Compound Name
SLU-PP-332
Reviewed April 2026
Written by Garret Grant
Founder & Lead Researcher · B.S. Civil Engineering, UCLA
Last updated: April 2026
Human-researched and AI-assisted with full editorial review. I verify sources, protocol interpretation, and final judgments personally. See methodology.
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Research guide for SLU-PP-332, the pan-ERR agonist often framed as an exercise mimetic. This page covers published murine dosing, reconstitution math, side-effect limits, and how it differs from appetite-driven compounds like Semaglutide and Tirzepatide, plus mitochondrial comparators like MOTS-c and AOD-9604.
Half-life
Human PK unpublished
Published dose
25-50 mg/kg IP
Status
Preclinical only
Class
Pan-ERR agonist
Need to calculate reconstitution and dosing units? Use the dose to units converter.
Compound Name
SLU-PP-332
Aliases
SLU-PP 332, 4-Hydroxy-N'-(naphthalen-2-ylmethylene)benzohydrazide, SLU32
Category / Class
Pan-ERR Agonist / Small-Molecule Exercise Mimetic
Half-Life
Not formally published in humans; plasma and muscle exposure confirmed at 6 hours post-IP injection in mice (0.2 uM plasma, 0.6 uM muscle at 30 mg/kg).
Dosing Frequency
Twice daily in preclinical studies; once daily with oral community formulations, not clinically validated.
Dose Range
Preclinical: 25-50 mg/kg IP in mice. No human-validated dose. Community oral protocols: 250 mcg to 20 mg per day.
Common Vial Sizes
5 mg injection vial; oral capsules commonly sold in 250 mcg, 500 mcg, 1 mg, 5 mg, 10 mg, and 20 mg strengths.
Route of Administration
Intraperitoneal in published animal studies; oral capsule and subcutaneous use in community settings, not validated.
Regulatory Status
Not FDA-approved. Research use only. No human clinical trials as of April 2026. Not WADA-scheduled as a named compound, but ERR agonists fall under WADA class S4.5 metabolic modulators.
Developer
Thomas P. Burris lab (Saint Louis University, later Washington University in St. Louis / University of Florida Genetics Institute).
Key Stat
About 4-fold greater potency at ERRalpha (EC50 98 nM) than ERRgamma (EC50 430 nM), with 50 mg/kg BID in mice reducing fat mass and improving insulin sensitivity without requiring exercise.[1][2]
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SLU-PP-332 is a synthetic small-molecule pan-agonist of the estrogen-related receptors (ERRalpha, ERRbeta, and ERRgamma) - a family of orphan nuclear receptors that sits upstream of mitochondrial biogenesis, fatty acid oxidation, and the aerobic gene program activated by endurance exercise. In plain terms, SLU-PP-332 flips many of the same intracellular switches that training flips, which is why it is often described as an exercise mimetic. The compound was identified by the Thomas P. Burris lab, and the lead publications are Billon et al. in ACS Chemical Biology (2023) and Journal of Pharmacology and Experimental Therapeutics (2024).[1][2]
Structurally, SLU-PP-332 is not a peptide at all - it is a small organic molecule built on a benzohydrazide scaffold, with formula C18H14N2O2, molecular weight 290.3 g/mol, and CAS 303760-60-3.[3][12] It is included on PDP because the peptide-research community treats it as a peptide-adjacent metabolic tool and frequently stacks or compares it with true peptides. In cell assays it activates all three ERR isoforms but is roughly four-fold more potent at ERRalpha than ERRgamma, with ERRbeta in between.[1][3]
The current research program is entirely preclinical. Four published in-vivo studies in mice cover exercise capacity, metabolic syndrome and obesity, pressure-overload heart failure, and age-related kidney dysfunction.[1][2][4][5] No human clinical trial has been registered or completed as of April 2026. The compound is sold by research suppliers as injection vials and oral capsules, but there is no established human safety or efficacy profile. This page is an educational research reference only.
The short version: SLU-PP-332 binds to ERRalpha, and to a lesser extent ERRbeta and ERRgamma, which are transcription factors in the nucleus that control how many mitochondria a cell builds, how efficiently those mitochondria burn fat, and how much oxidative capacity the cell has. When you run, muscle cells upregulate these same receptors. SLU-PP-332 does it pharmacologically. Think of ERRalpha as the master volume knob for a cell's aerobic machinery - SLU-PP-332 turns that knob up.
ERRalpha is highly expressed in energy-demanding tissues such as skeletal muscle, heart, brown adipose tissue, and liver.[1][3] When ERRalpha is activated it switches on genes for mitochondrial biogenesis, oxidative phosphorylation, the TCA cycle, and fatty acid beta-oxidation. In the Billon 2023 paper, a single 25 mg/kg intraperitoneal dose in mice was enough to induce an acute aerobic exercise transcriptional signature in muscle within hours.[1] After 15 days of dosing at 25 mg/kg, treadmill endurance increased measurably.
ERRalpha works in partnership with PGC-1alpha, the master coactivator of mitochondrial biogenesis. Together they drive expression of nuclear-encoded mitochondrial genes, increasing both the number and efficiency of mitochondria inside muscle and cardiac tissue.[1] In the Billon 2023 study, 50 mg/kg BID for 28 days increased succinate dehydrogenase-positive oxidative muscle fibers and raised OXPHOS complex protein levels.[1]
In diet-induced obese mice and ob/ob mice, 50 mg/kg BID for 28 days increased whole-body energy expenditure and fatty acid oxidation, reduced fat mass, lowered cholesterol and triglycerides, and improved insulin sensitivity without changing food intake.[2] That is a metabolic-rate mechanism, not an appetite-suppression mechanism like Semaglutide or Tirzepatide.
In the pressure-overload heart-failure model, 6 weeks of SLU-PP-332 IP dosing improved ejection fraction, reduced fibrosis, and increased survival. The authors attributed the effect primarily to ERRgamma engagement in cardiomyocytes, which normalized fatty acid metabolism and mitochondrial function without reversing hypertrophy itself.[4] The practical takeaway is that ERRalpha appears to drive most skeletal-muscle effects, while ERRgamma carries more of the cardiac signal.
Put together, SLU-PP-332 reproduces many of the cellular adaptations of endurance training at the transcriptional level. What it does not reproduce is the mechanical loading of actual exercise, so tendon, bone, and connective-tissue adaptations are not part of the promise. It is a metabolic research tool, not a substitute for training.
Here is the core caveat before any numbers: every published in-vivo dose for SLU-PP-332 is a mouse dose. There is no human titration schedule, no human pharmacokinetic study, no human safety margin, and no FDA-approved label. Dosing figures circulating in the research community are either human-equivalent-dose extrapolations from mouse protocols or vendor-driven capsule suggestions with no primary-source backing.
The table below summarizes the published murine regimens researchers actually cite, plus the two unvalidated community dosing patterns that show why the human-dose question remains unresolved.
Billon 2023 - Endurance
15 days
25 mg/kg IP once daily
Increased treadmill endurance and induced an acute aerobic exercise transcriptional signature in muscle.[1]
Billon 2023 - Chronic
28 days
50 mg/kg IP twice daily
Raised oxidative muscle fibers and OXPHOS complex proteins, with longer running distance before exhaustion.[1]
Billon 2024 - DIO mice
28 days
50 mg/kg IP twice daily
Reduced fat mass, improved glucose tolerance, and lowered triglycerides in diet-induced obesity.[2]
Billon 2024 - ob/ob mice
12 days
50 mg/kg IP twice daily
Improved metabolic markers in the ob/ob model using the same BID dosing framework.[2]
Xu 2024 - Heart failure
6 weeks
IP dosing per Burris-lab standard
Improved ejection fraction, reduced fibrosis, and increased survival in the TAC model.[4]
Wang 2023 - Aging kidney
8 weeks
25 mg/kg IP once daily
Reduced albuminuria, preserved podocin, and restored mitochondrial function in aging kidney tissue.[5]
Community patterns
Unvalidated
250 mcg-1.5 mg oral QD or ~650 mg/day HED math
Low-dose vendor capsule protocols and high-dose HED extrapolations differ by roughly 500-1000x, highlighting how unresolved human dosing remains.
Protocol Notes
Evidence quality: The published dosing above comes from Tier 1 primary murine publications. It is accurate for the mouse models described, but it should not be mistaken for a validated human regimen.
Pattern A - Low-dose oral capsule: Typical capsule products come in 250 mcg, 500 mcg, 1 mg, 5 mg, 10 mg, or 20 mg strengths. Community protocols suggest 250 mcg to 1.5 mg once daily, often justified with a simple 'start low, see how you feel' logic. There is no primary-source efficacy data supporting those human doses, and oral bioavailability has not been formally published.
If you convert the published 100 mg/kg/day mouse dose to an 80 kg human using standard allometric scaling, the human equivalent lands around ~650 mg/day. This is the pattern sometimes cited by biohacker commentators. It has no safety data whatsoever and sits orders of magnitude above vendor capsule protocols.
Missed dose guidance: With no published human half-life, there is no validated missed-dose rule. In murine BID protocols, doses were spaced about 12 hours apart; community oral users generally omit a skipped dose rather than doubling up.
Cycling: Published murine studies ran 2-8 weeks continuously. Community protocols often use 8-12 weeks on and 4 weeks off, but the rationale for cycling remains theoretical because long-term receptor desensitization has not been measured.
Timing and route: Morning dosing is common in community use because of circadian metabolism. Oral absorption in humans is under-characterized, and all published efficacy data used IP injection in mice. If you compare oral and injectable use, understand that the published literature will not resolve bioavailability for you.
Here is how much water to add to a SLU-PP-332 vial and what dose to draw afterward. SLU-PP-332 is a small molecule, not a peptide, so it behaves somewhat differently in solution than a typical lyophilized peptide. Published lab preparations often use DMSO-containing vehicles for animal work, while community reconstitution protocols usually use bacteriostatic water for subcutaneous research use.
Math shown: Concentration in mcg/mL = total compound in mcg divided by water volume in mL. U-100 syringe units = volume in mL x 100. Example: 5 mg vial + 2 mL water = 5,000 mcg / 2 mL = 2,500 mcg/mL. A 500 mcg dose is 500 / 2,500 = 0.20 mL = 20 units on a U-100 insulin syringe.
Capsule note: Many vendors now sell SLU-PP-332 as oral capsules in 250 mcg to 20 mg strengths. If using capsules, there is no reconstitution required. The table above applies to injection vials only.
Vial Size: 5 mg
BAC Water Added: 1.0 mL
Concentration: 5.0 mg/mL (5,000 mcg/mL)
250 mcg: 5 units (0.05 mL)
500 mcg: 10 units (0.10 mL)
1 mg: 20 units (0.20 mL)
5 mg: 100 units (1.00 mL)
Vial Size: 5 mg
BAC Water Added: 2.0 mL
Concentration: 2.5 mg/mL (2,500 mcg/mL)
250 mcg: 10 units (0.10 mL)
500 mcg: 20 units (0.20 mL)
1 mg: 40 units (0.40 mL)
5 mg: Full vial
Vial Size: 5 mg
BAC Water Added: 3.0 mL
Concentration: 1.67 mg/mL (1,667 mcg/mL)
250 mcg: 15 units (0.15 mL)
500 mcg: 30 units (0.30 mL)
1 mg: 60 units (0.60 mL)
5 mg: -
Vial Size: 10 mg
BAC Water Added: 2.0 mL
Concentration: 5.0 mg/mL (5,000 mcg/mL)
250 mcg: 5 units (0.05 mL)
500 mcg: 10 units (0.10 mL)
1 mg: 20 units (0.20 mL)
5 mg: 100 units (1.00 mL)
Vial Size: 10 mg
BAC Water Added: 5.0 mL
Concentration: 2.0 mg/mL (2,000 mcg/mL)
250 mcg: 12.5 units (0.125 mL)
500 mcg: 25 units (0.25 mL)
1 mg: 50 units (0.50 mL)
5 mg: -
Vial Size: 20 mg
BAC Water Added: 5.0 mL
Concentration: 4.0 mg/mL (4,000 mcg/mL)
250 mcg: 6.25 units (0.0625 mL)
500 mcg: 12.5 units (0.125 mL)
1 mg: 25 units (0.25 mL)
5 mg: 125 units (1.25 mL)
The honest bottom line: there is no human safety data for SLU-PP-332. No Phase 1 trial has been conducted, no human pharmacokinetic study has been published, and no incidence percentages for human side effects exist. Everything below comes from either mouse studies at preclinical doses or uncontrolled community observations.
In the Billon 2023 and Billon 2024 studies, mice dosed at 25-50 mg/kg IP for up to 28 days showed no overt toxicity, no sickness-related weight loss, no liver-enzyme signal at the doses tested, and no cardiac dysfunction.[1][2] In the Xu 2024 heart-failure study the compound improved cardiac function rather than worsening it, and in the Wang 2023 kidney study it was renoprotective rather than nephrotoxic.[4][5]
Serious adverse events: No serious adverse events have been reported in any published rodent study of SLU-PP-332 at the doses and durations tested. No long-term toxicology study beyond 12 weeks has been published in any species.
Discontinuation and washout: No published discontinuation rates exist because there are no human trials. The short exposure window observed in mice suggests washout may be relatively fast, but that remains an animal-PK inference rather than a human fact.
For a cross-class safety comparison, see the PepPal Peptide Side Effects Guide.
Here is a straightforward table of the four major published in-vivo studies of SLU-PP-332. These are all animal studies - there are no human trials to report.
Billon et al., ACS Chem Biol 2023 [1]
Preclinical in vivo • 15-28 days
C57BL/6J mice (n = 8-10 per group)
25 mg/kg IP for 15 days increased treadmill endurance; 50 mg/kg BID for 28 days raised oxidative muscle fibers and OXPHOS proteins.
Billon et al., JPET 2024 [2]
Preclinical in vivo • 12-28 days
DIO C57BL/6J and ob/ob mice (n = 7-8 per group)
50 mg/kg BID reduced fat mass, lowered cholesterol and triglycerides, reduced adipocyte size, and improved glucose tolerance.
Xu et al., Circulation 2024 [4]
Preclinical in vivo • 6 weeks
C57BL/6J mice, pressure-overload TAC heart-failure model
Improved ejection fraction, reduced fibrosis, and increased survival, with effects mediated mainly via ERRgamma in cardiomyocytes.
Wang et al., Am J Pathol 2023 [5]
Preclinical in vivo • 8 weeks
Aged mice, aging-kidney model
25 mg/kg/day reduced albuminuria, preserved podocin, and reversed mitochondrial dysfunction and inflammation.
Status as of April 2026: there is still no registered human trial for SLU-PP-332 on ClinicalTrials.gov.[11] The compound remains a preclinical research tool. The 2024 Circulation paper is the most advanced translational study so far because it showed functional benefit in a clinically relevant heart-failure model, but translating from mouse IP dosing to a human oral or subcutaneous regimen still requires a Phase 1 PK and safety study that has not been initiated.
For context, the fat-mass reductions reported in Billon 2024 - roughly 25-30% in diet-induced obese mice over 28 days without exercise - are large for a preclinical metabolic agent and explain why the 'exercise mimetic' label stuck.[2] But until human PK and safety work exists, all efficacy claims should be treated as mouse-only.
SLU-PP-332 is a small molecule rather than a peptide, so it is generally more stable than fragile lyophilized peptides at ambient conditions. Storage still depends on whether you are holding dry powder, a BAC-water solution, oral capsules, or a laboratory DMSO stock.
Lyophilized / powder form
-20 C (-4 F)
Long-term storage
Lyophilized / powder form
2-8 C (36-46 F)
Weeks to months
Reconstituted solution
2-8 C (36-46 F)
Typically 2-4 weeks
Oral capsules
Cool, dry room temperature
Per vendor expiration
DMSO stock solution
-80 C or -20 C
Up to 6 months at -80 C or 1 month at -20 C
Protect reconstituted solutions from light, avoid freeze-thaw cycles, and keep oral capsules in a cool, dry, dark location. For laboratory DMSO stocks, aliquot before storage so repeated thawing does not degrade the compound.
These three compounds are often discussed together because they all show up in metabolic and fat-loss research conversations, but they are not interchangeable. SLU-PP-332 is the nuclear-receptor-level lever, MOTS-c is the mitochondrial peptide with AMPK-linked signaling, and AOD-9604 is a GH-fragment-derived lipolysis tool.
Class
SLU-PP-332: Synthetic small-molecule pan-ERR agonist
MOTS-c: Mitochondrial-derived peptide (16 aa)
AOD-9604: Modified GH fragment (aa 176-191)
Primary target
SLU-PP-332: ERRalpha / beta / gamma nuclear receptors
MOTS-c: AMPK activation and mitochondrial signaling
AOD-9604: Lipolysis pathways without GH-receptor signaling
Half-life
SLU-PP-332: Not formally published; 6-hour exposure seen in mouse plasma/muscle
MOTS-c: ~3 hours (mouse plasma)
AOD-9604: ~2-4 hours (rodent data)
Dosing frequency
SLU-PP-332: BID preclinical; QD community oral
MOTS-c: Daily SC, often 5 days on / 2 off
AOD-9604: Daily SC
Max studied dose
SLU-PP-332: 50 mg/kg BID (mouse, 28 days)
MOTS-c: 5-15 mg/kg (mouse)
AOD-9604: 1-5 mg/day in human Phase 2
Peak efficacy metric
SLU-PP-332: ~25-30% fat-mass reduction in DIO mice over 28 days
MOTS-c: Improved insulin sensitivity in aged mice
AOD-9604: Modest fat-loss signal in human Phase 2, then failed primary endpoint
Route in humans
SLU-PP-332: Oral capsule or SC in community use; no validation
MOTS-c: SC in community use; no human efficacy trials
AOD-9604: SC in clinical trials
FDA status
SLU-PP-332: Not approved; no human trials
MOTS-c: Not approved; no native human trials
AOD-9604: Not approved for fat loss; Phase 2 failed primary endpoint
Unique advantage
SLU-PP-332: Only pan-ERR agonist with demonstrated in-vivo exercise-mimetic activity
MOTS-c: Endogenous mitochondrial peptide with AMPK-focused signaling
AOD-9604: Most human clinical history of the three
These compounds are not interchangeable. [SLU-PP-332](/protocol/slu-pp-332) is the nuclear-receptor-level lever, directly switching on the exercise transcriptional program. [MOTS-c](/protocol/mots-c) works further downstream through AMPK, while [AOD-9604](/protocol/aod-9604) belongs to a different fat-loss category altogether.
If "exercise mimetic" is the goal, SLU-PP-332 is the class-defining compound. If "mitochondrial signaling in aging" is the goal, MOTS-c is the literature favorite. If "clinical trial history" matters, AOD-9604 is the only one with Phase 2 human data. Also worth keeping in the same conversation is Tesamorelin, which works through the GHRH -> GH -> IGF-1 axis rather than ERR signaling.
See the MOTS-c protocol, AOD-9604 protocol and Tesamorelin protocol for compound-specific guides.
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There is no human-validated starting dose. Published murine studies used 25-50 mg/kg IP once or twice daily. Two community protocols circulate: a low-dose oral approach (250 mcg to 1.5 mg once daily) and a high-dose approach extrapolated from mouse HED math (hundreds of milligrams daily). These two patterns differ by roughly 500-1000x, which tells you how unresolved the dosing question is.
A formal human pharmacokinetic half-life has not been published. In the Billon 2023 paper, mice given 30 mg/kg IP still showed measurable plasma and muscle concentrations at 6 hours post-injection, which helps explain why twice-daily dosing was used in efficacy studies.[1]
From the published mouse data: increased treadmill endurance within 15 days at 25 mg/kg IP, fat-mass reduction of roughly 25-30% over 28 days at 50 mg/kg BID in diet-induced obese mice, improved glucose tolerance and lower triglycerides, improved cardiac function in heart-failure mice, and reduced kidney inflammation in aged mice.[1][2][4][5] Human results are not established.
For a standard 5 mg injection vial, add 2 mL of bacteriostatic water for a 2,500 mcg/mL concentration, where a 500 mcg dose equals 20 units on a U-100 syringe. For other vial sizes and concentrations, use the reconstitution table above or the PepPal reconstitution calculator.
No. SLU-PP-332 is not approved by the FDA for any indication. It is a research chemical with no registered or completed human clinical trials as of April 2026.
There is no human side-effect dataset. Published mouse studies did not report overt toxicity, liver-enzyme issues, or sickness-related weight loss at 25-50 mg/kg IP for up to 8 weeks.[1][2][5] Community reports describe mild appetite suppression or sleep disturbance in some users, but these are uncontrolled observations.
SLU-PP-332 works at the nuclear-receptor level through ERRalpha / beta / gamma. MOTS-c is a mitochondrial-derived peptide with AMPK-linked signaling, and AOD-9604 is a GH-fragment-derived lipolysis compound. SLU-PP-332 has the strongest preclinical exercise-mimetic signature of the three, but zero human clinical data.
For injection vials, 5 mg is the most common format, with some suppliers also offering 10 mg. For oral capsules, 250 mcg, 500 mcg, 1 mg, 5 mg, 10 mg, and 20 mg strengths are common.
For a 5 mg vial, 2 mL of BAC water gives a workable 2,500 mcg/mL concentration. Some users prefer 1 mL for smaller injection volume or 3 mL for easier low-dose measurement. There is no single correct answer - choose the concentration that gives you clean syringe-unit math.
In published mouse studies, 50 mg/kg IP twice daily for 28 days is the highest-dose, longest-duration regimen reported in peer-reviewed literature.[2] Human equivalent dose extrapolation from that protocol lands around 650 mg/day for an 80 kg adult, but no human has been studied at any dose in a published trial.
Store reconstituted SLU-PP-332 at 2-8 C, protected from light, and avoid freeze-thaw cycles. Because it is a small molecule rather than a peptide, it may be somewhat more stable in aqueous solution than fragile peptides, but formal stability studies for community reconstitution protocols have not been published.
There is no clinical trial program as of April 2026. ClinicalTrials.gov has no registered Phase 1 or later studies for SLU-PP-332, so the compound remains a preclinical research tool.[11]
~3 hours
Mitochondrial Peptide
View protocol~2-4 hours
GH Fragment / Lipolysis
View protocol~20-40 minutes; IGF-1 effect sustained
GHRH Analog
View protocolVariable
Cofactor / Mitochondrial Support
View protocol~6 days
Triple Agonist (GLP-1/GIP/Glucagon)
View protocol~7 days
GLP-1 Agonist
View protocolConvert this protocol into exact units and save it in Pep Pal with the peptide reconstitution calculator.
The information on this page is for educational and research reference purposes only. SLU-PP-332 is an experimental research compound with no FDA-approved indication and no human clinical trial program. No compounds discussed on this site are intended for human consumption. This is not medical advice.
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