Important limitations
- Safety Concerns & Translational Barriers: What still limits translation from animal research to human use
- Future Research: Where the field is likely heading next
SLU-PP-332
SLU-PP-332 is a synthetic small molecule rather than a peptide, developed in Thomas Burris's medicinal chemistry laboratory at Saint Louis University as the first usable.
Dosing & scaling, explained
No mass-based amount example with adequate calculation context is available for this compound. This is educational source context, not a protocol or recommendation.
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No independently verified schedule
Evidence context
No clinical amount or schedule is inferred from this material. Source verification is pending, and every displayed amount remains educational context rather than guidance.
Storage, handling and interpretation
Product identity
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Storage & handling
Follow the product label, certificate and validated laboratory SOP; no universal storage assumption is applied here.
Prepared solutions
Label concentration and preparation date, use sterile technique where applicable, and follow a validated stability protocol.
Reported protocols for SLU-PP-332
What published studies and recent community write-ups report about amounts, timing and course length. 3 preclinical and 3 community-reported rows, each linked to its source. These are descriptions of what others report, not instructions, and nothing here is medical advice.
| Context | Dose | Frequency | Route | Course | Source |
|---|---|---|---|---|---|
| Preclinical3 rows | |||||
| Preclinical exercise capacity and muscle remodellingThree-month-old male C57BL/6J mice, 6 to 8 per group | 50 mg/kg (30 mg/kg for the pharmacokinetic measurement) | Twice daily | Intraperitoneal injection in a DMSO and surfactant vehicle | 7 days before treadmill testing, 10 days for gene expression, 15 days for muscle histologyNot applicable | ACS Chemical Biology (PubMed Central)2023 |
| After 7 days of dosing, sedentary mice ran about 70% longer and 45% further than vehicle controls, and 15 days produced more oxidative type IIa fibres, more mitochondria and higher mitochondrial DNA content. At 2 hours after a 30 mg/kg dose, levels reached about 0.6 micromolar in skeletal muscle against 0.2 micromolar in plasma, and 10 days of twice-daily dosing produced no overt toxicity, normal blood counts and no change in creatine kinase. | |||||
| Preclinical diet-induced obesity model20-week-old male C57BL/6 mice kept on a 60% fat diet for 8 weeks beforehand, 7 per group | 50 mg/kg | Twice daily, timed to Zeitgeber time 0 and 12 | Intraperitoneal injection, with the high-fat diet maintained throughout | 28 daysNot applicable | Journal of Pharmacology and Experimental Therapeutics (PubMed Central)2024 |
| Treated mice weighed about 12% less after 28 days and gained under 0.5 g of fat mass against roughly 5 g in controls, with no difference in food intake and no loss of lean mass. Total cholesterol, HDL and triglycerides fell, liver enzymes did not rise, and fasting glucose and insulin were lower, with respiratory exchange ratio showing a shift toward fat as fuel. | |||||
| Preclinical leptin-deficient obesity modelThree-month-old male ob/ob mice on a chow diet, 8 per group | 50 mg/kg | Twice daily | Intraperitoneal injection at thermoneutrality | 12 daysNot applicable | Journal of Pharmacology and Experimental Therapeutics (PubMed Central)2024 |
| This arm was deliberately shortened from 28 days because the animals tolerated twice-daily intraperitoneal injection poorly, which is itself a limit on how far the regimen can be pushed. Total body weight only trended down over 12 days, but adiposity and liver weight fell significantly, with higher fatty acid oxidation and resting energy expenditure. | |||||
| Community-reported3 rows | |||||
| Community subcutaneous dosing chart | 500 mcg per day at the low end, 1 mg typical, 1.5 mg at the high end | Once daily, or split twice daily to mirror the mouse schedule | Subcutaneous from a lyophilised vial reconstituted with bacteriostatic water, 5 mg in 1 mL giving 5 mg/mL | 4-8 weeks4-8 weeks off | Community resource2026 |
| This 2026 chart is open about the arithmetic it is working from: body-surface-area scaling of the 25 mg/kg mouse dose lands near 140-160 mg per day for a 75 kg adult, so the community figures sit about a hundredfold lower, chosen for cost and caution. It states that either the low dose is producing real receptor activation or the reported effects are largely placebo, and that no published human pharmacokinetic data can settle it. | |||||
| Community oral tablet planning | One 30 mg capsule or 50 mg tablet per day, or a low-dose pattern of 250 mcg to about 1.5 mg daily | Once daily | Oral capsule or tablet | 8-12 weeks4 weeks off | Community resource2026 |
| Oral tablets are the most common consumer format, yet this guide notes that oral bioavailability in humans has never been published and that published murine work used intraperitoneal injection twice daily. It describes the cycling rationale as theoretical because long-term receptor desensitisation has not been measured in people. | |||||
| Community low-dose oral titration | 250 mcg per day to start, titrated toward 500 mcg or 1 mg | Once daily, in the morning or 30 to 60 minutes before cardio | Oral capsule | 8-12 weeksA break of similar length to the course | Community resource2026 |
| This 2026 overview explains that the low end of the range is reverse-engineered from the capsule sizes vendors happen to sell rather than from any dose-finding work. It points out that the human half-life has never been measured, that vendor pages quote anything from 1.5 to 16 hours with no published source, and that the cycling structure is a cautious instinct rather than an evidence-based protocol. | |||||
How a course is commonly described
- Week 1 in micePreclinical
Seven days of 50 mg/kg twice daily was enough to change treadmill performance in sedentary mice, so the functional effect arrives quickly at that exposure. Gene expression changes in muscle were measurable 3 hours after a dose.
- Days 7-14 of community useCommunity-reported
Community reports place a subjective endurance shift at 7 to 14 days and a body-composition signal at 3 to 4 weeks. There is no human pharmacokinetic study to anchor either claim, and the doses involved are roughly a hundredth of the scaled mouse equivalent.
- Day 28: the longest published exposurePreclinical
The 28-day obesity study is the longest continuous dosing on record, and it ended with about 12% lower body weight, almost no fat gain on a high-fat diet, lower fasting glucose and insulin, and no rise in liver enzymes. Nothing has been dosed longer than a month in any species.
- Weeks 8-12 and the breakCommunity-reported
Community courses run 4 to 12 weeks and then pause for a similar period. The stated reason is that ERR receptors are expressed in heart, liver, kidney and muscle and nobody has studied what sustained pan-agonism does in a person, so the break is a precaution rather than a finding.
- There is no human data of any kind: no registered trial, no published pharmacokinetics, no dose-finding work and no safety follow-up. Every human figure in circulation is extrapolated from mouse studies that used twice-daily intraperitoneal injection.
- The originating laboratory developed the successor SLU-PP-915 specifically because the parent compound lacks oral bioavailability, which contradicts the oral capsules and tablets sold as SLU-PP-332 and means the most popular route is also the least supported.
- SLU-PP-332 is not FDA-approved, is not on the list of bulk substances pharmacies may compound, and although it is not named on the 2026 WADA prohibited list, community and compound-reference sources advise athletes to treat an endurance-enhancing metabolic modulator as prohibited.
Sources for this section (8)
- Synthetic ERR alpha/beta/gamma Agonist Induces an ERR alpha-Dependent Acute Aerobic Exercise Response and Enhances Exercise Capacity
- A Synthetic ERR Agonist Alleviates Metabolic Syndrome
- An orally active estrogen receptor-related receptor agonist, SLU-PP-915, enhances aerobic exercise capacity
Plus 5 community resources (dosing guides, forum threads and vendor write-ups), reported above but not linked.
How SLU-PP-332 is being studied to work
This process map organizes available educational context. Individual claims remain subject to source-level verification.
- 1
Mechanism of Action
How SLU-PP-332 is thought to mimic parts of the exercise response
- Activates ERRα-related transcriptional programs
- Associated with increased PGC-1α signaling
- Supports mitochondrial biogenesis and respiration research
- Promotes fatty acid oxidation and energy expenditure pathways
Overview
SLU-PP-332 is a synthetic small molecule rather than a peptide, developed in Thomas Burris's medicinal chemistry laboratory at Saint Louis University as the first usable agonist of all three estrogen-related receptors. Because those receptors sit downstream of PGC-1 alpha and control mitochondrial biogenesis and fatty acid oxidation, the compound switches on much of the gene programme that aerobic training switches on, which is why it is described as an exercise mimetic. Every published study is in mice or cell lines: no human trial has been registered, there is no FDA approval or investigational application, and the compound does not appear on the FDA list of bulk substances that pharmacies may compound. It reached the research-chemical market after a 2023 conference presentation and is sold as oral tablets, capsules and occasional injectable preparations, despite the originating laboratory reporting that the parent compound lacks oral bioavailability.
What researchers are exploring
These themes organize the educational information currently available. Individual claims remain under source review and are not treatment claims.
- 1
Mechanism of Action
How SLU-PP-332 is thought to mimic parts of the exercise response
- 2
Preclinical Metabolic Research
Findings from obesity, glucose control, and fat metabolism models
- 3
Mitochondrial Function, Endurance & Exercise Mimicry
Why SLU-PP-332 is often described as an exercise mimetic
- 4
Cardiometabolic and Organ Research
Potential relevance to heart, liver, kidney, and brown adipose tissue research
What is known and what still needs verification
Available context is organized without assigning unsupported study models or evidence grades.
- Not graded
Research Status & Administration Notes
Important context about current evidence and why no dosing guide is presented
- Not graded
Mechanism of Action
How SLU-PP-332 is thought to mimic parts of the exercise response
- Not graded
Preclinical Metabolic Research
Findings from obesity, glucose control, and fat metabolism models
- Not graded
Mitochondrial Function, Endurance & Exercise Mimicry
Why SLU-PP-332 is often described as an exercise mimetic
Chemistry identifiers
Sequence, synonyms and registry identifiers as recorded in PubChem, the National Library of Medicine's open chemistry database. Formula, mass and CAS number are summarized at the top of the page.
Also listed as
SLU-PP-332, ERR pan-agonist 332, 4-Hydroxy-N'-(naphthalen-2-ylmethylene)benzohydrazide, CHEMBL4208749, UNII 5YW57G7ADL, SR9861, HY-155673, STK082756
InChIKey
RNZIMBFHRXYRLL-XDHOZWIPSA-N
IUPAC name
4-hydroxy-N-[(E)-naphthalen-2-ylmethylideneamino]benzamide
Limitations and unknowns
Sources
0 links carried over from the earlier page, awaiting verification.