SLU-PP-332
SLU-PP-332 is a synthetic pan-ERR agonist (ERR alpha, beta, gamma) developed in the Thomas Burris lab. The only major dataset is Billon et al. 2023 in Cell Reports Medicine, which showed a roughly 50 percent increase in running endurance and metabolic-syndrome reversal in sedentary mice after 8 days of daily injection. Zero human trials have completed. All current human use is gray-market research-chemical resale.
SLU-PP-332 scored 5.3 / 10 (⚖️ Neutral) on the BioHarmony scale as a Substance → Research Compound.
What It Is
SLU-PP-332 is a small-molecule synthetic agonist of all three estrogen-related receptors (ERR alpha, ERR beta, ERR gamma) developed in the Thomas Burris lab at Saint Louis University. ERRs are orphan nuclear receptors that partner with the PGC-1 alpha coactivator to drive mitochondrial biogenesis, fatty acid oxidation, slow-twitch muscle fiber conversion, and hepatic lipid handling. This is the same gene expression program that endurance training activates, which is why SLU-PP-332 is called an exercise mimetic. The single major dataset is Billon 2023 in Cell Reports Medicine: sedentary mice injected intraperitoneally at 25-50 mg/kg for 8 days ran roughly 50 percent longer on a treadmill test, and obese mice on high-fat diet showed reversal of metabolic syndrome markers. Zero human trials have completed.
Type: Research compound (pan-ERR agonist; preclinical animal data only; gray-market resale with no clinical trials).
Current status: Not FDA-approved for any indication. No publicly filed Investigational New Drug application, no Phase 1 safety trial, no ClinicalTrials.gov registration. The compound is sold by a small number of gray-market research-chemical vendors labeled "for research use only, not for human consumption." Human use is entirely outside the regulatory framework. No cGMP manufacturing oversight, no independent lot-release testing, no recall mechanism, no adverse-event reporting, and no consumer protection. Nick tried two cycles, experienced progressive fatigue within about two weeks each time, stopped the compound, and currently rates it 5.5 based on intellectual interest in the mechanism offset by personal tolerance and evidence concerns.
Terminology
- ERR: Estrogen-related receptor. Orphan nuclear receptor family distinct from classical estrogen receptors (ERα, ERβ). Three isoforms: ERR alpha, ERR beta, ERR gamma.
- ERR alpha: Dominant metabolic isoform; highly expressed in heart, skeletal muscle, brown adipose, kidney.
- ERR beta: Less characterized; overlapping function with alpha and gamma in skeletal muscle.
- ERR gamma: Metabolic isoform; drives oxidative fiber phenotype in muscle.
- Pan-agonist: Ligand that activates all isoforms of a receptor family simultaneously. SLU-PP-332 is a pan-ERR agonist.
- PGC-1 alpha: Peroxisome proliferator-activated receptor gamma coactivator 1-alpha. Master transcriptional coactivator for mitochondrial biogenesis; partners with ERRs.
- Mitochondrial biogenesis: Formation of new mitochondria inside cells, increasing oxidative capacity.
- Exercise mimetic: Drug class that activates exercise-responsive gene programs without requiring physical training.
- Research compound: Chemical sold explicitly for laboratory research use, not approved for human consumption.
- Gray-market: Commerce that operates outside the FDA regulatory framework but is not explicitly prosecuted against individual buyers.
- IND: Investigational New Drug application. FDA filing required before legally dosing humans in a clinical trial.
- FDA: US Food and Drug Administration. Regulator of drugs, foods, and supplements.
- Orphan nuclear receptor: Nuclear receptor whose endogenous ligand is unknown or absent.
- Allometric scaling: Mathematical conversion of animal drug doses to human-equivalent doses, based on surface area or metabolic rate. Unreliable for novel mechanisms.
- cGMP: Current Good Manufacturing Practices. FDA regulatory standard for pharmaceutical manufacturing quality.
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 capsule (gray-market research compound) | 1-10 mg/day oral | ||
| Oral powder (gray-market research compound) | 1-10 mg/day measured powder |
Protocols
Hypothetical biohacker extrapolation Anecdotal
- Dose
- 3-5 mg/day oral
- Frequency
- daily
- Duration
- 4-8 weeks
Gray-market community midpoint derived from uncritical allometric scaling off mouse IP studies. No clinical validation. Assumes human oral bioavailability is nonzero and target-tissue exposure resembles mouse injection, neither of which is established.
Pre-workout exercise mimetic use Anecdotal
- Dose
- 5 mg oral pre-training
- Frequency
- training days only
- Duration
- cycles of 4-8 weeks
Motivated by the Billon 2023 endurance data. No human pharmacokinetic rationale for timing, no RCT support for any dose, no evidence that pre-workout timing outperforms daily dosing. Intellectually coherent with the mechanism, empirically unvalidated.
Use-Case Specific Dosing
| Use Case | Dose | Notes |
|---|---|---|
How this score is calculated →
Upside (2.03 / 5.00)
| Dimension | Weight | Score | Visual | Weighted |
|---|---|---|---|---|
| Efficacy | 25% | 3.5 | 0.875 | |
| Breadth of Benefits | 15% | 4.0 | 0.600 | |
| Evidence Quality | 25% | 2.0 | 0.500 | |
| Speed of Onset | 10% | 4.0 | 0.400 | |
| Durability | 10% | 2.0 | 0.200 | |
| Bioindividuality Upside | 15% | 3.0 | 0.450 | |
| Total | 3.025 |
Upside Rationale
Efficacy (3.5/5.0): The Billon 2023 mouse data is striking. Sedentary male mice injected IP at 25-50 mg/kg daily for 8 days ran approximately 50 percent longer on a treadmill endurance test versus vehicle, with upregulated mitochondrial and oxidative fiber markers on muscle biopsy. Obese mice on high-fat diet showed metabolic syndrome reversal, reduced adiposity, improved glucose handling, and reversed hepatic steatosis. The gene-expression signature resembles chronic aerobic training. But every single efficacy data point is preclinical rodent. Zero human RCTs exist as of 2026-04. Translation from mouse IP injection to human oral dosing involves three major uncertainties (species, route, chronic exposure) that routinely kill promising preclinical molecules. The score weights mouse evidence heavily by human translation risk.
Breadth (4.0/5.0): Pan-ERR agonism hits mitochondrial biogenesis, fatty acid oxidation, slow-twitch fiber conversion, hepatic lipid handling, and systemic glucose metabolism simultaneously. The mechanism touches endurance performance, body composition, metabolic syndrome, fatty liver, and theoretically healthspan through the PGC-1 alpha mitochondrial axis. In mice the breadth shows up as coordinated improvements across multiple organ systems in a single 8-day protocol. If the compound translates to humans, the theoretical reach is wider than almost any single supplement or drug. Score stays at 4.0 (not 5.0) because demonstrated breadth is mouse-only; the mechanism could fail to cover any one of these domains in humans for reasons that only a clinical program will reveal.
Evidence (2.0/5.0): The Burris lab is credible and has published foundational ERR-beta and ERR-alpha pharmacology for over a decade. Billon 2023 is a well-executed rodent study in a reputable journal. But the entire evidence base is: one major mouse paper, supporting ERR biology reviews (Giguere 2018, Audet-Walsh 2015, Wang 2022), and chemical characterization (PubChem). No human trials, no human pharmacokinetics, no human safety data, no MTD, no Cochrane review, no meta-analysis, no independent replication outside the originating lab group. Industry integrity anchor is near-floor: no commercial sponsor, no completed safety program, gray-market sourcing with zero cGMP oversight. Score at 2.0 reflects a credible mechanism with a single rodent dataset as the only major empirical support.
Speed (4.0/5.0): In the mouse studies gene expression changes appear within hours of dosing and endurance phenotype emerges within 8 days of daily injection. If human oral bioavailability is reasonable and target-tissue exposure tracks the mouse data, onset in humans would plausibly be fast relative to structural interventions like strength training or fasting adaptation. Caveat is heavy: human speed is entirely extrapolated and could easily be slower because oral bioavailability, plasma half-life, and target-tissue distribution are all unvalidated. Score reflects the theoretical onset profile of a small-molecule nuclear receptor agonist, anchored by mouse timing, with substantial downside risk on actual human translation.
Durability (2.0/5.0): Effects in the mouse models fade quickly after discontinuation. Mitochondrial gene expression returns toward baseline within days to a few weeks of stopping, and endurance phenotype regresses. This is expected for a pure transcriptional-throughput intervention: the ERR-PGC-1 alpha axis runs while the ligand is present and idles when it is not. Unlike endurance training (which produces structural mitochondrial remodeling that persists for weeks to months after detraining), SLU-PP-332 does not appear to produce durable adaptation. Maintenance dosing would be required indefinitely to hold the benefit, which amplifies cumulative safety exposure in a compound with no long-term human safety data.
Bioindividuality (3.0/5.0): Unknown in humans. Theoretically the ERR mechanism is broadly conserved across human populations, but without human data there are zero data on responder profiles, baseline-dependent effect sizes, genetic variants in ERR or PGC-1 alpha, age or sex effects, or lifestyle interactions. Nick's personal response (fatigue rather than energy) on two cycles hints that individual response may be heterogeneous in ways the mouse monoculture does not predict. Community reports are sparse and heavily confounded by gray-market product identity. Score at 3.0 is a placeholder reflecting mechanistic universality offset by total lack of human responder data.
Downside (2.67 / 5.00)
| Dimension | Weight | Score | Visual | Weighted |
|---|---|---|---|---|
| Safety Risk | 30% | 4.0 | 1.200 | |
| Side Effect Profile | 15% | 2.5 | 0.375 | |
| Financial Cost | 5% | 3.0 | 0.150 | |
| Time/Effort Burden | 5% | 2.5 | 0.125 | |
| Opportunity Cost | 5% | 2.5 | 0.125 | |
| Dependency / Withdrawal | 15% | 2.5 | 0.375 | |
| Reversibility | 25% | 2.5 | 0.625 | |
| Total | 2.975 | |||
| Harm subtotal × 1.4 | 3.605 | |||
| Opportunity subtotal × 1.0 | 0.400 | |||
| Combined downside | 4.005 | |||
| Baseline offset (constant) | −1.340 | |||
| Effective downside penalty | 2.665 |
Downside Rationale
Safety (4.0/5.0): Zero human safety data. No MTD, no long-term exposure studies, no drug-drug interaction profile, no organ-system toxicology package in humans, no pregnancy or lactation data, no cancer-signal monitoring over years. This is the dominant downside dimension. Chronic pan-ERR agonism has theoretical cancer-biology implications because ERRs participate in tumor metabolic reprogramming (Audet-Walsh 2015), and while no animal carcinogenicity signal has been published, the human translation is unstudied. Gray-market sourcing adds independent risk: product identity and purity are buyer-verified at best, with no cGMP oversight, no recall mechanism, no adverse-event reporting infrastructure, and no regulatory consumer protection. Score at 4.0 is the high-risk anchor appropriate for a preclinical research compound with no human safety data, sold outside the regulatory framework.
Side Effects (2.5/5.0): Mouse data shows mild and transient effects at the doses tested. Nick's personal experience on two cycles was progressive fatigue, drained feeling, and loss of motivation within about two weeks, the opposite of the expected exercise-mimetic phenotype, resolving within days of discontinuation. Community reports are sparse and heavily confounded by uncertain product identity. The honest position is that human side-effect profile is simply not characterized; Nick's fatigue could be the compound, could be an impurity from gray-market sourcing, could be individual bioindividuality, or could be an unrelated confound. Score at 2.5 is mid-range because the tail of possible side effects is wide and uncharacterized in a compound with no human clinical base.
Cost (3.0/5.0): Gray-market research-chemical pricing runs roughly $30-80/month at typical community dosing. Absolute dollar figure is modest compared to high-end supplements or peptides, but the cost analysis is corrupted by the product-identity risk: a $50/month spend on a product that may not contain what the label claims is functionally wasted money on top of the downside risk. Independent HPLC verification costs multiples of the product price. Score at 3.0 reflects the dollar figure adjusted upward for the quality-control overhead a responsible user would need to absorb.
Effort (2.5/5.0): Oral capsule or measured powder swallowed once per day. Minimal adherence friction if the user trusts the product. Real effort comes from due diligence: sourcing from less-disreputable vendors, ideally sending samples for independent HPLC identity and purity testing, weighing powders accurately with a research-grade scale, and monitoring subjective and objective response indicators closely because no established biomarker guides dosing. Effort is higher than a mainstream supplement because the user has to do the quality control that pharma infrastructure normally provides.
Opportunity (2.5/5.0): The evidence-backed alternatives for endurance and metabolic health (structured zone-2 training, resistance training, caloric and protein management, sleep optimization, creatine monohydrate) produce larger and more durable effects than any speculative exercise mimetic, with a known safety profile and zero sourcing risk. Spending attention, budget, and personal risk-capacity on SLU-PP-332 while lifestyle fundamentals are unoptimized is a clearly poor allocation. Score at 2.5 reflects a real but not catastrophic opportunity cost: a biohacker interested in the Burris lab mechanism for intellectual reasons can run a personal n-of-1 without displacing lifestyle foundations, and the financial allocation is modest compared to many device purchases.
Dependency (2.5/5.0): No data either way in humans. Mechanistically, ERR agonism is not an addictive or reward-pathway intervention, so pharmacological dependency is not expected. Possible functional reliance (user feels dependent on the compound to hold metabolic or endurance gains) is untested. No withdrawal syndrome documented in mouse discontinuation data. Score at 2.5 is the neutral anchor for an uncharacterized compound with no mechanistic reason to expect dependency but no empirical demonstration of its absence in humans.
Reversibility (2.5/5.0): Mouse data suggests rapid washout with effects fading within days to a few weeks of discontinuation. Plasma pharmacokinetics appear short-lived, and the mitochondrial gene-expression signature regresses without the ligand. Nick's two cycles also resolved subjectively within days of stopping. These signals are consistent with a reversible intervention, but the honest position is that long-term reversibility (whether chronic pan-ERR agonism leaves any persistent tissue signature over months or years in humans) is completely uncharacterized. Score at 2.5 is mid-range reflecting short-term reversibility signals from limited data, offset by total absence of long-term human reversibility evidence.
Verdict
✅ Best for: Advanced biohackers with medical supervision who are actively studying exercise-mimetic pharmacology as a research interest, who have exhausted structured endurance training and nutrition optimization, and who explicitly accept that the evidence base is rodent-only with unknown human safety. Researchers working in metabolic pharmacology who are following the Burris lab program. Nobody else.
❌ Avoid if: You want any human clinical evidence before exposure. You are under 25, pregnant, breastfeeding, or trying to conceive. You have any cardiovascular condition, active or historical cancer, or any current medication (no drug interaction data exists). You cannot verify product identity and purity through independent testing. You expect a regulatory safety net to protect you (this is a research compound with no approved human use). You are substituting SLU-PP-332 for structured training and lifestyle fundamentals. You want a safety profile you can point to.
Use Case Breakdown
The overall BioHarmony score reflects the intervention's primary evidence profile. These subratings are independent assessments per use case.
| Use Case | Score | Summary |
|---|---|---|
| 💪 Mitochondrial | 7.0 | ERR alpha/gamma/beta agonism directly upregulates mitochondrial biogenesis and oxidative phosphorylation genes in preclinical models |
| 👍 Endurance / Cardio | 6.5 | Mouse studies show increased running endurance and muscle oxidative capacity without exercise |
| 👍 Metabolic Health | 6.5 | ERR agonism shifts metabolism toward fat oxidation; mouse obesity models show improvement in glucose and lipid handling |
| 👍 Body Composition / Fat Loss | 6.0 | Exercise-mimetic effects reduce fat mass in sedentary mice; no human data |
| ⚖️ Cardiovascular | 5.5 | Improved metabolic profile and endurance capacity may benefit CV health indirectly; no human CV outcome data |
| ⚖️ Blood Sugar / Glycemic Control | 5.5 | Enhanced fatty acid oxidation improves insulin sensitivity in animal models |
| ⚖️ Energy / Fatigue | 5.5 | Theoretical energy boost from enhanced mitochondrial function; Nick experienced the opposite subjectively |
| ⚖️ Liver / Detoxification | 5.0 | ERR signaling active in liver; may support hepatic fatty acid oxidation; mouse steatosis reversal documented |
| ⚖️ Kidney Function | 5.0 | No kidney-specific data; ERR expressed in kidney but unstudied for this compound |
| ⚖️ Healthspan | 5.0 | Exercise-mimetic concept is promising for healthspan but entirely preclinical |
| ⚖️ VO2 Max | 5.0 | Mouse endurance gains suggest VO2max improvement; no human cardiopulmonary testing |
| ○ Longevity / Lifespan | 4.5 | Exercise mimetics theoretically extend lifespan but no longevity studies exist for SLU-PP-332 |
| ○ Anti-Inflammatory | 4.5 | ERR activation modulates inflammatory gene expression in preclinical models |
| ○ Geriatric / Aging Population | 4.5 | Exercise mimetic could benefit sedentary elderly; purely theoretical, no age-stratified data |
| ○ Cellular Senescence | 4.0 | Mitochondrial improvement may slow senescence; speculative connection |
| ○ Recovery / Repair | 4.0 | Enhanced oxidative metabolism may support recovery; no direct evidence |
| ○ Strength / Power | 3.5 | Muscle fiber type shifting toward oxidative may not benefit strength or power output |
| ○ Antioxidant / Oxidative Stress | 3.5 | ERR upregulates some antioxidant defense genes; modest indirect effect |
| ○ Muscle Growth / Hypertrophy | 3.5 | Fiber type shifting rather than hypertrophy; may favor endurance over size |
| ○ Bone / Joint Health | 3.0 | Exercise benefits bone but unclear if mimetic replicates mechanical loading effects |
| ○ Autophagy | 3.0 | Exercise activates autophagy; ERR agonism may partially replicate this via PGC-1 alpha axis |
Frequently Asked Questions
What exactly is SLU-PP-332 and how does it work mechanistically?
SLU-PP-332 is a small molecule that activates all three estrogen-related receptors (ERR alpha, ERR beta, ERR gamma) simultaneously. ERRs are orphan nuclear receptors that partner with the PGC-1 alpha coactivator to drive mitochondrial biogenesis, fatty acid oxidation, and slow-twitch muscle fiber conversion. This is the same gene-expression program that endurance training activates, which is why SLU-PP-332 is called an exercise mimetic. ERRs are distinct from classical estrogen receptors (ERα and ERβ), so SLU-PP-332 does not produce estrogenic effects. The compound came out of Thomas Burris's lab at Saint Louis University.
Why are there no human trials yet?
SLU-PP-332 is a preclinical research tool. As of 2026 there is no publicly filed Investigational New Drug application, no Phase 1 safety trial, no registered ClinicalTrials.gov entry. The compound needs toxicology packages, formal pharmacokinetic characterization, and a commercial sponsor willing to fund a multi-hundred-million-dollar development program before humans can be legally dosed. Exercise-mimetic pharmacology has a graveyard of near-misses (GW501516, AICAR) that killed investor appetite. The Burris lab compounds remain academic research tools. Human data may be years away and may never arrive.
What did Billon 2023 actually show in the mouse study?
Billon et al. 2023 in Cell Reports Medicine reported that sedentary male mice injected with SLU-PP-332 at 25-50 mg/kg IP daily for 8 days ran roughly 50 percent longer on a treadmill endurance test versus vehicle controls. Obese mice on high-fat diet showed reversal of metabolic syndrome markers, reduced fat mass, improved glucose handling, and reversed hepatic steatosis. Muscle biopsies showed upregulation of oxidative fiber markers and mitochondrial genes. This is compelling preclinical proof of concept, but the dose is intraperitoneal injection in rodents, the timeframe is 8 days, and the species is mouse. Human translation is unvalidated.
Is gray-market SLU-PP-332 safe to buy and use?
No, it is not. Gray-market vendors operate outside cGMP manufacturing standards, and independent HPLC or mass-spec verification of identity and purity is rare. Products labeled SLU-PP-332 may contain the wrong compound, degradation products, or contaminants from sloppy synthesis. There is no recall mechanism, no adverse-event reporting system, no lot-release testing, and no legal consumer protection. Even if the compound were safe in humans at a known dose (unproven), the supply chain introduces independent risk. Nick's personal experience of unexplained fatigue on two cycles may have been the compound, may have been an impurity, or may have been something else entirely.
What are realistic benefits versus internet hype?
The hype claim is "50 percent more endurance without exercise." The reality is that 50 percent figure is from sedentary mice injected intraperitoneally for 8 days, not humans swallowing capsules. Human exercise-mimetic history (GW501516 cancer signal, AICAR failure) suggests even if SLU-PP-332 translates, effect sizes in trained humans will likely be far smaller than the mouse data implies, and long-term safety is completely uncharacterized. A reasonable prior is that the compound may produce modest mitochondrial upregulation in some users, may produce unexpected fatigue in others (like Nick), and has a nonzero cancer risk that cannot be quantified without human data.
Why did Nick try it and then stop?
Nick ran two cycles based on the theoretical mechanism and the mouse endurance data. Both times he reported becoming progressively fatigued, drained, and unmotivated within about two weeks, the opposite of the expected exercise-mimetic effect. Symptoms resolved within days of discontinuation both times. He still finds the Burris lab mechanism interesting and wants to see human data eventually, but he stopped using the compound personally because the subjective outcome was negative, the sourcing was gray-market, and the long-term safety was unknowable. His 5.5 rating reflects intellectual interest in the mechanism offset by personal tolerance and evidence concerns.
Is possession or use actually legal?
SLU-PP-332 is not a scheduled controlled substance in the US, so personal possession is not a criminal matter under drug-scheduling law. However, sale or distribution for human consumption is illegal under the FDCA, which is why vendors label products "for research use only." That label does not create a safe harbor for buyers who intend to self-administer. The compound is a gray area: not prosecuted against individuals in practice, but not legal to market or sell for human use. Anyone using it is outside the FDA regulatory framework with no consumer protection, no labeling guarantees, and no clinical supervision infrastructure.
Who should absolutely avoid SLU-PP-332?
Anyone who requires any level of human safety data before exposure should avoid SLU-PP-332 entirely. That category includes anyone with active or historical cancer (ERR signaling has tumor-biology implications), anyone with cardiovascular disease, anyone taking prescription medications (zero drug-interaction data), anyone pregnant or trying to conceive, anyone under 25, and anyone who cannot absorb catastrophic downside risk from an unknown long-term adverse event. For endurance and metabolic goals, the evidence-backed alternatives (structured zone-2 training, resistance training, caloric management, sleep, and creatine) outperform any speculative exercise mimetic by a wide margin with a known safety profile.
How This Score Could Change
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.
| Scenario | Dimensions Affected | Recalculated Score | New Tier |
|---|---|---|---|
| First human Phase 1 RCT released with clean 12-week safety data | Evidence 2.0 to 3.0; Safety 4.0 to 3.0 | ~6.1 | Worth trying (supervised) |
| Phase 2 efficacy trial confirms endurance or metabolic endpoint in humans | Evidence 2.0 to 3.5; Efficacy 3.5 to 4.0; Safety 4.0 to 2.5 | ~7.4 | Strong recommend |
| Human cancer signal emerges in long-term ERR agonist users | Safety 4.0 to 5.0; Evidence 2.0 to 1.5 | ~3.8 | Avoid |
| Gray-market adverse-event cluster (hepatotoxicity, cardiac event) reported | Safety 4.0 to 5.0; Side Effects 2.5 to 4.0 | ~4.2 | Avoid |
| FDA files warning letter or enforcement action against research-chemical vendors | Legal only (grey_area to illegal) | ~5.0 | Neutral (access blocked) |
| Independent replication of Billon 2023 endurance phenotype in a second animal model | Evidence 2.0 to 2.5 | ~5.5 | Neutral |
| Clean Phase 1 plus Phase 2 plus cGMP commercial formulation with IND | Evidence 2.0 to 4.0; Safety 4.0 to 2.0; Efficacy 3.5 to 4.0 | ~8.0 | Strong recommend |
BioHarmony v0.5 methodology. Date scored: 2026-04-18. Author: Nick Urban, CHEK Functional Health Coach Level 1.
Key Evidence Sources
- Billon C et al. 2023. A synthetic ERR agonist alleviates metabolic syndrome. Cell Reports Medicine (Burris lab). Mouse endurance and metabolic syndrome reversal, 25-50 mg/kg IP daily.. Foundational and essentially only major SLU-PP-332 paper. Preclinical proof of concept. The entire SLU-PP-332 human-use narrative rests on this single rodent study.
- Wang T et al. 2022. Estrogen-related receptors in metabolism and cancer. Endocrine Reviews. Comprehensive review of ERR biology, ligand pharmacology, and tumor implications.. Background on ERR signaling. Essential for understanding the mechanism SLU-PP-332 targets and the cancer-biology concerns around chronic ERR activation.
- Giguere V. 2018. Transcriptional control of energy homeostasis by the estrogen-related receptors. Endocrine Reviews. Foundational review of the ERR nuclear receptor family from the lab that discovered them.. Authoritative review of ERR family biology. Establishes the mechanistic rationale for targeting ERRs for metabolic and endurance phenotypes.
- Audet-Walsh E, Giguere V. 2015. The multiple universes of estrogen-related receptor alpha and gamma in metabolic control and related diseases. Acta Pharmacologica Sinica.. Reviews ERR alpha and gamma roles including tumor biology. Cancer-signal concern for chronic pan-ERR agonism rests partly on this literature.
- PubChem CID 146025: SLU-PP-332 chemical structure, reported activity, and vendor listings.. Structural and basic property reference for the compound as a research chemical.
Other interventions for Mitochondrial
See all ratings →📊 How BioHarmony scoring works
BioHarmony translates a weighted expected-value calculation into a reader-facing 0–10 score. 5.0 is neutral (benefits and risks balance). Above 5 = benefits outweigh risks; below 5 = risks outweigh benefits.
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 = 2.025 − 2.665 = -0.640
EV ranges from −5 to +5. Adding 7 shifts to 2–12, dividing by 12 normalizes to 0–1, then ×10 gives the 0–10 score.
Score = ((-0.640 + 7) / 12) × 10 = 5.3 / 10
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