ERR Pan-Agonist · Exercise Mimetic · Retired September 2026
Why We Retired SLU-PP-332
Rx Peps Direct stopped selling SLU-PP-332 on September 20, 2026. The Saint Louis University group that created the molecule reported that it improves aerobic performance in mice but lacks oral bioavailability, and built a different compound to get around that. Every form we sold was an oral capsule. This page stays up because the reasoning belongs on the record.
- Status
- Retired from the Rx Peps Direct catalog
- Retired
- September 20, 2026
- Reason
- Not orally bioavailable, per its developers
- Human trials
- Still zero
Our promise: We follow the evidence. When the lab that invented SLU-PP-332 published that it is not orally bioavailable, we retired our oral capsules and updated this page to explain why.
Medically reviewed by Dr. Jonathan Snipes, MD. Last reviewed September 20, 2026.On this page
The update
Why We Retired It
The sentence that ended this product is in a 2025 paper from Thomas Burris and colleagues, the lab behind the molecule. Introducing a successor compound, they describe the original in plain terms: it improves aerobic performance in mice but lacks oral bioavailability. That is not a rival group taking a shot. It is the inventors explaining why they had to build something else, and the something else, SLU-PP-915, is chemically distinct and was designed specifically to survive being swallowed.
Route of administration is not a detail. A swallowed drug has to get through the gut wall and then through the liver before it reaches the rest of the body, and the liver can clear most of a dose on that first pass. Separate work from an anti-doping laboratory, published in 2026, ran SLU-PP-332 through human liver preparations and identified nine metabolites: six phase-one transformations and three phase-two conjugates. Human liver tissue takes this molecule apart. The mouse studies that made SLU-PP-332 famous injected it, which skips that trip entirely.
The ERR biology is real and the mouse results are real. The limitation is delivery: every product we offer has to make sense in the form a patient receives it, and an oral capsule of a compound that does not survive oral delivery no longer met that standard. On September 20, 2026 we retired it.
2
SKUs retired: SLU-PP-332 and SLU-PP-332/BAM-15
9
Metabolites identified in human liver preparations
0
Human trials of SLU-PP-332, then and now
915
The successor its developers built to be orally active
Section 01
What SLU-PP-332 Actually Is
SLU-PP-332 is a synthetic small molecule, not a peptide. It was designed by chemists at Saint Louis University and the Burris lab (the SLU in the name stands for Saint Louis University) and first described in 2023. Its job is narrow and specific: it activates the estrogen-related receptors, a family of three orphan nuclear receptors called ERRalpha, ERRbeta, and ERRgamma. These receptors are master switches for mitochondrial metabolism and for the genes muscle turns on in response to aerobic exercise.
That is why SLU-PP-332 gets called an exercise mimetic. In the original work, a single dose triggered an ERRalpha-dependent gene program in mouse muscle that looks like the program triggered by an acute bout of aerobic exercise, and treated mice ran farther and longer than untreated mice. Follow-up work in obese mice showed increased energy expenditure, more fat oxidation, and less fat mass. The mechanism is real and the animal data is consistent.
What SLU-PP-332 has not done is be tested in a single human being. There is no clinical trial, no published human pharmacokinetics, no human safety data, and no FDA approval for any use. Everything claimed about endurance, fat loss, or metabolic health in people is an extrapolation from mouse and cell studies. That is the single most important fact on this page.
3
ERR subtypes targeted (alpha, beta, gamma); highest potency at ERRalpha
2023
Year SLU-PP-332 was first characterized (ACS Chem Biol)
0
Human trials completed or published to date
Retired
Pulled from the Rx Peps Direct catalog on September 20, 2026
Section 02
Who It Was Studied For
Every row in this table is a hypothesis drawn from the animal mechanism, not a tested indication in people. It is kept here for reference and is not a recommendation.
| Profile | Primary Motivation | Evidence Basis | Fit |
|---|---|---|---|
| Endurance and Exercise Capacity Seeker | Improve aerobic capacity and fat oxidation | Mouse running-endurance data. No human data. | Hypothesis Only |
| Recovery / Limited-Mobility User | Capture exercise-like adaptations when training is limited by injury | Mechanistically plausible, animal-only, never trialed for this use. | Exploratory |
| Metabolic / Body-Composition User | Fat loss, energy expenditure, glycemic support | Obese-mouse metabolic data. No human metabolic data. | Speculative |
| Longevity / Biohacking User | Mitochondrial and aging-pathway benefits | Extrapolated from cell and animal mitochondrial work. | Speculative |
| Athlete Subject to Anti-Doping Testing | Performance support during training | Already flagged by anti-doping labs as a doping-potential compound. | High Risk, Confirm First |
Profile
Primary Motivation
Evidence Basis
Fit
Profile
Primary Motivation
Evidence Basis
Fit
Profile
Primary Motivation
Evidence Basis
Fit
Profile
Primary Motivation
Evidence Basis
Fit
Profile
Primary Motivation
Evidence Basis
Fit
Section 03
How SLU-PP-332 Works
SLU-PP-332 is a pan-agonist of the ERR family, with its strongest activity at ERRalpha. When it binds these receptors, it drives a transcriptional program centered on mitochondrial biogenesis, oxidative phosphorylation, and fatty acid oxidation. In animals, that program overlaps with the one acute aerobic exercise produces.
ERRalpha-Dependent Gene Program
In mouse muscle, SLU-PP-332 induced an acute aerobic-exercise gene signature that depended specifically on ERRalpha, including Ddit4, a gene that acute exercise switches on. Knock out the receptor and the endurance benefit disappears, which is how the researchers tied the effect to the target.
Mitochondrial and Fat-Oxidation Drive
In a skeletal-muscle cell line, SLU-PP-332 increased mitochondrial function and cellular respiration. In obese mice it raised energy expenditure and fatty acid oxidation. The throughline is metabolism: the molecule pushes cells toward burning fuel oxidatively.
Oxidative Fiber Shift
Treated mice showed an increase in type IIa oxidative muscle fibers, the fatigue-resistant fiber type endurance training favors, alongside improved running distance and duration. This is a structural adaptation, not just an acute signal.
Autophagy via TFEB
A separate cardiac study found ERR agonists induce TFEB, a master regulator of the autophagy-lysosome recycling pathway. This is part of why the receptor family is being explored for heart failure and aging, all of it still in animal and cell models.
Section 04
What the Evidence Shows
This is the section that decides whether SLU-PP-332 is right for you, because the entire evidence base is preclinical. Here is the actual published record, in order, with the species made explicit every time.
| Study | Model | Key Finding | Strength |
|---|---|---|---|
| Billon 2023 (ACS Chem Biol) [1] | Cells and mice | Identified SLU-PP-332 as an ERR pan-agonist; induced an ERRalpha-dependent acute-exercise gene program, increased type IIa fibers, and enhanced running endurance in mice. | Foundational, Preclinical |
| Billon 2024 (JPET) [2] | Diet-induced obese mice | Increased energy expenditure and fatty acid oxidation, reduced fat mass, and improved insulin sensitivity in metabolic-syndrome models. | Animal Metabolic |
| Losby 2024 (Mol Pharmacol) [3] | Cardiomyocytes and rodent cells | ERR agonists induce autophagy through TFEB, a mechanism relevant to heart failure and aging. Mechanistic, cell-level. | Mechanistic, Preclinical |
| Billon 2025 (JPET) [4] | Mice | Built SLU-PP-915 because SLU-PP-332 lacks oral bioavailability; the orally active successor matched its exercise-mimetic activity by mouth in mice. | Highlights the Oral Gap |
| Moller 2026 (Rapid Commun Mass Spectrom) [5] | Human liver fractions, in vitro | Characterized SLU-PP-332 metabolites for anti-doping detection, explicitly framing it as a compound with doping potential. | Anti-Doping Flag |
| de Souza-Lima 2026 (Rev Med Chil) [6] | Systematic review | Reviews the pan-ERR agonist field and concludes the strategy is promising but states plainly that clinical trials are still needed to confirm efficacy and safety in humans. | Review, Calls for Trials |
Study
Model
Key Finding
Strength
Study
Model
Key Finding
Strength
Study
Model
Key Finding
Strength
Study
Model
Key Finding
Strength
Study
Model
Key Finding
Strength
Study
Model
Key Finding
Strength
Section 05
Realistic Expectations
We cannot give you a human timeline because there are no human studies to draw one from. What follows is framed honestly as a reasonable-monitoring schedule, not a promise of results. If you and your prescriber decide to proceed, this is the lens to evaluate it through.
No Reliable Felt Effect
SLU-PP-332 acts on a gene-expression program, not on a receptor that produces an immediate sensation. Expect to feel nothing obvious early. In animals the effects are metabolic and structural, the kind of change that would accrue quietly rather than announce itself.
Watch, Do Not Assume
If anything translates to humans, this is the window to start paying attention to perceived exercise capacity and recovery. Track it honestly, because expectation effects are powerful and there is no placebo-controlled human data to separate signal from belief.
Reassess With Your Prescriber
A sensible point to check in. If you are seeing nothing meaningful, that is fully consistent with the absence of human evidence and is a reason to stop, not to push the dose higher.
Course Decision Point
Decide with your prescriber whether to continue, pause, or stop. Because long-term human safety is entirely uncharacterized, shorter, supervised courses are the conservative default.
Side Effects and How to Manage Them
There is no human safety data for SLU-PP-332. None. The side effects below are extrapolated from mouse studies and the known pharmacology of ERR agonism. They are informed inferences, not clinical findings. This matters, both because it should inform your decision to start, and because it means your provider cannot tell you how common any of these events are.
| Side Effect | Frequency | When | Mitigation |
|---|---|---|---|
| GI discomfort (nausea, loose stools) | Unknown: animal data only | First 2 to 4 weeks | Take with food. Animal studies showed GI tolerance at therapeutic doses; human GI response is entirely uncharacterized. |
| Fatigue or muscle weakness | Unknown: animal data only | Weeks 1 to 4 | Mitochondrial activation can produce adaptation symptoms. Track energy weekly. Report persistent or worsening fatigue. |
| Liver enzyme elevation | Unknown: no human metabolic data | Ongoing | Baseline LFTs and follow-up at 4 and 12 weeks are required given the absence of human pharmacokinetic data. Report any jaundice, right-side abdominal pain, or dark urine immediately. |
| Unknown long-term risks | Uncharacterized: no human data exists | All timeframes | Not a known risk: an unknown risk. Your provider set a monitoring schedule specifically because we cannot predict what we have not yet observed. |
Side Effect
Frequency
When
Mitigation
Side Effect
Frequency
When
Mitigation
Side Effect
Frequency
When
Mitigation
Side Effect
Frequency
When
Mitigation
Section 08
Safety and Side Effects
The honest safety statement is short: there is no human safety data for SLU-PP-332. In animal studies it was tolerated without obvious toxicity, but animal tolerability does not establish human safety, and no formal toxicology in people has been done. Everything below is precautionary.
| Consideration | Detail | Action |
|---|---|---|
| No human safety data | Tolerability is known only from rodent studies | Treat as investigational. Use only under clinician supervision. |
| Metabolic and cardiovascular effects | ERR agonism touches energy metabolism and cardiac pathways | Share your full cardiac and metabolic history with your prescriber. |
| Pregnancy / lactation | No safety data | Avoid. |
| Anti-doping tested athletes | Already characterized by anti-doping labs as a doping-potential agent | Confirm status with your governing body before use. Treat as high risk. |
Consideration
Detail
Action
Consideration
Detail
Action
Consideration
Detail
Action
Consideration
Detail
Action
Weekly Self-Monitoring Protocol
Your monitoring log is not a formality. With no human clinical data, systematic tracking of your response is the only way Rx Peps Direct can detect patterns. Report anything that changes, including things you do not think are related.
| Metric | Frequency | Tool | Signal to Report |
|---|---|---|---|
| Energy and exercise tolerance (0-10) | Weekly | Phone note | Unexpected fatigue worsening beyond week 4, or inability to maintain normal exercise: report immediately |
| GI symptoms (nausea, bloating, stool changes) | Weekly | Phone note | Persistent GI symptoms beyond week 2: discuss timing or dose adjustment |
| Systemic symptoms (jaundice, dark urine, fatigue with abdominal pain) | Any occurrence | Clinical assessment | STOP the protocol. Contact provider or emergency care immediately |
Metric
Frequency
Tool
Signal to Report
Metric
Frequency
Tool
Signal to Report
Metric
Frequency
Tool
Signal to Report
Section 11
Legal Access in 28 States + DC
503A Licensed Pharmacy
Licensed U.S. 503A compounding pharmacy
Clinician Prescription Required
Compounded medication, Rx only
Investigational Compound
Preclinical only, no FDA approval
Compounded, Not FDA Approved
Prescribed patient-specifically under Section 503A
SLU-PP-332 is an investigational compound. It has not been studied in humans and is not FDA-approved for any indication. In the United States it is available through 503A patient-specific compounding under a prescription. The 503A pathway is the documented legal route for compounded access. Rx Peps Direct prescribers serve patients in 28 states plus Washington, DC. Athletes subject to testing should note that anti-doping authorities are already tracking this compound.
Section 12
Community Q&A
Is there any human data on SLU-PP-332?
No. There are zero human trials. Every published result is from mice or cultured cells, and the foundational studies come from the lab that designed the molecule. Treat all human benefits as hypothesis, not fact.
Does SLU-PP-332 replace exercise?
No. In mice it turned on some of the same genes acute aerobic exercise turns on and improved running endurance. That is not the same as replacing the cardiovascular, neurological, and musculoskeletal benefits of training, and it has never been tested in a person. Best thought of as a tool studied alongside exercise, not a substitute.
Is it banned for drug-tested athletes?
Treat it as high risk. Anti-doping laboratories have already characterized SLU-PP-332 specifically and built methods to detect it and its metabolites. Exercise mimetics fall under the metabolic-modulator category that anti-doping programs watch closely. Confirm with your governing body before use.
Why did you stop selling it?
Because it is not orally bioavailable and every form we sold was an oral capsule. The research group that created the molecule reported in 2025 that SLU-PP-332 improves aerobic performance in mice but lacks oral bioavailability, which is why they built a chemically distinct, orally active successor, SLU-PP-915. We retired both SLU-PP-332 SKUs on September 20, 2026. The reason is absorption, not safety.
How long is a course?
There is no trial-derived course length, because there are no trials. Rx Peps Direct courses are kept short and supervised, with your prescriber reassessing before any extension, precisely because long-term human safety is uncharacterized.
Section 13
The Rx Peps Direct Model
Pharmacy: Licensed U.S. 503A
A licensed U.S. 503A compounding pharmacy compounds every Rx Peps Direct prescription under a patient-specific order, USP <797>standards, and federal 503A oversight. SLU-PP-332 is no longer among the products we send them.
Medical Service: Rx Peps Direct Clinicians
A licensed clinician reviews your history, screens for contraindications, designs your protocol, and writes your prescription. Rx Peps Direct bills the $39 medical review for this service.
Transparent Safety Communication
When the developing lab published that SLU-PP-332 lacks oral bioavailability, we retired the product and updated this page with the evidence, so anyone searching for it gets the facts.
Legal Access in 28 States + DC
Every shipment is a compounded prescription medication filled by a 503A licensed pharmacy under a prescription.
References
- Billon C, Sitaula S, Banerjee S, et al. Synthetic ERRalpha/beta/gamma Agonist Induces an ERRalpha-Dependent Acute Aerobic Exercise Response and Enhances Exercise Capacity. ACS Chem Biol. 2023. PMID: 36988910
- Billon C, Schoepke E, Avdagic A, et al. A Synthetic ERR Agonist Alleviates Metabolic Syndrome. J Pharmacol Exp Ther. 2024. PMID: 37739806
- Losby M, Hayes M, Valfort A, et al. The Estrogen Receptor-Related Orphan Receptors Regulate Autophagy through TFEB. Mol Pharmacol. 2024. PMID: 39168657
- Billon C, Appourchaux K, Cote I, Burris TP. An orally active estrogen receptor-related receptor agonist, SLU-PP-915, enhances aerobic exercise capacity. J Pharmacol Exp Ther. 2025. PMID: 41421047
- Moller T, Krug O, Thevis M. In Vitro Metabolism and Analytical Characterization of SLU-PP-332 and SLU-PP-915: Novel Pan-ERR Agonists With Doping Potential. Rapid Commun Mass Spectrom. 2026. PMID: 41588687
- de Souza-Lima J, Astrosa-Martin BD, Galaz-Rodriguez CA, et al. Pharmacological Activation of ERRalpha/beta/gamma as an Exercise Mimetic: Potential Therapeutic Applications. Rev Med Chil. 2026. PMID: 42024694
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