SLU-PP-915 and SLU-PP-332 are synthetic pan-ERR agonists built by the same research program, and they differ in chemical scaffold, oral pharmacokinetics, and how much published research sits behind each one. SLU-PP-332 came first and established that activating estrogen-related receptors can switch on the gene expression signature of aerobic exercise, while SLU-PP-915 is a chemically distinct follow-up designed around oral dosing.
Most comparisons stop at a single line about oral bioavailability. The more useful story is what the medicinal chemists changed, and what happened in the studies where both compounds ran through the same experiment.
Both remain research compounds. Every finding below comes from animal models, cell culture, or analytical chemistry, and neither compound has published human clinical trial results.
Key Takeaways
The Short Version
SLU-PP-915 and SLU-PP-332 are synthetic pan-ERR agonists from the same laboratory, both studied as exercise mimetics in animal and cell models.
SLU-PP-332 has the broader research base, with published rodent work spanning skeletal muscle, heart, kidney, and metabolic syndrome models.
SLU-PP-915 sits on a different chemical backbone, a thiophene ring carrying a boronic acid group, which is what gave it oral bioavailability in rodents.
Neither compound has completed human trials, so identity verification and third-party analysis matter more here than in any established supplement category.
Two Compounds From One Research Program
SLU-PP-332 and SLU-PP-915 came out of the same drug discovery effort, and the naming tells you they are siblings rather than competitors. Both target the estrogen-related receptors ERRα, ERRβ, and ERRγ. These are orphan nuclear receptors, meaning no natural hormone has been found that switches them on. What they do is control the genes behind mitochondrial biogenesis, fatty acid oxidation, and cellular energy production. A pan agonist is simply a molecule that activates all three subtypes rather than picking one.
SLU-PP-332 was reported first in ACS Chemical Biology. Researchers identified it as a pan agonist hitting all three ERR subtypes with the highest potency at ERRα, which had proven unusually hard to activate with small molecules. In a skeletal muscle cell line it increased mitochondrial function and cellular respiration. In mice it raised the proportion of type IIa oxidative muscle fibers and improved exercise endurance, and the effect disappeared without ERRα.
SLU-PP-915 arrived from a separate chemical series, built through structure-based design around 2,5-disubstituted thiophenes rather than the acyl hydrazide template behind SLU-PP-332.
| Factor | SLU-PP-332 | SLU-PP-915 |
|---|---|---|
| Chemical class | Acyl hydrazide scaffold | 2,5-disubstituted thiophene with a boronic acid group |
| Receptor profile | Pan-ERR, highest potency at ERRα | Pan-ERR, roughly equivalent activity across α, β, and γ |
| First published | 2023, ACS Chemical Biology | 2023, European Journal of Medicinal Chemistry |
| Oral activity in rodents | Not orally bioavailable | Orally bioavailable |
| Research breadth | Muscle, heart, kidney, metabolic syndrome, human myoblasts | Heart failure, exercise capacity, metabolite characterization |
| Human trial data | None published | None published |
The Chemistry Behind 915’s Oral Activity
SLU-PP-915 is orally active because of a boronic acid group, and that one structural decision is the reason the compound exists at all.
The team started from a known acyl hydrazide template and the ERRγ agonist GSK-4716, then worked through a series of thiophenes. Several were potent ERRγ agonists in cell-based co-transfection assays, and direct binding to ERRγ was confirmed by NMR. The breakthrough was structural. Swapping the phenolic or aniline group for a boronic acid moiety held onto receptor activity while improving metabolic stability in microsomal assays.
That stability is what carried through to whole-animal dosing. In the 2025 characterization of SLU-PP-915, researchers described SLU-PP-332 as improving aerobic performance in mice while lacking oral bioavailability, and reported that SLU-PP-915 held comparable efficacy when given by mouth once systemic exposure was accounted for.
None of this makes SLU-PP-332 the weaker molecule. A 2026 structure-activity analysis of the SLU-PP-332 scaffold tested a wide set of analogues and still described SLU-PP-332 as a strong benchmark for ERR activation, with some analogues matching its transcriptional output while improving solubility or ligand efficiency. It remains the reference compound the field measures against.
What Happened When Both Ran Through the Same Experiment
The cleanest comparison of the two compounds comes from a Circulation study that put both through an identical animal protocol.
Researchers designed and synthesized both agonists, then tested them in a pressure overload model of heart failure in mice. Both improved ejection fraction, reduced fibrosis, and increased survival, without changing cardiac hypertrophy.
The molecular work went deeper. RNA sequencing and metabolomics showed broad activation of fatty acid metabolism and mitochondrial genes. Genetic dependency experiments then pinned the cardioprotective effect specifically on ERRγ.
The exercise comparison points the same direction. In the 2025 exercise capacity study, SLU-PP-915 raised running distance and duration in mice to a similar extent as SLU-PP-332 when both were injected, and it kept comparable efficacy when given orally.
Read together, the two compounds behave in animal models like the same pharmacology delivered through two different routes.
Ddit4, the Gene That Says a Workout Happened
Ddit4 is the readout researchers use to check whether an ERR agonist produced a genuinely exercise-like response rather than a vague metabolic shift.
DNA damage-inducible transcript 4 is induced by a single bout of aerobic exercise. In the 2025 mouse work, both compounds strongly induced Ddit4, reaching or exceeding the levels produced by treadmill running depending on which muscle was sampled. A systematic review of the pan-ERR agonist literature describes the same ERRα-dependent program, with Ddit4 and Slc25a25 as the signature genes.
One finding separates the two compounds. SLU-PP-915 synergized with exercise training, pushing Ddit4 and mitochondrial gene expression higher than training alone. In that model the compound and the training added to each other rather than one standing in for the other, which is a more interesting result than a straight substitution would have been.
ERR activation sits alongside the machinery behind mitophagy, the clearing of damaged mitochondria, and works through the same PGC-1α coactivator that exercise and AMPK activation supplements rely on.
The Research That Reaches Past Skeletal Muscle
Almost all of the non-muscle research used SLU-PP-332, because it arrived first and became the standard chemical probe for ERR activation.
Metabolic syndrome and obesity
In diet-induced obese mice, SLU-PP-332 increased energy expenditure and fatty acid oxidation and reduced fat mass accumulation. The same animal work reported improved insulin sensitivity in metabolic syndrome models.
Kidney aging
ERR expression drops in aging human and mouse kidneys, and stays higher in mice kept on lifelong caloric restriction. Eight weeks of pan-ERR agonist treatment in 21-month-old mice reversed age-related increases in albuminuria, podocyte loss, mitochondrial dysfunction, and inflammatory cytokines, working through the cGAS-STING and STAT3 pathways.
Human muscle cells
The closest thing to human data comes from a 2025 pilot study using muscle biopsies taken during hip replacement surgery in 20 women. Muscle from the inactive women showed a more oxidized, less mitochondrially active protein profile than muscle from the active women.
Researchers then cultured myoblasts from the inactive group and treated them with SLU-PP-332. In that cell-based research the pattern flipped back, with lower oxidative stress and senescence markers and more myotube formation.
That last study is worth flagging precisely. It is human tissue, but the compound was applied to cells in a dish, not to people. It tells us the receptor pathway behaves in human muscle cells the way it behaves in mouse muscle, which is a meaningful step and not a clinical outcome.
Why Anti-Doping Labs Are Watching Both
Both compounds are now characterized for sports drug testing, and the detection methods are published.
A 2026 analytical study profiled SLU-PP-332 and SLU-PP-915 by liquid chromatography-high resolution tandem mass spectrometry and mapped how human liver enzymes break each one down. Nine metabolites were identified for SLU-PP-332, six Phase I and three Phase II conjugates. SLU-PP-915 produced seven metabolites, all Phase I, with three confirmed by chemical synthesis and NMR.
The authors were explicit that the work was motivated by the doping potential of exercise mimetics. If you compete under any anti-doping authority, treat both compounds as detectable and check your sport’s prohibited list before going anywhere near them.
What Quality Verification Looks Like for a Compound This New
For a molecule with an analytical standard only a few years old, confirming identity is the whole game. Purity percentages mean nothing if the material in the capsule is not the compound on the label.
Four things separate a verifiable product from a guess.
| What to look for | Why it matters |
|---|---|
| The exact compound designation | SLU-PP-332 is a specific molecule. “Exercise mimetic blend” tells you nothing you can check. |
| A stated amount per capsule | A proprietary blend total cannot be compared against any published study. |
| Mass spectrometry identity confirmation | A purity figure is meaningless if the material was never confirmed as the right compound. |
| A readable Certificate of Analysis | It should be tied to a batch number you can match to the bottle in your hand. |
Worth clearing up a common mix-up. Neither compound is a peptide. Both are synthetic small molecules that bind a nuclear receptor, which is a different class of chemistry from the peptides the category is often lumped in with. Our ingredients library breaks down what sits in which category.
BioLongevity publishes Certificates of Analysis for its catalog, and every batch is analyzed by HPLC with mass spectrometry for molecular identity and purity. ShredMAX is the single-compound SLU-PP-332 capsule at 100 mg per capsule, in a vegetarian shell with a three-item excipient list. SHREDX takes a different approach, combining SLU-PP-332 with GW-501516 and AOD-9604 across three separate metabolic pathways.
If your interest is mitochondrial and metabolic support with a longer research history behind it, BioAmp uses the pan-AMPK activator ATX-304 instead, and our roundup of longevity supplements ranked by evidence covers the ingredients with human trial data.
Frequently Asked Questions
Is SLU-PP-915 stronger than SLU-PP-332?
Not in the published animal work, no. Injected into mice in the same study, both raised running distance and duration to a similar extent, and SLU-PP-915 held comparable efficacy dosed orally once systemic exposure was matched. The difference is route, not raw potency.
Are SLU-PP-332 and SLU-PP-915 peptides?
No. Both are synthetic small molecules that act as agonists at the estrogen-related receptors, a family of nuclear receptors. They are frequently sold and discussed alongside research peptides, but they are a completely different class of chemistry.
Has SLU-PP-915 been tested in humans?
No. There aren’t any published human clinical trials for either compound. A 2026 systematic review of pan-ERR agonists concluded that clinical trials are still needed to establish efficacy and safety in people.
Which compound has more research behind it?
SLU-PP-332, by a wide margin. It appears in published work on skeletal muscle, heart failure, kidney aging, metabolic syndrome, and human myoblast culture. SLU-PP-915 shows up in four papers so far.
Can an ERR agonist replace exercise?
The animal research does not support that framing. In the 2025 mouse study, SLU-PP-915 added to the effect of exercise training rather than substituting for it, raising Ddit4 and mitochondrial gene expression above what training produced on its own.
Is SLU-PP-915 sold in capsule form?
BioLongevity does not carry SLU-PP-915. The catalog’s ERR agonist products use SLU-PP-332, which has the deeper published research base of the two.
Ready to look at the compound with the broader evidence file behind it? ShredMAX delivers SLU-PP-332 as a single-compound capsule with the amount printed on the label and analytical documentation available, and you can compare it against the rest of the metabolic support and fat loss collection before you decide.
Ask a qualified clinician before starting any supplement if you are pregnant, nursing, taking medication, or managing a medical condition. If you compete in tested sport, confirm the current status of any metabolic modulator with your governing body first.
These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure, or prevent any disease.
References
- Billon C, Sitaula S, Banerjee S, et al. Synthetic ERRα/β/γ agonist induces an ERRα-dependent acute aerobic exercise response and enhances exercise capacity. ACS Chemical Biology. 2023;18(4):756-771. DOI
- Hampton CS, Sitaula S, Billon C, et al. Development and pharmacological evaluation of a new chemical series of potent pan-ERR agonists, identification of SLU-PP-915. European Journal of Medicinal Chemistry. 2023;258:115582. DOI
- Billon C, Appourchaux K, Côté I, Burris TP. An orally active estrogen receptor-related receptor agonist, SLU-PP-915, enhances aerobic exercise capacity. The Journal of Pharmacology and Experimental Therapeutics. 2025;393(1):103787. DOI
- Okda HE, Zhao P, Hayes M, et al. Chemical optimization of the exercise mimetic SLU-PP-332 enables insight into estrogen-related receptor signaling. International Journal of Biological Macromolecules. 2026;355:151450. DOI
- Xu W, Billon C, Li H, et al. Novel pan-ERR agonists ameliorate heart failure through enhancing cardiac fatty acid metabolism and mitochondrial function. Circulation. 2024;149(3):227-250. DOI
- de Souza-Lima J, Astrosa-Martin BD, Galaz-Rodríguez CA, et al. Pharmacological activation of ERRα/β/γ as an exercise mimetic: potential therapeutic applications. Revista Médica de Chile. 2026;154(2):237-245. DOI
- Billon C, Schoepke E, Avdagic A, et al. A synthetic ERR agonist alleviates metabolic syndrome. The Journal of Pharmacology and Experimental Therapeutics. 2024;388(2):232-240. DOI
- Wang XX, Myakala K, Libby AE, et al. Estrogen-related receptor agonism reverses mitochondrial dysfunction and inflammation in the aging kidney. The American Journal of Pathology. 2023;193(12):1969-1987. DOI
- Bonanni R, Falvino A, Matticari A, et al. Targeting ERRs to counteract age-related muscle atrophy associated with physical inactivity: a pilot study. Frontiers in Physiology. 2025;16:1616693. DOI
- Möller T, Krug O, Thevis M. In vitro metabolism and analytical characterization of SLU-PP-332 and SLU-PP-915: novel pan-ERR agonists with doping potential. Rapid Communications in Mass Spectrometry. 2026;40(8):e70039. DOI