SLU-PP-915
SLU-PP-915 scored 4.7 / 10 (⚖️ Neutral) on the BioHarmony scale as a Research chemical (ERR nuclear receptor agonist, exercise mimetic).
SLU-PP-915 is an orally active pan-ERR agonist, a later analog of the injection-only SLU-PP-332. Its one real advance is the oral route. Its own demonstrated effect is narrow, oral exercise-capacity parity with injected 332 plus a five-day brown-fat gene signal, and it has never been tested in a human.
What is SLU-PP-915?
SLU-PP-915 is an experimental compound that switches on the genetic programs endurance exercise normally triggers, by activating the estrogen-related receptors. In mice it improves aerobic capacity when taken by mouth.
It comes from the Burris lab at Saint Louis University, the same group behind SLU-PP-332, and 915 is the later analog. It belongs to a class marketed as exercise mimetics.
The reason 915 exists is the route. SLU-PP-332 has to be injected because it is poorly absorbed by mouth.
915 was built on a different chemical scaffold so it works orally while matching 332's effect on exercise capacity when exposure is adjusted (Billon et al. 2026). That oral route is the single real advance.
The 915-specific data is thin even for a preclinical compound. Its own demonstrated effects are oral exercise-capacity parity with injected 332 and a five-day brown-fat gene signal in mice (Johansen et al. 2025).
The richer story, fat loss, insulin sensitivity and body-weight reduction, belongs to 332, not 915 (Billon et al. 2024). Vendor copy that sells 915 as a proven fat-loss compound is borrowing 332's papers.
What does not exist, at all, is a single human. There is no pharmacokinetic study, no dose-finding, no safety data. It is sold only as an unregulated research chemical.
The score of 4.7 is not a verdict on the mechanism. It is a statement that a compound nobody has dosed in a person, with thin 915-specific animal data, cannot be recommended to one.
Terminology
A handful of terms decide how to read every claim about SLU-PP-915, and most of the confusion comes from blurring 915 with its older sibling. The single most important distinction is which compound a given finding actually used, because the weight-loss data belongs to one and the oral route to the other.
It also matters whether a result is a gene-expression readout in one tissue or a measured whole-body outcome, since almost everything on 915 is the first kind. The receptor vocabulary is worth having straight before weighing any selectivity claim.
- Estrogen-related receptors (ERRs): A family of orphan nuclear receptors, alpha, beta and gamma, with no known natural ligand, that drive mitochondrial and fat-burning gene programs.
- Pan-ERR agonist: A drug that activates all three ERRs rather than one. Primary sources describe 915 this way, at an EC50 near 400 nM.
- PGC-1alpha: The master coactivator of mitochondrial biogenesis that ERR agonism works through.
- Exercise mimetic: A compound meant to reproduce training adaptations pharmacologically. The marketing frame for the whole SLU-PP series.
- Ddit4 (REDD1): A stress-response gene induced in muscle by both 915 and treadmill running, used as a readout of the exercise program.
- Brown adipose tissue: The heat-producing fat depot where 915 induced the thermogenic gene Gpr3.
- Intraperitoneal (IP): Injection into the abdominal cavity, the route SLU-PP-332 needs and 915 was engineered to avoid.
- Oral bioavailability: How much of a swallowed dose reaches circulation. Improving it is the main advertised advance of 915 over 332.
SLU-PP-915 is orally bioavailable and enhances aerobic exercise capacity, matching intraperitoneally dosed SLU-PP-332 when adjusted for systemic exposure. Billon and colleagues, Journal of Pharmacology and Experimental Therapeutics
How do you take SLU-PP-915?
Dosing & Protocols
Dosing information is summarized from published research and community reports. This is not a prescribing guide. Consult a healthcare provider before starting any protocol.
Routes & Forms
| Route | Form | Clinical Range | Community Range |
|---|---|---|---|
| Oral | Powder, dissolved or in capsule (gray-market research chemical) | None established in humans The oral route matched injected SLU-PP-332 on exercise capacity in mice when adjusted for systemic exposure | Vendor and forum figures repackage mouse mg/kg, units and basis unverified There is almost no independent, non-vendor self-experimentation reported for 915 specifically |
| Injection (intraperitoneal) | Solution, animal research use | None established in humans 20 mg/kg twice daily for five days induced brown-fat thermogenic genes in wild-type mice | None Not a human route |
Protocols
Animal exercise-capacity protocol (reference only) Clinical
- Dose
- Oral and intraperitoneal, exposure-matched to injected SLU-PP-332
- Frequency
- Repeated dosing
- Duration
- Days to weeks
This is the mouse paradigm that produced exercise-capacity parity and muscle Ddit4 induction. It is not a human dose and cannot be scaled by body weight.
Animal thermogenesis protocol (reference only) Clinical
- Dose
- Roughly 20 mg/kg twice daily
- Frequency
- Twice daily
- Duration
- Five days
The short window that induced brown-fat Gpr3 and thermogenic genes. It is a gene-induction readout in one tissue, not a body-composition result.
How this score is calculated →
What are the benefits of SLU-PP-915?
Upside contribution: 1.09
| Dimension | Weight | Score | Visual | Weighted |
|---|---|---|---|---|
| Efficacy | 25% | 2.3 | 0.575 | |
| Breadth | 15% | 2.4 | 0.360 | |
| Evidence | 25% | 1.7 | 0.425 | |
| Speed | 10% | 2.5 | 0.250 | |
| Durability | 10% | 1.8 | 0.180 | |
| Bioindividuality | 15% | 2.0 | 0.300 | |
| Total | 2.090 | |||
| Baseline offset (constant) | −1.000 | |||
| Effective upside contribution | 1.090 |
Upside Rationale
The upside for SLU-PP-915 comes from one real advance and one narrow demonstrated effect. It is orally active where its predecessor needs injection, and in mice it improves aerobic exercise capacity through a coherent mitochondrial mechanism.
What the upside cannot include is human confirmation, a broad demonstrated benefit, or the fat-loss dataset that vendor copy borrows from 332. The dimensions below credit the oral route and the exercise signal while holding evidence and breadth low, because 915's own record is two studies.
Efficacy (2.3/5.0): 915's demonstrated effect is narrow. In mice it matched injected SLU-PP-332 on aerobic exercise capacity when exposure-adjusted, and induced the muscle gene program training normally triggers (Billon et al. 2026).
Efficacy is scored on the magnitude of the observed effect, and the honest observed effect for 915 is exercise-capacity parity plus one brown-fat gene readout. It stays low because that is a single-domain animal result with no human benefit to tie it to, and the larger fat-loss numbers are 332's, not 915's.
Breadth of Benefits (2.4/5.0): The mechanism is systemic, since every cell runs on mitochondria, but 915's own demonstrated endpoints are few. It has an exercise-capacity result and a brown-fat gene-induction result, and that is close to the whole 915-specific list (Johansen et al. 2025).
The metabolic-syndrome, insulin and weight breadth that makes the series look versatile is 332's dataset (Billon et al. 2024). Crediting 915 with that breadth would be crediting it with another compound's work.
Evidence Quality (1.7/5.0): 915's evidence is two primary studies plus supporting chemistry, all preclinical, which caps it hard. One shows oral exercise capacity, one shows a five-day brown-fat gene signal, and a third is analytical liver-metabolism work for doping detection (Moller et al. 2026).
There is not one human trial, no pharmacokinetic data in people, and no toxicology package. The evidence dimension asks how confident a real person can be that 915 will work for them, and with animal-only data on two endpoints the answer is very low.
Speed of Onset (2.5/5.0): In the thermogenesis study the gene response was measured after five days of dosing, and the exercise work used repeated dosing rather than a single dose (Johansen et al. 2025).
Because the mechanism is a transcriptional switch, some gene-level change appears within days, but a felt or measurable performance change in a person has never been timed because no person has been dosed. The score reflects a days-to-weeks mechanism discounted by the absence of any human onset data.
Durability (1.8/5.0): 915's benefit is a continuous signal, not a permanent change. ERR agonism drives gene programs only while the drug is present, so the effect should depend on ongoing dosing.
No washout or durability-after-stopping data exists for 915 in any species, so the expectation that the effect fades when dosing stops is inference from the mechanism rather than a measured finding. That places durability near the floor, where interventions whose benefit tracks continued use sit.
Bioindividuality Upside (2.0/5.0): Because the mechanism runs through mitochondria present in every cell, it should in principle apply broadly rather than to a narrow subgroup, which is a point in 915's favor.
But bioindividuality asks the odds a specific person responds, and with no human data there is no responder profile, no predictor and no variance estimate. The score reflects a plausibly universal mechanism offset by the complete absence of human evidence about who actually responds.
What are the risks & downsides of SLU-PP-915?
Downside contribution: 1.36 (safety risks weighted extra)
| Dimension | Weight | Score | Visual | Weighted |
|---|---|---|---|---|
| Safety | 30% | 2.8 | 0.840 | |
| Side effects | 15% | 2.2 | 0.330 | |
| Cost | 5% | 3.0 | 0.150 | |
| Effort | 5% | 1.6 | 0.080 | |
| Opportunity | 5% | 2.5 | 0.125 | |
| Dependency | 15% | 1.2 | 0.180 | |
| Reversibility | 25% | 1.3 | 0.325 | |
| Total | 2.030 | |||
| Harm subtotal × 1.4 | 2.345 | |||
| Opportunity subtotal × 1.0 | 0.355 | |||
| Combined downside | 2.700 | |||
| Baseline offset (constant) | −1.340 | |||
| Effective downside penalty | 1.360 |
Downside Rationale
The dominant downside for SLU-PP-915 is not a demonstrated toxicity. It is a mechanism that acts as a systemic metabolic switch with no established safe level, paired with a total absence of human data and a gray-market supply.
No intrinsic catastrophic effect has been shown, which keeps safety off the floor reserved for proven life-threatening compounds. But hepatic metabolism is confirmed with no liver-safety study, the cardiac pathway is untested in people, and dose accuracy from unregulated vendors cannot be assumed.
The dimensions below keep safety elevated while keeping demonstrated side-effect, dependency and reversibility concerns low.
Safety Risk (2.8/5.0): 915 has no demonstrated intrinsic catastrophic effect, which keeps it below the floor reserved for compounds with a proven life-threatening signal. The animal studies reported the intended metabolic effects without a flagged toxicity in their short windows.
What keeps safety elevated is an untested mechanism. Pan-ERR agonism has no established correct activation level in a living human, hepatic metabolism is confirmed with no hepatotoxicity study (Moller et al. 2026), and the cardiac fatty-acid pathway the mechanism touches has never been checked in a person.
Side Effect Profile (2.2/5.0): There is no human side-effect data to report, so this dimension reflects a mechanism-expected profile rather than a measured complaint rate. In the short animal windows, the studies described the target metabolic effects without a distinct toxicity syndrome.
The realistic human concerns, if 915 were ever dosed, would be the thermogenic and metabolic-rate effects of the mechanism rather than a specific proven organ toxicity, which places side effects toward the low end while acknowledging the profile is unmeasured.
Financial Cost (3.0/5.0): There is no legitimate channel to price, because 915 is neither an approved drug nor a supplement. The only route is a research-chemical vendor selling powder for laboratory use, which lands mid-range on the dollar figure but carries the no-legitimate-channel problem that pushes the score up.
A buyer pays an ordinary research-chemical price for a product with no manufacturing oversight and no guarantee it contains what the label claims, which is a poor value proposition regardless of the number on the invoice.
Time and Effort Burden (1.6/5.0): Oral dosing is simple in principle, a small daily commitment rather than an appointment or a procedure, and the oral route removes the injection burden that 332 carries.
Anyone using gray-market powder still has to weigh and prepare doses without an approved product. On balance this is a low-burden intervention to administer, with the caveat that self-preparation adds an error surface a labeled product would not.
Opportunity Cost (2.5/5.0): For endurance or body composition, 915 competes against better-evidenced options, from actual training and diet to approved metabolic drugs like semaglutide and tirzepatide, and against its own better-studied sibling SLU-PP-332.
Choosing an animal-only research chemical over any of those means accepting unknown risk for an unproven human benefit, which is a real opportunity cost even though 915 does not physically block other interventions. The score reflects concrete, better-established alternatives for the same goals.
Dependency and Withdrawal (1.2/5.0): 915 has no addictive mechanism, no craving, no tolerance and no withdrawal syndrome. It is a metabolic-gene manipulation, so stopping it simply returns the gene program toward baseline. The loss of benefit on stopping is a durability matter, scored above, rather than a dependency one. This places dependency at the floor.
Reversibility (1.3/5.0): 915 appears to act as a live transcriptional signal that stops when the compound clears, with no evidence of a permanent structural change and no taper described.
Because the mechanism is a switch rather than a lasting rewrite, stopping is clean in the sense that matters for this dimension. The score sits near the floor, with the honest caveat that clean washout is inferred from the mechanism and from mouse dosing rather than measured in people.
Is SLU-PP-915 worth it?
SLU-PP-915 is a real chemical advance on an interesting compound and one of the worse things a person could buy right now, and both come from the same fact. The oral route is a legitimate improvement over 332, and the 915-specific evidence behind it is two mouse studies.
The mechanism is coherent, the oral bioavailability is a published result rather than a marketing line, and the exercise-capacity parity with injected 332 is real in mice (Billon et al. 2026). That is where the good news stops.
There is no human data, no dose, no safety package, and the fat-loss story vendors attach to 915 actually belongs to SLU-PP-332. The more-selective claim is unverified. Score it as a compound to watch through its first real toxicology and human work, not one to source from a research-chemical vendor and dose by guesswork.
✅ Best for: Researchers and coaches tracking the ERR-agonist exercise-mimetic class who want a reference point for where oral 915 sits against injected 332. People who want the honest state of the 915-specific evidence rather than the vendor version that blends it with 332's fat-loss data.
Anyone comparing the SLU-PP series who needs the distinction between the two compounds drawn clearly. Writers and analysts covering the exercise-mimetic space who want the primary literature separated from the marketing.
❌ Avoid if: You are looking for a fat-loss compound to take, since 915's own data shows exercise capacity and one brown-fat gene, not weight loss, and no human has ever been dosed. You would be buying research-chemical powder, which carries no purity guarantee, no dose verification and no recourse.
You have any cardiac concern, since the mechanism touches cardiac fuel metabolism and has never been tested in a human heart. You are inclined to weight-scale a mouse dose to your own body, which is guesswork with no pharmacokinetic basis for 915 in people.
What is SLU-PP-915 best for?
The overall BioHarmony score reflects the intervention's primary evidence profile. These subratings are independent assessments per use case.
| Use Case | Score | Summary |
|---|---|---|
| ○ Endurance / Cardio Primary | 3.5 | The strongest 915-specific signal, and still mouse-only. Orally dosed 915 matched injected SLU-PP-332 on aerobic exercise capacity when exposure-adjusted, and induced muscle Ddit4 and mitochondrial genes that synergized with training (Billon et al. 2026). No human exercise data exists, which caps this well below 5.0. |
| ○ Body Composition / Fat Loss Primary | 3.0 | Extrapolated, not demonstrated for 915. Chronic fat-mass and body-weight reduction is an SLU-PP-332 finding (Billon et al. 2024); for 915 there is only a five-day brown-fat gene signal (Johansen et al. 2025), a plausible bridge but no body-composition study. |
| ○ Metabolic Health Primary | 3.0 | Insulin-sensitivity and glucose improvement belong to the 332 dataset (Billon et al. 2024), not to a dedicated 915 trial. Mechanistically shared, but 915-specific metabolic evidence is thin. |
| ○ Mitochondrial Primary | 3.5 | Direct mechanism. Pan-ERR agonism drives PGC-1alpha-coactivated mitochondrial biogenesis and oxidative phosphorylation, and 915 induced mitochondrial genes in muscle (Billon et al. 2026). Preclinical only. |
| ○ VO2 Max | 3.0 | Aerobic-capacity gains in mice imply an oxygen-uptake benefit, but no VO2 max was measured in any species and no human data exists (Billon et al. 2026). |
Frequently Asked Questions
Does SLU-PP-915 actually cause fat loss?
Not on any 915 data. The chronic body-weight and fat-mass reduction people cite is the SLU-PP-332 dataset (Billon et al. 2024), not 915. For 915 itself, the only adipose finding is a five-day brown-fat gene signal in mice (Johansen et al. 2025), which is upstream of any measured fat loss. Vendor copy that promises 915 fat loss is borrowing the 332 papers, not showing a completed 915 body-composition study.
How is SLU-PP-915 different from SLU-PP-332?
The one real advance is the route. SLU-PP-332 needs intraperitoneal injection because of poor oral uptake, and 915 was built on a different scaffold to be orally active while matching 332 on exercise capacity (Billon et al. 2026). Beyond the oral route, 915 has thinner evidence of its own. The weight-loss, insulin and energy-expenditure work all sits with 332, so calling 915 a straight upgrade overstates what has been shown.
Has SLU-PP-915 been tested in humans?
No. Every primary paper uses mice or mouse tissue, and no clinical-trial registration exists for 915 or 332. There is no human pharmacokinetic study, no dose-finding, and no safety margin. The only human-tissue work is a test-tube liver-metabolism study run to build anti-doping assays (Moller et al. 2026), which tells you the compound is metabolized in the liver and nothing about whether it is safe to take.
Is SLU-PP-915 more ERR-alpha selective than SLU-PP-332?
The selectivity claim is unverified. Some vendor blogs frame 915 as more ERRalpha-selective, but the primary and chemical-catalog characterization describes it as a pan-ERR agonist hitting alpha, beta and gamma at an EC50 near 400 nM (Billon et al. 2026). That is less potent than 332's reported ERRalpha figure, not more selective. Treat the more-selective framing as marketing until a primary selectivity paper confirms it.
Can you buy SLU-PP-915, and is it legal?
Only as an unregulated research chemical. It is not approved as a drug or supplement, so the only route is a gray-market vendor selling powder labeled not for human use. There is no pharmaceutical-grade product, no dose-verified capsule and no recourse if a vial contains the wrong thing. That sourcing risk sits on top of the fact that no human dose has ever been established, so any amount discussed online is guesswork from mouse figures.
What dose of SLU-PP-915 do people use?
There is no established human dose. The animal work used roughly 20 mg/kg twice daily over a short window (Johansen et al. 2025), and the exercise study exposure-matched oral to injected drug. Those numbers cannot be scaled to a person by body weight, and no allometric or pharmacokinetic justification for a human dose of 915 has been published. Any milligram figure sold or posted online is unsupported extrapolation, not a protocol.
Does SLU-PP-915 work as an exercise mimetic?
In mice, it improves aerobic capacity, and that is its best-supported effect. Orally dosed 915 matched injected 332 on exercise capacity and induced the muscle gene program endurance training normally triggers, synergizing with actual training (Billon et al. 2026). It does not replace training in the data, it amplifies a training signal. There is no human exercise-capacity study, so the exercise-in-a-pill framing remains a mouse finding, not a demonstrated human benefit.
Is SLU-PP-915 safe?
Nobody knows, because there is no toxicology package and no human exposure. The mechanism is a systemic metabolic switch with no established safe activation level, hepatic metabolism is confirmed with no liver-safety study (Moller et al. 2026), and there is no repeat-dose, genotoxicity or reproductive data. On top of the molecule, gray-market sourcing adds contamination and mislabeling risk. Treat every safety claim as unmeasured rather than reassuring.
What could change SLU-PP-915's score?
BioHarmony scores are living assessments. New research, regulatory changes, or personal context can shift the score up or down. These are the most likely scenarios that would change this intervention's rating.
The single event that would move 915's score is real 915-specific data in a higher species or a human, and it could move in either direction by roughly a point. A clean toxicology package plus a first human pharmacokinetic study would lift Evidence out of the floor and raise confidence toward Moderate.
A dedicated 915 body-composition study confirming the fat-loss bridge from the brown-fat signal (Johansen et al. 2025) would raise Efficacy and Breadth together.
Running the other way, a safety signal in the cardiac or hepatic pathway, or a first human study showing the mouse effect does not translate, would cut Efficacy and Evidence and drop it into caution.
| Scenario | Dimension shifts | New Score |
|---|---|---|
| A first toxicology package plus human pharmacokinetics land clean | Evidence 1.7 to 2.8, Safety 2.8 to 2.5, confidence Low to Moderate | 5.4 / 10 ⚖️ Neutral |
| A dedicated 915 body-composition study confirms the fat-loss bridge | Efficacy 2.3 to 3.2, Breadth 2.4 to 3.0, Evidence 1.7 to 2.4 | 5.6 / 10 ⚖️ Neutral |
| A primary paper confirms real ERRalpha selectivity over 332 | Efficacy 2.3 to 2.8, Evidence 1.7 to 2.2 | 5.1 / 10 ⚖️ Neutral |
| A first human exercise study confirms the mouse effect translates | Efficacy 2.3 to 3.4, Evidence 1.7 to 2.8, confidence rises | 5.9 / 10 👍 Worth trying |
| A cardiac or hepatic safety signal surfaces in a repeat-dose study | Safety 2.8 to 3.6, Evidence 1.7 to 2.2 | 4.1 / 10 ⚠️ Caution |
| The mouse effect fails to translate in an early higher-species study | Efficacy 2.3 to 1.6, Evidence 1.7 to 2.2 | 4.3 / 10 ⚠️ Caution |
📊 How BioHarmony Scoring Works
SLU-PP-915 upside total 1.09, downside total 1.360, giving a net of -0.27 and a score of 4.7 out of 10.Every intervention is rated 1 to 5 on six upside dimensions and seven downside dimensions, then weighted. A score of 5.0 out of 10 means the upside and the downside cancel out, not that the intervention is average. Harm-type downsides carry a 1.4 multiplier because a health risk is not interchangeable with a cost or an inconvenience; cost, effort and opportunity cost count at face value.| Upside dimension | Weight | SLU-PP-915 | |---|---|---| | Efficacy | 25% | 2.3 | | Breadth of benefits | 15% | 2.4 | | Evidence quality | 25% | 1.7 | | Speed of onset | 10% | 2.5 | | Durability | 10% | 1.8 | | Bioindividuality | 15% | 2.0 || Downside dimension | Weight | SLU-PP-915 | |---|---|---| | Safety risk | 30% | 2.8 | | Side effect profile | 15% | 2.2 | | Financial cost | 5% | 3.0 | | Time and effort | 5% | 1.6 | | Opportunity cost | 5% | 2.5 | | Dependency | 15% | 1.2 | | Reversibility | 25% | 1.3 || Tier | Range | Meaning | |---|---|---| | ✅ Top-tier | 8.8 to 10.0 | Worth building a routine around | | 💪 Strong recommend | 7.0 to 8.7 | Clear net benefit for most people | | 👍 Worth trying | 5.8 to 6.9 | Favourable odds, worth a personal test | | ⚖️ Neutral | 4.5 to 5.7 | Upside and downside roughly cancel | | ⚠️ Caution | 3.0 to 4.4 | Downside usually wins | | 🚫 Skip | 0.0 to 2.9 | Not worth it |
This report is informational and is not medical advice. SLU-PP-915 is an unapproved research chemical that has never been tested in humans. Nothing here is a recommendation to obtain or use it. Talk to your own clinician before making any change to medication or treatment.
BioHarmony Engine v2.0
Key Evidence Sources
- Billon et al. 2026, Journal of Pharmacology and Experimental Therapeutics: an orally active ERR agonist, SLU-PP-915, enhances aerobic exercise capacity. The primary 915 characterization. This 2026 study shows oral bioavailability, exercise-capacity parity with intraperitoneally dosed SLU-PP-332 when exposure-adjusted, muscle Ddit4 and mitochondrial gene induction, and synergy with exercise training in mice.
- Johansen et al. 2025, Molecular Metabolism: cold exposure induces the thermogenic receptor GPR3 via ERRalpha and ERRgamma, with SLU-PP-915 as the tool agonist. The 915-specific thermogenesis data point. In this study SLU-PP-915 at 20 mg/kg twice daily for five days induced brown-fat Gpr3 expression in wild-type mice via adipocyte ERRalpha and ERRgamma, reproducing part of the cold response without cold exposure.
- Moller et al. 2026, Rapid Communications in Mass Spectrometry: in vitro metabolism and analytical characterization of SLU-PP-332 and SLU-PP-915, pan-ERR agonists with doping potential. A 2026 analytical study identifying seven phase-I metabolites of 915 in human liver preparations to build anti-doping detection assays. It confirms hepatic metabolism occurs but is not a safety study and gives no signal on hepatotoxicity.
- Billon et al. 2024, Journal of Pharmacology and Experimental Therapeutics: a synthetic ERR agonist alleviates metabolic syndrome. The chronic body-weight, fat-mass, energy-expenditure and insulin-sensitivity dataset for the series, over 15 to 28 days in obese and ob/ob mice. Related compound, this is SLU-PP-332, cited to show where the weight-loss evidence actually lives rather than with 915.
- Billon et al. 2023, ACS Chemical Biology: a synthetic ERRalpha/beta/gamma agonist induces an ERRalpha-dependent acute aerobic exercise response and enhances exercise capacity. The foundational 2023 SLU-PP-332 study, reporting an ERRalpha EC50 of 98 nM and no mention of 915, which postdates it. Related compound, included for mechanistic context and as the series precursor 915 was engineered from.
- PubChem CID 142532359: SLU-PP-915 compound record, molecular formula C17H13BFNO3S. The authoritative structural and identifier record for 915, confirming the fluorinated boronic-acid thiophene scaffold, CAS 2285432-92-8 and molecular weight near 341, distinct from the 332 scaffold. Verified 2026.
- TargetMol 2026, chemical vendor listing: SLU-PP-915, CAS 2285432-92-8, pan-ERR agonist, EC50 near 400 nM. A research-chemical vendor listing that corroborates the pan-ERR (not selective) characterization and the EC50 near 400 nM, contradicting secondary vendor blogs that frame 915 as more ERRalpha-selective. A 2026 catalog record, not a study.
- Wikipedia 2026, SLU-PP-332 encyclopedia entry. The tertiary reference for the series, confirming no human-trial data exists for 332 and that 915 is absent from the encyclopedic literature as of this 2026 review, which supports the finding that 915 is thin even in secondary sources. Related compound context.
What does the evidence say about SLU-PP-915?
Evidence on this intervention is summarized across three complementary streams: contemporary clinical research, pre-RCT-era pharmacology and observational use, and the traditional medical systems that documented it first. Convergence across streams signals higher confidence; divergence is surfaced honestly.
Modern Clinical Research
Confidence: Emerging
Citations: Billon 2026, Johansen 2025, Moller 2026, Billon 2024
What to Track If You Try This
These are the data points that matter most while running a 30-day Experiment with this intervention.
How to read this section
- Pre
- Test or score before starting the protocol. Anchors a baseline.
- During
- Track while running the protocol so you can see if anything is changing.
- Post
- Re-test after a full cycle to confirm the change held.
- Up
- The marker should rise. For most positive outcomes, that is a good sign.
- Down
- The marker should fall. For most positive outcomes, that is a good sign.
- Stable
- The marker should hold steady. Big swings in either direction are a yellow flag.
- Watch
- Direction depends on dose, timing, and your baseline. Pay close attention to the trend.
- N/A
- No expected direction. The entry is there to anchor a baseline reading.
- Primary
- The Pulse dimension most likely to shift. Track this first.
- Secondary
- Also relevant, but a smaller or less consistent shift. Track if Primary is unclear.
Bloodwork to Order
Open These Markers In Your Dashboard
- ALT During | Expected Watch
- AST During | Expected Watch
- Resting Heart Rate During | Expected Watch
- hs-CRP During | Expected Watch
- Creatine Kinase During | Expected Watch
- Lactate During | Expected Watch
Pulse Dimensions to Watch
- Energy During | Expected Watch | Primary
- Body During | Expected Watch | Secondary
Subjective Signals (Daily Voice Card)
- Exercise capacity and time to fatigue Scale 1-5 | During | Expected Up
- Resting heart rate on waking Scale 1-5 | During | Expected Watch
- Overheating or unusual sweating Scale 1-5 | During | Expected Watch
Red Flags: Stop and Consult
- Chest pain, palpitations or any cardiac symptom: stop immediately and seek care, since the mechanism modulates cardiac fatty-acid metabolism and no human cardiac safety data exists.
- Jaundice, dark urine or right-upper-quadrant pain: stop and get liver function checked, since hepatic metabolism is confirmed and no hepatotoxicity study exists.
- Any product from a vendor without a verified certificate of analysis: do not take it, because no approved supply of SLU-PP-915 exists anywhere.
Other interventions for Endurance / Cardio
See all ratings →📊 How BioHarmony scoring works
BioHarmony translates a weighted expected-value calculation into a reader-facing 0–10 score. Tier bands: Skip 0–2.9, Caution 3.0–4.4, Neutral 4.5–5.7, Worth Trying 5.8–6.9, Strong Recommend 7.0–8.7, Top-tier 8.8–10.0.
Harm-type downsides (safety risk, side effects, reversibility, dependency) carry a 1.4× precautionary multiplier. Harm weighs more than benefit. Opportunity-type downsides (financial cost, time/effort, opportunity cost) are subtracted at face value.
Use case subratings are independent assessments of how well the intervention addresses specific health goals. They are not components of the overall score. Each subrating reflects the scorer's judgment based on use-case-specific evidence, safety, and effect sizes.
Every dimension is evaluated on a 1–5 scale, and the baseline (1) is subtracted before weighting. A perfect intervention with zero downsides contributes zero penalty rather than a residual floor, so top-tier scores are actually reachable.
EV = Upside − Downside
EV = 1.090 − 1.360 = -0.270
Formula v2.0 maps EV = 0 to score 5.0. Above neutral, EV = +4.00 reaches 10.0; below neutral, EV = −5.36 reaches 0.0. Both sides use the full 5-point half-scale.
Score = 5 + (-0.270 / 5.36) × 5 = 4.7 / 10
