SLU-PP-332
Also known as: SLU-PP-332
A small-molecule pan-agonist of estrogen-related receptors (ERR alpha/beta/gamma) developed academically. In mice, it produces exercise-like adaptations and meaningful fat loss. In humans, there is zero clinical data. Treat it as the experimental tool it actually is.
Overview
SLU-PP-332 came out of a Saint Louis University group's work on the ERR family of nuclear receptors. The 2023 Nature Communications paper showed that dosing it into mice triggered mitochondrial biogenesis in skeletal muscle, raised endurance capacity, and reduced fat mass in diet-induced obese animals without changing food intake. The media wrote it up as an exercise pill. The actual situation is a single research compound, a small number of academic groups working on it, no IND filings in public registries, and a grey-market industry that started selling it within weeks of the paper hitting the press. The mechanism is interesting and the mouse data is real. Anyone telling you what dose to use in humans is extrapolating from rodent allometry, full stop.[1]
Evidence quality
The foundational paper is Billon et al., Nature Communications 2023, from the Burris lab at Saint Louis University. Additional work has come from the same group and a handful of collaborators. There are zero registered human clinical trials of SLU-PP-332 as of this writing. The mechanism (pan-ERR agonism producing mitochondrial biogenesis) is well-validated in cell and rodent models. Whether the same effect appears in humans, at what dose, with what safety margin, is genuinely unknown.
Benefits & timeline
Benefits
- Strong rodent data for mitochondrial biogenesis and oxidative-fibre conversion in skeletal muscle - the cleanest exercise-mimetic mechanism published to date
- Reduced fat mass in obese mice without appetite suppression, suggesting an energy-expenditure rather than intake mechanism
- Improved endurance capacity in mouse running-wheel and treadmill assays
- Mechanistically distinct from GLP-1 incretins, which means in principle it could complement them - but there is zero human stack data to lean on
Timeline
Week 1-4
No reliable human pharmacokinetic data exists. Whatever you feel is either novelty effect or you are dosing wrong for human physiology.
Week 8
In mice, peak adaptations land here. In humans, this is purely a guess.
Week 12
If you are running it this long, you are gambling on a compound with no chronic-toxicology data in humans.
Off-cycle
Long off-cycle. There is no safety data justifying continuous use. Months of pause between any repeat is the cautious pattern.
Dosage protocols
Advanced
4 mg
daily
Investigational; preclinical data only.
Beginner
1 mg
daily
Standard
2 mg
daily
Titration & adjustment
No human titration data exists. Animal-derived starting estimates suggest 1 mg/day for 2 weeks, then assess subjective tolerance before increasing. Given the lack of safety data, the prudent approach is to stay at the lowest dose that produces a measurable effect and cycle off after 8–12 weeks.
Injection timing
No human data on optimal timing — extrapolating from animal studies, dosing pre-workout amplifies the exercise-mimetic effect. Do not dose late evening: the energetic effect can disrupt sleep.
Side effects & contraindications
- severeNo human safety data of any kind. You are the trial. There is no published profile of what dose causes what problem in humans.
- moderateTheoretical cardiac concern - ERR-gamma activation in cardiac tissue affects metabolism in ways that have not been characterised under chronic agonism in primates.
- moderateTheoretical hepatic concern - ERR receptors are expressed in liver and the chronic effect of pan-agonism on hepatic metabolism in humans is unknown.
- mildInjection-site reaction in users who reconstitute and inject. The molecule was studied in rodents via oral gavage; the subcutaneous route in humans is improvised.
Contraindications
- Pregnancy or breastfeeding - obvious, no data
- Cardiovascular disease - the cardiac ERR-gamma role is not characterised under chronic agonism
- Active cancer - nuclear receptor pan-agonism in a tumour-permissive environment is the exact wrong direction
- Anyone who is not comfortable being an N-of-1 experiment on themselves - the honest contraindication that no other vendor will write down for you
Reconstitution & injection
There is no approved formulation. Grey-market vials typically contain 5-10 mg of powder. A 5 mg vial reconstituted in 2 ml bacteriostatic water gives 2.5 mg per ml. A 1 mg dose draws 0.4 ml, or 40 units on a U-100 insulin syringe. Doses circulating online are extrapolated from mouse allometry without human PK data; treat the numbers as rough guesses, not protocols. Subcutaneous abdomen is the convention. None of this is grounded in human trial design.
Open calculator pre-filledStorage after reconstitution
Research-grade powder — reconstitute small batches. Refrigerate at 2–8 °C after mixing, light-protected. Stability is poorly characterised; conservative window is 14 days at fridge temperature in BAC water. Given the lack of clinical safety data, the best practice is to mix only what you will use in 1–2 weeks and discard the rest rather than stretch one vial.
Cost & sourcing red flags
Typical price range: $80–200 per 10 mg vial from research-chemical suppliers; oral capsule formats $100–250 per 30–60 count bottle. There is no legitimate pharmaceutical-grade source — every vial on the market is research-use-only.
Red flags
- Any vendor describing SLU-PP-332 as 'clinically studied in humans' or quoting human-trial efficacy numbers — there are no human trials. Every efficacy claim in human terms is extrapolation from rodent data.
- No batch HPLC or LC-MS certificate of analysis tied to the lot number. SLU-PP-332 is a small molecule synthesised in a wet lab; expect a chromatogram and mass-spec trace, not a peptide-style purity sheet.
- Vials marketed as 'injectable SLU-PP-332' without any buffer specification. The published in vivo work used DMSO-PEG-saline vehicles; a vendor shipping a lyophilised cake with no reconstitution guidance is leaving the user to guess at solubility.
- Listings that conflate SLU-PP-332 with established exercise mimetics (AICAR, GW501516) or with peptides like MOTS-c. They have different chemistry and different risk profiles; cross-listing them suggests the vendor is not synthesising or sourcing rigorously.
- Pricing under $50 per 10 mg vial — synthesising a research-grade ERR agonist with verified purity costs more than that at scale, so deep discounts likely reflect underdosed product or substituted material.
Pricing rots fast and varies by region and supplier. We list no vendors.
Common mistakes
Treating mouse doses as a starting point for human protocols.
Better approach: Allometric scaling from rodents to humans is the worst kind of guess - mouse metabolism is faster than ours, mouse surface-area-to-mass is different, and mouse studies dosed orally with vehicle, not subcutaneously. If you choose to use this compound, accept that any dose you pick is uninformed.
Stacking it with stimulants or thyroid agonists.
Better approach: The mechanism amplifies oxidative metabolism. Stacking it with anything else that does the same (T3, clenbuterol, high-dose caffeine) compounds cardiac strain risk in a compound where the cardiac safety profile is unknown. Run it alone if you run it at all.
Running it longer than 8 weeks.
Better approach: There is no chronic-toxicity data in any species at the doses people use. 4-8 weeks on, months off, is the cautious pattern - and honestly the better answer is to wait for human trials.
Sourcing from random online vendors.
Better approach: There is no approved manufacturing standard. If you are determined to try this, source from a vendor who provides third-party HPLC and mass-spec analysis on the batch you receive. Without it, you have no idea what powder is in the vial.
Real-world tips
- Honestly, the best tip is to wait. The human trial that will define this molecule has not been run. Whatever you learn from your own N-of-1 will be replaced by data in a few years.
- If you proceed anyway, track an objective endurance metric weekly (5k time, VO2 estimate, 1-mile pace) so you can tell whether the mechanism is doing anything for you.
- Avoid cardiovascular stress amplifiers in the same window - no high-stim pre-workouts, no thyroid pushing, no heavy alcohol use.
- Baseline labs at minimum: liver panel, CK, cardiac troponin if accessible, and a resting ECG. Repeat at week 4 and week 8.
- Stop immediately if you notice unusual chest discomfort, persistent tachycardia, or any new sign your heart is working harder than it should. The mechanism touches cardiac tissue.
What users report
SLU-PP-332 is preclinical-only — there are no human clinical trials and almost no real-world user base. The few reports that exist come from early-adopter biohacker forums and are anecdotal in the strongest sense.
Onset: The handful of self-reports describe a subtle warmth and slight uptick in workout endurance within 30–60 minutes of an oral or injected dose, but the signal is small and frequently indistinguishable from placebo.
Common reports
- Few real-world user reports exist for this compound — the published reports are limited to early-adopter biohacker forums and a small number of YouTube self-experimenters.
- Reported acute effects (when reported at all) cluster around a transient body-temperature rise, mild sweating, and a subjective sense of easier cardio output lasting 1–2 hours post-dose.
Where reports diverge from theory: This is the central honest caveat for SLU-PP-332: all of the impressive efficacy data — 20–30% improvements in mouse treadmill running, increased type IIa oxidative fibres, reduced adipose mass, improved insulin sensitivity — comes from rodent models. None of it has been replicated in humans. There is no published human pharmacokinetic data, no human safety data, no dose-finding study, and no long-term toxicology read in humans. The anecdotal forum reports of 'feels like an exercise mimetic' are uncontrolled n=1 experiments at doses derived by allometric scaling from mouse studies. Treat every claim about human SLU-PP-332 effects, positive or negative, as preliminary. The clinical literature does not yet exist.
When something else is the better tool
Actual endurance training
Use instead when: Always, before any exercise mimetic. The molecule that simulates training does not exist; SLU-PP-332 produces some of the muscle-level adaptations but does not deliver the cardiovascular, neural, and behavioural benefits of training. If you are running it because you do not want to train, the wrong tool is the one you are reaching for.
MOTS-c or AICAR
Use instead when: You want an exercise-mimetic peptide with a marginally longer anecdotal track record in the community, while still acknowledging that human data is thin. Different mechanisms, similar uncertainty, slightly more known about each.
Semaglutide or Tirzepatide
Use instead when: The fat-loss arm is the actual goal. The incretins have Phase 3 evidence; SLU-PP-332 has rodent data. Different evidence quality by an order of magnitude.
Based on 1 peer-reviewed study
- Has anyone done a human trial?
- Not in any public registry as of this writing. The compound is academic; the path to a human trial requires an IND, funding, and a sponsor. None of those are visible.
- Is it really like exercise?
- In mice, it produces a subset of exercise adaptations - mitochondrial biogenesis, oxidative fibre profile changes, fat mass reduction. It does not replicate the cardiovascular, neural, and metabolic benefits of actual exercise. The 'exercise in a bottle' headline is journalism, not pharmacology.
- What dose should I use?
- Honest answer: nobody knows. The doses circulating online are extrapolations from mouse experiments. If you must, start lower than any vendor suggests, monitor labs, and stop at any signal.
- Is it safe?
- There is no human safety data. The honest answer is unknown. The mechanism touches tissues (cardiac, hepatic) where chronic pan-receptor agonism could plausibly cause problems. Wait for trials, or accept that you are running one.
- What about the other ERR agonists I see online?
- The grey market has started selling several research compounds in this class. Same answer applies to all of them: interesting mechanism, no human data, uncharacterised long-term effects. The mechanistic story is not a substitute for trials.
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