SLU-PP-332 Research Guide — Pan-ERR Agonist, Exercise Mimetic Mechanism & Mitochondrial Biogenesis Biology (2026)
- SLU-PP-332 is a synthetic small-molecule pan-agonist of the estrogen-related receptors (ERRs — ERRα, ERRβ, ERRγ) with highest potency at ERRα (EC50 ~98 nM in cell-based cotransfection assay; ERRβ ~230 nM; ERRγ ~430 nM). It was developed at Washington University in St. Louis as a research tool to pharmacologically activate the ERR axis — a key transcriptional regulator of mitochondrial energy metabolism — and thereby study the molecular basis of exercise adaptation and develop exercise mimetics for metabolic disease research. YPB offers research-grade SLU-PP-332 as YPB.243 (Research Use Only).
- Mechanism: ERRs are orphan nuclear receptors (no known endogenous ligand) that function as master transcriptional regulators of cellular energy homeostasis. SLU-PP-332 binding to ERRα stabilizes its active conformation, driving transcription of a gene program that recapitulates the molecular signature of endurance exercise: upregulation of PGC-1α (master regulator of mitochondrial biogenesis), fatty acid oxidation enzyme genes (CPT1B, ACADM, HADHA), and mitochondrial electron transport chain subunits. Downstream physiological effects in published mouse data: increased type IIa oxidative skeletal muscle fibers, enhanced running endurance, increased resting energy expenditure, improved glucose tolerance, and reduced adiposity.
- Landmark publications: Billon et al. (2023) ACS Chem Biol — ERRα-dependent acute aerobic exercise genetic program; type IIa fiber induction; endurance enhancement in mice. Second study (2024) J Pharmacol Exp Ther — metabolic syndrome models: increased energy expenditure, improved glucose tolerance, reduced adiposity at 50 mg/kg twice-daily for 28 days. Third application: cardiac protection against pressure-overload heart failure in mouse models (GCGR fatty acid oxidation program in heart).
- Important classification note: SLU-PP-332 is a small molecule (MW ~382 Da; not a peptide). YPB.243 is classified in the YPB research compound catalog alongside peptide products. WADA has identified pan-ERR agonists and exercise mimetics as compounds with doping potential; metabolic modulator/exercise mimetic category under monitoring. No human clinical trial as of April 2026. Research Use Only (RUO). Updated April 2026.
What Is SLU-PP-332 and What Makes It a Unique Research Tool?
Exercise Mimetic Small Molecule
PGC-1α/Mitochondrial Biogenesis
SLU-PP-332 is a synthetic small molecule (MW ~382 Da; not a peptide) developed as an exercise mimetic research tool through rational compound design targeting the estrogen-related receptor family. Updated April 2026. It emerged from research at Washington University in St. Louis aimed at solving a longstanding pharmacological challenge: designing synthetic agonists for ERRα, an orphan nuclear receptor that genetic evidence had established as a key regulator of exercise capacity, but for which no selective small-molecule agonist existed. ERRα loss-of-function mice show dramatically reduced muscle oxidative function and running endurance — demonstrating that ERRα is not merely present during exercise adaptation but functionally required for it. Pharmacologically activating ERRα was therefore predicted to recapitulate key aspects of exercise adaptation without the exercise itself.
SLU-PP-332 activates all three ERR subtypes (pan-agonist) with highest potency at ERRα. The landmark characterization (Billon et al., 2023, ACS Chem Biol) established that SLU-PP-332 induces an ERRα-specific acute aerobic exercise genetic program in skeletal muscle, increases type IIa oxidative muscle fibers, and enhances running endurance in mice — confirming the exercise mimetic hypothesis at the molecular and physiological levels.
Key Characteristics
| Parameter | Value |
|---|---|
| Classification | Synthetic small molecule; pan-ERR agonist; exercise mimetic; NOT a peptide (MW ~382 Da) |
| YPB SKU | YPB.243 |
| Receptor Targets | ERRα (EC50 ~98 nM), ERRβ (~230 nM), ERRγ (~430 nM); highest potency at ERRα; all three are orphan nuclear receptors |
| Receptor Class | Orphan nuclear receptors (no known endogenous ligand); ligand-binding domain shares structural similarity with estrogen receptors but ERRs do not bind estrogens |
| Mechanism | ERRα stabilization → PGC-1α upregulation → mitochondrial biogenesis gene program: fatty acid oxidation (CPT1B, ACADM, HADHA), ETC subunits, DDIT4, Slc25a25 induction |
| Functional Outcome (Mouse) | Type IIa oxidative muscle fiber increase; enhanced running endurance; increased resting energy expenditure; improved glucose tolerance; reduced adiposity; cardiac protection |
| Landmark Publication | Billon et al. (2023) ACS Chem Biol (exercise mimetic characterization); second study (2024) JPET (metabolic syndrome models) |
| Key Downstream Genes | PGC-1α, DDIT4, Slc25a25, CPT1B, ACADM, HADHA (fatty acid oxidation); UQCRC2, ATP5A1 (ETC) |
| Half-Life | Sufficient for in vivo use (published twice-daily dosing at 50 mg/kg in mouse studies confirms adequate pharmacokinetics) |
| FDA Status | Not research-grade. No human clinical trial as of April 2026. Research Use Only (RUO). |
| WADA Status | Exercise mimetics and metabolic modulators under WADA monitoring; pan-ERR agonists specifically identified as having doping potential in published WADA metabolomics literature (2026) |
| Storage | Lyophilized: −20°C. DMSO stock (75 mg/mL): −20°C up to 3 months. Not freely water-soluble; reconstitute in DMSO first, then dilute to aqueous buffer (≤0.1% final DMSO for cell assays) |
The ERR Axis: Why Orphan Nuclear Receptors Are the Master Switch for Exercise Adaptation
To understand SLU-PP-332’s significance as a research tool, it is necessary to understand what ERRα does at the molecular level and why pharmacologically activating it constitutes a genuine exercise mimetic approach rather than merely a metabolic stimulant.
ERRs: Orphan Nuclear Receptors Without a Known Endogenous Ligand
The estrogen-related receptors (ERRα, ERRβ, ERRγ) are members of the nuclear receptor superfamily that share structural similarity with the classical estrogen receptors (ERα, ERβ) but do not bind estrogens. They are designated “orphan receptors” because no endogenous ligand has been identified; ERRs appear to be constitutively active and regulated primarily through coactivator interactions rather than ligand binding. ERRα is the most studied and is highly expressed in metabolically active tissues: skeletal muscle, heart, brown adipose tissue, and liver. Genetic loss-of-function studies established that ERRα (and ERRγ) are required for normal oxidative muscle function and endurance; ERRα-null mice exhibit markedly reduced exercise capacity.
ERRα and the PGC-1α Axis: Transcriptional Engine of Exercise Adaptation
During endurance exercise, AMPK activation (from ATP depletion) and increased NAD+ levels (from oxidative metabolism) activate SIRT1, which deacetylates and activates PGC-1α — the master transcriptional coactivator of mitochondrial biogenesis. PGC-1α then coactivates ERRα on the promoters of mitochondrial biogenesis genes, creating a feed-forward loop: ERRα + PGC-1α together drive transcription of the genes that build more mitochondria, upregulate fatty acid oxidation enzymes, and remodel skeletal muscle toward oxidative (type IIa/slow-twitch) fiber phenotypes. SLU-PP-332 engages ERRα directly — bypassing the upstream AMPK/SIRT1 signaling cascade and stabilizing ERRα’s active conformation, driving the same downstream PGC-1α-associated gene program that exercise would trigger through the AMPK pathway.
What Research Applications Has SLU-PP-332 Been Studied For?
Skeletal Muscle Oxidative Remodeling and Exercise Endurance
The primary published application (Billon et al., 2023) is skeletal muscle exercise adaptation research. SLU-PP-332 induces a shift toward type IIa (fast oxidative glycolytic) muscle fiber phenotype — the fiber type predominantly increased by endurance exercise training. This involves upregulation of oxidative enzyme expression, mitochondrial biogenesis, and fatty acid oxidation capacity. Enhanced running endurance was documented in treated vs. vehicle mice in treadmill exhaustion assays, with ERRα knockout mice failing to show the endurance enhancement (confirming ERRα mediation). The acute exercise genetic program induced by SLU-PP-332 overlaps substantially with the gene expression signature of endurance exercise, validating its classification as a molecular exercise mimetic.
Metabolic Syndrome and Obesity Research
A follow-up study (2024, JPET) examined SLU-PP-332 in diet-induced obesity and metabolic syndrome mouse models at 50 mg/kg twice daily for 28 days. Key findings: increased resting energy expenditure (indirect calorimetry; whole-body fatty acid oxidation increase); improved glucose tolerance (OGTT); reduced adiposity. These effects mirror metabolic improvements from aerobic exercise training, validating SLU-PP-332 as a pharmacological tool for studying the mechanisms by which increased oxidative metabolism protects against metabolic syndrome pathology.
Cardiac Research (Pressure Overload)
In cardiac pressure overload models (which induce pathological hypertrophy and heart failure), SLU-PP-332 demonstrated cardioprotective effects by transcriptionally activating the same metabolic gene program (fatty acid oxidation, mitochondrial function) in cardiac tissue. The failing heart characteristically shifts from fatty acid oxidation toward glucose metabolism; ERRα activation maintains or restores the fatty acid oxidation program, preserving energy efficiency in stressed cardiac tissue.
Muscle Atrophy and Aging Research
Published data (Frontiers Physiol, 2025) examined SLU-PP-332 as a potential counter-measure for age-related muscle atrophy associated with physical inactivity. ERRα activation drives expression of key molecules (NOX4, FNDC5, SIRT1, PGC-1α) that are downregulated during aging and inactivity, identifying SLU-PP-332 as a candidate research tool for studying sarcopenia mechanisms.
What Does the Preclinical Research Data Show?
| Study / Application | Model / Design | Key Finding & Adverse Events | Year |
|---|---|---|---|
| Billon et al. — Exercise mimetic characterization | In vitro (C2C12 myotubes) + in vivo (C57BL/6 mice; ERRα KO controls) | SLU-PP-332 induced ERRα-dependent acute aerobic exercise gene program; increased type IIa oxidative muscle fibers; enhanced running endurance vs. vehicle; effect abrogated in ERRα KO mice. Well tolerated at studied doses. (ACS Chem Biol, 2023) | 2023 |
| Metabolic syndrome / obesity models | In vivo (diet-induced obesity mice; 50 mg/kg twice-daily × 28 days) | Increased resting energy expenditure (whole-body fatty acid oxidation); improved glucose tolerance (OGTT); reduced adiposity. Metabolic adaptations consistent with aerobic exercise training. Well tolerated at 28-day dosing. (JPET, 2024) | 2024 |
| Cardiac pressure overload | In vivo (pressure overload heart failure mouse model) | Cardioprotective effects: maintained fatty acid oxidation gene program in cardiac tissue; attenuated pathological hypertrophy. ERRα activation in cardiac cells proposed as mechanism. Well tolerated. | 2023–2024 |
| Human clinical trial | No published trial as of April 2026 | No published Phase 1 or Phase 2 human clinical trial. All efficacy and safety data from in vitro and mouse models. Human pharmacokinetics, safety profile, and efficacy are unknown. WADA has identified ERR pan-agonists as having doping potential (published 2026 doping-control metabolism study). | N/A |
How Does SLU-PP-332 Compare to Other Metabolic and Exercise Biology Research Compounds?
| Parameter | SLU-PP-332 | AICAR | MOTS-c | AOD 9604 |
|---|---|---|---|---|
| Classification | Small molecule; pan-ERR agonist; nuclear receptor | Nucleotide analogue; AMPK activator | Mitochondria-derived peptide (16 AA); AMPK pathway | HGH fragment peptide; proposed β3-AR lipolytic |
| Primary Target | ERRα/β/γ (orphan nuclear receptors; transcriptional) | AMPK (AMP kinase; metabolic sensor); also AICAR ribotide activates purine synthesis | AMPK activation; mitochondrial FOXO1/DAF-16 | Proposed β3-adrenergic receptor / adipose lipolysis |
| Position in Exercise Pathway | Downstream: directly activates ERRα transcriptional output (PGC-1α program); bypasses AMPK/SIRT1 upstream signaling | Upstream: AMPK activation → SIRT1 → PGC-1α → ERRα; physiological metabolic stress mimic | Upstream/mitochondrial: AMPK + FOXO1; distinct mitochondrial peptide signaling | Peripheral: lipolysis and fat mobilization; no mitochondrial biogenesis mechanism |
| Muscle Fiber Remodeling | Yes — type IIa oxidative fiber increase confirmed (Billon 2023) | Indirect; AMPK activation drives some fiber remodeling | Yes — metabolic reprogramming in muscle | No published fiber-type remodeling data |
| Published Landmark Paper | Billon et al. (2023) ACS Chem Biol (exercise endurance + gene program) | Merrill et al. (2002) Diabetes AICAR exercise mimetic characterization | Lee et al. (2015) Cell Metab MOTS-c mitochondrial signaling | Heffernan et al. (2001) J Endocrinol AOD 9604 lipolytic activity |
| YPB SKU | YPB.243 — see product | YPB.250 — see guide | YPB.227 — see guide | YPB.248 — see guide |
SLU-PP-332 and AICAR target the same exercise-adaptation pathway at different levels, making them complementary pharmacological tools: AICAR activates AMPK upstream of ERRα (see the AICAR Research Guide); SLU-PP-332 activates ERRα directly, downstream. MOTS-c (see the MOTS-c Research Guide) activates AMPK through a distinct mitochondrial peptide pathway. Together these three compounds enable researchers to dissect the full AMPK/SIRT1/PGC-1α/ERRα exercise adaptation cascade at multiple intervention points.
What Should Researchers Know About SLU-PP-332 Handling?
Solubility: DMSO-First Protocol Required
SLU-PP-332 has limited aqueous solubility. The standard preparation protocol: first dissolve in DMSO at 75 mg/mL to create a stock solution; then dilute into aqueous buffer or cell culture medium to working concentration. For cell-based assays, keep final DMSO concentration at ≤0.1% to avoid cytotoxicity from the vehicle. DMSO stocks at −20°C are stable for up to 3 months; avoid repeated freeze-thaw cycles from the DMSO stock. Lyophilized material: −20°C for up to 2 years.
ERRα Knockout Control Requirement
Billon et al. (2023) definitively confirmed ERRα mediation by demonstrating that the endurance enhancement was abrogated in ERRα knockout mice. For research protocols claiming ERRα-mediated effects, ERRα knockdown or knockout controls (siRNA in cell studies; KO mice for in vivo) are the appropriate mechanistic validation. Without ERRα loss-of-function controls, observed effects could reflect ERRβ/γ activation or off-target activities.
COA Verification
HPLC purity (≥98%) and MS confirmation at ~382 Da. As a small molecule, SLU-PP-332 should show a single, clean HPLC peak; multiple peaks indicate impurities that could confound ERR binding assays. All YPB SLU-PP-332 batches include lot-traceable COA documentation through the COA Library.
Key Research Findings
- Pan-ERRα/β/γ agonist, highest potency at ERRα (EC50 ~98 nM): First synthetic compound to effectively target ERRα in vivo; ERRα knockout mice fail to show endurance enhancement, confirming ERRα is the functionally critical subtype.
- Billon et al. (2023) ACS Chem Biol: ERRα-dependent acute aerobic exercise genetic program; type IIa oxidative muscle fiber increase; enhanced running endurance in mice. Landmark exercise mimetic characterization.
- Metabolic syndrome models (2024 JPET): 50 mg/kg twice-daily × 28 days: increased resting energy expenditure, improved glucose tolerance, reduced adiposity — reproducing metabolic adaptations of aerobic exercise training in mice.
- Mechanism: ERRα → PGC-1α → mitochondrial biogenesis gene program: CPT1B, ACADM, HADHA (fatty acid oxidation); DDIT4, Slc25a25 (mitochondrial function); ETC subunits. Same gene set upregulated by endurance exercise via AMPK/SIRT1/PGC-1α.
- Downstream of AMPK; complementary to AICAR: AICAR activates AMPK upstream; SLU-PP-332 activates ERRα downstream. Parallel use in research enables cascade dissection.
- No human clinical trial published (April 2026): All data from in vitro and mouse models. Human PK, safety, and efficacy unknown.
- WADA doping potential identified (2026): Published metabolism characterization for doping-control purposes confirms WADA awareness; exercise mimetics/metabolic modulators category under monitoring.
- Small molecule, not a peptide: DMSO-first reconstitution required; MW ~382 Da; not water-soluble without vehicle.
Browse the Full Research Catalog
Market Demand and Research Interest
| Demand Indicator | SLU-PP-332 Data Point |
|---|---|
| Search context | Exercise mimetic; ERR agonist; pan-ERR compound; exercise in a pill research; metabolic disease pharmacology |
| Landmark publications | Billon et al. (2023) ACS Chem Biol; metabolic syndrome study (2024) JPET; cardiac study (2023–2024); WADA metabolism characterization (2026) |
| Unique catalog position | Only ERR agonist in YPB catalog; only small-molecule nuclear receptor agonist; only compound with published type IIa fiber remodeling mechanism |
| Exercise biology audience | Muscle physiology; metabolic disease; aging muscle; cardiac metabolism; endurance exercise biology — each an active funded research area |
| WADA context | WADA monitoring of exercise mimetics drives both regulatory attention and commercial interest as a research tool; doping-control metabolism paper published 2026 |
| Keyword difficulty range | Very low (KD <5); specialized but rapidly growing |
How Can Researchers Offer SLU-PP-332 Under Their Own Brand?
Wholesale Pricing & Margin Analysis
| SKU | Compound | Premier ($497/mo) | Core ($297/mo) | Suggested MSRP | Premier Margin |
|---|---|---|---|---|---|
| YPB.243 (RUO) | SLU-PP-332 (pan-ERR agonist) | TBC Premier | TBC Core | TBC | TBC at Premier tier |
Contact the YPB team for confirmed Premier and Core tier pricing. Use the YPB Profit Calculator to model projected revenue. White-label brands offering SLU-PP-332 alongside AICAR and MOTS-c provide the most mechanistically complete exercise biology and metabolic research toolkit available: direct ERRα transcriptional activation (SLU-PP-332) + AMPK upstream activation (AICAR) + mitochondrial AMPK peptide signaling (MOTS-c). Together these three tools cover the entire exercise-adaptation signaling cascade from three non-redundant intervention points. Download the full catalog for all exercise biology category pricing.
Methodology & Data Sources
Methodology & Data Sources
Scientific literature: PubMed searched for “SLU-PP-332,” “ERR alpha agonist exercise mimetic,” “pan-ERR agonist,” and “estrogen-related receptor exercise.” Search conducted through April 2026.
Key sources: Billon et al. (2023) ACS Chem Biol (landmark exercise mimetic characterization; PMC11584170); ERR agonist metabolic syndrome study (2024) JPET (PMC10801787); Frontiers Physiology (2025) ERR and aging muscle atrophy; WADA-related metabolite characterization (Möller et al., Rapid Commun Mass Spectrom, 2026).
Limitations: SLU-PP-332 is a small molecule with all efficacy data from cell culture and mouse models; no human clinical trial as of April 2026. Long-term safety of ERRα pan-agonism in humans is unknown. ERRα has roles in multiple tissues including reproductive biology and cancer (ERRα is upregulated in multiple cancer types); chronic systemic ERRα activation merits oncology safety monitoring in chronic in vivo protocols. WADA has identified exercise mimetics and metabolic modulators as compounds with doping potential. This article is for educational purposes only.
References
- Billon, C., Murray, M. H., Bhatt, D., et al. (2023). Synthetic ERRα/β/γ agonist induces an ERRα-dependent acute aerobic exercise response and enhances exercise capacity. ACS Chem Biol, 18(4), 756–772. PMC11584170.
- Murray, M. H., Billon, C., Bhatt, D., et al. (2024). A synthetic ERR agonist alleviates metabolic syndrome. J Pharmacol Exp Ther. PMC10801787.
- Dufour, C. R., Wilson, B. J., Huss, J. M., et al. (2007). Genome-wide orchestration of cardiac functions by the orphan nuclear receptors ERRα and γ. Cell Metab, 5(5), 345–356. (ERR cardiac biology context.)
- Möller, T., Krug, O., & Thevis, M. (2026). In vitro metabolism and analytical characterization of SLU-PP-332 and SLU-PP-915: novel pan-ERR agonists with doping potential. Rapid Commun Mass Spectrom. (WADA doping-control metabolite study.)
- Huss, J. M., Garbacz, W. G., & Xie, W. (2015). Constitutive activities of estrogen-related receptors mediate cell type-specific expansion of intestinal epithelium. J Biol Chem, 290(19), 12273–12284.
- Giguere, V. (2008). Transcriptional control of energy homeostasis by the estrogen-related receptors. Endocr Rev, 29(6), 677–696. PMID: 18664618 (ERR axis biology foundational review.)
- Arany, Z., Lebrasseur, N., Morris, C., et al. (2007). The transcriptional coactivator PGC-1beta drives the formation of oxidative type IIX fibers in skeletal muscle. Cell Metab, 5(1), 35–46. (PGC-1/fiber type context.)
- Frontiers in Physiology (2025). Targeting ERRs to counteract age-related muscle atrophy associated with physical inactivity: a pilot study. (SLU-PP-332 sarcopenia context.)
- Merrill, G. F., Kurth, E. J., Hardie, D. G., & Winder, W. W. (2002). AICA riboside increases AMP-activated protein kinase, fatty acid oxidation, and glucose uptake in rat muscle. Am J Physiol Endocrinol Metab. (AICAR comparison context.)
Frequently Asked Questions
SLU-PP-332 is a synthetic small molecule (MW ~382 Da; not a peptide; YPB.243) that functions as a pan-agonist of the estrogen-related receptors (ERRα EC50 ~98 nM; ERRβ ~230 nM; ERRγ ~430 nM), with highest potency at ERRα. In research models, it directly activates ERRα transcriptional output, upregulating PGC-1α and a downstream mitochondrial biogenesis/fatty acid oxidation gene program (CPT1B, ACADM, HADHA, DDIT4, Slc25a25, ETC subunits) that recapitulates the molecular signature of endurance exercise. Published mouse data: increased type IIa oxidative muscle fibers, enhanced running endurance (Billon et al., 2023 ACS Chem Biol); increased resting energy expenditure, improved glucose tolerance, reduced adiposity in metabolic syndrome models (2024 JPET); cardiac protection in pressure-overload models. ERRα knockout mice do not show endurance enhancement, confirming ERRα specificity. No human clinical trial as of April 2026. WADA exercise mimetics monitoring. Research Use Only (RUO). Updated April 2026.
ERRs (estrogen-related receptors — ERRα, ERRβ, ERRγ) are members of the nuclear receptor superfamily that share structural similarity with the classical estrogen receptors (ERα, ERβ) in their DNA-binding and ligand-binding domains. They are designated “orphan receptors” because, despite intensive research, no endogenous ligand has been identified that binds and activates them in the classical ligand-receptor manner. ERRs appear to be constitutively active, regulated primarily through coactivator interactions (particularly with PGC-1α) rather than ligand binding. This makes designing synthetic agonists challenging — there is no natural ligand pharmacophore to model from. SLU-PP-332 was designed through rational structural approaches to stabilize ERRα’s active conformation despite the absence of a known natural ligand template, making it a significant methodological advance for ERR biology research.
Both SLU-PP-332 and AICAR are classified as exercise mimetics and both ultimately drive PGC-1α-dependent mitochondrial biogenesis, but they intervene at different levels of the same signaling cascade. AICAR activates AMPK by mimicking AMP (the high-energy-depletion metabolic signal generated during exercise). AMPK then activates SIRT1, which deacetylates PGC-1α, which in turn coactivates ERRα to drive the mitochondrial gene program. AICAR therefore activates the full AMPK/SIRT1/PGC-1α/ERRα cascade from the top, mimicking the upstream metabolic stress signal of exercise. SLU-PP-332 activates ERRα directly, at the bottom of this cascade, bypassing AMPK and SIRT1 entirely. The research significance: comparing parallel studies with AICAR (upstream) and SLU-PP-332 (downstream) allows researchers to identify which exercise-adaptation effects require the full signaling cascade vs. which can be achieved by directly engaging ERRα transcriptional output. Effects seen with SLU-PP-332 but not AICAR suggest non-ERRα AMPK-dependent pathways; effects seen with AICAR but not SLU-PP-332 suggest ERRα-independent AMPK signaling. This cascade dissection is not possible with either compound alone.
Skeletal muscle contains distinct fiber types defined by their metabolic and contractile properties. Type I (slow oxidative) fibers: high mitochondrial content, fatigue-resistant, fatty acid oxidation primary fuel, adapted for sustained low-intensity activity. Type IIa (fast oxidative glycolytic) fibers: intermediate — high mitochondrial content and oxidative capacity like type I, but faster contraction speed; well-adapted for sustained moderate-to-high intensity aerobic exercise. Type IIx/IIb (fast glycolytic) fibers: low mitochondrial content, high-force, fatigue quickly, primarily glycolytic. Endurance exercise training shifts skeletal muscle composition from type IIx/IIb toward type IIa — increasing oxidative capacity, fatigue resistance, and metabolic flexibility. SLU-PP-332’s documented increase in type IIa fibers at the expense of fast glycolytic fibers directly recapitulates this endurance training adaptation at the tissue level, confirming that ERRα activation is sufficient to drive the fiber-type remodeling that makes trained muscle more oxidative and fatigue-resistant. This is a qualitatively different endpoint than simply increasing metabolic gene expression — it demonstrates structural remodeling of muscle tissue.
SLU-PP-332 safety considerations fall into two categories. First, known study-specific data: at the doses used in published mouse studies (50 mg/kg twice-daily for 28 days in metabolic syndrome models), the compound was reported as well tolerated with no prominent adverse event documentation. However, these are acute-to-subacute rodent studies; long-term safety is unknown. Second, theoretical concerns: ERRα is expressed in multiple tissues beyond skeletal muscle, including the liver, brown adipose tissue, and importantly, several cancer types where ERRα is overexpressed and proposed to support tumor metabolism. Chronic systemic ERRα pan-agonism in the context of pre-existing malignancy or in oncologically predisposed models requires appropriate safety monitoring. Additionally, WADA has identified pan-ERR agonists as having doping potential (published 2026 metabolomics/doping-control study), placing SLU-PP-332 in the exercise mimetic/metabolic modulator category for which regulatory monitoring is increasing. No human data exists for safety assessment. All YPB SLU-PP-332 is Research Use Only.
Yes. YourPeptideBrand.com provides white-label dropship for SLU-PP-332 as YPB.243 (Research Use Only). White-label storefronts include pre-built RUO-compliant product pages with pan-ERR agonist mechanism descriptions, exercise mimetic research context, DMSO reconstitution protocol, WADA classification notes, and COA library links. Contact the YPB team for confirmed Premier and Core pricing, and use the profit calculator to model projected revenue.
Every SLU-PP-332 batch includes a lot-specific COA: HPLC purity (≥98%), MS confirmation at ~382 Da (small molecule; single clean peak confirming defined compound identity; multiple HPLC peaks would indicate impurities that could confound ERR binding assays), NMR structural confirmation where available, endotoxin (<1 EU/mg), and TAMC/TYMC. For small-molecule research compounds, NMR is the gold-standard identity confirmation beyond MS; request NMR data if precise structural identity is critical for publication. All lots are traceable through the batch-specific COA library.
SLU-PP-332 is a small molecule, not a peptide, but it belongs in the same exercise biology and metabolic research catalog as AICAR, MOTS-c, and AOD 9604 because it addresses the same research questions. Position it as the ERRα transcription-level exercise mimetic: the compound that directly activates the nuclear receptor transcriptional machinery responsible for encoding exercise adaptation into muscle, rather than signaling through the upstream metabolic stress pathway (AICAR/AMPK) or mitochondrial peptide axis (MOTS-c). For researchers studying muscle metabolism, exercise adaptation, or metabolic disease, SLU-PP-332 is the most mechanistically specific tool available for isolating ERRα-dependent gene programs. The WADA exercise mimetic designation adds a layer of research interest from sports science and anti-doping communities in addition to the metabolic disease and aging biology audiences.
Key Takeaways
Research Takeaways
- Pan-ERRα/β/γ agonist (highest potency ERRα EC50 ~98 nM): First synthetic compound to effectively activate ERRα in vivo; ERRα is an orphan nuclear receptor with no known endogenous ligand.
- Billon et al. (2023) ACS Chem Biol: ERRα-dependent acute aerobic exercise gene program; type IIa oxidative muscle fiber increase; enhanced running endurance in mice; abrogated in ERRα KO (confirms ERRα specificity).
- Mechanism: ERRα → PGC-1α → mitochondrial biogenesis: CPT1B, ACADM, HADHA (fatty acid oxidation); DDIT4, Slc25a25; ETC subunits. Downstream of AMPK/SIRT1 exercise cascade.
- Downstream of AICAR/AMPK; complementary research tool: Parallel use with AICAR enables dissection of AMPK-dependent vs. ERRα-specific exercise adaptation effects.
- DMSO reconstitution required: 75 mg/mL DMSO stock; ≤0.1% final DMSO in cell assays; aqueous solubility limited.
- No human clinical trial (April 2026): All data from in vitro and mouse models; WADA exercise mimetic monitoring; ERRα cancer biology context warrants oncology safety monitoring in chronic in vivo protocols.
- Small molecule, not a peptide: MW ~382 Da; HPLC single-peak and MS at ~382 Da are primary quality criteria.
Business Takeaways
- Only ERR agonist in YPB catalog — unique nuclear receptor mechanism; no overlap with any other guide.
- WADA exercise mimetic designation drives interest from sports science, anti-doping, and metabolic disease research communities simultaneously.
- SLU-PP-332 + AICAR + MOTS-c exercise biology trio covers the full exercise-adaptation signaling cascade at three intervention points from a single research buyer audience.
- Contact YPB for confirmed pricing on YPB.243.
Ready to add SLU-PP-332 to your research catalog? Book a consultation with the YPB team.
[ypb_studies peptide=”slu-pp-332″]