The Longevity Desk
12 min readMitochondria

SLU-PP-332: The Mice Got It Injected Into the Abdomen, and It Is Sold as a Capsule

The mice really did run about 70 percent longer, and the people who made the compound have written in print that it does not get from the gut into the blood.


What it is

SLU-PP-332 is not a peptide, whatever shelf it is sold from. It is a small synthetic molecule of 290.3 daltons, PubChem entry 5338394, CAS number 303760-60-3, with no amino acids in it and no peptide bonds. The chemists took GSK4716, a GlaxoSmithKline compound that switches on two of the three estrogen related receptors but not the third, and redesigned it for the one it was missing, gaining fifty fold potency there. (PMID 36988910)

Those receptors, written ERRα, ERRβ and ERRγ, are proteins inside the cell nucleus that switch on the genes for building new mitochondria, for burning fat, and for the chemical loop that turns food into cellular fuel. They are called orphan receptors, because no natural substance that switches them on has been identified, and despite the name they are not estrogen receptors. The compound turns all three on and is too blunt to separate them.

Three of its authors disclose that they hold stock in a company built on this receptor family. Correct behaviour, and still worth knowing.

What the trials found

I could find no trial in the sense of people. What follows is four mouse studies, every one injecting the compound into the abdominal cavity, the space the organs sit in.

Billon and colleagues published the primary paper in ACS Chemical Biology in 2023. Six male C57BL/6J mice per arm, 12 weeks old, got 50 mg per kilogram or a dummy injection once a day for six days, then ran on a treadmill. The treated animals ran about 70 percent longer, and their fatigue resistant muscle fibres increased. In mice with the alpha receptor deleted from skeletal muscle, at 25 mg per kilogram for 15 days, five per group, that gain did not appear. The only pharmacokinetics in the paper, meaning where the compound goes once it is in the body, is one tissue distribution experiment in a handful of mice: no half life, no peak concentration, no bioavailability figure, nothing by mouth. (PMID 36988910)

The obesity paper followed a year later: twenty week old males fattened for eight weeks on a 60 percent fat diet, then 50 mg per kilogram twice daily for 28 days, seven per group. The untreated mice put on about 5 grams of fat, the treated ones less than 0.5 grams. That is fat gained, not fat lost, and on ordinary chow the same dosing moved body weight not at all. (PMID 37739806)

Two more, same route. Xu and colleagues, Circulation 2024: six weeks at 25 mg per kilogram twice daily improved survival in mice with heart failure, and I could find no group size for it (PMID 37961903). Wang and colleagues, American Journal of Pathology 2023: eight weeks at 25 mg per kilogram a day reversed age related kidney changes in 21 month old mice, five to six per group (PMID 37717940).

Then the searching. PubMed returns ten records unfiltered and none at all with the clinical trial filters applied, and the American and European registers return nothing, for the compound or for the receptor class. Go and run it: open ClinicalTrials.gov and search SLU-PP-332. This site has found forged registry records before, and here there is no record at all, real or fake.

Whose evidence it is

Three substitutions are already in circulation, each moving evidence onto this compound from somewhere else.

One. The only paper I found with human beings in it gave the compound to none of them. Bonanni and colleagues enrolled twenty women having hip replacement surgery, took muscle tissue during the operation, grew muscle cells from the tissue of the ten who reported being inactive, and put the compound on those cells in a dish. The title carries the words pilot study. Nothing here is easier to misread as a human trial. (PMID 40692696)

Two. The 2026 paper from the same laboratory says they previously developed SLU-PP-332, which improves aerobic performance in mice but lacks oral bioavailability, and then characterises SLU-PP-915, a chemically distinct compound that is orally available. Do not tidy that into a story about chemists going back to the bench after the capsule failed. 915 was in print in the 2024 heart failure paper and named alongside 332 in 2021. (PMID 41421047)

Three. The line about these receptors being essential for muscle adaptation to aerobic exercise, the basis of the whole exercise mimetic idea, comes from genetics rather than from this drug. Seller pages run the receptor biology and the compound data together so the weight of the first lands on the second, and the 2026 metabolite papers from two anti-doping laboratories, run in liver enzyme preparations rather than in people, get read the same way. They exist so a urine test can be built. (PMID 41688415, PMID 41588687)

How it compares

The comparison worth making is against what the World Anti-Doping Agency does name. I searched the full 26 page 2026 Prohibited List: the strings "SLU", "estrogen-related receptor" and "exercise mimetic" appear nowhere in it.

On the 2026 Prohibited List
SLU-PP-332Not named, and neither is its receptor family
AICARNamed by example, as an activator of AMPK
MOTS-cNamed on the same line, also as an AMPK activator
GW501516Named by example, as a PPAR delta agonist
SR9009 and SR9011Named by example, as Rev-erb alpha agonists

The last row is the interesting one. SR9009 and SR9011 came out of the same senior author's laboratory as this compound, Thomas Burris's, aimed at a different nuclear receptor. An earlier series from that laboratory got onto the list by name and this one has not. Several seller pages state flatly that SLU-PP-332 is listed as a metabolic modulator. That is not what the document says, though it does carry a catch all section reaching anything in development with no approval anywhere.

Where the dose came from

Nowhere I could find. No approved labelling, and no human dose finding study.

What is sold does not agree with itself. One seller lists capsules at 250 micrograms and another at 50 milligrams under a research use only disclaimer, two hundred fold apart on the label, and a third sells 5 mg of freeze dried powder in a vial for injection. That is a disagreement about what the thing in the capsule is.

The protocol pages are no steadier. One carries three incompatible regimens at once, reported here as convention, not recommendation: 250 to 1,500 micrograms a day under the skin, 1 to 5 mg a day under the skin, and 400 to 800 mg a day by mouth. The same page concedes that whether the compound survives gastric acid in people is not established.

I could find no published derivation, so I ran the standard conversion myself. Using the regulator's body surface area factors, the mouse regimen of 100 mg per kilogram a day comes out at roughly 570 mg a day for a 70 kilogram adult, inside that oral band. So the high number looks like scaling of a mouse dose, applied to a route its own inventors say does not work. The 250 microgram capsule sits about 2,300 times below it, derived from nothing I could find.

What could go wrong

The only toxicity assessment I found is ten days long: no obvious toxicity in mice at 50 mg per kilogram twice daily into the abdomen, with normal blood counts, normal electrolytes and a normal level of creatine kinase, an enzyme that leaks out of damaged muscle. That is an observation inside an efficacy study, not a toxicology package. Mice have been dosed for longer with no formal toxicology endpoints attached: six weeks at 25 mg per kilogram twice daily in the heart study, which did report increased survival, and eight weeks at 25 mg per kilogram a day in the kidney one. I could find no repeat dose toxicology study, no test of whether the compound damages DNA, no safety pharmacology work of the kind that precedes a first human dose, and no published human safety data at all. An empty file is not a clean one.

The receptor has been pursued in the opposite direction. A 2023 medicinal chemistry review covers inverse agonists at the alpha receptor, compounds designed to turn it down, and describes it as strongly expressed in breast cancer cells, with high levels linked to poor outcomes in one subtype, triple negative breast cancer. Whether that matters to someone taking a compound that turns the same receptor up is not established, and I found no study addressing it. (PMID 37190810)

And I could find no independent measurement of what is in the jars. The UCLA laboratory identified 22 breakdown products in liver preparations, the metabolites a liver makes of the compound, none I could find characterised for activity or toxicity, and the only certificates on grey market material come from the sellers.

What nobody knows

Whether swallowing it does anything at all in a person, which is the entire question for a product sold as a capsule. I could find no study measuring where a swallowed dose goes, in a person or in any other species. Whether either compound has an open application to begin human testing, since those filings are not public. And whether turning this receptor up for months is safe in a person.

My take

The capsule is what bothers me. Every other gap here is ordinary for a research compound: mouse data only, and a convention with no derivation behind it. This one is different. The sentence that undermines the product is the opening line of an abstract written by the people who invented the molecule.

Two hundred fold between two capsules of the same name is the second thing. A buyer cannot fix that by being careful, because there is no correct number to be careful about.

The mouse work itself I have no complaint with. Four studies, one species, every dose into an abdomen.

If you have seen SLU-PP-332 sold as a capsule, I want to know what strength was printed on the bottle, and whether the page said anything about how much of a swallowed dose reaches the blood.

Frequently asked

Has SLU-PP-332 been tested in humans?

I could find no study, published or registered, that gave SLU-PP-332 to a person by any route. The American and European trial registers return no record of it, and a literature search restricted to clinical trials returns nothing. The one published paper I found with human participants took muscle tissue from twenty women during hip replacement surgery and put the compound on cells grown in a dish from the tissue of the ten who reported being inactive, not on any of the women themselves.

Does SLU-PP-332 work if you swallow it?

The scientists who made it wrote in a 2026 paper that the compound lacks oral bioavailability, meaning it does not get from the gut into the blood, and the orally available molecule they describe is a chemically distinct compound called SLU-PP-915. I could find no oral bioavailability figure for SLU-PP-332 in any species and no human study of the swallowed route. Most of what is sold is a capsule.

How much did the mouse studies use?

Published mouse studies used 25 to 50 milligrams per kilogram of body weight, once or twice daily, injected into the abdominal cavity, for periods of six days to eight weeks. Those are mouse doses, given by a route I did not see any seller describe, and no human dose has been established in any study I could find.

Why is the same product sold at 250 micrograms and at 50 milligrams?

I do not know, and neither figure has a human study behind it. One seller lists capsules of 250 micrograms and another lists capsules of 50 milligrams under the same compound name, which is a two hundred fold difference on the label. The oral figures of 400 to 800 milligrams a day that circulate bracket the roughly 570 milligrams a day that a body surface area conversion of the mouse dose produces, which is arithmetic rather than evidence, and they are reported here as convention rather than as a recommendation.

Is SLU-PP-332 banned in sport?

It is not named on the World Anti-Doping Agency's 2026 Prohibited List, and neither is its receptor family. The list's catch-all section covers any substance in preclinical or clinical development with no approval from any health authority, which describes this compound, and two anti-doping laboratories published methods in 2026 for detecting it. Only an athlete's own anti-doping organisation can answer this question for them.

What are the side effects of SLU-PP-332?

I could find no published human safety data of any kind. The only toxicity assessment I could find is ten days in mice given 50 milligrams per kilogram twice daily into the abdominal cavity, which reported normal blood counts, normal electrolytes and a normal level of a muscle damage enzyme. Seller pages list fatigue, stomach upset, sleep changes and injection site reactions, and those are unsourced reports rather than trial findings.


This content is for educational and informational purposes only and is not medical advice. Peptides discussed are research compounds and may not be approved for human use. Nothing here should be used to diagnose, treat, cure, or prevent any disease. Always consult a qualified healthcare professional before starting any peptide, supplement, or protocol. Individual responses vary. Do not self-administer compounds without proper medical supervision.

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