SLU-PP-332 sits in the usual grey zone where half the internet projects fantasies onto a molecule designed to torment lab mice. ERRα agonist, high purity, priced like a novelty item for hobby scientists. People treat it like a secret metabolic accelerator when the only thing it has proven is that rodents can be bullied into outperforming their baseline.
Data is straightforward: activate ERRα, push PGC-1α expression, increase mitochondrial count and oxidative capacity. Fat oxidation rises. Glucose sparing improves insulin sensitivity. Liver fat drops in steatosis models. Endurance jumps by roughly seventy percent in controlled trials like Patch 2017 and Benoit 2021. Muscle phenotype shifts toward slow twitch dominance. Neuroprotection shows up in ischemia models with reduced toxicity markers.
Protocols stay in the microscopic and animal ranges. Cell studies at 0.1 to 5 micromolar for 1 to 3 days with DMSO under 0.1 percent. Mice at 5 to 15 milligrams per kilogram by IP or gavage. Rats at 3 to 10. Keep total DMSO under 1% or you will see cytotoxicity.
The story is always the same: a compound shows strong mitochondrial effects in rodents and suddenly every forum attracts users who think they discovered a hidden upgrade. They never bother checking that none of the research crosses into human safety or efficacy. They skip the part where ERRα signaling sits inside complex transcriptional networks that no one has mapped fully in humans.
SLU-PP-332 is a tool for metabolic studies. Nothing more. It gives researchers controlled levers to modulate mitochondrial biogenesis, substrate preference, and endurance traits in animals so they can understand disease pathways. Anyone treating it as a personal performance enhancer is doing it out of impatience or ignorance.
Data is straightforward: activate ERRα, push PGC-1α expression, increase mitochondrial count and oxidative capacity. Fat oxidation rises. Glucose sparing improves insulin sensitivity. Liver fat drops in steatosis models. Endurance jumps by roughly seventy percent in controlled trials like Patch 2017 and Benoit 2021. Muscle phenotype shifts toward slow twitch dominance. Neuroprotection shows up in ischemia models with reduced toxicity markers.
Protocols stay in the microscopic and animal ranges. Cell studies at 0.1 to 5 micromolar for 1 to 3 days with DMSO under 0.1 percent. Mice at 5 to 15 milligrams per kilogram by IP or gavage. Rats at 3 to 10. Keep total DMSO under 1% or you will see cytotoxicity.
The story is always the same: a compound shows strong mitochondrial effects in rodents and suddenly every forum attracts users who think they discovered a hidden upgrade. They never bother checking that none of the research crosses into human safety or efficacy. They skip the part where ERRα signaling sits inside complex transcriptional networks that no one has mapped fully in humans.
SLU-PP-332 is a tool for metabolic studies. Nothing more. It gives researchers controlled levers to modulate mitochondrial biogenesis, substrate preference, and endurance traits in animals so they can understand disease pathways. Anyone treating it as a personal performance enhancer is doing it out of impatience or ignorance.
