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 (%) ?

Join me for our October Live Q&A on Saturday, October 25 at 12:00 p.m. EST. We’ll dig into peptides, mitochondrial medicine, training and recovery design, and real-world protocol troubleshooting. Bring your questions (big or small), wins, sticking points, and labs or metrics you want decoded. Come ready to learn, take notes, and leave with clear next steps you can use the same day. To submit a question in advance, reply to this post with “Q&A” at the top and a concise summary of your question; live questions will be taken in order after pre-submissions. Save the date, invite a friend who’d benefit, and I’ll see you Saturday at noon. Here is the link to watch the replay of the Q&A thank you everone for joining and thank you for sending your questions in! https://us06web.zoom.us/rec/share/pcj7EkP9JA9hgj2SIcHeiFFgml4klErn_CRj33Nbb10OM0gmzh7itR_vKyHGXXwd.Cs3mioaqFw2jbYHe?startTime=1761407862000 Passcode: e4T2tR!l

Why are we (the collective “we”) not talking about Cardarine more? It’s effective, and it’s cheap as hell, win win IMO. I get that these peptides, small molecules and whatnot are the hot topic nowadays, rightfully so, but why isn’t Cardarine in that discussion? I’ve personally seen good results with using carnitine and Cardarine together, and now I’m looking at bringing in SLU and the other mitochondrial players. How would I use Cardarine along with carnitine, SLU, mots c, etc.? I’ve used carnitine and Cardarine pre training with good success, but like all of us here, I want to keep improving Like I mentioned, I’ve used carnitine and cardarine pre training (substrate session) thinking that I’ll spare muscle glycogen, therefore improving performance, by enhancing fat usage and stimulating PGC-1 in a training environment would help make sure those new mitochondria are exposed to that environment. But if I’m looking to build my glycolytic system, maybe that’s not the best approach, and keep those players on more metabolic days? @Anthony Castore

Plasmalogens are one of the oldest, most fundamental molecules inside the human body, yet almost no one talks about them. If you imagine the cell as a city, plasmalogens are the shock-absorbing pavement, the insulation around every electrical wire, and the structural glue that determines how well the buildings hold up under stress. They make up a significant portion of the membranes around our cells, especially in the brain, heart, immune system, and mitochondria. They’re not used as fuel, they’re not signaling hormones, and they’re not vitamins they are architectural lipids, meaning their entire purpose is to create the “physical environment” inside which every biochemical reaction occurs. When this architecture is strong, cells communicate clearly, mitochondria keep up with energy demands, neurons fire smoothly, and tissues age more slowly. When plasmalogens decline as they do with aging, chronic inflammation, metabolic disease, and overtraining the whole system becomes more fragile. Surfaces become leaky. Signals get distorted. Energy becomes harder to make. And we see it clinically as brain fog, slower recovery, impaired metabolism, chronic fatigue, mood instability, and higher disease risk. To understand plasmalogens, you first need to understand the membrane. The membrane is the barrier between chaos and order. It keeps the inside of the cell different from the outside. But it’s not a hardened shell; it’s a flexible, dynamic, constantly-moving layer of phospholipids, cholesterol, proteins, and microdomains. Think of it like a high-tech trampoline. Every receptor sits in this trampoline. Every transporter is anchored to it. Every signal, from insulin binding to the NMDA receptor firing, depends on how stable and well-organized that trampoline is. Plasmalogens sit inside this membrane like reinforced beams with a special vinyl-ether bond. This bond is unique: it actually absorbs oxidative damage like a sacrificial shield. Instead of letting free radicals tear up the membrane, plasmalogens get hit first and protect the surrounding structure. This is why they are most concentrated in tissues with the highest oxidative stress—neurons, muscle, heart, immune cells, and mitochondria. When plasmalogens are low, cell membranes become thinner, more fragile, and more prone to dysfunction. Receptors do not cluster properly, inflammation becomes easier to trigger, and mitochondria lose their tight coupling between electron flow and ATP production. In other words, membranes lose intelligence.

SLU-PP-332 is one of the most misunderstood compounds in the entire performance and longevity space, and nowhere is that misunderstanding more obvious than in the topic of water retention. People experience it, panic, and immediately assume “estrogen,” “bad purity,” “toxicity,” or “my body isn’t responding to SLU correctly.” But when you break down what’s actually happening at the cellular level, the explanation is far more interesting, far more predictable, and far more fixable than people realize. Water retention with SLU isn’t random. It’s not a flaw in the compound. It’s a message from your system saying, “Your signaling is mismatched.” In this article, we’re going to break down what that means, why it happens, how SLU interacts with AMPK, ERRα, and renal sodium handling, and what the body is actually trying to do. By the end, beginners will understand the big picture clearly, and advanced clinicians and coaches will be able to teach it to others. To understand SLU and water retention, you first need to understand what SLU is actually doing. SLU is not a fat burner. It is not a stimulant. It is not a thermogenic drug. SLU is a pan-ERR agonist meaning it activates estrogen-related receptors alpha, beta, and gamma. These receptors live inside the nucleus and act like metabolic switchboards. They determine which genes get turned on to burn fat, use oxygen, increase mitochondrial respiration, create new mitochondria, and shift fuel preference. ERRα in particular is a master regulator of mitochondrial function. It influences everything from oxidative phosphorylation to uncoupling protein expression to metabolic adaptation under stress. When SLU binds to these receptors, it triggers the same gene programs normally activated by aerobic exercise: DDIT4, which senses metabolic stress and tells the cell to adapt, and SLC25A25, which helps shuttle fuel across the inner mitochondrial membrane so you can produce energy more efficiently. These genes are not surface-level actors. They’re deep in the machinery. They’re the electricians rewiring the power grid.