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 analogue 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 programme — agonising 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 characterised |
| Half-life | Not characterised 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 analogue 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 programme — agonising 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.
Human clinical evidence
- No human trials. It never left preclinical development, so the ceiling on what anyone can claim is a rodent model — and rodent models of this endpoint have a poor record of transferring.
📊 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 nothing at all about efficacy: nobody posts the cycle where they felt no different, so what survives is a filtered sample that will always look better than the truth.
🧪 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.
These tiers tell you how much human evidence exists — not how well something works. This is the research space, and most of what’s in here is new rather than disproven. Something sitting at “theoretical” usually means nobody has funded the trial, not that the trial was run and failed.
The trap runs the other way too: something can be clinically validated and still do very little for you specifically. A statistically significant result in a study population is not a promise about your body.
- ✅ Clinically validated — human randomised trials or meta-analyses support it. The strongest footing available.
- 📊 Correlative — observational or epidemiological data. Suggestive, and genuinely useful for direction, but it cannot establish cause.
- 🧪 Theoretical / mechanistic — the mechanism is understood and often demonstrated in cells or animals, and the human trial doesn’t exist yet. Unproven is not the same as ineffective. Plenty of what’s standard practice today sat here five years ago.
✗ is a safety flag, not a grade. Where you see it, the concern is harm — not a disappointing trial. A compound tested for one purpose and found not to help there can still be worth studying somewhere else, so a negative result never gets rendered as a cross. It sits alongside the tier, because something can be both well-studied and genuinely risky.
My job is to tell you which one you’re looking at, and let you make the call. Grading something low isn’t me dismissing it — it’s me refusing to oversell it. This is the research space, and being able to reason forward from a mechanism matters as much as waiting for the trial.
SLU-PP-915 — safety, predicted from mechanism
Much of this compound class has never been through a human safety trial. Rather than say nothing — or print a generic warning — this is what its known mechanism predicts could go wrong, and what you can do about it. Predictions are labelled as predictions.
What the mechanism predicts
Derived from what this molecule does, not from a trial.
- These act on mitochondrial function, NAD+ availability, sirtuin signalling 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
Each of these follows from the 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, not a guess about the drug.
- 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-signalling reasoning above.
- Pregnancy — uncharacterised.
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 catalogue 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.
Where to get SLU-PP-915
Buy SLU-PP-915 at Disguised Alpha →SLU-PP-915 — interference & stacking
Predicted from mechanism, not from an interaction study. There are no trials of these combinations — what follows is what the biology implies, so treat it as a reason to watch something, not as a finding.
What SLU-PP-915 moves on your bloodwork
These are the markers this compound is expected to move, and which direction. Knowing that in advance is mostly about NOT panicking: some of these moving is the compound working.
- 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.
- 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
Get the complete breakdown for SLU-PP-915 — inside the Academy alongside the full interactive Vault.
Unlock in the Academy — $10/mo →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
Get the complete breakdown for SLU-PP-915 — inside the Academy alongside the full interactive Vault.
Unlock in the Academy — $10/mo →Bloodwork to run alongside SLU-PP-915
Run these before you start, and again after 8–12 weeks. A baseline you didn’t take is one you can never go back for.
| 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 102 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 analogue 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 programme — agonising 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 the Academy.
What is the half-life of SLU-PP-915?
SLU-PP-915 has an approximate half-life of Not characterised 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.
Want Coach Cam's exact SLU-PP-915 protocol?
Dosing schedules, stacking, cycle timing and my personal notes live inside the Academy — plus the full interactive Vault of 237 compounds & 350 supplements.
Join the Academy — $10/mo →What SLU-PP-915 is used for
SLU-PP-915 appears under 2 goals in the Vault’s goal router, grouped by the mechanism it works through rather than by how much trial evidence exists. Each link opens that pathway in full, with the alternatives beside it and the bloodwork that tests it.