An Orally Active ERR Agonist, SLU-PP-915, Enhances Aerobic Exercise Capacity (1 December 2025) The authors stress that 332 is NOT orally bioavailable. "We previously developed a ERR pan-agonist, SLU-PP-332 (332), which improve aerobic performance in mice but lacks oral bioavailability. Here, we characterize SLU-PP-915 (915), a chemically distinct ERR pan-agonist that is orally bioavailable and exhibits potent in vivo exercise mimetic activity." Who can help to get the full paper and interpret the findings? Specifically , is there any new data on how much exactly SLU-PP-332 orally bioavailable (%) ?

Redox “being stuck” means electrons are not cycling smoothly through your mitochondria and antioxidant systems. Instead of a flexible rhythm of mild oxidation and reduction, the system is trapped in one zone: either chronically over-oxidized (too much damaging ROS, not enough repair) or over-reduced (too much electron pressure, not enough safe places to send them). When redox is moving again, you see better pulse: you can increase energy output when needed, return to baseline efficiently, and labs, performance, and symptoms all start to show more adaptability rather than flatness or chaos. For objective markers of a stuck redox system, blood lactate is one of the simplest and most meaningful. At rest, most healthy people will sit around 0.5–1.5 mmol/L. If you consistently see resting lactate above about 2.0 mmol/L without clear cause (e.g., infection, metformin, sepsis, big training session an hour ago), that often means mitochondria are struggling to pass electrons down the respiratory chain, so pyruvate is being shunted to lactate. If you do very low-intensity work, like easy cycling at a conversational pace, and lactate still jumps above 3–4 mmol/L and stays there, that suggests redox is “pressure-locked” rather than flowing. When redox starts to move again, resting lactate drifts back below 1.5 mmol/L, and at low workloads it stays under about 2 mmol/L with a faster return to baseline in the 10–20 minutes after exercise. The lactate-to-pyruvate ratio can add nuance. Lactate and pyruvate are cousins in energy metabolism, and their ratio reflects how much the cell is “leaning” toward reduction or oxidation. A typical fasting lactate:pyruvate ratio is roughly in the 10–20:1 range. A ratio persistently above about 25–30 can indicate a more hypoxic or electron-traffic-jam state, where NADH is high, oxygen can’t be used efficiently, or parts of the respiratory chain are blocked. When redox starts moving again, that ratio tends to normalize toward the mid-teens, especially if total lactate also comes down and overall energy tolerance improves.

If you’ve ever watched a great coach or a great clinician work, you’ll notice something they don’t stare harder; they see differently. They aren’t simply looking for more data; they’re trying to understand the rhythm beneath the data. Biology, especially mitochondrial biology, is a dance long before it becomes a number on a lab report. This article is about learning to see that dance. To understand how SS-31, methylene blue, ketone esters, and even your training decisions interact with real cellular dynamics, you need to know one thing above all else: Biology doesn’t run on quantity, it runs on phase. This is the part that confuses even very smart people. We’re trained to think that oxidative stress = bad, antioxidants = good, more oxygen = good, more ATP = good. But life is rhythmic, not linear. Your mitochondria aren’t furnaces they’re oscillators. They need to pulse. They need to switch between states. They need to signal, respond, tighten, release, and tighten again. This is why a supplement, a peptide, or a drug can work beautifully in one phase of physiology and completely derail things in another. To understand this, we need to talk about one of the most underrated molecules in all of human physiology: cardiolipin. CARDIOLIPIN: THE CONDUCTOR OF THE MITOCHONDRIAL ORCHESTRA Cardiolipin is a special lipid that lives almost exclusively in the inner mitochondrial membrane. If the mitochondrial membrane were a concert hall, cardiolipin would be the acoustic paneling that allows the orchestra to play in tune. It has four fatty acid tails, which is extremely rare most lipids have two. That design allows it to shape the membrane into cristae, those elegant folds where electron transport happens. These folds aren’t random architecture; they control the spacing, alignment, and speed of electron flow. Without cardiolipin, the ETC complexes would be like a bunch of musicians sitting in the wrong seats. Even more importantly, cardiolipin is both a sensor and a switch. When it is oxidized in the right way, it helps signal adaptation. When it is oxidized in the wrong way, it collapses mitochondrial membrane potential, releases cytochrome c, and pushes the cell toward apoptosis. This is why tools that interact with cardiolipin like SS-31 are profoundly powerful but profoundly phase-dependent. They’re not like taking creatine or magnesium; they actively alter the structural language of the mitochondria.

Since they all work on mitochondria in different ways if you wanted to do the three in what order would you do the Epitalon and Ss-31? I’m sure mots would be the final stage. How would you run a cycle like this and why? And where would SLU-pp-331 come into play?

I just got some and would like to know what a good starting dose is as a general mitochondrial dose.