Informational only. Not medical advice.INFORMATIONAL PLATFORM ONLY — NOT MEDICAL ADVICE, DIAGNOSIS, OR TREATMENT
Informational only. Not medical advice.INFORMATIONAL PLATFORM ONLY — NOT MEDICAL ADVICE, DIAGNOSIS, OR TREATMENT
Two pan-ERR agonist “exercise mimetics” from the Burris lab at Saint Louis University, compared: isoform potency, oral bioavailability, and what the peer-reviewed rodent studies actually show — versus what gray-market marketing claims.
Not peptides, and no human data.Both are synthetic small molecules (not peptides). Neither is FDA-approved, has an IND, or has any registered human clinical trial. Every efficacy and safety figure comes from mouse or in-vitro studies. Sold “for research use only.”
| Attribute | SLU-PP-332 | SLU-PP-915 |
|---|---|---|
| Generation | Prototype (2023) | Successor (2025) |
| ERR isoform profile | Pan-agonist, modest ERRα preference (~2–4×) | Balanced pan-agonist (~400 nM each) |
| Oral bioavailability | No — dosed intraperitoneally | Yes — orally active |
| Chemistry | C18H14N2O2 (MW 290.3) | Boronic acid, C17H13BFNO3S (MW 341.16) |
| Key in-vivo finding | ↑ type IIa fibers, ↑ endurance, ↑ fatty-acid oxidation (mice) | Matches 332's endurance gain — orally (mice) |
| Human data | None | None |
| Status | Gray-market research chemical | Gray-market research chemical |
The estrogen-related receptors (ERRα, ERRβ, ERRγ) are orphan nuclear receptors. Despite the name, they do not bind estrogen. They act as master transcriptional regulators of oxidative metabolism — driving mitochondrial biogenesis, oxidative phosphorylation, fatty-acid oxidation, and the TCA cycle, largely as partners of the PGC-1 coactivators. In skeletal muscle this program is carried mainly by ERRα and ERRγ (ERRβ protein is nearly undetectable there).
Aerobic exercise switches on much of this same gene program. A molecule that activates it pharmacologically is therefore called an “exercise mimetic.” SLU-PP-332 and SLU-PP-915 were built to test that idea. Important framing: this is a preclinical concept demonstrated in mice. No ERR agonist is an approved therapy, and “exercise mimetic” describes a mechanism, not a proven human benefit.
Prototype pan-ERR agonist — potent but not orally bioavailable
ERR isoform profile
Pan-ERR agonist with a modest ~2–4 fold potency preference for ERRα (roughly 0.22 µM at ERRα vs 0.59 µM at ERRγ). Best described as a pan-agonist, not a selective drug.
Oral bioavailability
Not orally bioavailable — dosed intraperitoneally in every in-vivo study.
Chemistry
Small molecule, C18H14N2O2 (MW 290.3), CAS 303760-60-3, PubChem CID 5338394. Not a peptide.
Mechanism
Activates ERRα/β/γ to drive the PGC-1α aerobic gene program: mitochondrial biogenesis, oxidative phosphorylation, and fatty-acid oxidation. Shifts skeletal-muscle composition toward oxidative type IIa fibers.
Preclinical finding
In mice (Billon et al., 2023), ~13 days of treatment increased oxidative type IIa fibers and improved treadmill endurance (treated mice ran markedly farther and longer to exhaustion). In diet-induced obese mice it raised fatty-acid oxidation by ~25% and blunted fat-mass gain. All intraperitoneal, mouse-only.
Key studies
Billon C, et al. Synthetic ERRα/β/γ Agonist Induces an ERRα-Dependent Acute Aerobic Exercise Response and Enhances Exercise Capacity. ACS Chem Biol. 2023 (PMID 36988910). Billon C, et al. A Synthetic ERR Agonist Alleviates Metabolic Syndrome. J Pharmacol Exp Ther. 2023 (PMID 37739806).
Orally bioavailable successor — balanced pan-ERR agonist
ERR isoform profile
Roughly balanced pan-ERR agonist — EC50 ~400 nM at each of ERRα, ERRβ, and ERRγ. More evenly balanced across isoforms than the ERRα-preferring SLU-PP-332.
Oral bioavailability
Orally bioavailable — the design goal that motivated its development.
Chemistry
Chemically distinct boronic-acid small molecule, C17H13BFNO3S (MW 341.16), CAS 2285432-92-8, PubChem CID 142532359. Not a peptide.
Mechanism
Same ERR/PGC-1α target program as SLU-PP-332. The phenol and aniline groups of earlier agonists were replaced with a boronic-acid moiety on a disubstituted thiophene, preserving receptor activity while improving microsomal stability and oral exposure. Upregulates PGC-1α, LDHA, PDK4, and DDIT4.
Preclinical finding
In mice (Billon et al., 2025), oral SLU-PP-915 enhanced aerobic exercise capacity — running distance and duration — to an extent comparable to intraperitoneal SLU-PP-332 after adjusting for systemic exposure. Metabolite profiling (Möller et al., 2026) found 7 exclusively Phase-I metabolites, versus 9 for SLU-PP-332 (including 3 Phase-II conjugates). Mouse and in-vitro only.
Key studies
Billon C, et al. An orally active estrogen receptor–related receptor agonist, SLU-PP-915, enhances aerobic exercise capacity. J Pharmacol Exp Ther. 2025 (PMID 41421047). Möller GM, et al. In Vitro Metabolism and Analytical Characterization of SLU-PP-332 and SLU-PP-915. Rapid Commun Mass Spectrom. 2026 (DOI 10.1002/rcm.70039).
SLU-PP-332 came first and established the pharmacology: a pan-ERR agonist that reproduced parts of the aerobic-exercise gene program in mice. But it could only be given by intraperitoneal injection — it lacked the oral absorption a practical drug would need. SLU-PP-915 exists to solve exactly that. Swapping the earlier phenol/aniline chemistry for a boronic-acid group on a thiophene scaffold preserved ERR activity while improving metabolic stability and oral exposure, yielding a more evenly balanced pan-agonist that works when taken by mouth in mice.
The gap between what is being sold and what is actually known is unusually wide for these two compounds. SLU-PP-332 has been sold as a research chemical for some time, and SLU-PP-915 has more recently appeared on the gray market as well — both while the entire evidence base remains mouse-only.
These are small molecules, not peptides, so verification differs from a peptide COA. Key signals:
SLU-PP-332 vs SLU-PP-915 — side by side
The full data-driven comparison with chemical identity, references, and vendor COA quality for each compound.
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MOTS-c
A mitochondrial-derived peptide that also acts as an exercise mimetic via AMPK — a peptide counterpart to the ERR-agonist approach.
5-Amino-1MQ
A small-molecule NNMT inhibitor studied for metabolic and body-composition endpoints — another non-peptide metabolic research compound.
No. Despite being sold alongside research peptides and sometimes mislabeled as such, both SLU-PP-332 and SLU-PP-915 are synthetic small molecules — not peptides. They are agonists of the estrogen-related receptors (ERRα, ERRβ, ERRγ), a family of orphan nuclear receptors. SLU-PP-332 has the molecular formula C18H14N2O2 (CAS 303760-60-3, PubChem CID 5338394); SLU-PP-915 is a chemically distinct boronic-acid-containing molecule with the formula C17H13BFNO3S (CAS 2285432-92-8, PubChem CID 142532359). Because they are small molecules rather than peptides, identity verification relies on mass spectrometry and reference-standard comparison rather than the HPLC retention-time methods used for peptide chains.
SLU-PP-332 is the prototype (first-generation) pan-ERR agonist. It activates all three ERR isoforms with only a modest (roughly 2–4 fold) potency preference for ERRα, and in mouse studies it increased oxidative type IIa muscle fibers, raised skeletal-muscle fatty-acid oxidation, and improved treadmill endurance. Its central limitation is that it is not orally bioavailable — every in-vivo study dosed it by intraperitoneal injection. SLU-PP-915 is the second-generation successor engineered to fix that: a medicinal-chemistry redesign replaced the earlier phenol and aniline groups with a boronic-acid moiety on a thiophene scaffold, producing a more evenly balanced pan-agonist (EC50 ~400 nM at each isoform) that is orally bioavailable while matching SLU-PP-332's exercise-performance benefit in mice after adjusting for systemic exposure. In short: 915 is the orally active version of the same idea.
The estrogen-related receptors (ERRα, ERRβ, ERRγ) are orphan nuclear receptors — despite the name, they do not bind estrogen. They act as master transcriptional regulators of oxidative metabolism, driving mitochondrial biogenesis, oxidative phosphorylation, fatty-acid oxidation, and the TCA (Krebs) cycle, largely as partners of the PGC-1 coactivators. Because aerobic exercise activates much of this same gene program, a drug that switches it on pharmacologically is described as an "exercise mimetic." SLU-PP-332 and SLU-PP-915 were developed as tools to test that concept. Note that this is a preclinical research concept: no ERR agonist is an approved therapy, and "exercise mimetic" describes a mechanism in mice, not a demonstrated benefit in humans.
No. As of 2026 there is zero human data for either compound. Neither has FDA approval, an Investigational New Drug (IND) application, or any registered human clinical trial, and no human pharmacokinetic or safety data has been published. Every efficacy, pharmacokinetic, and safety figure in the literature comes from mouse and in-vitro studies. Vendor safety data sheets for SLU-PP-332 list "no data available" for every toxicology endpoint — acute toxicity, mutagenicity, carcinogenicity, reproductive toxicity, and organ toxicity. Any dosing figure circulating online is extrapolated from rodent studies and has not been validated in humans.
Both originate in the laboratory of Thomas Burris at Saint Louis University — the "SLU" prefix denotes Saint Louis University — with collaborators including the Patti lab. SLU-PP-332 was first characterized in Billon et al. (ACS Chemical Biology, 2023) and a follow-up metabolic-syndrome study (J. Pharmacol. Exp. Ther., 2023). SLU-PP-915 was introduced as the orally bioavailable successor in a 2025 J. Pharmacol. Exp. Ther. paper. A separate 2026 analytical study (Möller et al., Rapid Communications in Mass Spectrometry) characterized the in-vitro metabolism of both compounds and explicitly flagged them as having doping potential, anticipating misuse as exercise mimetics.
Both are sold in the United States as "research use only" chemicals that are explicitly labeled not for human consumption — a legal framing gray-market vendors use for unapproved compounds. They are not FDA-approved for any use. SLU-PP-332 has been available this way for some time; SLU-PP-915 has more recently appeared on the gray market as well. For athletes, both have been flagged in anti-doping research as metabolic modulators / exercise mimetics with doping potential; substances in this class are generally prohibited under WADA's S4 category (hormone and metabolic modulators), so athletes subject to testing should assume they are banned. This guide does not endorse human use of either compound.
Because these are small molecules rather than peptides, the verification approach differs from a peptide COA. Identity is best confirmed by mass spectrometry against a certified reference standard, matching the exact molecular formula (C18H14N2O2 for SLU-PP-332; C17H13BFNO3S for SLU-PP-915) and monoisotopic mass — the boron and fluorine in SLU-PP-915 give it a distinctive isotope pattern. Purity is assessed by HPLC. Two specific risks in this market: mislabeling (a small molecule sold as a "peptide," or one SLU-PP compound substituted for the other) and reliance on a vendor-supplied COA with no independent confirmation. Disclosed Labs' position is that identity and purity claims should be independently verified against a reference standard, not taken from a vendor's own paperwork.
Disclosed Labs