---
title: "SLU-PP-332: Dosing & Vendor Prices | BodyHackGuide"
url: https://www.bodyhackguide.co/compound/slu-pp-332
description: "SLU-PP-332: dosing protocols, mechanism & side effects, 8 PubMed results. Compare 4 current vendor prices."
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# SLU-PP-332

Performance (https://www.bodyhackguide.co/wiki#cat-performance)Preclinical

Also known as: SLU PP 332

SLU-PP-332 is the first-generation synthetic pan-agonist of the estrogen-related receptors (ERRα, ERRβ, ERRγ) developed by the laboratory of Thomas Burris at Saint Louis University and reported in a landmark 2023 publication that established ERR pan-agonism as a pharmacologically tractable exercise-mimetic drug mechanism. The compound is the chemical scaffold from which the second-generation, orally bioavailable successor SLU-PP-915 was developed, and the SLU-PP-332 story is essential context for understanding the ERR agonist field because SLU-PP-332's original rodent pharmacology is what generated the initial enthusiasm for this drug class and its limitations (specifically its poor oral bioavailability) are what motivated the second-generation development program.

R

Featured vendor

$5.33/mg $79.99 for 15mg

at ResearchChemHQ ·

Buy at RC: https://researchchemhq.co/product/slu-pp-332/?ref=oyxnywoz

CAS: 2264906-88-2 8 PubMed results (https://pubmed.ncbi.nlm.nih.gov/?term=SLU-PP-332%20ERR%20agonist)

Last reviewed: May 4, 2026

## Overview

### At A Glance

Mechanism

SLU-PP-332 acts through pan-agonism of the three estrogen-related receptors (ERRα/NR3B1, ERRβ/NR3B2, ERRγ/NR3B3), a subfamily of orphan nuclear receptors that regulate oxidative metabolism, mitochondrial biogenesis, and exercise-responsive gene expression. The ERRs are constituti…

Dose Range

Research compound — no established human doses. Animal studies: 10-50 mg/kg

Potential Benefits

Exercise mimicry without physical exertion Enhanced fat oxidation Increased mitochondrial biogenesis Improved endurance capacity Muscle fiber type conversion Metabolic health improvement

### Mechanism of Action

SLU-PP-332 acts through pan-agonism of the three estrogen-related receptors (ERRα/NR3B1, ERRβ/NR3B2, ERRγ/NR3B3), a subfamily of orphan nuclear receptors that regulate oxidative metabolism, mitochondrial biogenesis, and exercise-responsive gene expression. The ERRs are constitutively active transcription factors without well-characterized endogenous ligands, so pharmacologic "activation" means improving coactivator recruitment and transcriptional output rather than turning on a receptor that was otherwise off. SLU-PP-332 binds the ligand-binding domain of all three ERR isoforms and stabilizes receptor conformations that preferentially recruit coactivators including PGC-1α (peroxisome proliferator-activated receptor gamma coactivator 1-alpha), the master regulator of mitochondrial biogenesis and oxidative metabolism. The downstream transcriptional response produces a coordinated program of mitochondrial biogenesis, fatty acid oxidation enzyme expression, oxidative phosphorylation complex synthesis, and slow-twitch muscle fiber marker upregulation — the gene expression signature of endurance exercise. The specific genes induced by ERR/PGC-1α complex activation include mitochondrial biogenesis factors (NRF1, NRF2, TFAM for mitochondrial DNA replication and maintenance), fatty acid oxidation enzymes (CPT1A and CPT1B for fatty acid transport into mitochondria, ACADM and ACADL and ACADVL for fatty acyl-CoA dehydrogenation, HADHA and HADHB for fatty acyl-CoA β-oxidation), TCA cycle enzymes, components of all four electron transport chain complexes, ATP synthase subunits, mitochondrial fusion and fission machinery (MFN1, MFN2, OPA1, DRP1), and slow-twitch myosin heavy chain (MYH7) and troponin isoforms. The coordinated upregulation of this gene program shifts cellular metabolism toward oxidative phosphorylation from carbohydrate-dominated glycolysis, increases mitochondrial content and function, and produces a muscle phenotype resembling that of endurance-trained tissue. The pan-agonist profile — hitting ERRα, ERRβ, and ERRγ simultaneously — distinguishes SLU-PP-332 from selective isoform-specific ligands. Each ERR isoform has tissue-enriched expression: ERRα is broadly expressed with highest levels in metabolically active tissues (skeletal muscle, heart, brown adipose tissue, liver, kidney); ERRβ is most prominent in undifferentiated cells and specific neural populations; ERRγ is most enriched in heart, slow-twitch muscle, and brown adipose tissue. Pan-activation captures the full tissue-distributed metabolic program rather than a restricted subset. Published rodent studies with SLU-PP-332 demonstrated functional consequences consistent with this mechanism: increased treadmill running endurance in mice without prior training, elevated expression of oxidative metabolism genes in skeletal muscle at both mRNA and protein levels, increased mitochondrial content measured by electron microscopy and respirometry, elevated fatty acid oxidation rates in isolated muscle and heart tissue, and improved whole-body oxygen consumption during activity. In diet-induced obesity models, SLU-PP-332 produced reductions in fat mass and improvements in metabolic parameters. In pressure-overload cardiac hypertrophy and heart failure models, SLU-PP-332 preserved or improved cardiac function, reduced pathological remodeling, and improved exercise tolerance. The cardiac effects specifically reflect the dependence of the heart on fatty acid oxidation and the critical role of ERRα/γ in cardiac energetics. Beyond the core transcriptional mechanism, SLU-PP-332 produces secondary effects through interactions with other nuclear receptor pathways and metabolic signaling networks. The coactivator PGC-1α is a shared coactivator for multiple nuclear receptors including PPARs, thyroid hormone receptor, and glucocorticoid receptor, and pharmacologic recruitment of PGC-1α by ERR agonism affects the overall balance of nuclear receptor signaling. AMPK signaling is also relevant because AMPK directly phosphorylates and activates PGC-1α, and the interplay between SLU-PP-332's pharmacologic activation of PGC-1α-dependent transcription and endogenous AMPK signaling during exercise or fasting creates a context where effects can be additive or saturating depending on baseline state. The mechanism has important limitations that should be understood. First, driving tissues toward oxidative metabolism pharmacologically produces a transcriptional signature similar to exercise but does not reproduce the mechanical loading, cardiovascular conditioning, or neuroendocrine effects of actual exercise. SLU-PP-332 is a transcriptional exercise mimetic, not an actual exercise replacement. Second, sustained pharmacologic ERR activation may produce adaptive regulatory changes that attenuate the effect over time through homeostatic mechanisms — receptor downregulation, coactivator redistribution, or compensatory changes in metabolic sensors. The timescale and magnitude of such adaptation in humans is unknown. Third, the effects of chronic ERR activation on tissues where fibrotic fibrosis or remodeling could be adverse (cardiac ventricle under chronic load, renal tissue with glomerular disease) are not comprehensively characterized, and pharmacologic ERR agonism could have tissue-specific effects that differ from the net-positive rodent picture. Fourth, the specific pharmacological limitations of SLU-PP-332 — poor oral bioavailability, rapid clearance, need for IP administration in rodent studies — restrict both its clinical development potential and its practical use by self-experimenters. These limitations are specifically addressed by the second-generation compound SLU-PP-915 (https://www.bodyhackguide.co/compound/slu-pp-915), which is why most users interested in this drug class have migrated to the newer compound. Users considering SLU-PP-332 specifically should understand they are working with the first-generation molecule with known PK limitations.

### Overview

SLU-PP-332 is the first-generation synthetic pan-agonist of the estrogen-related receptors (ERRα, ERRβ, ERRγ) developed by the laboratory of Thomas Burris at Saint Louis University and reported in a landmark 2023 publication that established ERR pan-agonism as a pharmacologically tractable exercise-mimetic drug mechanism. The compound is the chemical scaffold from which the second-generation, orally bioavailable successor SLU-PP-915 (https://www.bodyhackguide.co/compound/slu-pp-915) was developed, and the SLU-PP-332 story is essential context for understanding the ERR agonist field because SLU-PP-332's original rodent pharmacology is what generated the initial enthusiasm for this drug class and its limitations (specifically its poor oral bioavailability) are what motivated the second-generation development program. The original publication from the Burris group established that SLU-PP-332 administration to mice produces a transcriptional, functional, and physiological signature that overlaps substantially with the effects of endurance exercise — enhanced running endurance on treadmill testing, increased mitochondrial biogenesis in skeletal muscle, shifts in muscle fiber type toward slow-twitch oxidative phenotype, elevated fatty acid oxidation, favorable body composition changes in diet-induced obesity models, and cardiac functional improvements in pressure-overload heart failure models. These effects are mediated through coordinated activation of the three ERR isoforms (ERRα, ERRβ, ERRγ), nuclear receptor transcription factors that sit at the top of the regulatory cascade controlling oxidative metabolism, and through recruitment of PGC-1α and other transcriptional coactivators that together drive expression of the exercise-responsive gene program. SLU-PP-332 specifically attracted intense scientific and popular media attention in 2023-2024 because the rodent data was presented in accessible terms — "a drug that mimics the effects of exercise" — and the social and medical appeal of such a compound for patients who cannot exercise due to frailty, cardiac disease, orthopedic limitations, or other constraints is obvious. The public discussion outran the evidence in typical fashion: the rodent data is real and consistent, but human validation of the exercise-mimetic premise requires clinical trials that have not been conducted for SLU-PP-332 or any related compound. SLU-PP-332's major pharmacological limitation, documented in the published work, is poor oral bioavailability. Every published rodent study with SLU-PP-332 used intraperitoneal (IP) injection as the route of administration, not oral dosing. IP administration in mice is routine in preclinical research but is obviously not a viable route for human chronic therapy, and this limitation was the specific motivation for the Burris group to develop the second-generation compound SLU-PP-915 (https://www.bodyhackguide.co/compound/slu-pp-915) with improved oral PK. The practical reality in April 2026 is that SLU-PP-332 remains a first-generation research chemical that has been largely superseded by SLU-PP-915 (https://www.bodyhackguide.co/compound/slu-pp-915) for self-experimentation purposes where oral dosing is preferred, though SLU-PP-332 continues to be sold by research-chemical vendors and used by a subset of biohackers who prefer the first-generation compound either for cost reasons, availability reasons, or preference for the more extensively characterized parent molecule. No human clinical trials of SLU-PP-332 have been registered or published, no IND applications for it have been publicly disclosed, and no pharmaceutical-grade supply exists. This entry covers the detailed mechanism of ERR pan-agonism as established in the original SLU-PP-332 work, the specific preclinical pharmacology including cardiovascular, metabolic, and musculoskeletal endpoints, the context provided by the broader ERR biology literature, the theoretical and practical concerns with self-administration of an unvalidated nuclear receptor agonist, how SLU-PP-332 differs practically from SLU-PP-915 (https://www.bodyhackguide.co/compound/slu-pp-915) for self-experimenters, and how SLU-PP-332 fits into the stacking landscape alongside other metabolic and exercise-mimetic interventions like 5-Amino-1MQ (https://www.bodyhackguide.co/compound/5-amino-1mq), BAM15 (https://www.bodyhackguide.co/compound/bam15), Humanin (https://www.bodyhackguide.co/compound/humanin), L-Carnitine (https://www.bodyhackguide.co/compound/l-carnitine), Semaglutide (https://www.bodyhackguide.co/compound/semaglutide), Tirzepatide (https://www.bodyhackguide.co/compound/tirzepatide), Retatrutide (https://www.bodyhackguide.co/compound/retatrutide), and Tesofensine (https://www.bodyhackguide.co/compound/tesofensine). The core takeaway is that SLU-PP-332 established a mechanistically compelling drug class for exercise-mimetic pharmacology, demonstrated consistent preclinical efficacy, and is limited in its current self-experimentation role by PK properties that are specifically addressed by the second-generation successor compound.

## Chemical Information

IUPAC Name

Not yet available

CAS Number

2264906-88-2

Molecular Formula

C23H20F3N3O4S2

Molecular Mass

535.54 g/mol

Image: SLU-PP-332 molecular structure (https://pubchem.ncbi.nlm.nih.gov/rest/pug/compound/cid/146816027/PNG)

View on PubChem: https://pubchem.ncbi.nlm.nih.gov/compound/146816027

## Dosing & Protocols

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## Research

### Unlock the research summary

- A summary of the key research
- Safety and side effects
- A link to the PubMed results

## Interactions

### Interaction Matrix

### Contraindications

SLU-PP-332's mechanism as a pan-ERR agonist creates a contraindication profile similar to that of its successor SLU-PP-915 (https://www.bodyhackguide.co/compound/slu-pp-915) reflecting concerns about cardiovascular disease, hormone-sensitive conditions, cancer, reproductive function, and cardiometabolic medication interactions. Active or recent cardiovascular disease is a major contraindication because ERR agonism directly affects cardiac energetics and vascular function. Patients with recent myocardial infarction (within 6 months), unstable angina, decompensated heart failure, uncontrolled hypertension, or significant arrhythmias should not use SLU-PP-332 outside of clinical trial participation. Stable cardiovascular disease on optimal medical management may be compatible with cautious self-experimentation under physician supervision, but the absence of human cardiovascular safety data makes this high-risk. Hormone-sensitive cancer history or current disease is a relative-to-absolute contraindication. ERRs share structural homology with estrogen receptors and ERRα activity has been associated with unfavorable breast cancer phenotypes in preclinical studies. Women with history of hormone-receptor-positive breast cancer should not use SLU-PP-332 without oncology consultation. Similar concerns apply to endometrial, ovarian, and prostate cancer. Pregnancy and breastfeeding are absolute contraindications. Nuclear receptor agonists cross the placenta and could disrupt fetal development, placental function, and metabolic programming. Breastfeeding is similarly contraindicated. Women trying to conceive should discontinue at least several weeks before attempting. Children and adolescents should not use SLU-PP-332 because nuclear receptor biology contributes to normal growth, development, and tissue maturation during these periods. Thyroid disease with unstable control is a relative contraindication because of combined effects on metabolic rate. Uncontrolled diabetes is a relative contraindication because altered substrate utilization could affect glucose homeostasis. Significant hepatic impairment warrants caution. Significant renal impairment warrants consideration because of the general principle of avoiding uncharacterized compounds in complex regimens. Autoimmune disease on immunomodulatory therapy is a relative contraindication. Known hypersensitivity to SLU-PP-332 or preparation components is an absolute contraindication. Drug-drug interactions are uncharacterized. Theoretical concerns include: other nuclear receptor agonists; CYP450 substrates; cardiac medications; diabetes medications; anticoagulants; and statins (due to shared effects on mitochondrial biology). Users on complex medication regimens should discuss with physician and pharmacist. The final and most important contraindication is absence of clinical oversight. Self-experimentation with an unvalidated nuclear receptor agonist without a physician who can monitor response, order appropriate labs, and evaluate adverse events does not meet minimum safety standard for SLU-PP-332's risk profile. This infrastructure contraindication applies regardless of personal health status.

Research Disclaimer

This interaction data is compiled from published research and community reports. It may not be exhaustive. Always consult a healthcare professional before combining compounds.

Best Price

$69.99

up to $149.00

Best $/mg

$1.3998

Vendors

4

Listings

5

vial, capsule

Dosage

Form

Sort

| Vendor | Product | Form | Qty | Price | $/mg | Coupon | |
| --- | --- | --- | --- | --- | --- | --- | --- |
| Image: ResearchChemHQ logo (https://staging.researchchemhq.co/wp/wp-content/uploads/2024/08/cropped-RCHQ-Invert-Logo-e1724477505900.png) ResearchChemHQ (https://www.bodyhackguide.co/vendors/researchchemhq) 100: https://www.bodyhackguide.co/vendor-trust-scorecard 🇺🇸 US | SLU-PP-332 Capsules 60ct | capsule | 60 capsules ● In Stock | $79.99 | $5.33 | REDDIT | Buy: https://researchchemhq.co/product/slu-pp-332/?ref=oyxnywoz |
| Image: BHG Labs logo (https://bhglabs.co/store/wp-content/uploads/2026/06/logo-full.png) BHG Labs (https://www.bodyhackguide.co/vendors/bhg-labs) 70: https://www.bodyhackguide.co/vendor-trust-scorecard 🇺🇸 US | SLU-PP-332 500mcg, 60 Dry-Fill Units | capsule | 60 dry-fill units ● In Stock | $99.99 | $3.33 | BHG20 | Buy: https://bhglabs.co/product/slu-pp-332-500mcg-60-dry-fill-units/?ref=zmgqyxku&coupon=BHG20 |
| Image: Ion Peptide logo (https://ionpeptide.com/wp-content/uploads/2025/08/ion-peptide-logo-1-300x148.jpg) Ion Peptide (https://www.bodyhackguide.co/vendors/ion-peptide) 70: https://www.bodyhackguide.co/vendor-trust-scorecard 🇺🇸 US 🌍 International | SLU-PP-332 5mg | vial | 1 vial ● Out of Stock | $39.00 | $7.80 | — | View: https://ionpeptide.com/product/slu-pp-332-10mg/?ref=reddit15 |
| Image: Ion Peptide logo (https://ionpeptide.com/wp-content/uploads/2025/08/ion-peptide-logo-1-300x148.jpg) Ion Peptide (https://www.bodyhackguide.co/vendors/ion-peptide) 70: https://www.bodyhackguide.co/vendor-trust-scorecard 🇺🇸 US 🌍 International | SLU-PP-332 30mg | vial | 1 vial ● In Stock | $149.00 | $4.97 | — | Buy: https://ionpeptide.com/product/slu-pp-332-10mg/?ref=reddit15 |
| Image: VANDL Labs logo (https://halfnattys.shop/wp-content/themes/halfnattys/assets/img/logo.webp) VANDL Labs (https://www.bodyhackguide.co/vendors/vandl-labs) 50: https://www.bodyhackguide.co/vendor-trust-scorecard 🇺🇸 US | SLU-PP-332 50mg | vial | 50mg vial ● In Stock | $69.99 BEST | $1.40 | CHON | Buy: https://www.vandl-labs.com/product/slu-pp-332/?ref=choncho |

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Current low

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Tracking since Apr 6, 2026 · 4 data points

## Price History

3 data points

### Vendors Selling SLU-PP-332

#### Ion Peptide

4.5

2 listings · from $39.00
https://www.bodyhackguide.co/vendors/ion-peptide

#### VANDL Labs

1 listing · from $69.99
https://www.bodyhackguide.co/vendors/vandl-labs

#### ResearchChemHQ

4.7

1 listing · from $79.99
https://www.bodyhackguide.co/vendors/researchchemhq

#### BHG Labs

4.8

1 listing · from $99.99
https://www.bodyhackguide.co/vendors/bhg-labs

How we score these vendors

Every supplier above is graded 0 to 100 on COA verification, payment transparency, shipping, reviews, and active listings. Methodology published, no pay-to-rank.

View Scorecard (https://www.bodyhackguide.co/vendors/scorecard)

### Related Compounds

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### ITPP

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ITPP (myo-inositol trispyrophosphate, sometimes written myo-inositol tripyrophosphate or OXY111A in NormOxys trial documents) is a small-molecule allosteric effector of hemoglobin designed to increase the amount of oxygen red blood cells release to tissues.

Research compound — IV infusion in studies, no established oral doses

36 PubMed View Profile
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### LGD-4033 (Ligandrol)

Performance Phase 2

LGD-4033, usually sold as ligandrol, is a nonsteroidal selective androgen receptor modulator that Viking Therapeutics took into clinical development under the code VK5211 (NCT02578095).

t½ Long elimination half-life in humans with dose-proportional accumulation over 21 days of daily dosing in healthy young men; the report describes the profile without giving a single value in its summary (PMID: 22459616)

Preclinical View Profile
https://www.bodyhackguide.co/compound/lgd-4033

### Ostarine (Enobosarm, MK-2866)

Performance Phase 3

Ostarine is the market name for enobosarm, a nonsteroidal selective androgen receptor modulator first developed by GTx Inc under the codes GTx-024, MK-2866 and S-22.

t½ Not established from a retrieved human report; in rats the mean elimination half-life of radiolabeled GTx-024 was 0.6 h in males and 16.4 h in females (PMID: 24074268). Human plasma pharmacokinetics were characterized in phase 1 drug-interaction studies (PMID: 27105861)

Preclinical View Profile
https://www.bodyhackguide.co/compound/ostarine

### PEG-MGF

Performance Preclinical

PEG-MGF (Pegylated Mechano Growth Factor) is a synthetic, PEGylated form of Mechano Growth Factor (MGF) — an alternatively spliced variant of IGF-1 produced locally in muscle and other tissues in response to mechanical loading or damage.

t½ Native MGF: very short (minutes) due to rapid proteolysis. PEG-MGF: PEGylation is intended to extend this substantially (community estimates up to roughly 1 day), but there are no published human pharmacokinetic data to confirm a specific value. 200 mcg

Preclinical View Profile
https://www.bodyhackguide.co/compound/peg-mgf

### RAD-140 (Testolone)

Performance Phase 1

RAD-140, sold as testolone and given the international nonproprietary name vosilasarm, is a nonsteroidal selective androgen receptor modulator developed at Radius Health, whose scientists reported the first-in-human trial (PMID: 34565686), and first described in the medicinal chemistry literature as a compound with an oxadiazole core designed for oral androgen receptor activity with tissue selectivity (PMID: 24900290).

t½ Terminal half-life 44.7 hours in humans, measured in a first-in-human phase 1 study in postmenopausal women with metastatic breast cancer (PMID: 34565686)

Preclinical View Profile
https://www.bodyhackguide.co/compound/rad-140

### YK-11

Performance Preclinical

YK-11 is a synthetic steroid, not a nonsteroidal SARM, despite being sold alongside them.

t½ Not established. In a human elimination study using deuterium-labeled YK-11, no intact parent compound was seen in urine; unconjugated metabolites disappeared within 24 hours and glucuronidated and sulfated metabolites remained traceable beyond 48 hours (PMID: 30379415)

Preclinical View Profile
https://www.bodyhackguide.co/compound/yk-11

View Full Dosage Guide →

Protocols, calculator & safety for SLU-PP-332
https://www.bodyhackguide.co/guides/dosage/slu-pp-332

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### Featured Price

⚗️

ResearchChemHQ

$79.99($5.33/mg)

4 vendors · 5 listings

### Research Score

31

8 PubMed results

### Quality Indicators

Data Completeness

100%

Description

Mechanism of Action

Chemical Data

Dosing Protocols

Safety Profile

PubMed Results

Interactions

Vendor Listings

COA Verification

6

Verified COAs

1

Vendors w/ COA

High verification rate (100%)

Latest test: 12/5/2024

Research Volume

8 PubMed results

Limited research available

### Quick Facts

Molecular Weight

535.54 g/mol

CAS Number

2264906-88-2

Trial Phase

Preclinical

0

Research Disclaimer

This information is for educational and research purposes only. Not intended as medical advice. Consult a healthcare professional before use.

## Frequently Asked Questions

What is SLU-PP-332?

SLU-PP-332 is the first-generation synthetic pan-agonist of the estrogen-related receptors (ERRα, ERRβ, ERRγ) developed by the Thomas Burris laboratory at Saint Louis University and reported in 2023. It was the first compound to establish ERR pan-agonism as a pharmacologically tractable exercise-mimetic drug mechanism, demonstrating that pharmacologic ERR activation produces the transcriptional and functional signature of endurance exercise in rodent models.

What is the difference between SLU-PP-332 and SLU-PP-915?

SLU-PP-332 and SLU-PP-915 (https://www.bodyhackguide.co/compound/slu-pp-915) are both pan-agonists of the same ERR receptors and produce similar biological effects in rodent studies. The key difference is oral bioavailability — SLU-PP-332 has poor oral PK and required intraperitoneal injection in rodent studies, while SLU-PP-915 was designed as the second-generation compound with improved oral absorption and meaningful systemic exposure from oral dosing. Most users preferring oral dosing have migrated to SLU-PP-915.

Has SLU-PP-332 been tested in humans?

No. As of April 2026, no Phase 1 or later clinical trials of SLU-PP-332 have been published, no IND applications have been publicly disclosed, and no registered trials appear on ClinicalTrials.gov. The evidence base is entirely preclinical — cell culture assays and rodent pharmacology primarily from the Burris laboratory.

How does SLU-PP-332 mimic exercise?

SLU-PP-332 activates the three ERR isoforms (ERRα, ERRβ, ERRγ), nuclear receptor transcription factors that regulate mitochondrial biogenesis, fatty acid oxidation, and oxidative metabolism. Combined with PGC-1α (the master regulator of mitochondrial biogenesis), ERR activation drives the gene-expression program that overlaps with the transcriptional response to endurance exercise. This produces increased mitochondrial content, enhanced fatty acid oxidation capacity, and improved running endurance in rodent studies. It does not reproduce mechanical loading, cardiovascular conditioning, or neuroendocrine effects of actual exercise.

Can you take SLU-PP-332 orally?

No, not effectively. SLU-PP-332 has poor oral bioavailability established in the original rodent pharmacology studies. Every published rodent study used intraperitoneal injection, and oral dosing is not expected to produce meaningful systemic exposure. Users who want oral ERR pan-agonist activity should consider SLU-PP-915 (https://www.bodyhackguide.co/compound/slu-pp-915) instead, which was specifically designed to have adequate oral bioavailability.

What dose of SLU-PP-332 do people use?

Self-report community doses range from 3-20 mg per injection subcutaneously or intramuscularly, typically once daily or every other day. Beginners usually start at 3-5 mg every other day; intermediate users run 5-10 mg daily; advanced users go up to 10-20 mg daily. These doses are extrapolated from rodent IP dosing and have no clinical validation in humans.

Should I use SLU-PP-332 or SLU-PP-915?

For most users, SLU-PP-915 (https://www.bodyhackguide.co/compound/slu-pp-915) is the better choice because of its oral bioavailability — the injection burden of SLU-PP-332 is substantial and most users don't want to inject an exercise mimetic daily for 6-12 week cycles. SLU-PP-332 remains relevant for users who specifically prefer the first-generation compound, have cost or availability constraints, or have established experience with it. Both compounds produce similar biological effects in rodent studies, so the choice is largely about practical dosing considerations.

What are the main side effects of SLU-PP-332?

Human side effects are undocumented because no clinical trials exist. Theoretical concerns based on mechanism include cardiovascular effects, hormonal effects (ERR homology with estrogen receptors), metabolic effects on glucose homeostasis, and uncharacterized effects on cancer risk in hormone-sensitive tissues. Self-report community users describe occasional GI effects, headaches, and no consistent severe adverse patterns in short-term use. Injection-related reactions are typical for SC/IM dosing.

Does SLU-PP-332 actually work in people?

Unknown. Rodent studies consistently show positive effects on endurance, mitochondrial content, and metabolic markers. Whether these effects translate to humans at tolerable doses has not been tested. Self-report community users describe subjective improvements but these reports are uncontrolled and confounded. Objective endurance testing during and after SLU-PP-332 cycles would provide better data than subjective impressions.

Where can I read the published research on SLU-PP-332?

The foundational SLU-PP-332 work was published by Billon and colleagues from the Burris laboratory at Saint Louis University in peer-reviewed journals. Searching PubMed for 'SLU-PP-332' and 'Burris' or 'ERR agonist' returns the primary literature. Related publications are also indexed on ScienceDirect with DOI links to full text. The compound has been discussed extensively in longevity and metabolic pharmacology reviews since 2023.

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## Related Compounds

### ITPP

Performance Preclinical

### LGD-4033 (Ligandrol)

Performance Phase 2

### Ostarine (Enobosarm, MK-2866)

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### PEG-MGF

Performance Preclinical

### RAD-140 (Testolone)

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### YK-11

Performance Preclinical

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      "description": "SLU-PP-332 is the first-generation synthetic pan-agonist of the estrogen-related receptors (ERRα, ERRβ, ERRγ) developed by the laboratory of Thomas Burris at Saint Louis University and reported in a landmark 2023 publication that established ERR pan-agonism as a pharmacologically tractable exercise-mimetic drug mechanism. The compound is the chemical scaffold from which the second-generation, orally bioavailable successor SLU-PP-915 was developed, and the SLU-PP-332 story is essential context for understanding the ERR agonist field because SLU-PP-332's original rodent pharmacology is what generated the initial enthusiasm for this drug class and its limitations (specifically its poor oral bioavailability) are what motivated the second-generation development program. The original publication from the Burris group established that SLU-PP-332 administration to mice produces a transcriptional, functional, and physiological signature that overlaps substantially with the effects of endurance exercise — enhanced running endurance on treadmill testing, increased mitochondrial biogenesis in skeletal muscle, shifts in muscle fiber type toward slow-twitch oxidative phenotype, elevated fatty acid oxidation, favorable body composition changes in diet-induced obesity models, and cardiac functional improvements in pressure-overload heart failure models. These effects are mediated through coordinated activation of the three ERR isoforms (ERRα, ERRβ, ERRγ), nuclear receptor transcription factors that sit at the top of the regulatory cascade controlling oxidative metabolism, and through recruitment of PGC-1α and other transcriptional coactivators that together drive expression of the exercise-responsive gene program. SLU-PP-332 specifically attracted intense scientific and popular media attention in 2023-2024 because the rodent data was presented in accessible terms — \"a drug that mimics the effects of exercise\" — and the social and medical appeal of such a compound for patients who cannot exercise due to frailty, cardiac disease, orthopedic limitations, or other constraints is obvious. The public discussion outran the evidence in typical fashion: the rodent data is real and consistent, but human validation of the exercise-mimetic premise requires clinical trials that have not been conducted for SLU-PP-332 or any related compound. SLU-PP-332's major pharmacological limitation, documented in the published work, is poor oral bioavailability. Every published rodent study with SLU-PP-332 used intraperitoneal (IP) injection as the route of administration, not oral dosing. IP administration in mice is routine in preclinical research but is obviously not a viable route for human chronic therapy, and this limitation was the specific motivation for the Burris group to develop the second-generation compound SLU-PP-915 with improved oral PK. The practical reality in April 2026 is that SLU-PP-332 remains a first-generation research chemical that has been largely superseded by SLU-PP-915 for self-experimentation purposes where oral dosing is preferred, though SLU-PP-332 continues to be sold by research-chemical vendors and used by a subset of biohackers who prefer the first-generation compound either for cost reasons, availability reasons, or preference for the more extensively characterized parent molecule. No human clinical trials of SLU-PP-332 have been registered or published, no IND applications for it have been publicly disclosed, and no pharmaceutical-grade supply exists. This entry covers the detailed mechanism of ERR pan-agonism as established in the original SLU-PP-332 work, the specific preclinical pharmacology including cardiovascular, metabolic, and musculoskeletal endpoints, the context provided by the broader ERR biology literature, the theoretical and practical concerns with self-administration of an unvalidated nuclear receptor agonist, how SLU-PP-332 differs practically from SLU-PP-915 for self-experimenters, and how SLU-PP-332 fits into the stacking landscape alongside other metabolic and exercise-mimetic interventions like 5-Amino-1MQ, BAM15, Humanin, L-Carnitine, Semaglutide, Tirzepatide, Retatrutide, and Tesofensine. The core takeaway is that SLU-PP-332 established a mechanistically compelling drug class for exercise-mimetic pharmacology, demonstrated consistent preclinical efficacy, and is limited in its current self-experimentation role by PK properties that are specifically addressed by the second-generation successor compound.",
      "activeIngredient": "SLU-PP-332",
      "mechanismOfAction": "SLU-PP-332 acts through pan-agonism of the three estrogen-related receptors (ERRα/NR3B1, ERRβ/NR3B2, ERRγ/NR3B3), a subfamily of orphan nuclear receptors that regulate oxidative metabolism, mitochondrial biogenesis, and exercise-responsive gene expression. The ERRs are constitutively active transcription factors without well-characterized endogenous ligands, so pharmacologic \"activation\" means improving coactivator recruitment and transcriptional output rather than turning on a receptor that was otherwise off. SLU-PP-332 binds the ligand-binding domain of all three ERR isoforms and stabilizes receptor conformations that preferentially recruit coactivators including PGC-1α (peroxisome proliferator-activated receptor gamma coactivator 1-alpha), the master regulator of mitochondrial biogenesis and oxidative metabolism. The downstream transcriptional response produces a coordinated program of mitochondrial biogenesis, fatty acid oxidation enzyme expression, oxidative phosphorylation complex synthesis, and slow-twitch muscle fiber marker upregulation — the gene expression signature of endurance exercise. The specific genes induced by ERR/PGC-1α complex activation include mitochondrial biogenesis factors (NRF1, NRF2, TFAM for mitochondrial DNA replication and maintenance), fatty acid oxidation enzymes (CPT1A and CPT1B for fatty acid transport into mitochondria, ACADM and ACADL and ACADVL for fatty acyl-CoA dehydrogenation, HADHA and HADHB for fatty acyl-CoA β-oxidation), TCA cycle enzymes, components of all four electron transport chain complexes, ATP synthase subunits, mitochondrial fusion and fission machinery (MFN1, MFN2, OPA1, DRP1), and slow-twitch myosin heavy chain (MYH7) and troponin isoforms. The coordinated upregulation of this gene program shifts cellular metabolism toward oxidative phosphorylation from carbohydrate-dominated glycolysis, increases mitochondrial content and function, and produces a muscle phenotype resembling that of endurance-trained tissue. The pan-agonist profile — hitting ERRα, ERRβ, and ERRγ simultaneously — distinguishes SLU-PP-332 from selective isoform-specific ligands. Each ERR isoform has tissue-enriched expression: ERRα is broadly expressed with highest levels in metabolically active tissues (skeletal muscle, heart, brown adipose tissue, liver, kidney); ERRβ is most prominent in undifferentiated cells and specific neural populations; ERRγ is most enriched in heart, slow-twitch muscle, and brown adipose tissue. Pan-activation captures the full tissue-distributed metabolic program rather than a restricted subset. Published rodent studies with SLU-PP-332 demonstrated functional consequences consistent with this mechanism: increased treadmill running endurance in mice without prior training, elevated expression of oxidative metabolism genes in skeletal muscle at both mRNA and protein levels, increased mitochondrial content measured by electron microscopy and respirometry, elevated fatty acid oxidation rates in isolated muscle and heart tissue, and improved whole-body oxygen consumption during activity. In diet-induced obesity models, SLU-PP-332 produced reductions in fat mass and improvements in metabolic parameters. In pressure-overload cardiac hypertrophy and heart failure models, SLU-PP-332 preserved or improved cardiac function, reduced pathological remodeling, and improved exercise tolerance. The cardiac effects specifically reflect the dependence of the heart on fatty acid oxidation and the critical role of ERRα/γ in cardiac energetics. Beyond the core transcriptional mechanism, SLU-PP-332 produces secondary effects through interactions with other nuclear receptor pathways and metabolic signaling networks. The coactivator PGC-1α is a shared coactivator for multiple nuclear receptors including PPARs, thyroid hormone receptor, and glucocorticoid receptor, and pharmacologic recruitment of PGC-1α by ERR agonism affects the overall balance of nuclear receptor signaling. AMPK signaling is also relevant because AMPK directly phosphorylates and activates PGC-1α, and the interplay between SLU-PP-332's pharmacologic activation of PGC-1α-dependent transcription and endogenous AMPK signaling during exercise or fasting creates a context where effects can be additive or saturating depending on baseline state. The mechanism has important limitations that should be understood. First, driving tissues toward oxidative metabolism pharmacologically produces a transcriptional signature similar to exercise but does not reproduce the mechanical loading, cardiovascular conditioning, or neuroendocrine effects of actual exercise. SLU-PP-332 is a transcriptional exercise mimetic, not an actual exercise replacement. Second, sustained pharmacologic ERR activation may produce adaptive regulatory changes that attenuate the effect over time through homeostatic mechanisms — receptor downregulation, coactivator redistribution, or compensatory changes in metabolic sensors. The timescale and magnitude of such adaptation in humans is unknown. Third, the effects of chronic ERR activation on tissues where fibrotic fibrosis or remodeling could be adverse (cardiac ventricle under chronic load, renal tissue with glomerular disease) are not comprehensively characterized, and pharmacologic ERR agonism could have tissue-specific effects that differ from the net-positive rodent picture. Fourth, the specific pharmacological limitations of SLU-PP-332 — poor oral bioavailability, rapid clearance, need for IP administration in rodent studies — restrict both its clinical development potential and its practical use by self-experimenters. These limitations are specifically addressed by the second-generation compound SLU-PP-915, which is why most users interested in this drug class have migrated to the newer compound. Users considering SLU-PP-332 specifically should understand they are working with the first-generation molecule with known PK limitations.",
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        "name": "What is SLU-PP-332?",
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          "@type": "Answer",
          "text": "SLU-PP-332 is the first-generation synthetic pan-agonist of the estrogen-related receptors (ERRα, ERRβ, ERRγ) developed by the Thomas Burris laboratory at Saint Louis University and reported in 2023. It was the first compound to establish ERR pan-agonism as a pharmacologically tractable exercise-mimetic drug mechanism, demonstrating that pharmacologic ERR activation produces the transcriptional and functional signature of endurance exercise in rodent models."
        }
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        "@type": "Question",
        "name": "What is the difference between SLU-PP-332 and SLU-PP-915?",
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          "@type": "Answer",
          "text": "SLU-PP-332 and SLU-PP-915 are both pan-agonists of the same ERR receptors and produce similar biological effects in rodent studies. The key difference is oral bioavailability — SLU-PP-332 has poor oral PK and required intraperitoneal injection in rodent studies, while SLU-PP-915 was designed as the second-generation compound with improved oral absorption and meaningful systemic exposure from oral dosing. Most users preferring oral dosing have migrated to SLU-PP-915."
        }
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        "@type": "Question",
        "name": "Has SLU-PP-332 been tested in humans?",
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          "@type": "Answer",
          "text": "No. As of April 2026, no Phase 1 or later clinical trials of SLU-PP-332 have been published, no IND applications have been publicly disclosed, and no registered trials appear on ClinicalTrials.gov. The evidence base is entirely preclinical — cell culture assays and rodent pharmacology primarily from the Burris laboratory."
        }
      },
      {
        "@type": "Question",
        "name": "How does SLU-PP-332 mimic exercise?",
        "acceptedAnswer": {
          "@type": "Answer",
          "text": "SLU-PP-332 activates the three ERR isoforms (ERRα, ERRβ, ERRγ), nuclear receptor transcription factors that regulate mitochondrial biogenesis, fatty acid oxidation, and oxidative metabolism. Combined with PGC-1α (the master regulator of mitochondrial biogenesis), ERR activation drives the gene-expression program that overlaps with the transcriptional response to endurance exercise. This produces increased mitochondrial content, enhanced fatty acid oxidation capacity, and improved running endurance in rodent studies. It does not reproduce mechanical loading, cardiovascular conditioning, or neuroendocrine effects of actual exercise."
        }
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        "@type": "Question",
        "name": "Can you take SLU-PP-332 orally?",
        "acceptedAnswer": {
          "@type": "Answer",
          "text": "No, not effectively. SLU-PP-332 has poor oral bioavailability established in the original rodent pharmacology studies. Every published rodent study used intraperitoneal injection, and oral dosing is not expected to produce meaningful systemic exposure. Users who want oral ERR pan-agonist activity should consider SLU-PP-915 instead, which was specifically designed to have adequate oral bioavailability."
        }
      },
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        "@type": "Question",
        "name": "What dose of SLU-PP-332 do people use?",
        "acceptedAnswer": {
          "@type": "Answer",
          "text": "Self-report community doses range from 3-20 mg per injection subcutaneously or intramuscularly, typically once daily or every other day. Beginners usually start at 3-5 mg every other day; intermediate users run 5-10 mg daily; advanced users go up to 10-20 mg daily. These doses are extrapolated from rodent IP dosing and have no clinical validation in humans."
        }
      },
      {
        "@type": "Question",
        "name": "Should I use SLU-PP-332 or SLU-PP-915?",
        "acceptedAnswer": {
          "@type": "Answer",
          "text": "For most users, SLU-PP-915 is the better choice because of its oral bioavailability — the injection burden of SLU-PP-332 is substantial and most users don't want to inject an exercise mimetic daily for 6-12 week cycles. SLU-PP-332 remains relevant for users who specifically prefer the first-generation compound, have cost or availability constraints, or have established experience with it. Both compounds produce similar biological effects in rodent studies, so the choice is largely about practical dosing considerations."
        }
      },
      {
        "@type": "Question",
        "name": "What are the main side effects of SLU-PP-332?",
        "acceptedAnswer": {
          "@type": "Answer",
          "text": "Human side effects are undocumented because no clinical trials exist. Theoretical concerns based on mechanism include cardiovascular effects, hormonal effects (ERR homology with estrogen receptors), metabolic effects on glucose homeostasis, and uncharacterized effects on cancer risk in hormone-sensitive tissues. Self-report community users describe occasional GI effects, headaches, and no consistent severe adverse patterns in short-term use. Injection-related reactions are typical for SC/IM dosing."
        }
      },
      {
        "@type": "Question",
        "name": "Does SLU-PP-332 actually work in people?",
        "acceptedAnswer": {
          "@type": "Answer",
          "text": "Unknown. Rodent studies consistently show positive effects on endurance, mitochondrial content, and metabolic markers. Whether these effects translate to humans at tolerable doses has not been tested. Self-report community users describe subjective improvements but these reports are uncontrolled and confounded. Objective endurance testing during and after SLU-PP-332 cycles would provide better data than subjective impressions."
        }
      },
      {
        "@type": "Question",
        "name": "Where can I read the published research on SLU-PP-332?",
        "acceptedAnswer": {
          "@type": "Answer",
          "text": "The foundational SLU-PP-332 work was published by Billon and colleagues from the Burris laboratory at Saint Louis University in peer-reviewed journals. Searching PubMed for 'SLU-PP-332' and 'Burris' or 'ERR agonist' returns the primary literature. Related publications are also indexed on ScienceDirect with DOI links to full text. The compound has been discussed extensively in longevity and metabolic pharmacology reviews since 2023."
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