SLU-PP-332 is marketed as an "exercise mimetic" — a compound that switches on some of the same energy-burning pathways as endurance exercise. But it is not a peptide (despite being sold in peptide circles), it is not FDA-approved, and crucially it has no human trials at all — every result is from mice or cell dishes. It's also poorly water-soluble, so it isn't a "reconstitute-with-bac-water" peptide, and the version sold doesn't even absorb well by mouth.
SLU-PP-332 is a synthetic pan-ERR agonist studied in mice for exercise-like transcriptional changes, increased fatty-acid oxidation, improved endurance, and obesity/metabolic-syndrome endpoints. Its evidence base is entirely preclinical; any human protocol is speculative and must not be presented as established therapy. It also lacks oral bioavailability — motivating the orally active analog SLU-PP-915.
SLU-PP-332 activates ERRα/β/γ nuclear receptors (most potent at ERRα, EC50 ~98 nM), driving PGC-1α-associated mitochondrial, oxidative-phosphorylation, TCA-cycle, and fatty-acid-oxidation gene programs. Translational limits: no human PK, poor oral bioavailability, aqueous-solubility/formulation problems, anti-doping relevance, and no controlled human trials. CAS 303760-60-3; C₁₈H₁₄N₂O₂; ~290.3 g/mol.
SLU-PP-332 occupies a distinct honesty tier in the atlas. Unlike tesofensine or enclomiphene — small molecules with genuine human trial evidence — SLU-PP-332 has none: every efficacy result comes from mice or cell culture. What's real and interesting is the mechanism and the preclinical signal: it's a synthetic pan-ERR agonist that, in mice, reproduces a chunk of the transcriptional and metabolic signature of aerobic exercise — more oxidative muscle fibers, better treadmill endurance, increased fatty-acid oxidation and energy expenditure, and improved metabolic-syndrome markers. That earns a Grade C (animal efficacy) / P (mechanism) ceiling — there is no A or B grade anywhere on this page, because there is no human data. Three honest cautions dominate: it is not a peptide (it's sold as one, but it's a small organic molecule that isn't water-soluble and isn't reconstituted with bacteriostatic water); its human dose, PK, and safety are entirely unestablished; and the form sold lacks oral bioavailability, so much of the marketing is mechanistically incoherent. The page treats any human "protocol" as a speculative research layer, not therapy.
SLU-PP-332's mechanism is genuinely elegant and is the best-supported thing about it — but it's established in cells and mice, not people. Estrogen-related receptors (ERRα/β/γ) are orphan nuclear receptors that, working with the coactivator PGC-1α, control the transcriptional program of oxidative metabolism: mitochondrial biogenesis, oxidative phosphorylation, TCA-cycle enzymes, and fatty-acid β-oxidation — essentially the gene network that endurance training turns on. SLU-PP-332 binds and activates all three ERRs (most potently ERRα), pharmacologically triggering that "acute aerobic exercise" signature. In mice this translates to more oxidative muscle fibers, better endurance, increased energy expenditure and fat-burning, improved metabolic-syndrome markers, and benefits in aging-kidney and heart-failure models. The honest framing: each node is real ERR biology (Grade C/P), but every step is preclinical, the human translation is unproven, and pan-activation of a master metabolic switch across many tissues carries unknown long-term and tissue-specific risks.
| Receptor | EC50 | Relative potency |
|---|---|---|
| ERRα | ~98 nM | Most potent |
| ERRβ | ~230 nM | Intermediate |
| ERRγ | ~430 nM | Least potent |
| Feature | SLU-PP-332 | A typical peptide |
|---|---|---|
| Structure | Small organic molecule (acylhydrazone) | Amino-acid chain |
| Target | Intracellular nuclear receptors | Often cell-surface receptors |
| Solubility | Poorly aqueous (needs DMSO/vehicle) | Often water/BAC-soluble |
| Reconstitution | Not BAC-water — solvent needed | BAC water typical |
Two hard facts shape this section. First, SLU-PP-332 has no approved human dose, no validated human PK, and no clinical safety database — every published dose is a mouse intraperitoneal regimen (e.g. 25 mg/kg/day for endurance, 50 mg/kg twice daily for metabolic models). Any human "protocol" is a speculative research-only hypothesis, not a recommendation. Second, this is not a water-soluble peptide: the standard bacteriostatic-water reconstitution calculator is chemically inappropriate, so the tool below is explicitly lab dilution math only, using a research solvent (e.g. DMSO) and a milligram working unit — never microgram "peptide-style" dosing. The human-equivalent-dose table exists specifically to debunk fake "250 mcg = mouse-equivalent" vendor claims, not to establish safe use.
| Band | Basis | Range | Human relevance |
|---|---|---|---|
| Low mechanistic | In-vitro receptor activity | nM–low µM | Cell culture only |
| Mouse endurance | Published i.p. work | 25 mg/kg/day | Animal only |
| Mouse exposure | Plasma/muscle at 6 h | 30 mg/kg | Animal PK only |
| Mouse metabolic | DIO / ob/ob work | 50 mg/kg BID | Animal only |
| Human dose | None | Not established | Do not infer |
| Body weight | HED from 25 mg/kg mouse | HED from 50 mg/kg single | HED from 50 mg/kg BID total |
|---|---|---|---|
| 55 kg | ~112 mg/day | ~223 mg/dose | ~446 mg/day |
| 75 kg | ~152 mg/day | ~304 mg/dose | ~608 mg/day |
| 95 kg | ~193 mg/day | ~385 mg/dose | ~770 mg/day |
| 105 kg | ~213 mg/day | ~426 mg/dose | ~851 mg/day |
Body-surface-area scaling (mouse Km 3 / human Km 37). This table exists to prevent fake "250 mcg = mouse-equivalent" claims — note the math lands in the hundreds of milligrams, not micrograms. It does NOT establish safe human use: route, formulation, toxicity, receptor occupancy, and human PK are all unknown.
| Trigger | Action | Rationale |
|---|---|---|
| No human protocol / no oversight | Do not initiate | No human safety or PK data |
| Resting HR rise, palpitations, chest pain | Hard stop + medical evaluation | ERR-driven cardiac energetics uncertain |
| ALT/AST >2–3× baseline | Hold | Unknown hepatic metabolism/toxicity |
| CK elevation + muscle pain | Hold | Possible muscle stress / rhabdo risk |
| Active malignancy | Avoid / hard stop | ERR signaling intersects cancer energetics |
| Unknown purity / no COA | Reject | Research-chemical contamination risk |
| Marker | Why considered | Validated? |
|---|---|---|
| Resting HR / BP / ECG | Cardiovascular response | No |
| CMP / ALT / AST | Liver/kidney safety | No |
| Creatinine / eGFR | Renal safety | No |
| Glucose / insulin / HOMA-IR | Metabolic effect | No |
| CK / hs-CRP | Muscle stress / inflammation | No |
| DEXA / VO2max / RMR | Functional readout | No |
| Vendor claim | Reality |
|---|---|
| "Orally active" | SLU-PP-332 has poor oral bioavailability |
| "Peptide" | Small molecule, no amino-acid sequence |
| Route | Status |
|---|---|
| Mouse i.p. | Published (animal) |
| Human SC / IM / IV / oral | Not established |
| Readout | Meaning |
|---|---|
| ERR reporter activity | Target engagement |
| Mito oxygen consumption | Functional respiration |
SLU-PP-332 is a poorly water-soluble small molecule, not a peptide — so this is lab dilution math only, using a research solvent (e.g. DMSO), not a bacteriostatic-water "peptide reconstitution" calculator. It converts a vial mass and stock concentration into volumes for bench/in-vitro work. It is not a human dose: there is no validated human dose, and units are milligrams (mouse mg/kg-scale), never micrograms.
Solvent volume = vial mass ÷ stock concentration. Use a research-appropriate solvent (e.g. DMSO) with proper vehicle controls — not bacteriostatic water alone. Bench/in-vitro math only; not a human dose.
Because SLU-PP-332 has no human data at all, every "stack" discussed in research-chemical circles is purely hypothetical — there is no human combination safety or efficacy evidence for any of them. The mechanistically coherent pairings would converge on the same mitochondrial/metabolic machinery: combining it with exercise itself (overlapping the very gene programs it mimics), with GLP-1/GIP agents (pairing an energy-expenditure pathway with an appetite pathway), with AMPK activators or other "exercise mimetics" (parallel energy-sensing), or with mitochondrial peptides like MOTS-c or SS-31. The honest read is that these are speculative research-interest pairings, not protocols — and the convergence is itself a caution, since stacking multiple metabolic activators could compound mitochondrial and cardiovascular stress in ways no one has measured. The hard constraints mirror the safety section: avoid entirely in active malignancy, cardiovascular disease, pregnancy, and competitive sport.
| Possibility | Concern |
|---|---|
| Additive endurance | vs overtraining stress |
| Pathway | Role |
|---|---|
| GLP-1 | Appetite ↓ |
| SLU-PP-332 | Energy expenditure ↑ (mice) |
| Convergence | Risk |
|---|---|
| Mitochondrial activation | Compounded stress |
| Agent | Node |
|---|---|
| SLU-PP-332 | Nuclear receptor (ERR) |
| MOTS-c / SS-31 | Mitochondrial peptide |
The defining safety fact for SLU-PP-332 is the absence of evidence: there is no human adverse-event database. Published work is animal and in-vitro, so any claim of "safe in humans" is unsupported, and recent toxicology work focuses on doping-control metabolite identification rather than clinical safety. What can honestly be discussed is a set of theoretical, mechanism-derived risks. Because ERR activation ramps up metabolism in high-energy tissues, cardiovascular stimulation (altered heart rate, oxygen demand, rhythm vulnerability) is a plausible concern; because ERR signaling participates in cellular energy metabolism, there's a theoretical concern in active malignancy; and the unknown human hepatic/renal handling, plus the solvents needed to dissolve a poorly water-soluble compound, add formulation and organ-burden uncertainty. Two practical risks are concrete rather than theoretical: poor water solubility creates real precipitation/inaccurate-dosing/injection-site hazards, and the research-chemical supply chain means purity and identity can't be assumed without a certificate of analysis. The honest bottom line: this is an unstudied-in-humans research chemical, and the safety section can only map plausible risks, not document them.
For most atlas compounds the safety section weighs known signals; here there is nothing human to weigh. The entire risk discussion is mechanism-derived inference, which means the honest stance is precaution, not reassurance — the absence of reported harms reflects the absence of human study, not a clean safety record.
Because SLU-PP-332 is poorly water-soluble, it can't be cleanly dissolved in bacteriostatic water like a peptide — it needs a research solvent. That creates concrete, non-theoretical hazards: precipitation in solution, inaccurate dosing, injection-site reactions, and exposure to vehicle solvents. The "peptide reconstitution" framing sold online is chemically wrong and a safety problem in itself.
ERRs sit at the top of the oxidative-metabolism program across muscle, heart, liver, and kidney. Activating all three isoforms everywhere is what produces the appealing exercise-like phenotype in mice — but it's also why long-term, whole-body pan-ERR activation could carry tissue-specific risks (cardiac energetics, cancer metabolism) that short mouse studies can't detect.
| Condition / scenario | Concern | Severity |
|---|---|---|
| Pregnancy / breastfeeding | No reproductive safety data | High |
| Active malignancy | ERR / metabolic-signaling uncertainty | High |
| Known arrhythmia | Unknown cardiac electrophysiology risk | High |
| Heart failure / ischemic heart disease | Cardiac energy-demand uncertainty | High |
| Severe liver disease | Unknown metabolism / solvent exposure | High |
| Severe kidney disease | Unknown clearance / renal effects | High |
| Competitive athlete | WADA non-approved / exercise-mimetic risk | High |
| No COA / unknown supplier | Contamination and identity risk | High |
| Eating disorder / severe underweight | Fat-mass loss / metabolic stress concern | High |
| Uncontrolled diabetes | Unknown glucose effects | Moderate–High |
SLU-PP-332's evidence base is the cleanest illustration in the atlas of "interesting mechanism, no human data." The human-trials row is genuinely empty — no clinical efficacy or safety study exists. What's there is a coherent preclinical story, all Grade C (animal) or P (mechanism): Billon 2023 (ACS Chemical Biology) showed that repeated intraperitoneal SLU-PP-332 induced an ERRα-dependent acute aerobic-exercise gene program, increased oxidative (type IIa) muscle fibers, and enhanced treadmill endurance in mice; Billon 2024 (JPET) extended this to diet-induced-obese and ob/ob mice with increased energy expenditure, fatty-acid oxidation, and reduced fat mass; an aging-kidney study reported reversal of mitochondrial dysfunction and inflammation; and a heart-failure study found improved cardiac fatty-acid metabolism and mitochondrial function (mainly via ERRγ). Recent 2026 work is analytical — characterizing SLU-PP-332's in-vitro metabolites for doping-control purposes, which is itself a signal that anti-doping authorities are treating it as a substance of concern. The honest GRADE summary: the strongest defensible claim is that SLU-PP-332 activates ERRα/β/γ and produces exercise-like effects in mice. There is no validated human dose, no human safety dataset, no approved indication, and no clinical biomarker protocol — so the page carries no A or B grade.
No credible human SLU-PP-332 clinical trial was identified, and ClinicalTrials.gov searches do not surface an SLU-PP-332 study. There is no human efficacy or safety data — the defining limitation of this compound and the reason its evidence ceiling is Grade C.
The foundational in-vivo study (ACS Chemical Biology): repeated intraperitoneal SLU-PP-332 induced an ERRα-dependent acute aerobic-exercise transcriptional program, increased type IIa oxidative muscle fibers, and enhanced treadmill endurance in mice, with measurable plasma (~0.2 µM) and muscle (~0.6 µM) exposure 6 h after 30 mg/kg. The basis for the "exercise mimetic" label.
A JPET study extending SLU-PP-332 to diet-induced-obese and ob/ob mice (50 mg/kg i.p. twice daily), reporting increased energy expenditure and fatty-acid oxidation, reduced fat-mass accumulation, and improved metabolic-syndrome markers — apparently via ERR-driven muscle/liver energy metabolism rather than appetite suppression.
An American Journal of Pathology study reporting that estrogen-related-receptor agonism (SLU-PP-332) reversed mitochondrial dysfunction and inflammation in an aging-kidney model — extending the mitochondrial-support rationale to a disease/aging context, in animals.
A study of pan-ERR agonists (SLU-PP-332 and SLU-PP-915) in pressure-overload heart failure, reporting improved cardiac fatty-acid metabolism and mitochondrial function and better pumping function in vivo — acting mainly through ERRγ. Preclinical cardiac evidence, with the flip side that it underscores cardiac-energetic effects.
A 2026 JPET study on SLU-PP-915, an orally active ERR-agonist analog developed specifically because SLU-PP-332 lacks oral bioavailability — enhancing aerobic exercise capacity in mice. Direct evidence that the SLU-PP-332 form sold for oral use is mechanistically mismatched.
A Trends in Pharmacological Sciences review of ERR biology — the orphan nuclear receptors regulating oxidative phosphorylation, mitochondrial biogenesis, fatty-acid oxidation, and substrate selection — providing the mechanistic context for why a pan-ERR agonist could act as an exercise mimetic, and — alongside medicinal-chemistry reviews of ERR-modulator selectivity and efficacy — the challenges of drugging this class.
A 2026 Drug Testing and Analysis study identifying SLU-PP-332's in-vitro metabolites and analytical signatures for doping-control purposes — not a safety study, but a clear signal that anti-doping authorities are preparing to test for it as an exercise-mimetic substance of concern.
Chemical-identity records (CAS 303760-60-3; C₁₈H₁₄N₂O₂; ~290.3 g/mol; IUPAC 4-hydroxy-N-[(Z)-naphthalen-2-ylmethylideneamino]benzamide) confirming SLU-PP-332 is a small organic molecule (acylhydrazone), not a peptide, and is supplied as a research reagent (e.g. Selleckchem / GLP Bio datasheets) — not an approved drug or compounding peptide.
The natural comparison set is the exercise-mimetic / mitochondrial-metabolic landscape. SLU-PP-332's closest relative is SLU-PP-915, the orally active successor from the same group, developed precisely because SLU-PP-332 doesn't absorb well by mouth — both are unapproved research chemicals. The most cautionary comparator is GW501516 (cardarine), a PPARδ exercise-mimetic with a different mechanism and a notorious safety history (its development was halted over cancer findings in animals, and it's banned in sport). MOTS-c and SS-31/elamipretide come from the mitochondrial-peptide world — mechanistically distinct from a nuclear-receptor agonist, but often discussed in the same "mitochondrial/metabolic" breath; SS-31 in particular has a far more formal clinical-development history than SLU-PP-332. Nuclear-receptor-based drug development for metabolic disease is an active but difficult field. The table keeps the throughline visible: SLU-PP-332 is animal-and-in-vitro-only, unapproved, and not a peptide — the least clinically mature row, despite the most elegant mechanism.
| Compound | Primary positioning | Mechanism class | Evidence tier | Route | Regulatory status |
|---|---|---|---|---|---|
| SLU-PP-332 | Exercise mimetic / metabolic research | Pan-ERR agonist (small molecule) | Animal + in-vitro only | Mouse i.p.; oral poor | Unapproved research chemical |
| SLU-PP-915 | Orally active successor analog | ERR agonist (small molecule) | Animal | Oral + i.p. (preclinical) | Unapproved research chemical |
| GW501516 (cardarine) | Endurance / lipid metabolism | PPARδ agonist | Animal + some human exposure; halted | Oral | Prohibited / unapproved (cancer signal) |
| MOTS-c | Mitochondrial signaling | Mitochondrial-derived peptide | Preclinical + limited exploratory | Injectable | Not FDA-approved |
| SS-31 / elamipretide | Mitochondrial dysfunction | Mitochondrial-targeted peptide | More formal clinical development | SC / IV | Investigational (further along) |
Because SLU-PP-332 is not a peptide, these are related compounds — exercise-mimetic and mitochondrial-metabolic relatives — rather than related peptides.
Evidence grades reflect the strength of support for the specific claim cited, not the prestige of the journal. SLU-PP-332's register has a distinctive shape: there is no Grade-A or Grade-B source anywhere, because there is no human trial. The highest grade is C — the preclinical mouse studies (Billon 2023 exercise capacity, Billon 2024 metabolic syndrome, the aging-kidney and heart-failure models, and the SLU-PP-915 oral-analog work). Mechanistic ERR-biology reviews and the doping-control analytical papers are Grade P, and identity, reagent, and regulatory/anti-doping records are Grade D. This is the honest fingerprint of a compound with an elegant, well-characterized mechanism and a genuinely interesting animal phenotype, but zero human evidence — the grade ceiling is exactly where the data stops.