SLU-PP-915
ERR-alpha selective agonist
SLU-PP-915 (ERR-alpha selective agonist) is a metabolic & fat loss research compound. A more ERR-alpha-selective analog of SLU-PP-332, from the same St. Louis University series. Estrogen-related receptors are orphan nuclear receptors that sit at the top of the mitochondrial biogenesis program — agonizing them upregulates oxidative metabolism and fatty acid oxidation, which is why the class gets called an 'exercise mimetic'. The selectivity is the point: SLU-PP-332 hits ERR alpha, beta and gamma, and the beta/gamma activity is where a lot of the cardiac concern sits.
SLU-PP-915 quick facts
| Reported research dose | 50mg-180mg (.5mg-2.6mg/kg, oral) |
| Route | Oral (in rodent studies) |
| Frequency | Not established — no dosing protocol has been characterized |
| Half-life | Not characterized in humans |
| Forms | Oral |
| Evidence level | Preclinical (rodent) only |
Genuinely interesting pharmacology and genuinely untested in people. There are no human trials, no human dosing, no human safety data and no way to know whether the rodent fat-loss effect transfers. ERR-alpha is heavily expressed in cardiac tissue, so 'more selective' does not automatically mean 'safer' — it means the risk profile is different and equally unmeasured. If you want the mechanism this is chasing, resistance training and zone 2 do it with a known safety profile.
How SLU-PP-915 works
A more ERR-alpha-selective analog of SLU-PP-332, from the same St. Louis University series. Estrogen-related receptors are orphan nuclear receptors that sit at the top of the mitochondrial biogenesis program — agonizing them upregulates oxidative metabolism and fatty acid oxidation, which is why the class gets called an 'exercise mimetic'. The selectivity is the point: SLU-PP-332 hits ERR alpha, beta and gamma, and the beta/gamma activity is where a lot of the cardiac concern sits.
Proposed benefits
Researched for fat oxidation, appetite and energy regulation, insulin sensitivity and endurance capacity.
Where to get SLU-PP-915
Buy SLU-PP-915 at Disguised Alpha →The evidence for SLU-PP-915
Graded by what exists behind each claim.
Human clinical evidence
- No human trials: development stopped at preclinical, so the ceiling on any claim here is a rodent model — and these transfer poorly.
📊 Correlative data
- Newer than SLU-PP-332 and with an even thinner record — there is essentially no practical use to report, and what circulates is extrapolation from the earlier compound rather than experience with this one.
- Beyond that the record is self-reported: community dosing logs are real information about tolerability and almost none about efficacy.
🧪 How the mechanism reads
- A selective ERRα agonist, developed from the SLU-PP-332 scaffold specifically to improve on it — better selectivity for ERRα over ERRβ and ERRγ, and improved pharmacokinetics.
- Reported to increase thermogenesis and drive conversion of white adipose toward a beige, thermogenic phenotype in rodent work.
- Selectivity is the design case and the untested claim. ERRγ is highly expressed in cardiac tissue, so sparing it is the argument for a better safety margin — which is a prediction from receptor binding data, not a demonstrated outcome.
Why an empty tier is not a verdict → · What community dosing logs are worth →
How to read these tiers: they say how much human evidence exists, not how well something works — and ✗ flags harm, never a disappointing trial. How the evidence tiers work →
What SLU-PP-915 actually does
Start with the thing this site's own card gets wrong. SLU-PP-915 is not an ERR-alpha-selective analog of SLU-PP-332. Both primary papers say the opposite in their titles: the paper that introduced it describes a new chemical series of potent pan-ERR agonists Hampton 2023, and the paper that characterized it in vivo calls it a chemically distinct ERR pan-agonist Billon 2025. The doping-control laboratory that later profiled it uses the same word Moller 2026. It is not a selective compound and it is not an analog of 332 — it is a different chemical series that hits the same three receptors.
What those receptors are. ERR-alpha, ERR-beta and ERR-gamma are orphan nuclear receptors. Orphan means no endogenous ligand has been identified: they sit on DNA constitutively active, and what normally regulates their output is not a hormone but the availability of a coactivator — PGC-1-alpha, the protein exercise itself induces. Their target genes are the mitochondrial program: biogenesis, oxidative phosphorylation, fatty acid oxidation, the Krebs cycle Billon 2025.
That is a genuinely unusual place to put a drug, and the unusualness is the risk. With a normal receptor agonist you are amplifying a signal the body already sends. With an orphan receptor there is no natural ligand exposure to reason from — no physiological range, no known feedback loop that shuts it off, no ‘this is what a big meal does’ comparison. You are creating a signal that did not previously exist.
The read-out that makes the exercise claim concrete. Both 915 and 332 robustly induce Ddit4 (REDD1), a gene switched on by acute aerobic exercise, to levels matching or exceeding treadmill running depending on the muscle examined — and 915 synergizes with exercise training to push Ddit4 and mitochondrial genes higher still Billon 2025. That is a specific, named transcript with a direction, which is a great deal more than ‘upregulates oxidative metabolism’.
And the pan part has consequences in tissues nobody is buying it for. ERR-gamma is heavily expressed in heart. Pan-ERR agonists from this same series were shown to improve cardiac fatty acid metabolism and mitochondrial function in heart failure Xu 2023, and a related compound alleviated metabolic syndrome Billon 2023. Those are the arguments for the class. They are also the reason ‘more selective’ is not the right frame: this molecule engages the cardiac receptor by design.
Cell, rodent, human — and where it stops
Step one, chemistry and cells. A medicinal chemistry series was built and screened against all three ERR subtypes, and SLU-PP-915 was the compound identified out of it Hampton 2023. Potency at the receptors is where this molecule's evidence is strongest, and it is also where it stops being about a person.
Step two, rodents, with the parent compound. SLU-PP-332 produced an ERR-alpha-dependent acute aerobic exercise response and enhanced exercise capacity in mice Billon 2023; a related ERR agonist alleviated metabolic syndrome in mice Billon 2023; and pan-ERR agonists improved outcomes in rodent heart failure Xu 2023. Three separate phenotypes, one receptor family, all in mice.
Step three, rodents, with this compound, and the route is the whole result. Billon 2025 compared intraperitoneal injection with oral dosing in mice. Given by injection, 915 enhanced running distance and duration to about the same extent as 332. Given by mouth — which 332 cannot usefully be, because it is not orally bioavailable — it maintained comparable efficacy adjusted for systemic exposure. Read that qualifier carefully: the oral route works, and it delivers less.
Step four, humans: there is no step four. No phase 1. No human pharmacokinetics. No safety database. No dose. The most recent publication on the compound is a doping-control method Moller 2026 — an anti-doping laboratory working out which metabolites to look for in urine. When the analytical chemistry for catching people using a drug is published before any human has taken it in a trial, that tells you where this compound actually sits.
The obstacles, named one at a time. (1) Every efficacy read-out is running capacity in a mouse, and mouse running capacity is not a validated surrogate for anything in a person. (2) The mechanism runs through a transcriptional program whose composition differs by tissue, so the same drug is simultaneously a heart-failure candidate Xu 2023 and a metabolic-syndrome candidate Billon 2023; nobody has shown which program dominates in a healthy adult. (3) Because the receptor is orphan and constitutively active, there is no natural exposure ceiling to calibrate a human dose against. (4) The dose ranges circulating in the research-compound market — this site's own card lists 50 mg to 180 mg orally — are not derived from any published human study, because none exists.
SLU-PP-915 pharmacokinetics — how much of it actually gets in
The honest headline: there is no human half-life for this compound because no human pharmacokinetic study has been published. Everything below is either rodent data or the arithmetic that bounds what a person is doing.
The oral barrier is the reason this molecule exists. SLU-PP-332, the compound that established the pharmacology, lacks oral bioavailability Billon 2025. That is why the rodent exercise work was done by intraperitoneal injection. SLU-PP-915 was developed as an orally active member of the series, and in mice its oral efficacy matched the injected route only after adjusting for systemic exposure — meaning oral dosing reaches the receptor at a lower concentration than injection does, and the gap has never been quantified in a person.
What degrades it. The one metabolism study is an in vitro one, run for anti-doping purposes: Moller 2026 characterized the in vitro metabolism of both 332 and 915 in order to identify the metabolites a urine test should target. In-vitro metabolism of a small molecule means liver preparations — the cytochrome-P450 oxidation and conjugation screen that normally precedes a first human dose. So the metabolic fate has been mapped in a tube, for the purpose of catching users, and never in a person for the purpose of dosing one. That is an unusual order to do things in.
The arithmetic a reader can actually do. The community dose range on this card is 50 mg to 180 mg by mouth, roughly 0.5 to 2.6 mg/kg. The published rodent work is dosed in mg/kg in mice, and mice clear small molecules several-fold faster than humans per kilogram, so a naive mg/kg transfer overshoots rather than undershoots. Without a measured human half-life there is no way to know whether a once-daily schedule produces a single spike, a steady-state plateau, or accumulation — and those three have very different consequences for a drug that rewrites a mitochondrial gene program.
What would have to be true, and how you would know it was not
Four predictions. The compound has no human data, so all four are genuinely open, and the second one is the one that would stop someone.
1. If it is an exercise mimetic, capacity should rise without a change in training. Measure VO2 max or a fixed time-trial before and after 8 weeks with training volume held deliberately constant. Prediction: a measurable rise in VO2 or time to exhaustion with no increase in sessions. If capacity only improves in people who also trained harder, the mouse result did not transfer — and note Billon 2025 found synergy with training, which makes the confound the default rather than the exception.
2. The one that cuts against it: high-sensitivity troponin must not rise. This is a pan-ERR agonist and ERR-gamma sits in cardiac tissue; the same chemical series is being developed to remodel metabolism in failing hearts Xu 2023. Nobody has asked what that program does to a healthy one. Draw hs-troponin and a resting ECG at baseline, week 4 and week 12. Any rise, or any new arrhythmia, is the signal to stop — and there is no published safety database to reassure you against it.
3. Metabolic markers should move if the metabolic-syndrome result transfers. Billon 2023 is a mouse metabolic-syndrome paper. So in an insulin-resistant person: HbA1c, fasting insulin and a lipid panel at baseline and 12 weeks. Prediction: if the mechanism operates in humans, fasting insulin falls before HbA1c does, because HbA1c lags red-cell turnover by about 90 days. If someone reports better endurance and nothing on this panel moves at all, the endurance is not coming from the advertised mechanism.
4. The mechanistic biomarker is Ddit4 and it is reachable. In mice, 915 induces Ddit4 in muscle to levels matching treadmill running Billon 2025. In a person that is a vastus lateralis biopsy and a qPCR at 1 and 4 hours after a single dose. It is the one measurement that would confirm the drug is doing the thing it is sold as doing, and it has never been made.
What nobody has tested yet
Nobody has given this compound to a person under observation. That sentence is the page. There is no phase 1, no maximum tolerated dose, no human half-life, no food effect, no drug-interaction work, and no adverse-event denominator. Every dose in circulation was reasoned from mouse milligrams per kilogram by people who are also the experiment.
Nobody has measured an ERR target gene in human muscle after any ERR agonist. The whole class rests on transcriptional output, and the direct translation experiment is small: one oral dose, a muscle biopsy at 1 and 4 hours, qPCR for Ddit4 and a mitochondrial panel, against an exercise-only comparator. Ten people would produce more information about whether this class works in humans than currently exists.
Nobody knows what the cardiac program does in a healthy heart. Xu 2023 makes the case that driving cardiac fatty acid oxidation helps a failing heart. The untested inverse — whether the same shift is neutral, useful or harmful in a normal one, over months — is the experiment that matters most and is hardest to run. An echocardiogram with strain imaging before and after 12 weeks in twenty users would at least generate a signal.
Nobody has checked what is in the vials. Vendor listings for SLU-PP-915 do not even agree on its CAS registry number — at least two different registry numbers are in circulation for the same advertised compound. An independent identity and purity check on a handful of market samples, by nuclear magnetic resonance and mass spectrometry against the structure in Hampton 2023, is a one-afternoon experiment that nobody has published.
SLU-PP-915 — its own safety story, not its class's
The specific safety story here is that there is no safety story. Not ‘a reassuring one’ — none. No human has been dosed in a published study, so there is no adverse-event table, no laboratory-abnormality rate, no discontinuation rate, and no denominator against which to judge an anecdote. Every safety statement anyone makes about this compound, positive or negative, is an extrapolation from mice.
The mechanistically predicted risk is cardiac, and it is not hypothetical hand-waving. This is a pan-ERR agonist Hampton 2023 Billon 2025, and ERR-gamma is a cardiac receptor whose program the same chemical series is being deliberately used to change in heart failure Xu 2023. A drug potent enough to be a cardiac metabolic therapy in a sick heart is potent enough to be a cardiac intervention in a well one. Nothing about ‘pan’ makes that safer than ‘selective’ would; it makes it broader.
The second predicted risk is the one every mitochondrial up-regulator carries: you cannot switch it off. The natural control on ERR output is coactivator availability, which the body ties to actual energetic demand. A ligand bypasses that link, driving the oxidative program whether or not the demand exists. In rodents that reads as improved endurance over weeks. Over years, in a person, nobody has looked at all — and the tissues with the highest ERR expression are heart, skeletal muscle and kidney, not fat.
The practical risks. A validated urine detection method now exists Moller 2026, so any tested athlete using this will be caught, and the compound's presence in an anti-doping journal is itself evidence that use is running well ahead of evidence. And because the material is sold as a research chemical with inconsistent registry information, the person taking it cannot confirm that the powder is the molecule in the papers — which means even the mouse extrapolation may not apply to what is in the capsule.
Sources read for this page
- Hampton CS, Sitaula S, Billon C, Haynes K, Avdagic A, Wanninayake U, Adeyemi CM, Chatterjee A, Griffett K, Banerjee S, Burris SL, Schoepke E, Boehm T, Bess A, de Vera IMS, Burris TP, Walker JK. Development and pharmacological evaluation of a new chemical series of potent pan-ERR agonists, identification of SLU-PP-915.. Eur J Med Chem 2023 · PMID 37421886
- 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
- Billon C. 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. A Synthetic ERR Agonist Alleviates Metabolic Syndrome.. J Pharmacol Exp Ther 2023 · PMID 37739806
- Xu W, Billon C, Li H, Wilderman A, Qi L, Graves A, Rideb JRDC, Zhao Y, Hayes M, Yu K, Losby M, Hampton CS, Adeyemi CM, Hong SJ, Nasiotis E, Fu C, Oh TG, Fan W, Downes M, Welch RD, Evans RM, Milosavljevic A, Walker JK, Jensen BC, Pei L, Burris T, Zhang L. Novel Pan-ERR Agonists Ameliorate Heart Failure Through Enhancing Cardiac Fatty Acid Metabolism and Mitochondrial Function.. Circulation 2023 · PMID 37961903
SLU-PP-915 — safety, predicted from mechanism
Predicted from mechanism, not from a human safety trial. How that reasoning works →
What the mechanism predicts
Derived from the molecule, not a trial.
- These act on mitochondrial function, NAD+ availability, sirtuin signaling or cellular clearance. The honest prediction is that acute harm is unlikely and the interesting risks are theoretical and long-range — which is a different shape of risk, not an absence of one.
- Growth and clearance signals cut both ways. Anything that improves the efficiency of cell survival is also improving it for cells you would rather not keep. Anything that pushes clearance hard is doing so indiscriminately.
- The near-term, practical ones: NAD+ precursors and infusions commonly cause flushing and a strong sensation if pushed fast, and several compounds in this class are stimulating enough to disrupt sleep.
What has actually been reported
- Generally well tolerated at studied doses. NAD+ infusion discomfort is rate-dependent and resolves by slowing down.
- The human evidence is mostly short trials with surrogate endpoints — a marker moved, not a life changed. That is worth knowing before you build a decade-long habit on it.
How to reduce the risk
Same mechanism as the prediction.
- Slow the infusion rate. Almost all NAD+ discomfort is rate, not dose. There is no prize for finishing quickly.
- Dose earlier in the day. Several of these are subtly stimulating, and sleep is where most of the repair you are paying for happens.
- Pick an endpoint you can actually measure, and take the baseline before you start. This is the class most prone to spending years on something with no way of knowing whether it did anything.
- Fix the basics first. Sleep, training and bloodwork move the same markers further than anything on this list, and they are free. A longevity compound stacked on four hours of sleep is a rounding error.
What it does to your bloodwork
A fact about the assay.
- There is no NAD+ assay worth ordering clinically. Judge this class on downstream markers — inflammatory markers, lipids, fasting glucose, and whatever your baseline panel showed as out of range.
Don't run this if
- Active malignancy, for the survival-signaling reasoning above.
- Pregnancy — uncharacterized.
The honest unknown
- Whether any of it extends healthspan in humans. Every honest person in this field is running on mechanism and animal data, and this catalog should say so rather than imply otherwise.
Not medical advice. If you take prescription medication or have a diagnosed condition, check this with a pharmacist or doctor.
SLU-PP-915 — interference & stacking
Predicted from mechanism, not from an interaction study. How mechanism-predicted claims are made →
What SLU-PP-915 moves on your bloodwork
Expected direction, not a measured one.
- hs-CRP (High-Sensitivity C-Reactive Protein) — ↓ expected to fall
Where these work, systemic inflammation is the plausible readout.
What to do: hs-CRP is cheap and moves. Baseline and 12 weeks. - HbA1c (Hemoglobin A1c) — ↓ expected to fall
Improved mitochondrial and metabolic function should show here if the effect is real at all.
What to do: The honest use of these markers is as a falsification test: if nothing moves in 12 weeks, the compound is not doing much for you. - Comprehensive Metabolic Panel (CMP) — ◆ worth watching
Liver and kidney function — the standard baseline for anything run long term.
What to do: Twice a year is enough on a stable protocol.
This class is where honest expectation-setting matters most: the markers above are how you find out whether anything happened, and for most of these compounds that question is genuinely open.
- How to work up to it, and when not to
- When to take it, and why that window
- Cycle length
- Time off between cycles
- Fasted or fed, and when in the day
- Coach Cam's personal notes
- Which compounds push the same lever, and why the dose adds up faster than people count
- What blunts it — the stacks that waste your money
- What compounds the risk, so a side effect arrives sooner than any one of them suggests
- Coach Cam's read on running it alongside the rest of your protocol
Everything above is free and stays free. Skool is where it becomes a plan — SLU-PP-915 in an order, with the rest of what you're running.
Unlock in Skool — $10/mo →Bloodwork to run alongside SLU-PP-915
Baseline first, then again at 8–12 weeks.
| Marker | What it’s watching for |
|---|---|
| HbA1c (Hemoglobin A1c) | Where you started, so you can prove the change was real |
| Fasting Insulin | Moves years before HbA1c does — the earliest signal you get |
| Lipid Panel (Cholesterol, HDL, LDL, Triglycerides) | Rapid fat loss shifts triglycerides fast, in both directions |
| Comprehensive Metabolic Panel (CMP) | Liver, kidney and electrolytes while intake is restricted |
The Metabolic Health & Prediabetes panel covers these in one order — 8 markers, $81.45 with the discount applied.
Check results you already have → · All 103 markers A–Z
SLU-PP-915 — frequently asked questions
What is SLU-PP-915?
SLU-PP-915 (ERR-alpha selective agonist) is a metabolic & fat loss research compound. A more ERR-alpha-selective analog of SLU-PP-332, from the same St. Louis University series. Estrogen-related receptors are orphan nuclear receptors that sit at the top of the mitochondrial biogenesis program — agonizing them upregulates oxidative metabolism and fatty acid oxidation, which is why the class gets called an 'exercise mimetic'. The selectivity is the point: SLU-PP-332 hits ERR alpha, beta and gamma, and the beta/gamma activity is where a lot of the cardiac concern sits.
Is the full SLU-PP-915 protocol on this page?
The reported research dose is on this page, along with how SLU-PP-915 works and the evidence behind it. The protocol — how to work up to it, frequency, cycle length, time off, what not to stack it with and Coach Cam's notes — is inside Skool.
What is the half-life of SLU-PP-915?
SLU-PP-915 has an approximate half-life of Not characterized in humans, which is part of what determines how often it's dosed.
What's the evidence behind SLU-PP-915?
Current evidence level: Preclinical (rodent) only. SLU-PP-915 is offered for research purposes only and is not an approved medicine.
What SLU-PP-915 is used for
SLU-PP-915 appears under 2 goals in the goal router.
Related Metabolic & Fat Loss compounds
Where this goes next
The pages here are the frameworks. The protocols — the dosing, the order to correct things in, the week-by-week schedule and what to retest — are inside Skool.