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SLU-PP-332

Last reviewed: May 6, 2026 by The Peptide Catalog Team

A small-molecule ERR receptor agonist that acts like exercise inside your cells — driving mitochondrial biogenesis, fat oxidation, and endurance gains without any actual training.

CategoryWeight Loss & Metabolic Peptides
Classmetabolic
GoalFat LossLongevity
Overview

Core Benefits

Key Advantages
70% endurance gain (mice)
Treated mice ran ~70% longer in time on treadmill tests.
12% body weight loss (mice)
DIO mice on 28-day IP protocol — 10× less fat gain than controls.
ERR pan-agonist
Activates all three estrogen-related receptors (ERRα/β/γ) — synthetic small molecule.
Mitochondrial biogenesis
Flips the same transcriptional program endurance training flips.
Type IIa fiber shift
Skeletal muscle phenotype shift — endurance, not hypertrophy.
Zero human trials
Mouse-only data; oral capsules may lack systemic exposure.

These are educational summaries of commonly discussed effects in wellness/regenerative contexts, not guarantees.

SLU-PP-332 Results Timeline

Progression
1
Week 1
Physical Changes
Subclinical transcriptional changes — no perceptible effect
Performance & Recovery
Mitochondrial biogenesis genes upregulating; PGC-1α program activating
Other Benefits
Mouse data: gene-expression changes within hours of single dose; phenotype takes weeks
2
Week 2–3
Physical Changes
Subjective endurance changes (injectable users); oral users often nothing
Performance & Recovery
Lower perceived exertion at familiar workloads; longer sets without fatigue
Other Benefits
Oral capsules: parent SLU-PP-332 lacks oral bioavailability per Billon 2025 (PMID 41421047)
3
Week 4
Physical Changes
Mouse 28-day endpoint — 12% body weight loss in DIO mice
Performance & Recovery
Mouse data peak: ~70% longer treadmill time vs controls
Other Benefits
Community injectable users report 1–3 lb fat loss per month at modest doses
4
Week 5–8
Physical Changes
Beyond published preclinical data window
Performance & Recovery
Stable endurance gains; plateau in fat-loss rate
Other Benefits
Most community cycles run 4–8 weeks before an off period

Timeline is illustrative and non-guaranteed. Outcomes vary and are commonly discussed alongside training, nutrition, sleep, and cycling practices.

Read the full SLU-PP-332 results timeline →

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Evidence at a glance

Two parallel grades per outcome — clinical RCT depth and real-world community adoption. See the Research Overview below for citations and detail.

OutcomeClinical EvidenceCommunity Evidence
Body weight reduction (mouse DIO)PreliminaryWeak
Aerobic exercise capacity (mouse)PreliminaryWeak
Cardiac function in heart failure (mouse)PreliminaryPreliminary
Body weight / endurance in humansPreliminaryWeak
How It WorksERR Pan-Agonist (Synthetic Small Molecule, Exercise Mimetic)

Receptor → PGC-1α Coregulation → Mitochondrial Biogenesis → Outcomes

1
Target

ERRα/β/γ Nuclear Receptors

SLU-PP-332 is a synthetic small molecule — not a peptide — that binds and activates all three estrogen-related receptors (ERRα, ERRβ, ERRγ), with highest potency at ERRα. Despite the name, ERRs do not bind estrogen; they are orphan nuclear receptors that share structural homology with classical estrogen receptors.

2
Cellular Signal

PGC-1α Coregulation → Mitochondrial Biogenesis Program

ERRα sits downstream of PGC-1α and regulates the transcriptional program governing mitochondrial biogenesis, fatty acid β-oxidation, and oxidative phosphorylation. SLU-PP-332 flips the same transcriptional switches that endurance training flips — pharmacologically.

3
Systemic Effect

↑ Mitochondrial Mass + ↑ Fatty Acid Oxidation + Type IIa Fiber Shift

In mice: more mitochondria per cell, increased substrate oxidation in skeletal muscle and adipose tissue, fiber-type shift toward type IIa oxidative fibers. The transcriptional fingerprint is what chronic endurance training produces.

4
What You Notice

Mouse Phenotype: 70% Endurance + 12% Body Weight Loss (No Human Data)

Treated DIO mice ran ~70% longer in time and gained ~10× less fat than controls (Billon 2023, PMID 37739806; PMID 36988910). Zero human trials. Every "human dose" reference is allometric extrapolation from mouse data.

What Makes This Peptide Different

SLU-PP-332 is the cleanest pharmacological tool for studying ERR pan-agonism — distinct from cardarine (PPARδ) and MOTS-c (mitochondrial-derived peptide, AMPK activator). The catch: the Billon 2025 paper (PMID 41421047) introducing SLU-PP-915 explicitly identifies the parent SLU-PP-332 as lacking oral bioavailability — meaning oral capsules and tablets sold under this name may not reproduce the IP-route preclinical pharmacology.

Research overview

Outcome-by-outcome look at what the evidence actually supports for SLU-PP-332, including human vs. animal study counts and our editorial take on each.

Body weight reduction in diet-induced obesity (mouse)

Clinical:PreliminaryCommunity:Weak

DIO mice on 25–50 mg/kg IP twice daily for 28 days lost approximately 12% body weight, gained ~10× less fat than vehicle controls on the same high-fat diet, and improved glucose tolerance. The effect is mouse-only — no human trial has tested SLU-PP-332.

0 human studies · 2 animal studies

Key findings & citations
  • ~12% body weight loss over 28 days at 25 mg/kg IP BID in DIO mice (Billon 2024).
  • ~10× less fat gain than vehicle controls on a matched high-fat diet.
  • Increased resting energy expenditure and improved glucose tolerance.
  • Zero human trials registered as of May 2026.

Our take

Striking mouse data, zero human data. The lab's own development trajectory now points to the orally bioavailable sibling SLU-PP-915, not SLU-PP-332, as the likely clinical candidate.

Aerobic exercise capacity (mouse)

Clinical:PreliminaryCommunity:Weak

Mice on SLU-PP-332 ran ~70% longer in time and ~45% farther in distance than vehicle controls on a treadmill protocol. The effect required ERRα — knockout mice showed no benefit, confirming the gain is ERRα-transcription-dependent rather than off-target.

0 human studies · 1 animal study

Key findings & citations
  • ~70% longer treadmill time-to-exhaustion vs vehicle (Billon 2023).
  • ~45% greater treadmill distance vs vehicle.
  • Effect abolished in ERRα knockouts — confirms target dependency.
  • Shift toward type IIa oxidative skeletal muscle fibers, mimicking endurance training.

Our take

The single benefit with the strongest preclinical signal — and the one community oral-capsule users most often fail to reproduce, consistent with the published bioavailability finding for the parent compound.

Cardiac function in heart failure (mouse)

Clinical:PreliminaryCommunity:Preliminary

In a pressure-overload mouse heart failure model, pan-ERR agonism via SLU-PP-332 (and SLU-PP-915) improved ejection fraction, reduced cardiac fibrosis, and improved survival without inducing pathological hypertrophy. ERRγ was the main mediator of cardioprotection.

0 human studies · 1 animal study

Key findings & citations
  • Improved ejection fraction in pressure-overload heart failure (Xu 2023).
  • Reduced cardiac fibrosis and improved survival vs vehicle.
  • No pathological cardiac hypertrophy at the doses tested.
  • ERRγ — not ERRα — was the dominant cardioprotective receptor.

Our take

A single positive cardiac safety + efficacy datapoint in a disease model — not a clearance for chronic ERR pan-agonism in healthy human hearts.

What SLU-PP-332 doesn't do

Claims that current evidence does not support. Worth knowing before you set expectations.

SLU-PP-332 Vendors

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Price
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Amount
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$10.00/mg
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Dosing ProtocolFat Loss / Endurance Research (ERR Pan-Agonist)

Educational reference only. Individual responses vary. Consult healthcare provider before use.

Vial Size
5 mg or 30 mg lyophilized vial
Reconstitution
1 mL BAC water (5 mg vial → 5 mg/mL); 3 mL BAC water (30 mg vial → 10 mg/mL)
Dose
Mouse-only published doses: 25 mg/kg IP twice daily — no human dose established
Timing
AM and PM (mouse protocol BID)
Frequency
Twice daily IP in published mouse work
Duration
Up to 28 days continuous in published mouse work
Protocol Notes
Synthetic small molecule (not a peptide) — ERRα/β/γ pan-agonist. Zero human clinical trials. Billon 2025 (PMID 41421047) explicitly identifies the parent compound as lacking oral bioavailability — injectable lyophilized vials are the only format consistent with published preclinical pharmacology.

Why This Dosing Protocol

Why mouse-only doses? Published preclinical dosing is 25–50 mg/kg IP twice daily in mice. No human pharmacokinetics, no Phase 1 — every "human dose" is allometric extrapolation.

Why injectable over oral? Billon 2025 explicitly identifies the parent SLU-PP-332 as lacking oral bioavailability (the rationale for developing the orally active sibling SLU-PP-915). Injectable lyophilized vials are the only format consistent with the published preclinical pharmacology.

Why twice-daily? All published preclinical dosing is BID, consistent with a short estimated plasma half-life. Community once-daily oral protocols have no published pharmacokinetic basis.
Full Dosing GuideReconstitution CalculatorCycle Cost Calculator

Reconstitution Calculator

Dilution math and unit conversions. Prefilled using a common vial size for this peptide.

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Storage & Handling

Storage at a glance

Proper storage temperatures, shelf life, reconstitution best practices, and travel tips for lyophilized and reconstituted peptides.

Powder: Freezer
1+ year at -20°C
Reconstituted: Fridge
4 weeks max at 2-8°C
View Complete Storage Guide

Handling specifics

Educational overview on storage, labeling, and traceability considerations for lab environments. Consult primary literature and vendor documentation for specifics.

Powder storage (very stable)
  • Freezer (-20°C): 1+ year
  • Refrigerator (2-8°C): 1-3 months
  • Room temperature: 2-3 weeks (emergency only)
Reconstituted storage (fragile)
  • MUST refrigerate at 2-8°C
  • 4-week maximum shelf life
  • NEVER freeze after reconstitution
  • Use bacteriostatic water for multi-dose

FAQ

Is SLU-PP-332 a peptide?

No. SLU-PP-332 is a synthetic small molecule (molecular formula C22H21N5O3, ~419.4 Da) developed at Saint Louis University by the Burris lab. It activates the estrogen-related receptors ERRα/β/γ. The site lists it under the Small Molecule category alongside 5-amino-1MQ and tesofensine.

Does SLU-PP-332 really work like exercise?

In mice, yes — it induces an ERRα-dependent acute aerobic exercise transcriptional program and increases treadmill endurance by ~70% (Billon 2023, PMID 36988910). It flips the same transcriptional switches endurance training flips. Whether the effect translates to humans has not been tested — there are zero human clinical trials of SLU-PP-332.

What dose did the published mouse studies use?

25 mg/kg intraperitoneal (IP) twice daily. The Billon 2023 metabolic syndrome paper (PMID 37739806) ran this dose for 28 days. Earlier exercise-capacity work used a 25–50 mg/kg IP range. No human dose has been established. See our SLU-PP-332 Dosing Guide for the full breakdown.

Is oral SLU-PP-332 effective?

The Billon 2025 paper (PMID 41421047) introducing SLU-PP-915 explicitly states that the parent SLU-PP-332 "lacks oral bioavailability" — that is the published reason an orally active sibling compound was developed. Oral capsules and tablets sold as SLU-PP-332 may produce no systemic exposure. Injectable lyophilized vials are the only format consistent with the published preclinical pharmacology.

How does SLU-PP-332 compare to MOTS-c?

Both are described as exercise mimetics. SLU-PP-332 is a synthetic small molecule that activates ERR nuclear receptors. MOTS-c is a 16-amino-acid peptide encoded inside mitochondrial DNA that activates AMPK. Different upstream signals, both converging on mitochondrial biogenesis. Full breakdown: SLU-PP-332 vs MOTS-c.

Has SLU-PP-332 ever been tested in humans?

No. ClinicalTrials.gov shows no registered SLU-PP-332 trial as of May 2026. There is no published human pharmacokinetic, safety, or efficacy data. The compound has been characterized only in cell and mouse models.

Are there any side effects to know about?

Published mouse studies reported no overt toxicity at 25–50 mg/kg IP for up to 28 days. There is no human safety data of any kind — no Phase 1, no carcinogenicity studies, no long-term cardiac monitoring. ERRα and ERRγ are highly expressed in cardiac tissue, which is the most-discussed theoretical concern. See our SLU-PP-332 Side Effects guide.

Is SLU-PP-332 legal?

SLU-PP-332 is sold as a research chemical and is broadly available from research-peptide vendors in the US. It is not approved by the FDA and has not entered any human clinical trial. Vendor products are labeled "for research use only — not for human consumption." Possession or use outside an authorized research setting may be illegal in some jurisdictions.

How does it stack with retatrutide?

The mechanisms are non-overlapping — retatrutide drives appetite suppression and modest energy-expenditure increase via GLP-1/GIP/glucagon, SLU-PP-332 drives mitochondrial output via ERR pan-agonism. Community references frame the pairing as "eat less + burn more" through different signals. No published trial has tested the combination. Full guide: SLU-PP-332 + Retatrutide Stack.

Scientific Sources

The following peer-reviewed studies and official resources provide additional scientific context for this peptide:

SLU-PP-332 Research Articles

guides

SLU-PP-332 Dosage Chart: 500 mcg–1.5 mg Daily SC

Community SubQ protocols run 500–1,500 mcg/day, derived from mouse-to-human dose scaling. Why oral capsules likely fail and how the math gets there.

comparison

SLU-PP-332 vs MOTS-c: Two Exercise Mimetics

Synthetic ERR pan-agonist vs mitochondria-encoded AMPK activator. Same goal, opposite philosophies, and the stack rationale that ties them.

side-effects

SLU-PP-332 Side Effects: Zero Human Data, Mouse Signals

No human Phase 1, no incidence rates. What the mouse studies and ERR receptor expression actually predict — cardiac, hepatic, and the unknown long tail.

stacking

SLU-PP-332 + Retatrutide Stack: Eat Less, Burn More

Triple-agonist appetite suppression + ERR pan-agonist mitochondrial output. Why community references frame it as the cleanest mechanistic pair.

Compare SLU-PP-332 to alternatives

Side-by-side mechanism, dose, half-life, and vendor pricing.

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