SLU-PP-332

Volume Pricing

Price per pack (10 vials). Discount applies to this compound only – no mix and match.

SLU-PP-332 — Dual ERRα/γ Agonist Small Molecule for Mitochondrial Biogenesis Research

SLU-PP-332 is a synthetic small-molecule agonist of estrogen-related receptors alpha and gamma (ERRα and ERRγ), developed in the laboratory of Thomas Burris at Saint Louis University (the SLU prefix refers to this origin). The compound was first described in a 2023 Nature Communications publication demonstrating that ERRα/γ co-activation produces transcriptional changes in skeletal muscle and cardiac tissue that substantially overlap with the gene expression signature induced by endurance exercise — including upregulation of genes governing mitochondrial biogenesis, oxidative phosphorylation, and fatty acid beta-oxidation. ERRα and ERRγ are constitutively active nuclear receptors; they do not require endogenous ligand binding for basal activity, but their transcriptional output is significantly amplified by agonist binding. SLU-PP-332 is distinct from peptide-based research compounds in this catalog: it is a small molecule with oral bioavailability data in rodent studies, and its mechanism is entirely transcriptional rather than receptor-signaling or endocrine.

Why SLU-PP-332’s ERRα/γ Dual Agonism Matters

ERRα and ERRγ function as direct transcriptional regulators of PGC-1α target genes without requiring PGC-1α itself — they bind to ERRE (estrogen-related receptor response element) sequences in the promoters of TFAM, NRF1, NRF2, MCAD, HADH, and other mitochondrial biogenesis and fatty acid oxidation genes. This positions ERR agonism as a pathway that can activate mitochondrial gene programs even in contexts where PGC-1α expression is reduced, such as in aged or disease-affected tissue. The dual ERRα/ERRγ profile of SLU-PP-332 is significant because ERRα predominates in energy-demanding tissues (skeletal muscle, heart, brown adipose) while ERRγ is enriched in cardiac and neural tissue — co-activation of both receptors produces a broader transcriptional footprint than selective agonists for either alone.

Research Applications

SLU-PP-332 is used in studies examining:

• Mitochondrial biogenesis — TFAM, NRF1, NRF2 expression; mitochondrial copy number and density in muscle and cardiac tissue
• Exercise mimetic biology — transcriptomic overlap with endurance exercise; VO₂max surrogate markers in sedentary models
• Fatty acid oxidation — substrate flux, CPT1 activity, MCAD expression in energy-demanding tissues
• Cardiac metabolism — ERRγ-mediated oxidative capacity in failing and aged myocardium; metabolic flexibility under stress
• Type 2 diabetes and metabolic syndrome models — glucose uptake, insulin sensitivity in skeletal muscle
• ERR nuclear receptor biology — ERRE binding, co-activator recruitment, ERRα vs. ERRγ selectivity profiling
• Human-equivalent dose scaling research — interspecies PK/PD translation from rodent 100mg/kg oral studies

Specifications

Reconstitution

SLU-PP-332 arrives as lyophilized powder and is water-soluble; reconstitute with bacteriostatic water prior to use. Use the formula:

Total mg ÷ Volume added (mL) = Concentration (mg/mL)

Example: 5mg vial + 1mL BAC water = 5mg/mL solution

Reconstituted solution should be stored at 2–8°C and used within 28–30 days.

Protocol Notes

Published rodent studies and ongoing dose-scaling research provide the following reference frameworks — not instructions for use:

• Dose range: 100mg/kg oral (gavage) in the 2023 Nature Communications efficacy studies; human-equivalent dose scaling is an active research area without established consensus
• Frequency: Once daily oral administration in primary rodent studies
• Study duration: 4–8 weeks in metabolic and cardiac model studies; transcriptional changes detectable within 24–72h of initial dosing in rodent data

Research Stacks

SLU-PP-332 is commonly paired in research settings with:

• MOTS-c — MOTS-c activates AMPK and promotes mitochondrial biogenesis via nuclear translocation; SLU-PP-332 activates ERRα/β/γ, which share transcriptional targets with AMPK-regulated programs. Researchers pair both to study convergent regulation of oxidative metabolism and mitochondrial gene expression.
• SS-31 — SS-31 localizes to the inner mitochondrial membrane and reduces electron leak and cardiolipin oxidation, preserving ATP synthesis efficiency. Combined with SLU-PP-332’s ERR-driven transcriptional upregulation of oxidative phosphorylation components, the pairing is used to study complementary structural and transcriptional support of mitochondrial function.
• NAD+ — NAD+ is a cofactor essential for sirtuin activity and the electron transport chain; SLU-PP-332 drives transcription of oxidative metabolism genes that depend on NAD+ availability. The pairing is studied to examine whether substrate supply and transcriptional demand can be modulated in tandem.

Purity Guarantee

Every batch is ≥99% purity. If you independently test your compound and the results don’t match — send us the COA and we’ll issue store credit, no questions asked.