SLU-PP-332: Dose, Evidence, and Why It Is Not a Peptide

Nuclear receptors sit inside the cell and switch genes on. Estrogen-related receptors (ERRα, ERRβ, ERRγ) are three of them, and despite the name they do not bind estrogen. They govern mitochondrial biogenesis, fatty acid oxidation, and the oxidative fiber program in skeletal muscle.

Picture the lighting board in a theatre. Endurance exercise walks along the board and pushes up a specific bank of sliders: mitochondrial genes, fat-burning enzymes, PGC-1α. SLU-PP-332 reaches over and pushes up one of those sliders directly, with nobody on stage. Literally: it binds ERRα and stabilizes the active conformation, transcribing a gene program that resembles the molecular signature of acute aerobic exercise (Billon et al., ACS Chem Biol, 2023).

That mechanism is real chemistry, verified in cells and in mice. It is also completely unlike how a peptide works. Peptides such as MOTS-c or BPC-157 are short amino acid chains that act on membrane receptors or signaling cascades. SLU-PP-332 is a 290-dalton lipophilic molecule that crosses into the nucleus. Selling it beside tirzepatide on a peptide storefront is a chemistry error, repeated until it became a search term.

"Exercise in a pill" is a headline written by science journalists in 2023. The compound is not a pill. It is not orally active, which is why the same lab built a separate, orally bioavailable follow-up (SLU-PP-915).

Two peer-reviewed studies carry the entire reputation of this compound. Both come from the Burris group. Both used mice.

Endurance (Billon et al., ACS Chem Biol, 2023;18(4):756-771). Untrained mice received 50 mg/kg by intraperitoneal injection, either once an hour before a treadmill test or twice daily for 10 days. Treated mice increased type IIa oxidative muscle fibers and ran measurably longer and farther than vehicle controls, without ever training.

Metabolic syndrome (Billon et al., J Pharmacol Exp Ther, 2024;388(2):232-240; PMID 37739806). Diet-induced obese mice received 50 mg/kg intraperitoneally twice daily for 28 days. Body weight fell roughly 12% versus vehicle. Fat mass gain over the study was under 0.5 g on drug against about 5 g on vehicle. Fatty acid oxidation rose about 25%, glucose tolerance improved, and hepatic triglycerides dropped. In leptin-deficient ob/ob mice dosed for 12 days, adiposity, liver weight, and hepatic steatosis all fell.

The safety observations in that paper amount to minor shifts in plasma cholesterol and liver enzymes with no frank hepatotoxicity, across 28 days, in mice. Pharmacokinetics: six hours after a single 30 mg/kg intraperitoneal dose, plasma exposure was 0.2 μM and muscle exposure 0.6 μM.

That is the complete efficacy record. No human dose-response curve exists. No human safety database exists. Nothing published tells you what SLU-PP-332 does to a person over eight weeks, because nobody has published it. Compare that to retatrutide, which has Phase 2 data in hundreds of humans, and the gap is not subtle. See how does retatrutide work.

Mice in both papers received 50 mg/kg twice daily, so 100 mg/kg per day. Converting animal doses to a human-equivalent dose uses body surface area, not body weight. The FDA's standard conversion divides the mouse dose by 12.3 (the ratio of the mouse Km factor of 3 to the human Km factor of 37).

Run the arithmetic. 100 mg/kg per day ÷ 12.3 = 8.1 mg/kg per day. For an 80 kg adult, that is roughly 650 mg per day, split into two doses of about 325 mg.

Now look at what the internet sells. The most repeated SLU-PP-332 dosage circulating on vendor blogs is 500 to 1,500 mcg per day subcutaneous. At the top of that range, 1.5 mg per day, you are taking about 430 times less than the surface-area-scaled equivalent of the dose that moved the needle in mice.

Both readings of that gap are bad. If 1.5 mg/day is meaningfully below any active threshold, buyers are injecting an unapproved research chemical for no pharmacological return, at $40 to $90 a vial. If it is active at that dose in humans, then human ERR pharmacology diverges wildly from mouse ERR pharmacology, and nobody has any idea where the ceiling is. There is no third possibility, because there is no human dose-response data to define one.

The fix: treat every published SLU-PP-332 dosing chart as a number someone invented, then reverse-engineered a justification for. Nobody titrated it in a person. If you want to see what a dose actually validated in humans looks like, read the retatrutide dosage escalation schedule or the peptide dosage chart.

Every efficacy number for this compound came from intraperitoneal injection, a needle into the abdominal cavity. Human medicine essentially never uses that route outside dialysis and certain chemotherapy. Zero published SLU-PP-332 data used subcutaneous injection, and every online protocol prescribes subcutaneous injection.

The solvent problem is worse. SLU-PP-332 has low aqueous solubility and lacks oral bioavailability, which the anti-doping literature states explicitly (Möller, Krug & Thevis, Rapid Commun Mass Spectrom, 2026;40(8):e70039). Peptides dissolve in bacteriostatic water because they are charged, water-loving amino acid chains. A naphthalene ring bolted to a hydroxybenzamide is greasy. It does not go into water the way semaglutide does.

So buyers add DMSO. DMSO is a powerful aprotic solvent and a tissue irritant; it also carries whatever else is dissolved in it straight across membranes, including contaminants from an unregulated vial. Subcutaneous injection of a DMSO-solubilized research chemical risks local irritation, injection-site necrosis, and systemic delivery of impurities that no certificate of analysis ever quantified.

A cloudy vial after adding bacteriostatic water is not "mixing wrong." It is the compound refusing to dissolve, and it means the volume you draw contains an unknown fraction of the labeled dose. If you have used our peptide reconstitution calculator for a real peptide, the math assumed full dissolution. That assumption fails here.

SLU-PP-332 is a pan-agonist. It does not select for muscle. It activates ERRα, ERRβ, and ERRγ in every tissue that expresses them, which includes heart, liver, kidney, and breast tissue.

ERRα is not a neutral target. Elevated ERRα expression associates with unfavorable biomarkers and worse prognosis in human breast cancer, while ERRγ associates with favorable ones (Ariazi, Clark & Mertz, Cancer Res, 2002;62(22):6510-6518). That is a statement about receptor biology. Whether SLU-PP-332 raises cancer risk in a human is unanswerable today, because no carcinogenicity study has ever been run on it.

Here is the timeline that should stop people. The longest published exposure to SLU-PP-332 in any species is 28 days, in mice. A typical online "cycle" is 8 to 12 weeks. At 12 weeks you are running an exposure three times longer than the longest experiment ever conducted on this molecule, in any animal, ever, while chronically agonizing a receptor with documented oncology associations.

Add the doping problem. Anti-doping laboratories have already built LC-HRMS/MS detection methods for SLU-PP-332 and its nine identified phase-I and phase-II metabolites (Möller, Krug & Thevis, Rapid Commun Mass Spectrom, 2026), with a parallel metabolite characterization published the same year (Avliyakulov et al., Drug Test Anal, 2026). WADA's S0 category prohibits any pharmacological substance not approved by any government health authority for human therapeutic use, at all times, in and out of competition. SLU-PP-332 sits squarely in S0. Tested athletes should read do peptides show up on drug tests.

The fix: if you are drug tested, this compound is a positive waiting for an assay rollout. If you are not, the exposure question remains unanswered and you are the experiment.

Most buyers glance at a certificate of analysis, see "99.2% purity," and stop. That number answers one narrow question and stays silent on four that matter more.

What HPLC purity actually means. High-performance liquid chromatography separates a sample and reports each peak as a percentage of total peak area. "99.2%" means 99.2% of the material that eluted and absorbed at the detector wavelength was one peak. It does not confirm which molecule that peak is.

Purity is not identity. Identity requires mass spectrometry matched against a reference standard, or NMR. Peptide vendors run HPLC-MS routinely. SLU-PP-332 is a small molecule, and a mass spec run without an authentic reference standard confirms a mass, not a structure. Ask whether the COA includes an MS trace and what standard it was compared against. Most cannot answer.

Purity says nothing about mass. A vial labeled 5 mg at 99% purity can contain 3 mg or 9 mg of powder. Assay by weight is a separate test. Almost no research chemical COA includes it.

Purity says nothing about sterility, endotoxin, or residual solvent. Nothing on a standard COA rules out bacterial endotoxin or leftover DMF, dichloromethane, or hydrazine from synthesis. Hydrazone chemistry starts from hydrazides. Residual hydrazine is genotoxic. No COA you will be shown tests for it.

Check the lot number. The COA must carry the same lot as the vial in your hand. A generic COA posted once on a product page and never updated tells you about a batch synthesized who knows when. If the lot does not match, the document describes someone else's powder.

Run the same skepticism on price. A 5 mg vial at $40 to $90 sits in the same range as legitimate research peptides, which tells you nothing about what is inside. Model total spend with the peptide cost calculator and read where to buy peptides in 2026 and the FDA peptide crackdown before you order anything from a research-chemical storefront.

One table, side by side. The left column is peer-reviewed. The right column is marketing.

Now place it against compounds with actual human evidence:

Two entries on that list are also small molecules dressed up as peptides. 5-Amino-1MQ is an NNMT inhibitor with the same evidence problem. We have flagged this pattern before with lipo-C, which is a MIC plus B12 blend, and pinealon, whose evidence base is preclinical and largely Russian. On these storefronts, the word "peptide" describes a shelf.

If endurance and mitochondrial function are the actual goal, the interventions with the most human support remain the boring ones: structured training, sleep, and the metabolic drugs carrying Phase 3 files. See peptides for recovery, peptides for energy, and peptides vs steroids for how these categories differ in evidence and risk.

Mistake 1: Calling it a peptide and reasoning from peptide rules. Peptide handling assumptions (dissolves in bacteriostatic water, degrades by proteolysis, subcutaneous depot absorption) all fail for a 290-dalton lipophilic small molecule. The consequence is a cloudy vial, an unknown drawn dose, and a solvent you did not plan for. The fix: treat it as a small-molecule research chemical, and stop using the peptide stacking guide logic on it.

Mistake 2: Believing a published dosing chart implies a validated dose. No SLU-PP-332 dose has ever been titrated in a human. Every chart online is either a scaled rodent number or a copied guess. The consequence: you are dosing 430x below the scaled effective dose, or somewhere unmapped above it. The fix: recognize that a confident table on a vendor blog is not evidence.

Mistake 3: Running 8 to 12 week cycles. The longest exposure in any published study is 28 days in mice. A 12-week run triples that, in a species with no toxicology data, on a receptor with oncology associations. The fix: nothing about this compound supports chronic use, and no protocol length is defensible from the literature.

Mistake 4: Assuming "research chemical" is a legal safe harbor. The label protects the seller, not the buyer. SLU-PP-332 is unapproved for human use anywhere, prohibited under WADA's S0 category, and sits in the exact market the FDA has been narrowing. Read are peptides legal and peptide therapy cost before treating any of this as routine.