Most fat-loss compounds work by suppressing appetite or speeding metabolism. SLU-PP-332 is in a different category. It is one of the only molecules shown to make a sedentary mouse behave like a trained athlete, without the mouse ever stepping on the wheel.
🔑 Key Takeaways
- SLU-PP-332 is a small molecule, not a peptide, despite being grouped with peptides in most online stores. It was developed at Saint Louis University in the Patti and Burris labs, hence the SLU prefix.
- It works by activating the estrogen-related receptors (ERR alpha, beta, gamma), a family of nuclear receptors that switch on the same metabolic genes that endurance training switches on.
- In mice, a single daily dose increased running time by up to 70%, raised fat oxidation, and produced 12% body weight loss in obese animals over 28 days, all without any change in diet or activity.
- No human clinical trials exist. There is no validated human dose, no human safety data, and no FDA approval.
- Online dosing recommendations vary by a factor of 1,000. Some vendors suggest 250 mcg per day, others suggest 400 to 800 mg per day. Both cannot be right.
- Half-life is short, around 1.5 hours, which is why most community protocols split the dose 2 to 3 times daily.
- The most commonly used community range is 1 to 5 mg per day subcutaneous, cycled 6 to 8 weeks on with at least 4 weeks off.
- SLU-PP-332 is on the WADA prohibited list as a metabolic modulator. Any tested athlete should not use it.
This page is the honest reference on SLU-PP-332. What it actually is, what the mouse data really shows, why the human dosing range online is broken, how it compares to MOTS-c and 5-Amino-1MQ, what the side effect picture looks like, and what to know before sourcing it.
What Is SLU-PP-332?
A synthetic small molecule, not a peptide.
SLU-PP-332 is a benzohydrazide-class small molecule developed by Dr. Thomas Burris and Dr. Bahaa Elgendy at Saint Louis University, with later work continuing at Washington University and the University of Florida. It was designed as a pan-agonist of the three estrogen-related receptors (ERR alpha, beta, gamma), with the strongest affinity for ERR alpha. The CAS number is 303760-60-3 and the molecular formula is C18H14N2O2.
SLU-PP-332 at a Glance
- Chemical class: Benzohydrazide small molecule (not a peptide)
- CAS: 303760-60-3
- Molecular formula: C18H14N2O2
- Molecular weight: 290.32 g/mol
- Primary target: ERR alpha (EC50 98 nM), with secondary activity at ERR beta and ERR gamma (EC50 430 nM)
- Developed by: Burris and Elgendy labs, Saint Louis University, first published 2020
- Half-life: Approximately 1.5 hours in mice
- Delivery routes used in studies: Intraperitoneal injection in mice. Human use is subcutaneous
- Research stage: Animal data only. No human trials
The "exercise mimetic" label comes from the fact that ERR alpha is one of the master switches activated by endurance training. Train hard for weeks, and ERR alpha activity climbs in skeletal muscle and heart tissue. SLU-PP-332 turns that switch on directly, without the training. In a sedentary mouse, the gene expression profile shifts toward what you would see in a trained one.
How SLU-PP-332 Works
The ERR receptors are the entry point.
The estrogen-related receptors are nuclear receptors that, despite the name, do not bind estrogen. They were called "estrogen-related" only because of structural similarity. Their actual job is to sit on DNA and regulate the expression of genes involved in mitochondrial biogenesis, fatty acid oxidation, and oxidative muscle fiber composition. ERR alpha is the dominant member of the family in skeletal muscle and heart tissue.
When SLU-PP-332 binds ERR alpha, it recruits the coactivator PGC-1 alpha, which is the same coactivator that exercise recruits. PGC-1 alpha then drives transcription of the mitochondrial biogenesis program: more mitochondria, longer mitochondria, better-functioning mitochondria. Downstream, fatty acid oxidation rises, the respiratory exchange ratio drops (meaning the body burns fat over carbs), and slow-twitch oxidative muscle fibers become the dominant phenotype. This is the structural change endurance training produces, on a faster timeline.
Why the comparisons to MOTS-c and AICAR are not interchangeable
SLU-PP-332 sits in a category called "exercise mimetics" along with MOTS-c, AICAR, GW501516 (cardarine), and 5-Amino-1MQ. The category is misleading because each compound activates a completely different pathway:
- SLU-PP-332: ERR receptors, drives mitochondrial biogenesis through PGC-1 alpha
- MOTS-c: AMPK activator, drives glucose uptake and metabolic flexibility
- AICAR: AMPK activator (more direct than MOTS-c)
- GW501516: PPAR delta agonist, drives fat oxidation through a different transcription program
- 5-Amino-1MQ: NNMT inhibitor, raises NAD+ availability and shifts cellular energetics
They produce overlapping outcomes in body composition and endurance, but the underlying biology is distinct, which matters for stacking and for predicting side effects.
SLU-PP-332 Benefits
What the mouse data actually shows.
Endurance, without training
This is the headline result. In the original Billon 2023 paper, untrained mice given SLU-PP-332 ran on a treadmill 70% longer before exhaustion than untrained controls. Total running distance climbed by roughly 45%. The mice were not trained at any point during the study. The compound alone shifted endurance capacity into a range close to that of conditioned animals.
Fat loss without dietary change
In the diet-induced obesity (DIO) mouse model, daily SLU-PP-332 dosing produced 10 to 12% body weight loss over 28 days while the mice continued eating the same high-fat diet that made them obese in the first place. Fat mass dropped by 25 to 30%. The respiratory exchange ratio shifted, indicating the mice were burning fat preferentially over carbohydrates throughout the day, not just during activity windows.
Mitochondrial biogenesis and metabolic flexibility
The mechanism that produces the endurance and fat-loss effects also makes muscle and heart tissue more metabolically flexible. Mice given SLU-PP-332 oxidized fatty acids more efficiently across feeding states, and their mitochondrial density in skeletal muscle increased. This is the kind of cellular change normally seen only after weeks of consistent endurance training.
Cardiac protection in heart failure models
In a pressure-overload model of heart failure, SLU-PP-332 administration improved cardiac substrate utilization and slowed the metabolic dysfunction associated with failing hearts. The cardiac angle is one of the most active research directions, distinct from the popular fat-loss positioning online.
What is not yet supported
Online sources sometimes claim SLU-PP-332 prevents COVID-19, reverses kidney disease, or replaces strength training. None of these claims are supported by the published research. Treat them as marketing language until human trials say otherwise.
SLU-PP-332 Dosage (And Why It Is Such a Mess)
The dosing question is where most online content fails.
Two dose ranges circulate online and they differ by three orders of magnitude. Both come from real reasoning, and both have problems.
The Two Dose Camps
- The microgram camp: 250 to 1,500 mcg per day, subcutaneous. This is the dose most vendors and protocol sites recommend. It is reverse-engineered from typical research peptide vial sizes (5 mg vials reconstituted to last weeks) rather than from any pharmacology data.
- The high-dose camp: 400 to 800 mg per day, oral or split injection. This is what you get when you do a strict human equivalent dose (HED) calculation off the published mouse studies. The mice received 25 to 50 mg/kg, which scales to roughly 200 to 600 mg for an 80 kg human after correcting for surface area.
Both numbers cannot be right. The microgram camp ignores the actual published doses. The HED camp assumes mouse pharmacology translates linearly to humans, which it usually does not for ERR agonists, and it also ignores that vendor-grade SLU-PP-332 is rarely produced at the purity needed to safely take 800 mg of anything.
The honest answer is that no validated human dose exists. The most commonly used community range, where users report effects without obvious side effects, sits at 1 to 5 mg per day subcutaneous, split 2 to 3 times to compensate for the short half-life. That range is not validated by trials, but it is what shows up most consistently in user reports.
Sample community protocol
This is what a typical community protocol looks like. It is not medical advice, and it is not validated.
| Phase | Daily dose | Schedule | Duration |
|---|---|---|---|
| Titration | 500 mcg | Once daily, 30 to 60 minutes pre-workout | Week 1 |
| Build-up | 1 mg | Split AM and pre-workout | Week 2 |
| Working dose | 2 to 3 mg | Split AM, midday, pre-workout | Weeks 3 to 8 |
| Off cycle | 0 | None | 4 weeks minimum |
Reconstitution: 5 mg vial plus 2 mL bacteriostatic water gives 2,500 mcg per mL. On a U-100 insulin syringe, 10 units (0.1 mL) delivers 250 mcg. Refrigerate after reconstitution. Use within 30 days.
SLU-PP-332 Side Effects
The honest picture is that we do not know.
No published human safety data exists. The mouse studies report no obvious toxicity at the doses used, including no liver enzyme elevation, no significant cardiac arrhythmia, and no behavior changes suggesting central nervous system effects. That is reassuring at the level of mouse pharmacology, but it does not establish a human safety profile.
Reported community side effects, from the user reports that exist, fall into a few buckets:
- Mild fatigue or "metabolic shift" feeling in the first 1 to 2 weeks, usually resolves on its own
- Mild GI discomfort in users dosing oral or sublingual
- Sleep changes, in both directions. Some users report deeper sleep, others report mild insomnia at higher doses
- Injection site reactions at typical subcutaneous frequencies
The theoretical concerns that have not been tested in humans are more interesting:
- Cardiac substrate switching in healthy hearts. ERR activation in a healthy heart may not produce the same benefit it produces in a failing one.
- ERR gamma off-target effects. ERR gamma is involved in skeletal development and immune function. Long-term agonism has not been studied in humans.
- Hormonal effects. Despite the name, ERR receptors do not bind estrogen, but they share regulatory networks with steroid hormone signaling. Whether this matters in practice is unknown.
- Anti-doping status. SLU-PP-332 is on the WADA prohibited list under section S4.5 (metabolic modulators). Any drug-tested athlete will fail a test if they use it.
SLU-PP-332 vs MOTS-c, 5-Amino-1MQ, and AOD-9604
This is the comparison that most online articles get wrong by treating these as interchangeable.
| Compound | Mechanism | Best for | Onset | Human data |
|---|---|---|---|---|
| SLU-PP-332 | ERR alpha agonist, drives mitochondrial biogenesis | Endurance, sustained fat oxidation, cardiac metabolism | 2 to 4 weeks | None |
| MOTS-c | AMPK activator, mitochondrial-derived peptide | Insulin sensitivity, metabolic flexibility | 2 to 6 weeks | Limited human data, some safety |
| 5-Amino-1MQ | NNMT inhibitor, raises NAD+ | Fat loss, energy, NAD+ restoration | 4 to 8 weeks | None |
| AOD-9604 | HGH fragment, lipolysis activator | Localized and systemic fat loss | 4 to 8 weeks | Some early human safety, no efficacy approval |
The simplest way to think about it: SLU-PP-332 is the endurance and cardiac compound, MOTS-c is the insulin-sensitivity compound, 5-Amino-1MQ is the NAD+ compound, and AOD-9604 is the lipolysis compound. They are not substitutes. They can theoretically stack, but stacking three or four metabolic modulators in a body that has never seen any of them is not a starting protocol.
Stacking SLU-PP-332
If you are going to stack, here is how the community typically combines it.
The most commonly described stack pairs SLU-PP-332 with a growth hormone secretagogue like CJC-1295 plus Ipamorelin. The logic is that GH peptides drive lipolysis and recovery, while SLU-PP-332 drives mitochondrial capacity and endurance. The two effects are non-overlapping. A second common pairing is with MOTS-c, on the theory that combining ERR activation with AMPK activation hits two parallel metabolic pathways.
The honest assessment is that no human data backs any of these stacks. They are conceptually reasonable and they are what users report doing. They are not validated, and stacking multiple unstudied compounds compounds the unknown.
Where to Buy SLU-PP-332
Sourcing matters more here than for most peptides.
Because SLU-PP-332 is a small molecule rather than a peptide, the synthesis route is different from peptide synthesis, and so is the impurity profile. A bad batch of a peptide is usually weak. A bad batch of a small molecule can contain genuinely problematic side products from the reaction. Vendor selection is not optional.
What to verify before buying:
- HPLC purity report showing 98% or higher, dated within the last 12 months
- Mass spectrometry confirming the compound matches the published structure (M+H 291.1)
- Third-party COA rather than only an in-house COA from the vendor
- Storage and shipping conditions appropriate for a small molecule (cool, dry, dark)
For broader sourcing standards across peptide and small-molecule vendors, see our peptide vendor guide and how to read a peptide COA.
Frequently Asked Questions
Frequently Asked Questions
Medical disclaimer. This article is informational only and does not replace individualized medical advice. SLU-PP-332 is not approved by the FDA for any human use. Every efficacy claim discussed here is based on animal studies. There is no validated human dose, no human safety data, and no regulatory clearance. Anyone considering use should speak with a qualified healthcare provider, understand the unknowns, and source any product through verified channels.