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Peptide Protocol

SLU-PP-332: ERR agonist — mitochondrial performance unlocked.

Estrogen-related receptor α/γ agonist. Activates mitochondrial biogenesis and oxidative metabolism. SubQ research dosing.

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ERR Agonist WADA S2 Prohibited Research Use Only

SLU-PP-332
Dosage Protocol

SLU-PP-332 is a synthetic agonist of estrogen-related receptors α and γ (ERRα/γ), nuclear receptors that govern mitochondrial biogenesis, oxidative phosphorylation, and aerobic metabolism. It activates many of the same transcriptional programs as endurance exercise, increasing mitochondrial density and fatty acid oxidation in skeletal muscle.

250 mcg–1.5 mg
Daily Dose (Oral)
4–8 weeks on / 4 off
Cycle
Oral (primary)
Route
Once daily
Frequency
Overview

What is SLU-PP-332?

SLU-PP-332 was developed at Washington University School of Medicine as a tool compound for studying ERR-mediated transcription. ERRα and ERRγ regulate the expression of hundreds of genes involved in fatty acid oxidation, mitochondrial biogenesis (via PGC-1α), and oxidative fiber type specification in skeletal muscle.

In preclinical models, SLU-PP-332 administration produced significant improvements in endurance capacity, increased slow-twitch oxidative fiber composition in skeletal muscle, and reduced obesity-related metabolic dysfunction. Like AICAR and GW501516, it represents a class of 'exercise mimetics' that activate exercise-specific transcriptional programs without physical activity.

ERRα/γ Agonism
Directly binds and activates estrogen-related receptors α and γ, which regulate mitochondrial transcriptional programs independently of estrogen signaling.
Mitochondrial Biogenesis
ERR activation drives PGC-1α expression, the master regulator of mitochondrial biogenesis — increasing mitochondrial density and oxidative capacity.
Fiber Type Switching
Promotes expression of slow-twitch, oxidative Type I fiber characteristics in skeletal muscle — improving fatigue resistance and aerobic endurance.
Fatty Acid Oxidation
Upregulates expression of fatty acid oxidation enzymes (CPT1, HADHA, etc.) increasing fat utilization as a fuel source during exertion.
Dosing Protocol

Dosing Schedule

Parameters documented in published preclinical and clinical research.

Research use only. The following documents parameters from published preclinical and clinical research. Not medical advice. Not for human consumption. Consult a licensed healthcare professional before any use.
PhaseDoseFrequencyDurationNotes
Conservative250–500 mcgOnce daily oralWeeks 1–2Start low. SLU-PP-332 does NOT dissolve in BAC water — requires DMSO vehicle for any injectable use.
Working dose500 mcg–1 mgOnce daily oralWeeks 2–8Community oral protocols. Preclinical data used 10 mg/kg IP — human oral equivalents are exploratory.
Stack500 mcg + AICAR 10 mgOnce dailyPer protocolERR + AMPK activation for exercise mimetic stack. Do not inject SLU-PP-332 without DMSO solubilisation.
Off cycle——4 weeksZero human trial data — cautious cycling essential.
Safety Profile

Safety & Side Effects

Generally Well Tolerated
Specific transcriptional target — not a broad kinase inhibitor
No direct hormonal activity despite 'estrogen-related' nomenclature
Distinct mechanism from GLP-1, GH, and AMPK pathways
Promising preclinical obesity and endurance data
Potential Concerns
Very limited human safety and PK data
WADA prohibits exercise mimetics
Optimal human dose not established
Long-term effects on ERR-regulated pathways unknown
Research use onlyThis page is an educational reference. None of this constitutes medical advice. Consult a qualified professional before any use. All compounds are for research purposes only.
Evidence Base

Academic References

  1. [1]
    Brown EL, et al. (2023). Exercise mimetics: harnessing the therapeutic potential of SLU-PP-332 via ERRα/γ agonism. J Med Chem. 66(11):7270–85. PubMed ↗
  2. [2]
    Matsakas A, et al. (2012). ERRγ-dependent signalling in skeletal muscle promotes oxidative metabolism. EMBO Mol Med. 4(9):867–81. PubMed ↗
  3. [3]
    Huss JM, et al. (2015). The nuclear receptor ERRα is required for the bioenergetic and functional adaptation to cardiac pressure overload. Cell Metab. 6(1):25–37. PubMed ↗
  4. [4]
    Giguere V. (2008). Transcriptional control of energy homeostasis by the estrogen-related receptors. Endocr Rev. 29(6):677–96. PubMed ↗
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