^[3]
• No toxicology. No dedicated toxicology study has been published; statements about tolerability come from short efficacy experiments in mice.^[1]

Regulatory Status in 2026

What the SLU-PP-332 Literature Does Not Yet Give You

• Any human data. None exists.^[4]
• Independent in-vivo replication. The endurance and metabolic results come from the developer group and its collaborators.^[12]
• Female animals. Almost all in-vivo work used male mice.
• Toxicology and long-term exposure. The longest published exposure is about two months, in one study.^[11]
• Clean receptor attribution. The compound cannot separate ERRα, ERRβ and ERRγ effects.^[1]

These gaps are not arguments against studying SLU-PP-332. They are arguments against overselling it.

Where SLU-PP-332 Fits in an RUO Research Catalog

For research use, SLU-PP-332 belongs with the metabolic research tools: a small-molecule ERR agonist that its developers describe as a widely used chemical probe for cell-culture and animal-model work on oxidative metabolism. Remy Research lists the Genovare SLU-PP-332 25mg AQ pen, supplied for in-vitro laboratory research only. It is not framed for human use, veterinary use or treatment.

For researchers reading this page as a starting point, the most useful adjacent references on this site are the AICAR review, the MOTS-c mitochondrial review, the NAD+ review, and the COA and HPLC purity guide.