Also known as: SLU PP 332 · ERRα/γ agonist · exercise mimetic compound
| Parameter | Value | Source |
|---|---|---|
| Elimination Half-Life (Human) | Not established — no published human PK study | — |
| Elimination Half-Life (Animal) | Not reported in primary literature | Washington Univ. 2023[1] |
| Time to Peak (Tmax) | No published data (any species) | — |
| Bioavailability | No published human data | — |
| Plasma Protein Binding | No published data | — |
| Route of Administration (Animal Studies) | Intraperitoneal (murine models) | Washington Univ. 2023[1] |
| Target | ERRα (estrogen-related receptor alpha) and ERRγ | Washington Univ. 2023[1] |
| Full Clearance (5 × t½) | Cannot be calculated — human t½ unknown | — |
| FDA Approval Status | Not approved | — |
| Data Quality | Animal Study — no published human PK study identified as of May 2026 | |
No published human pharmacokinetic study for SLU-PP-332 has been identified as of May 2026. The plasma half-life in humans is unknown. The primary published research on SLU-PP-332 — from Washington University School of Medicine, St. Louis (2023) — characterized the compound's pharmacodynamic effects on endurance and body composition in mice but did not report formal pharmacokinetic parameters including half-life, Tmax, or bioavailability in any species.[1]
SLU-PP-332 (the compound designation references Saint Louis University where early ERR ligand work was conducted) is a synthetic small molecule designed to selectively activate estrogen-related receptors alpha and gamma (ERRα and ERRγ) — nuclear receptors that regulate mitochondrial biogenesis and oxidative metabolism. As a small lipophilic molecule, SLU-PP-332 likely undergoes hepatic metabolism, but no ADME characterization has been published to confirm this.
A pharmacokinetic characterization of SLU-PP-332 would require a dedicated animal PK study with serial plasma sampling and validated LC-MS/MS quantification, followed by an IND-enabled Phase 1 human study. Neither has been published as of the review date for this page. The research community's focus has been on demonstrating pharmacodynamic proof-of-concept in animal models, which is the typical first step before advancing a compound to formal PK/toxicology evaluation.[1]
For nuclear receptor agonists like SLU-PP-332, the biological effect duration is likely to substantially outlast plasma clearance of the compound. ERRα/γ activation drives transcriptional reprogramming — changes in mitochondrial gene expression, PGC-1α targets, and fiber type composition — that persist because of the downstream biological cascades they initiate. mRNA and protein turnover timescales (hours to days) determine how long these transcriptional changes are maintained after the receptor agonist has cleared. This is a mechanistic inference relevant to all nuclear receptor ligands; no quantitative data exists for SLU-PP-332 specifically.
This cannot be answered with published data. No human or animal pharmacokinetic study has characterized the clearance timeline for SLU-PP-332. A clearance timeline table (1–5 half-lives) cannot be presented because no validated half-life value exists. Presenting such a table would require fabricating data, which Halflife Labs' editorial policy prohibits.
If a human half-life is established in future clinical research, this section will be updated with a full clearance timeline based on primary data.
Because no human PK data exists for SLU-PP-332, no evidence-based dosing frequency or dosing amount can be recommended. In murine studies, dosing was administered intraperitoneally — a route not used in human therapeutics — at doses that cannot be directly translated to humans using simple weight-based scaling without safety validation. Human dosing for SLU-PP-332 or any related ERR agonist has not been established in published clinical trials as of May 2026.[1]
| Compound | Primary Target | Human PK Data? | Primary Evidence | Development Status |
|---|---|---|---|---|
| SLU-PP-332 | ERRα / ERRγ agonist | No | Murine endurance study (WashU 2023) | Preclinical research |
| 5-Amino-1MQ | NNMT inhibitor | No | Murine adipocyte study (Kannt 2018) | Preclinical research |
| AICAR | AMPK activator | Yes (limited) | Human PK studies; used in cardiology research | Preclinical for performance; not approved |
| GW501516 (Cardarine) | PPARδ agonist | Yes (limited) | Murine endurance; abandoned due to carcinogenicity | Abandoned — carcinogen in animal studies |
| Route | Half-Life | Bioavailability | Notes |
|---|---|---|---|
| Intraperitoneal (murine studies) | Not reported | Not reported | Route used in Washington University 2023; not a human administration route |
| Oral (projected) | No published data | No published data | Lipophilic small molecule; oral absorption plausible but not validated |
| Subcutaneous | No published data | No published data | No study in any species |
| Intravenous | No published data | 100% (definitional) | No study in any species |
SLU-PP-332 is not included in any standard SAMHSA-5 workplace, military, or forensic drug panel. It is not a controlled substance in the United States as of May 2026.[1]
WADA's prohibited list includes metabolic modulators (S4 category), which covers compounds that activate AMPK and related pathways. ERR agonists may fall under this category in future list updates, particularly if the compound demonstrates performance-enhancing effects in athletes. No validated analytical method for detecting SLU-PP-332 or its metabolites in urine or blood has been published in forensic or doping control literature as of May 2026.
SLU-PP-332 is a synthetic ligand for estrogen-related receptor alpha (ERRα, NR3B1) and estrogen-related receptor gamma (ERRγ, NR3B3) — orphan nuclear receptors expressed at highest levels in tissues with high oxidative metabolic demand: skeletal muscle, heart, brain, and brown adipose tissue.[1]
ERRα and ERRγ are constitutively active nuclear receptors in the absence of known endogenous ligands — they regulate the expression of hundreds of nuclear-encoded mitochondrial genes, including those governing the electron transport chain, fatty acid oxidation, and mitochondrial biogenesis. Their activity is co-regulated by the transcriptional coactivator PGC-1α, which is the master regulator of the adaptive response to exercise in skeletal muscle. When humans or animals exercise, PGC-1α expression increases, which activates ERR-target genes to increase mitochondrial density, oxidative phosphorylation capacity, and type I (slow oxidative) muscle fiber proportion.[1]
SLU-PP-332 bypasses the need for exercise to activate this pathway by directly binding and activating ERRα and ERRγ in a ligand-dependent manner. By acting as an agonist, SLU-PP-332 drives expression of the same transcriptional program that exercise training normally induces, without the mechanical stimulus of exercise. In the Washington University 2023 research, sedentary mice treated with SLU-PP-332 showed:
The mechanistic rationale for why SLU-PP-332 might work as an exercise mimetic is grounded in established biology: ERRα/γ → PGC-1α target gene activation → mitochondrial biogenesis → increased type I fiber proportion → improved fat oxidation capacity → enhanced endurance. The question that remains unanswered is whether this translates from mice to humans, and at what dose and safety profile.[1]
Important limitations of the current evidence: (1) Mouse skeletal muscle physiology and fiber type composition differs substantially from humans; (2) The pharmacokinetics of SLU-PP-332 in mice (via IP route) are irrelevant to human oral or SC administration; (3) Long-term effects of chronic ERRα/γ agonism on cardiac function, liver, and other tissues have not been characterized; (4) No safety or toxicology data for SLU-PP-332 in humans has been published.
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