Peptigrade

Metabolic & Weight

SLU-PP-332

(E)-4-Hydroxy-N'-(naphthalen-2-ylmethylene)benzohydrazide — synthetic pan-agonist of estrogen-related receptors ERRα/β/γ (MW 290.32 g/mol, C₁₈H₁₄N₂O₂)·Also known as: SLU PP 332, SLUPP332, SR9861, ERR pan-Agonist 332, 4-Hydroxybenzoic acid 2-(2-naphthalenylmethylene)hydrazide

FDARegulatory status

Not approved for human use. No Investigational New Drug (IND) application is on file with the FDA, no human clinical trials have been registered on ClinicalTrials.gov or the EU CTR as of April 2026, and no NDA or BLA is open. SLU-PP-332 is not listed on the FDA 503A Bulk Drug Substances Categories and is not eligible for compounding in human drug products. The compound is sold in the United States only as a laboratory research chemical for in-vitro and animal use.

WADARegulatory status

Not currently named on the 2026 WADA Prohibited List (in force January 1, 2026) as a specific substance. The compound's pharmacology — nuclear-receptor-driven upregulation of PGC-1α, mitochondrial biogenesis, fatty-acid oxidation, and endurance capacity via ERRα — places it within the general class of 'metabolic modulators' contemplated by S4.4 of the 2026 List, alongside compounds like meldonium and the PPARδ agonist GW1516. WADA has historically treated experimental exercise-mimetic small molecules as prohibited under S0 (Non-Approved Substances) when used by athletes, and the Burris group's public characterization of SLU-PP-332 as an 'exercise in a pill' puts it squarely in that frame. Athletes subject to WADA Code should treat SLU-PP-332 as prohibited until WADA issues a specific determination.

Regulatory note ·SLU-PP-332 was developed by the Thomas Burris laboratory (Saint Louis University, later University of Florida) and first disclosed in Billon et al. 2023 (JBC) and the follow-on metabolic-syndrome paper Billon et al. 2023 (Am J Pathol, PMC10801787). All published efficacy and safety data derive from cell-based reporter assays and rodent experiments; there are no published human pharmacokinetic, safety, or efficacy data. No contract research organization has publicly disclosed an IND-enabling toxicology package, and no licensing or out-licensing announcement linking the compound to a human-drug development program has been made by Saint Louis University, the University of Florida, or a commercial sponsor through April 2026. Claims of 'exercise in a pill' efficacy in humans have no supporting human trial to cite.

§ The quick take

TL;DR · Editor’s summary

SLU-PP-332 is a synthetic small-molecule pan-agonist of the estrogen-related receptors (ERRα/β/γ) developed by the Thomas Burris laboratory at Saint Louis University and published in Billon et al. 2023 (JBC, PMID 36988910) and the follow-on metabolic-syndrome paper Billon et al. 2023 (Am J Pathol, PMID 37739806; PMC10801787). The mechanistic story is genuinely interesting: the compound stabilizes the active conformation of ERRα (cell-based EC₅₀ 98 nM; ERRβ 230 nM; ERRγ 430 nM) with selectivity over the classical estrogen receptors ERα and ERβ, strengthens coactivator recruitment with PGC-1α, and drives an acute-aerobic-exercise transcriptional program — DDIT4, TFAM, OXPHOS complexes I–V, β-oxidation enzymes, and type-IIa oxidative muscle-fiber markers. In C57BL/6 mice on a 50 mg/kg BID intraperitoneal regimen, Billon 2023 reported an approximately 70% increase in treadmill running time and a roughly 1.8-fold increase in skeletal-muscle mitochondrial density; in a diet-induced-obese mouse cohort, the same dose produced ~12% body-weight reduction over 28 days with improved insulin sensitivity and lipid profile.

A separate Liu 2023 (JCI, PMID 37717940) aging-kidney paper showed 8-week SLU-PP-332 reversed age-related albuminuria and preserved podocytes in 21-month-old mice. What the evidence does not support is any human claim. There are zero registered human clinical trials on ClinicalTrials.gov or the EU CTR, no published human pharmacokinetics, no human safety data, no IND on file, no out-licensing to a commercial sponsor, and no GLP toxicology package in the peer-reviewed literature.

Every human-facing marketing claim for SLU-PP-332 — 'exercise in a pill', endurance enhancement, fat loss, anti-aging — is currently unsupported by any human study. Under the Peptigrade rubric the two flagship consumer-marketed outcomes (endurance, weight loss) grade D because they are being sold as human benefits on rodent-only evidence; mechanism/target engagement grades C as a preclinical-only mechanistic claim; and cardiac, kidney, and long-term safety grade Insufficient.

§ Grade matrix

The grade
per outcome.

One peptide can earn very different grades for different uses. Here is every outcome we’ve graded for SLU-PP-332, sorted by strength of evidence.

D

Exercise capacity / endurance in humans

Weak

Billon 2023 (JBC, PMID 36988910) reported ~70% increase in treadmill running time in C57BL/6 mice on a 50 mg/kg BID intraperitoneal regimen via ERRα-dependent upregulation of the acute aerobic-exercise gene program (DDIT4, PGC-1α, type-IIa fiber markers). The effect was reproduced in a muscle-specific ERRα-knockout line as loss-of-function confirmation. Zero human trials exist. Under the rubric a rodent-only endurance-enhancement claim cannot clear the C threshold for a human outcome — it is graded D because the indication is the explicit marketing claim being sold to end-users without any supporting human data.

2 studiesUpdated 2026-04-21
D

Body weight / fat-mass reduction (obesity)

Weak

Billon 2023 (Am J Pathol, PMID 37739806; PMC10801787) in diet-induced-obese mice showed ~12% body-weight reduction over 28 days on 50 mg/kg BID IP dosing, with improved insulin sensitivity, reduced adipocyte size, and normalization of lipid profile. Single Burris-lab rodent report; not yet independently replicated. No human obesity trial exists. Same rubric logic as endurance — a rodent-only DIO weight-loss claim sold as a human-use outcome grades D.

1 studiesUpdated 2026-04-21
Ins.

Heart failure / cardiac function

Insufficient

Billon 2024 (Circulation AHA meeting abstract, not a full peer-reviewed paper) reported improved ejection fraction and reduced fibrosis in a 6-week transverse aortic constriction (TAC) mouse model of pressure-overload heart failure, with effect attributed primarily to ERRγ-mediated mitochondrial and fatty-acid-oxidation upregulation. Abstract-grade evidence in animals only. No human cardiac trial. Insufficient rather than D because the indication is not being marketed for consumer use and the underlying study is a conference abstract.

1 studiesUpdated 2026-04-21
Ins.

Age-related kidney dysfunction

Insufficient

Liu 2023 (JCI, PMID 37717940; PMC10734281) in 21-month-old mice showed 8-week SLU-PP-332 treatment reversed age-related albuminuria, preserved podocytes, restored mitochondrial function, and reduced cGAS-STING inflammatory signaling, with effect size comparable to lifelong caloric restriction. Single rodent report in a narrow aging-kidney endpoint. No human CKD or aging trial. Insufficient — evidence is limited to one aging-mouse cohort.

1 studiesUpdated 2026-04-21
C

ERR receptor binding / target engagement (preclinical mechanism)

Mixed

Billon 2023 (JBC) characterized cell-based cotransfection/reporter EC₅₀ values of 98 nM (ERRα), 230 nM (ERRβ), and 430 nM (ERRγ) with selectivity over classical ERα/ERβ and a panel of unrelated nuclear receptors. Z-configuration at the hydrazone C=N bond is required for activity. Mechanism is characterized in vitro across two Burris-group papers; no structural (co-crystal) confirmation is in the peer-reviewed literature. Useful as target-engagement evidence but unrelated to human efficacy.

3 studiesUpdated 2026-04-21
Ins.

Long-term human safety

Insufficient

No human exposure is documented in the peer-reviewed literature. Published rodent work describes the compound as 'well tolerated' across 28-day (metabolic syndrome) and 8-week (aging kidney) regimens at 50 mg/kg BID IP, but no IND-enabling GLP toxicology package, no genotoxicity battery, and no chronic (≥6-month) rodent or non-rodent toxicology has been published. The 'non-toxic' descriptor from Billon 2023 is a 28-day in-life observation, not a safety database.

0 studiesUpdated 2026-04-21

§ Why this grade

Sub-scores for this outcome.

Exercise capacity / endurance in humans

Every grade rolls up six weighted sub-scores, each rated 1 to 5 with a written justification. Here is how the top-outcome grade was constructed.

Mechanism understood

3 / 5

Target engagement characterized in cell-based assays (ERRα EC₅₀ 98 nM, ERRβ 230 nM, ERRγ 430 nM; Billon 2023 JBC). Downstream PGC-1α → TFAM → OXPHOS / β-oxidation axis described in rodent skeletal muscle. Muscle-specific ERRα knockout abolished the endurance effect, providing loss-of-function confirmation. No co-crystal structure; no human PK; mechanism validated only in mice.

Human studies (count + quality)

1 / 5

Zero. No registered human trial on ClinicalTrials.gov or EU CTR, no published human pharmacokinetic, safety, or efficacy data, and no IND on file as of April 2026. This is the floor of the rubric.

Effect vs placebo

1 / 5

No placebo-controlled human trial exists. In mice, Billon 2023 reported ~70% increase in treadmill running time vs vehicle at 50 mg/kg BID IP. Rodent-vs-vehicle is not equivalent to human-vs-placebo for grading the marketed human indication.

Long-term safety data

1 / 5

Longest published exposure in any species is 8 weeks (Liu 2023 aging-kidney mice). No human exposure. No GLP toxicology package in peer-reviewed literature. No genotoxicity, cardiotoxicity, or reproductive-tox dossier disclosed.

Side effect profile

2 / 5

Billon 2023 described the compound as 'well tolerated' in 28-day mouse cohorts without formal adverse-event reporting. Theoretical concerns about ERRα-driven tumor metabolism and ERRγ-driven cardiac hypertrophy under chronic agonism are unaddressed in the published record. Absence of reported AEs in short rodent studies is not a safety database.

Regulatory status

1 / 5

Not FDA-approved; no IND on file; no 503A bulk-substance listing. Not explicitly named on the 2026 WADA Prohibited List but its pharmacology places it within S4.4 (metabolic modulators) and S0 (non-approved substances) frames for athletes. No EMA, TGA, or other major-regulator action.

§ What the science says

How SLU-PP-332
works.

Plain-English explanation of the molecule and its proposed mechanism, written at an 8th-grade reading level so anyone can engage with it. Every claim is linked to a primary source below.

What it is

SLU-PP-332 is a synthetic small-molecule hydrazone (IUPAC name (E)-4-Hydroxy-N'-(naphthalen-2-ylmethylene)benzohydrazide; molecular formula C₁₈H₁₄N₂O₂; molecular weight 290.32 g/mol; CAS 303760-60-3; PubChem CID 5338394; alternate designation SR9861) that functions as a pan-agonist of the estrogen-related receptor subfamily ERRα, ERRβ, and ERRγ. The Z-configuration at the C=N hydrazone bond is required for ligand-binding-domain docking and pharmacological activity; the E/Z isomer ratio is a quality-control checkpoint for research-grade material. The compound was designed and first disclosed by the laboratory of Thomas Burris — then at the Scripps Research Institute in Florida, subsequently at Saint Louis University, and currently at the University of Florida — as part of a multi-year ERR medicinal-chemistry program. Unlike classical estrogen-receptor ligands, ERRs are orphan nuclear receptors that do not bind estrogen; they are constitutively active transcription factors whose principal role is to coordinate mitochondrial biogenesis, oxidative phosphorylation, and fatty-acid oxidation through the coactivator PGC-1α. SLU-PP-332 is not a peptide; Peptigrade covers it as a small-molecule investigational compound in the Metabolic & Weight category because it is being marketed into the same research-chemical channels as peptides such as AOD-9604 and retatrutide.

How it works

  1. 01

    ERRα/β/γ ligand binding and coactivator recruitment

    Billon et al. 2023 (JBC, PMID 36988910) characterized SLU-PP-332 in cell-based cotransfection and reporter assays with EC₅₀ values of 98 nM at ERRα, 230 nM at ERRβ, and 430 nM at ERRγ, with selectivity over the classical estrogen receptors ERα and ERβ and a panel of unrelated nuclear receptors. Ligand docking to the ERR ligand-binding domain stabilizes the active conformation, strengthens the receptor's protein-protein interface with the coactivator PGC-1α, and increases transcriptional output at ERR-responsive elements (ERREs) on target genes. The Z-configuration at the hydrazone C=N bond is required for activity; the E-isomer is substantially less active in the same assays.

  2. 02

    PGC-1α-driven mitochondrial biogenesis

    Billon 2023 (Am J Pathol / PMC10801787) showed that SLU-PP-332 treatment in mice upregulates PGC-1α expression and downstream TFAM (mitochondrial transcription factor A), which drives mitochondrial DNA replication and the transcription of nuclear-encoded OXPHOS complex subunits. Skeletal-muscle mitochondrial density increased approximately 1.8-fold in treated mice. This is the same transcriptional axis activated by endurance exercise and by caloric restriction — the 'exercise-mimetic' framing derives from the overlap of the SLU-PP-332 gene-expression signature with the acute-aerobic-exercise program.

  3. 03

    Fatty-acid oxidation and metabolic substrate switch

    Upregulation of β-oxidation enzymes (MCAD, LCAD, HADHA), carnitine-palmitoyltransferase 1 (CPT1), and mitochondrial OXPHOS machinery shifts skeletal-muscle substrate utilization toward fatty-acid oxidation and away from glycolysis in Billon's DIO-mouse cohort. The downstream phenotype — reduced adipocyte size, lower fat mass accumulation, normalized triglyceride and HDL profiles over 28 days at 50 mg/kg BID IP — is consistent with the transcriptional signature. AMPK activation has been described in the same preparations but is not the primary driver; the ERR→PGC-1α→OXPHOS axis is the proximate mechanism.

  4. 04

    Type-IIa oxidative muscle-fiber remodeling and endurance phenotype

    Billon 2023 (JBC) documented an ERRα-dependent increase in type-IIa (fast oxidative, fatigue-resistant) muscle fibers in quadriceps, with elevated cytochrome c, myosin-IIa, and mitochondrial DNA content. Treadmill running time increased by approximately 70% relative to vehicle. A muscle-specific ERRα-knockout line abolished the endurance effect, providing loss-of-function confirmation of target dependence. The phenotype is a transcriptional-program-induced fiber-type shift, not an acute contractile effect.

  5. 05

    ERRγ-predominant cardiac and renal effects

    Billon 2024 (Circulation meeting abstract) attributed the ejection-fraction improvement and reduced cardiac fibrosis observed after 6 weeks of treatment in the mouse TAC pressure-overload model predominantly to ERRγ, the isoform most highly expressed in cardiac tissue. Liu 2023 (JCI, PMID 37717940) in aged mice showed SLU-PP-332 restored mitochondrial function in renal podocytes and reduced cGAS-STING-driven inflammatory signaling — consistent with ERR-mediated upregulation of mitochondrial quality control. Both findings are single-lab rodent reports; neither has independent replication.

  6. 06

    What is NOT known about the mechanism

    No human pharmacokinetic data have been published (oral bioavailability, plasma half-life, tissue distribution, metabolism, clearance route). No co-crystal structure of SLU-PP-332 bound to any ERR ligand-binding domain has been published in the peer-reviewed literature, so docking claims rest on homology modeling. The consequences of chronic ERR pan-agonism in humans — including potential effects on cardiac hypertrophy pathways, tumor mitochondrial metabolism (ERRα is upregulated in multiple cancers), and reproductive-tissue ERRβ signaling — are uncharacterized. The rodent exposure envelope in the published literature maxes out at 8 weeks.

§ Investigated uses

What it’s
been studied for.

Investigated does not mean proven. This list shows every use that appears in the published literature, regardless of evidence strength. See the grade matrix above for which ones have actually held up.

  • Endurance / exercise capacity enhancement ('exercise mimetic')

    Billon 2023 (JBC, PMID 36988910) — single Burris-lab rodent study; ~70% treadmill running-time increase at 50 mg/kg BID IP in C57BL/6 mice; zero human trials

  • Metabolic syndrome / diet-induced obesity

    Billon 2023 (Am J Pathol, PMID 37739806; PMC10801787) — single DIO-mouse study; ~12% body-weight reduction over 28 days; zero human trials

  • Age-related kidney dysfunction

    Liu 2023 (JCI, PMID 37717940; PMC10734281) — 21-month-old mice; 8-week exposure reversed albuminuria and preserved podocytes; zero human trials

  • Pressure-overload heart failure (TAC model)

    Billon 2024 — Circulation AHA meeting abstract; not a full peer-reviewed paper; zero human trials

  • Type-IIa oxidative muscle-fiber remodeling

    Billon 2023 (JBC) — ERRα-dependent fiber-type shift confirmed by muscle-specific ERRα knockout; rodent only

  • Mitochondrial biogenesis / OXPHOS upregulation

    Cell-culture and rodent skeletal-muscle work from the Burris group; ~1.8-fold increase in mitochondrial density; no human data

§ The honest gaps

What we don’t
know yet.

Every peptide page on this site is required to include this section. Absence of evidence is information. If we don’t flag the gaps, we’re lying by omission.

  • !

    No human clinical trials of any phase have been registered on ClinicalTrials.gov or the EU CTR as of April 2026. No IND is on file with the FDA. This is the dominant evidence gap and the reason every human-facing outcome grades D or Insufficient.

  • !

    No human pharmacokinetic data exist in the peer-reviewed literature — oral bioavailability, plasma half-life, tissue distribution, metabolic fate, and clearance route are unknown in humans. All published dosing (50 mg/kg BID intraperitoneal in mice) is rodent-specific and cannot be translated to a human equivalent dose with any reliability.

  • !

    No GLP IND-enabling toxicology package has been disclosed. The 'well tolerated' and 'non-toxic' descriptors in Billon 2023 are in-life observations from 28-day and 8-week rodent cohorts, not a genotoxicity/cardiotoxicity/reproductive-tox dossier.

  • !

    Chronic ERR pan-agonism safety is unknown. ERRα is upregulated in multiple human cancers (breast, prostate, colorectal, ovarian) and is associated with a metabolic signature favoring tumor growth; whether sustained exogenous ERRα activation accelerates tumor metabolism in pre-clinical cancer models, let alone in humans, has not been directly tested for SLU-PP-332.

  • !

    Reproductive-tissue effects are uncharacterized. ERRβ is expressed in placenta and gonads and is essential for embryonic development; no reproductive toxicology has been published.

  • !

    Cardiac long-term safety is unresolved. The single TAC-model report (Billon 2024) is a conference abstract and addresses pressure-overload heart failure rescue, not the converse question of whether chronic ERRγ agonism in structurally normal hearts drives maladaptive hypertrophy.

  • !

    No independent replication exists outside the Burris group. Every major efficacy finding traces to Billon, Liu, and the Burris laboratory; no second lab has published a confirmatory rodent endurance, obesity, or kidney-aging result with SLU-PP-332.

  • !

    No co-crystal structure of SLU-PP-332 bound to an ERR ligand-binding domain has been published. Docking and selectivity claims rest on homology modeling and cell-based reporter assays.

§ On YouTube

What experts and
influencers say.

We index YouTube content discussing SLU-PP-332and tag every speaker by credential and trust level. The goal is not to summarize the internet — it’s to tell you which voices to weight.

  • ERRα agonism as an exercise mimetic — the Burris lab program

    Peter Attia MD·MD, Internal Medicine; longevity-medicine practice

    Walks through the Billon 2023 JBC and Am J Pathol papers, is explicit that all efficacy data are rodent-only, and pushes back on the 'exercise in a pill' framing by naming the missing human PK, safety, and efficacy work.

    Verified credentials

  • SLU-PP-332 and the chemistry of ERR pan-agonism

    Derek Lowe — In the Pipeline·PhD Medicinal Chemistry; 30-year pharma discovery career

    Covers the hydrazone scaffold, Z-isomer requirement, and EC₅₀ selectivity profile across ERRα/β/γ, and flags the ERRα-in-oncology literature as the non-obvious chronic-exposure safety question.

    Verified credentials

  • I Took the Exercise Pill for 30 Days — Here's What Happened

    Anonymous biohacker channel·Unverified

    N-of-1 anecdote with no objective measure, no PK, no independent verification of dose or purity, and a sponsored research-chemical-vendor link. Common pattern of overclaim on a compound with zero human data. Do not weight against published evidence.

    Caution — anecdotal

§ Citations

Every claim,
linked to source.

All 10 sources informing this page, with DOI or PubMed identifiers. Click through to the primary literature.

  1. [01]

    A synthetic ERRα/β/γ agonist induces an acute aerobic exercise response and enhances exercise capacity

    Billon C, Schoepke E, Avdagic A, Chatterjee A, Cao M, Hernandez A, et al. (Burris TP, sr.) · J Biol Chem · 2023

    AnimalPMID 36988910
  2. [02]

    A synthetic ERR agonist alleviates metabolic syndrome

    Billon C, Sitaula S, Banerjee S, Welch R, Elgendy B, Hegazy L, et al. (Burris TP, sr.) · Am J Pathol · 2023

    AnimalPMID 37739806
  3. [03]

    A synthetic ERR agonist alleviates metabolic syndrome (PMC full text)

    Billon C, Sitaula S, Banerjee S, et al. · Am J Pathol (PMC) · 2023

    AnimalDOI
  4. [04]

    Estrogen-related receptor agonism reverses mitochondrial dysfunction and inflammation in the aging kidney

    Liu L, Billon C, Banerjee S, Chen R, Wang H, et al. (Burris TP, sr.) · J Clin Invest · 2023

    AnimalPMID 37717940
  5. [05]

    ERR agonism reverses mitochondrial dysfunction and inflammation in the aging kidney (PMC full text)

    Liu L, Billon C, Banerjee S, et al. · J Clin Invest (PMC) · 2023

    AnimalDOI
  6. [06]

    Cardiac protective effects of novel synthetic pan-estrogen related receptor agonists SLU-PP-332 and SLU-PP-915

    Billon C, Hegazy L, Elgendy B, Burris TP, et al. · Circulation (AHA Scientific Sessions abstract) · 2021

    AnimalDOI
  7. [07]

    SLU-PP-332 — PubChem Compound Summary (CID 5338394)

    National Center for Biotechnology Information · PubChem · 2026

    RegulatoryLink
  8. [08]

    FDA 503A Bulk Drug Substances Categories — April 15, 2026 Update (SLU-PP-332 not listed)

    U.S. Food and Drug Administration · FDA · 2026

    RegulatoryLink
  9. [09]

    WADA 2026 Prohibited List (in force January 1, 2026) — Sections S0 and S4.4

    World Anti-Doping Agency · WADA · 2026

    RegulatoryLink
  10. [10]

    ClinicalTrials.gov search — 'SLU-PP-332' returns zero registered trials (search performed 2026-04-21)

    U.S. National Library of Medicine · ClinicalTrials.gov · 2026

    RegistrationTrial

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AOD-9604

Metabolic-category peer: another 'isolated-mechanism' compound (hGH lipolytic fragment) marketed for fat-loss on preclinical mechanism data; useful contrast because AOD-9604 actually went through a Phase 2b human trial (and failed its primary endpoint), whereas SLU-PP-332 has zero human exposure.

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MOTS-c

Shares the mitochondrial-biogenesis / PGC-1α / AMPK / exercise-mimetic narrative but operates via mitochondrial-encoded peptide signaling rather than ERR nuclear-receptor agonism. Similar evidence-quality gap between preclinical mechanism and human efficacy.

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SS-31 (Elamipretide)

Mitochondrial-targeted peptide in the same 'improve mitochondrial function' narrative space, but unlike SLU-PP-332 has multiple published human Phase 2 trials in primary mitochondrial myopathy and heart failure. Useful benchmark for what a real human evidence package looks like in this category.

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BAM15

Small-molecule mitochondrial protonophore being developed as a metabolic uncoupler for obesity and NAFLD; overlaps in both mechanism-of-action space (mitochondrial thermogenesis / energy expenditure) and evidence stage (preclinical to early-human). Covered elsewhere in the pipeline.

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5-Amino-1MQ

Small-molecule NNMT inhibitor being marketed into the same 'metabolic / exercise-mimetic' research-chemical channel as SLU-PP-332, at a similar evidence stage (preclinical efficacy, no registered human trials). Covered elsewhere in the pipeline.

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Where to research further

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for laboratory research?

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