SLU-PP-915

A synthetic small molecule — not a peptide — that activates all three estrogen-related receptors and, unlike its predecessor SLU-PP-332, is orally bioavailable, studied in mice as an exercise mimetic with no published human data.

Also referenced as: SLU PP 915, SLU-PP915, SLUPP915, 2285432-92-8, [3-[5-[(2-fluorophenyl)carbamoyl]thiophen-2-yl]phenyl]boronic acid

Also appears in: Performance

COAPublic product evidence4 certificate records mentioning this compound or product name0 provider-linked · 0 exact product matches→

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What is SLU-PP-915?

SLU-PP-915 is a synthetic small molecule — not a peptide. It is [3-[5-[(2-fluorophenyl)carbamoyl]thiophen-2-yl]phenyl]boronic acid, CAS 2285432-92-8, formula C17H13BFNO3S, molecular weight 341.2: a 2,5-disubstituted thiophene carrying a fluoroanilide on one side and a phenylboronic acid on the other. There are no amino acid residues in it and therefore no peptide bonds. It does contain a single amide, but that amide joins a thiophene carbonyl to a fluoroaniline rather than one amino acid to the next, which is what a peptide bond specifically is. Calling it a peptide is a category error, the same one made with 5-Amino-1MQ and ATX-304.

It came out of the same medicinal-chemistry program at Saint Louis University that produced SLU-PP-332 — the “SLU-PP” prefix is the university’s — and was designed as a chemically distinct successor to it. SLU-PP-332 is an acyl hydrazone; SLU-PP-915 is a thiophene carboxamide, reached by cyclizing the hydrazone into a bioisosteric replacement, so the two share a pharmacology rather than a scaffold. It appears in this database because the vendors that stock research peptides also stock it, marketed to the same audience under the same “exercise in a pill” framing.

How it works

• It activates all three estrogen-related receptors. ERRα, ERRβ, and ERRγ are orphan nuclear receptors that drive transcription of genes for mitochondrial biogenesis, oxidative phosphorylation, fatty acid oxidation, and the Krebs cycle, and they are required for skeletal muscle to adapt to aerobic exercise (Billon et al., Journal of Pharmacology and Experimental Therapeutics, 2026;393(1):103787). In cell-based luciferase reporter assays SLU-PP-915 activates all three with well-balanced potency and no pronounced isoform bias; the published potency table gives EC50 values of 0.41 μM at ERRα and 0.378 μM at ERRγ, with no ERRβ figure tabulated, and efficacy of roughly 90% at ERRα and 167% at ERRγ relative to SLU-PP-332. Selectivity profiling against the actual estrogen receptors ERα and ERβ found minimal off-target agonism (Radwan et al., RSC Chemical Biology, 2026;7(7):1265–1277).
• The downstream readout is an exercise gene program. In vitro and in mice, the compound upregulates ERR target genes including PGC-1α, LDHA, PDK4, and DDIT4 (Hampton et al., European Journal of Medicinal Chemistry, 2023;258:115582). DDIT4 is the specific marker used as the acute-exercise proxy: in treated mice its induction matched or exceeded what treadmill running produced, depending on which muscle was sampled. The compound also synergized with exercise training to raise DDIT4 and mitochondrial gene expression further — an additional finding, not a limitation, since 915 on its own improved exercise capacity in the same study (Billon et al., 2026, above).
• Two changes, not one, made it orally usable. Getting from SLU-PP-332 to SLU-PP-915 took both a scaffold hop — cyclizing the acyl hydrazone into a thiophene carboxamide bioisostere — and, within that new series, replacing the phenolic or aniline hydrogen-bond donor with a boronic acid. The boronic acid is the part credited with metabolic stability: it preserved pan-ERR activity and, in the developers’ own words, modestly improved stability in human and mouse liver microsomes, where SLU-PP-915 was stable with a half-life beyond 60 minutes. Oral bioavailability is the property that distinguishes it from SLU-PP-332, but attributing that to the boronic acid alone overstates a single substituent’s role in a two-step redesign (Hampton et al., 2023; Radwan et al., 2026, both above).
• Binding mode is modeled, not solved. SLU-PP-915 has not been co-crystallized with an ERR. Docking into ERRγ predicts a pose resembling the reference agonist GSK4716, with the boronic acid standing in for the phenol’s role — two hydrogen bonds to Asp328 — plus π-stacking against Tyr326 and Phe435 (Radwan et al., 2026, above).

Research status

SLU-PP-915 is preclinical, and thinner than its reputation. Three primary studies name it:

• Discovery and structure-activity work. Hampton et al. (European Journal of Medicinal Chemistry, 2023;258:115582) reported the 2,5-disubstituted thiophene series and identified SLU-PP-915 — compound 10s in that paper — as a potent pan-ERR agonist, confirmed target-gene induction in vitro and in vivo, and established direct ERRγ binding by NMR for the series.
• Heart failure in mice. Xu et al. (Circulation, 2024;149(3):227–250) tested both SLU-PP-332 and SLU-PP-915 in a pressure-overload heart failure model. Both improved ejection fraction, reduced fibrosis, and increased survival without affecting cardiac hypertrophy, with genetic dependency experiments identifying ERRγ as the main mediator.
• Oral exercise capacity in mice. Billon et al. (Journal of Pharmacology and Experimental Therapeutics, 2026;393(1):103787, published online December 2025) is the paper the compound’s positioning rests on. Given intraperitoneally, SLU-PP-915 improved treadmill run-to-exhaustion distance and duration about as much as SLU-PP-332. Given orally, it maintained “comparable efficacy” — but the authors’ own qualifier is adjusted for systemic exposure, meaning the oral and injected arms are matched on drug in the blood, not on dose administered. The paper demonstrates that an ERR agonist can work by mouth; it does not establish an oral dose.

One further study is analytical rather than therapeutic: Möller et al. (Rapid Communications in Mass Spectrometry, 2026;40(8):e70039) characterized both compounds by LC-HRMS/MS and mapped their in vitro metabolism in human liver microsomes and S9 fraction, finding seven Phase-I metabolites for SLU-PP-915 and no Phase-II conjugates, with three confirmed by chemical synthesis and NMR. The stated purpose is sports drug testing.

Every in vivo result above comes from the inventors. SLU-PP-915 is covered by Saint Louis University intellectual property with Thomas P. Burris named as an inventor; he is also a stockholder in Myonid Therapeutics and Pelagos Pharmaceuticals, both developing ERR agonists. The disclosure appears on the pivotal oral-exercise paper, and the discovery paper carries a related patent (WO2019036562) licensed to Myonid across most of its author list. That does not make the data wrong, but no independent laboratory has yet replicated the exercise-capacity finding.

Most of what circulates about SLU-PP-915 is actually SLU-PP-332’s data. The obesity and metabolic syndrome results — increased energy expenditure, increased fatty acid oxidation, decreased fat mass — are from Billon et al. (Journal of Pharmacology and Experimental Therapeutics, 2024;388(2):232–240) using SLU-PP-332. The oxidative muscle fiber shift and endurance gains are from Billon et al. (ACS Chemical Biology, 2023;18(4):756–771), again SLU-PP-332. The reversal of mitochondrial dysfunction and inflammation in aging kidneys is Wang et al. (American Journal of Pathology, 2023;193(12):1969–1987), also SLU-PP-332. A 2026 systematic review (de Souza-Lima et al., Revista Médica de Chile, 2026;154(2):237–245) discusses the two compounds together and attributes reduced adiposity, improved glycemic control, and increased basal energy expenditure to both; its literature search covered 2020 to 2024, and no primary study has reported an obesity, body-composition, or glycemic endpoint for SLU-PP-915 on its own.

No human trials. ClinicalTrials.gov returns no registered study listing SLU-PP-915, and none listing SLU-PP-332 either. There is no Phase 1, no published human pharmacokinetics, no published formal toxicology, and no regulatory approval in any jurisdiction. Every efficacy result above is in mice or in cells.

Common dosage forms

• Oral capsules, listed at 20 mg per capsule in 30-count bottles.
• Oral liquid in 30 mL bottles. Vendor listings can carry more than one strength under a single product name — one tracked listing offers two 30 mL options at very different prices with no concentration in the title — so the strength has to be read off the individual variant rather than the product name.
• No injectable or lyophilized vial presentation is characteristic of this compound. That is unusual for this market and consistent with the compound’s rationale: oral exposure is the entire point of SLU-PP-915 over SLU-PP-332, so a vial-and-solvent presentation would be at odds with why it exists.
• Certificates of analysis for it are small-molecule assays — HPLC purity plus identity confirmation — not peptide purity runs, and should be read as such.
• Availability is thin. Only a couple of listings track in this database at all, and capsule stock is intermittent, so the format picture rests on a small sample.

This section describes formats only and is not dosing guidance.

Key considerations

• It is not a peptide. Nothing about its handling, stability, storage, or purity testing follows from peptide conventions. A certificate of analysis showing a peptide-style purity panel would be the wrong test for this molecule.
• The evidence gap between 915 and 332 is the main thing to hold onto. SLU-PP-915 has three primary papers to its name: a chemistry paper, a heart failure model, and an exercise capacity study. The metabolic, body-composition, muscle-fiber, and kidney-aging findings widely repeated about it were generated with SLU-PP-332. The two compounds are not interchangeable in evidence even if they share a target.
• The boronic acid is a recognized liability, not just a feature. The developers’ own review flags the electrophilic boronic acid on the A-ring as capable of forming covalent bonds with off-target proteins, and recommends exploring tetrazole or carboxylic acid replacements — while noting the group is not expected to bond covalently inside the ERRγ pocket itself (Radwan et al., 2026, above). That review labels the group a “Michael acceptor,” which is loose terminology: aryl boronic acids are Lewis-acidic electrophiles that form reversible boronate adducts with nucleophiles, not conjugate-addition acceptors, and the review’s own wording elsewhere describes the risk as non-specific reversible covalent bonding. The off-target concern is real either way, and no in vivo toxicology has been published to bound it. That review is also co-authored by the compound’s inventor, so it is not an independent assessment.
• Anti-doping: absent from the 2026 list, explicitly proposed for the 2027 one. SLU-PP-915 is not named anywhere in the 2026 WADA Prohibited List — that document contains no mention of SLU-PP compounds, ERRs, or estrogen-related receptors, so claims that either compound is already a listed metabolic modulator are wrong. It is nonetheless already prohibited under class S0 (Non-Approved Substances), which captures any pharmacological substance not addressed elsewhere on the List and with no current approval by any governmental regulatory health authority for human therapeutic use — drugs under preclinical or clinical development are the named example — at all times, in and out of competition. That is set to change: WADA’s draft 2027 Prohibited List proposes adding SLU-PP-332 and SLU-PP-915 by name under S4 (Hormone and Metabolic Modulators), and the Dutch stakeholders’ July 2026 consultation response backs the addition. A draft list is not final until WADA publishes the 2027 List, and the S4 subclass would determine whether it stays a Specified substance, but the direction is unambiguous — and anti-doping laboratories have already published the metabolite maps needed to test for it. Anyone subject to testing should treat it as prohibited now.
• Two naming traps. “Estrogen-related receptor” is not the estrogen receptor — ERRs are a separate orphan receptor family that do not bind endogenous estrogens, and selectivity profiling found minimal activity at ERα and ERβ, so the name does not imply estrogenic activity. Separately, the SLU-PP prefix spans compounds with opposite pharmacology: SLU-PP-1072, from the same group, is a selective ERRα/γ inverse agonist studied for inhibiting the Warburg effect in prostate cancer cells (Schoepke et al., ACS Chemical Biology, 2020;15(9):2338–2345). Prefix-based searching returns unrelated compounds, and searching the bare number returns nothing useful at all.