~50% increase in running distance in mice [1]
The headline finding — untrained treated mice ran substantially further than controls, with increased mitochondrial content and a shift toward oxidative fibre types.
PrecisePep/Peptide Library/SLU-PP-332
Metabolic & Adipose Regulation
SLU-PP-332
ERR agonist · oestrogen-related receptor pan-agonist
A small molecule that switches on the transcriptional programme endurance exercise produces — the closest thing to a genuine exercise mimetic in this catalogue, and a compound no human has ever taken.
00 Overview
SLU-PP-332 is not a peptide and has never been given to a human. It is a synthetic small molecule that agonises the oestrogen-related receptors — ERRα, ERRβ and ERRγ — a family of orphan nuclear receptors that sit at the centre of the transcriptional response to endurance exercise, governing mitochondrial biogenesis, oxidative metabolism and fibre-type composition.
The headline mouse result is striking: treated animals ran roughly 50% further, with increased mitochondrial content and a shift toward oxidative muscle fibres, without training.[1] Subsequent work reported improvements in metabolic parameters and reduced adiposity in obese mouse models.[2]
What follows from that is much less than the marketing implies. The studies used intraperitoneal injection in mice; oral bioavailability is a known limitation the developing group has acknowledged. There is no human pharmacokinetics, no human safety data, no dose, and no trial. ERRs are transcription factors with broad tissue expression, which makes chronic pan-agonism a substantial unknown rather than a targeted intervention.
Newest is not best-evidenced
SLU-PP-332 is among the most recently publicised compounds in this catalogue, and it has the least human evidence of anything in it — which is to say none. Novelty and evidence run in opposite directions here, and the enthusiasm around it is driven by a genuinely interesting mouse result rather than by anything demonstrated in a person.
// Mechanism of action
ERR pan-agonism. The oestrogen-related receptors are orphan nuclear receptors — named for sequence similarity to oestrogen receptors, but they do not bind oestrogen and are not part of oestrogen signalling. ERRα in particular is a master regulator of mitochondrial biogenesis and oxidative metabolism.
The exercise transcriptional programme. ERRs partner with PGC-1α, the coactivator induced by endurance exercise, to drive expression of genes for mitochondrial biogenesis, fatty acid oxidation and oxidative fibre characteristics. Agonising ERRs directly activates part of that programme without the exercise.
Why "exercise mimetic" overstates it. Exercise produces mechanical loading, cardiovascular adaptation, neural adaptation, bone loading and systemic signalling that no transcription factor agonist reproduces. Activating one arm of one adaptive programme is not equivalent to training.
Broad tissue expression. ERRs are expressed in heart, kidney, liver, brain and elsewhere. A pan-agonist does not confine itself to skeletal muscle, and what sustained activation does in those tissues has not been examined.
01 Reported benefits
Effects that have been reported. A study-tier entry means a result was published — not that the effect is established, reproducible, or transferable from a rodent to a person.
Highest confidenceReported in peer-reviewed literature, registered clinical trials, or regulatory filings. Note the model: much peptide literature is in vitro or rodent work, not human trial data.
Improved metabolic parameters in obese mice [2]
Reported reductions in fat mass and improvements in glucose and lipid handling in diet-induced obesity models.
Increased mitochondrial biogenesis [1]
Consistent with the ERR/PGC-1α mechanism and demonstrated at the tissue level in the animal work.
Poor oral bioavailability is an acknowledged limitation [1]
The studies used intraperitoneal injection. The developing group has described improving oral properties as an objective, which means the compound as it exists is not optimised for the route people would use.
No human study of any kind
No pharmacokinetics, no safety, no dose, no trial.
Unproven — inference onlyExtrapolated from a known mechanism, receptor profile, or adjacent compound class. Biologically plausible but not directly demonstrated for this compound in this context.
Improved endurance and metabolic health in humans
The entire use case, resting on a mouse result obtained by a route humans would not use. The inference chain is as long as any in this library.
Fat loss without appetite suppression
Attractive as a complement to incretins. Untested.
Benefit where exercise is not possible
The genuinely interesting clinical hypothesis, and the one the developing group has articulated — heart failure, mitochondrial disease, immobility. Also the one that would require actual trials.
Concern: chronic nuclear receptor agonism
Transcription factors regulate large gene networks across many tissues. Sustained pan-agonism of a receptor family is a systemically broad intervention with no characterisation.
Concern: cardiac effects
ERRα is highly expressed in cardiac tissue and central to cardiac metabolism. Sustained activation there is unexamined and is not a tissue where surprises are welcome.
Uncontrolled reportsAggregated from research-community logs, forums, vendor literature and self-reported experience. Uncontrolled, unverified, subject to placebo, polypharmacy and product-purity confounds. Lowest evidentiary weight.
Improved endurance and work capacity
Reported by early adopters, in very small numbers, entirely uncontrolled, and about a compound with no established human dose.
Increased body temperature and sweating
Occasionally reported, plausibly consistent with increased oxidative metabolism.
Doses are guesswork
Community figures are back-calculated from mouse studies by allometric scaling — a procedure that has no validation for this compound and frequently misleads.
Very thin anecdotal base
One of the least-used compounds in this catalogue, so even the uncontrolled evidence is minimal.
02 Adverse effects & risks
Adverse effects, contraindications and unknowns. The grey-market tier is where under-reporting is worst: uncontrolled use produces no systematic safety surveillance at all, so absence of a reported harm is not evidence of safety.
Highest confidenceReported in peer-reviewed literature, registered clinical trials, or regulatory filings. Note the model: much peptide literature is in vitro or rodent work, not human trial data.
No human safety data
Nothing. No toxicology, no pharmacokinetics, no adverse-event data.
No reported toxicity in the mouse studies [1]
The published animal work does not report notable toxicity over the study durations used, which were short.
Unproven — inference onlyExtrapolated from a known mechanism, receptor profile, or adjacent compound class. Biologically plausible but not directly demonstrated for this compound in this context.
Cardiac consequences of chronic ERRα activation
ERRα is central to cardiac energy metabolism. Sustained pharmacological activation there is entirely uncharacterised.
Broad off-target transcriptional effects
ERRs regulate large gene networks in multiple tissues. A pan-agonist affects all of them.
Unknown interaction with training adaptation
Pre-activating the transcriptional programme exercise recruits may amplify or may blunt the adaptive signal from training. Nobody knows which.
Doses derived by unvalidated scaling
The most immediate practical risk is simply taking an amount nobody has any basis for.
Uncontrolled reportsAggregated from research-community logs, forums, vendor literature and self-reported experience. Uncontrolled, unverified, subject to placebo, polypharmacy and product-purity confounds. Lowest evidentiary weight.
Almost no adverse-effect data
Reflecting extremely low usage rather than any safety property.
03 Dosing ranges
Figures below are documented, not recommended. Study ranges come from published protocols in the stated model; grey-market ranges are what the research community reports using and carry no safety validation of any kind.
Highest confidenceReported in peer-reviewed literature, registered clinical trials, or regulatory filings. Note the model: much peptide literature is in vitro or rodent work, not human trial data.
Mouse dosing by intraperitoneal injection [1]
The published studies used weight-normalised intraperitoneal dosing in mice. Neither the route nor the scaling converts to a human oral dose by any validated method.
No human dose exists
None has been established, proposed in a trial, or tested.
Unproven — inference onlyExtrapolated from a known mechanism, receptor profile, or adjacent compound class. Biologically plausible but not directly demonstrated for this compound in this context.
There is no defensible dose to state
With no human pharmacokinetics and poor oral bioavailability acknowledged by the developers, any figure is arbitrary. That is worth saying plainly rather than filling the space with a number.
The injectable route is closer to the evidence than the oral one
The mouse studies dosed intraperitoneally, not orally, precisely because oral bioavailability is poor. Subcutaneous grey-market use is therefore — unusually for this library — nearer to what was actually studied. That is an argument about route only, and it says nothing about dose.
Uncontrolled reportsAggregated from research-community logs, forums, vendor literature and self-reported experience. Uncontrolled, unverified, subject to placebo, polypharmacy and product-purity confounds. Lowest evidentiary weight.
250–500 mcg daily, subcutaneous
The dominant grey-market figure, from 10 mg vials, back-calculated from mouse intraperitoneal dosing by allometric scaling. At 500 mcg daily a 10 mg vial is twenty days.
250–500 mcg daily, oral
Also circulated, and harder to defend given the acknowledged bioavailability problem — the same figure by a route the compound is known to handle badly.
1 mg or more daily
Reported, without any way to assess whether it is proportionate to anything.
| Approach | Dose | Route | Notes |
|---|---|---|---|
| Entry | 250 mcg daily | Subcutaneous | Scaled from mouse IP dosing |
| Standard | 500 mcg daily | Subcutaneous | 10 mg vial = 20 days |
| Oral variant | 250 – 500 mcg daily | Oral | Poor bioavailability acknowledged |
| Higher-end | 1 mg daily | Subcutaneous | No basis for proportionality |
Every number here is a guess
These figures come from allometric scaling of mouse intraperitoneal doses — a procedure with no validation for this compound and a poor track record generally. There is no human pharmacokinetic study, so there is no way to check whether 500 mcg is a tenth of an active dose or ten times one. The calculator will do the arithmetic accurately; the input is what is unreliable.
04 Synergy & interactions
Combination effects. Almost no peptide combination has been studied as a combination in humans; stack logic is overwhelmingly mechanistic inference and community practice. Each linked compound has its own page.
Highest confidenceReported in peer-reviewed literature, registered clinical trials, or regulatory filings. Note the model: much peptide literature is in vitro or rodent work, not human trial data.
No combination studies exist
None.
Unproven — inference onlyExtrapolated from a known mechanism, receptor profile, or adjacent compound class. Biologically plausible but not directly demonstrated for this compound in this context.
With MOTS-c
Both push toward mitochondrial biogenesis and oxidative metabolism by different routes — ERR transcription versus AMPK. Redundant or additive, unknown which.
With incretin agonists
Substrate utilisation alongside intake reduction. The common stack rationale, untested.
With actual endurance training
The only intervention here with unambiguous evidence for the outcome being sought — and the comparison that makes the rest of the page look thin.
Uncontrolled reportsAggregated from research-community logs, forums, vendor literature and self-reported experience. Uncontrolled, unverified, subject to placebo, polypharmacy and product-purity confounds. Lowest evidentiary weight.
Added to metabolic stacks
The typical context, in very small numbers.
05 Protocols
Whole schedules — dosing, titration, cycle length, and off-time — as documented in trials, as proposed from mechanism, and as circulated in the research community. Reproduced for study and comparison only.
Highest confidenceReported in peer-reviewed literature, registered clinical trials, or regulatory filings. Note the model: much peptide literature is in vitro or rodent work, not human trial data.
No human protocol exists
No registered trial of any kind.
Unproven — inference onlyExtrapolated from a known mechanism, receptor profile, or adjacent compound class. Biologically plausible but not directly demonstrated for this compound in this context.
This one is genuinely too early
A compound with a striking mouse result, an acknowledged bioavailability problem, no human pharmacokinetics and no safety data is at the stage where the honest position is to watch the literature rather than construct a protocol.
Uncontrolled reportsAggregated from research-community logs, forums, vendor literature and self-reported experience. Uncontrolled, unverified, subject to placebo, polypharmacy and product-purity confounds. Lowest evidentiary weight.
Daily oral courses of undefined length
What circulates, on no established basis.
Not part of either documented protocol
Neither documented protocol includes it.
05b Condition-specific interest
SLU-PP-332 is marketed on one phrase — "exercise in a bottle" — and the phrase is doing all of the work. This section is short because the evidence is.
No approval, no trial
No human data exists for SLU-PP-332 by any route, for any indication. It is a small molecule, not a peptide, and it is sold as a vial because oral bioavailability is poor — which is also why the animal studies injected it.
Theorized — mouse, and the framing overstates it
The exercise-mimetic claim
Pathophysiology
Exercise produces coordinated adaptation across muscle, cardiovascular, metabolic, skeletal, immune and neurological systems, mediated by hundreds of signalling molecules acting over years.
Mechanistic rationale
SLU-PP-332 is an agonist of the estrogen-related receptors, which regulate mitochondrial biogenesis and oxidative metabolism. In mice it increased running capacity and reduced adiposity without training. Reproducing one transcriptional arm of the exercise response is not reproducing exercise — it does not load bone, does not improve cardiac output through training adaptation, and does not produce the neurological or mood effects that account for much of exercise’s benefit. Exercise has mortality data. This has mice.
Community reports
Sold to people who train, which makes attribution impossible in the population using it.
Components carrying the argument: ERRα/β/γ agonism
Theorized — and the direction is unknown
Cardiac and metabolic effects — the unexamined question
Pathophysiology
Estrogen-related receptors are highly expressed in cardiac muscle, where they regulate the mitochondrial and metabolic programme that supports continuous contraction.
Mechanistic rationale
Systemic ERR agonism acts on the heart, and nobody has characterised what that does in a person. ERR signalling is altered in heart failure, and both agonism and antagonism have been proposed therapeutically in different contexts. A compound with no human pharmacokinetic data, acting on a receptor family central to cardiac metabolism, is not a compound whose cardiac effects can be assumed benign.
Community reports
Not raised in community discussion, where the framing is entirely about endurance and fat loss.
Components carrying the argument: ERR in cardiac tissue
| Question | Position |
|---|---|
| Human data? | None |
| Is it a peptide? | No — a small molecule |
| Evidence | Mice — running capacity, adiposity |
| Does it replace exercise? | No — one transcriptional arm of many |
| Cardiac effects | ERRs are central to cardiac metabolism — uncharacterised |
| Why a vial? | Poor oral bioavailability — which is why studies injected it |
What actually has evidence for these conditions
Exercise has mortality data, and it is the comparator here. Aerobic training improves cardiorespiratory fitness, which is among the strongest predictors of all-cause mortality there is. Resistance training preserves muscle and bone and improves function. Neither has been outperformed by any pharmacological agent for these outcomes, and the compounds that describe themselves as substitutes have been tested against nothing.
06 Handling, reconstitution & storage
Physical-chemistry reference for laboratory handling of the lyophilised material. Reproduced so that stability and concentration mathematics can be studied — see the calculator for the arithmetic and the reconstitution guide for sterile technique.
Reconstitution
A small molecule, commonly supplied as a 10 mg vial for subcutaneous use, or as capsules. Solubility differs from peptides — some suppliers specify a co-solvent rather than plain bacteriostatic water, and incomplete dissolution is reported. Follow the supplier specification rather than assuming peptide handling applies.
Storage
Dry, cool, protected from light. Small-molecule stability.
Common vial sizes
Commonly 10 mg vials or oral capsules.
Stability notes
Not subject to peptide degradation concerns.
07 Legal & regulatory status
Regulatory status changes and differs by country. This is a summary for orientation, not legal advice — check your own jurisdiction.
Not approved anywhere and never studied in humans. SLU-PP-332 is a pre-clinical research compound from an academic medicinal chemistry programme. It is not a peptide, not a supplement, and not a drug in any regulatory sense.
Regulatory and trial claims re-checked against primary sources on 16 August 2026. Checked: no human data and no regulatory status by any route. Approvals, trial readouts and compounding decisions move faster than anything else on this page — a date here means someone looked, not that nothing has changed since.
Anti-doping
Metabolic modulators and PPAR/ERR-axis agents are addressed under WADA S4. An exercise-mimetic transcriptional agonist should be assumed prohibited.
§ Sources & further reading
Links resolve to PubMed records, trial registries, publisher pages or primary documents. Where a body of work rather than a single paper is cited, the link opens a PubMed query so the full result set — including newer papers than this page — can be reviewed. Verify every claim against the primary source before relying on it.
- PubMed: SLU-PP-332 and ERR agonism — exercise mimetic and endurance findings (live query)Database or literature search
- PubMed: ERR agonism in obesity and metabolic models (live query)Database or literature search
- PubMed: ERRα, PGC-1α and the exercise transcriptional programme (live query)Database or literature search
Reminder
For educational and research reference only. Nothing on this site is medical advice, a recommendation, or an instruction to administer any substance to a human being. Every figure on this page is a record of what has been reported, not a recommendation. Full disclaimer.