Format
Explainers
Plain-language breakdowns of what a compound is and how it works.
36 articles
Metabolic health5-Amino-1MQ — the NNMT inhibitor and the body composition conversationYou do everything right for six months. The diet is clean — genuinely clean, not self-deceiving. The training is consistent. Sleep is adequate. The weight drops, but not the way you expected: mostly muscle along with the fat, so the body composition number barely moves, and the scale improvement feels borrowed rather than earned. You feel smaller but not different. The metabolic math doesn't seem to be working in your favor the way it worked when you were twenty-five.8 min readCognitive supportAdamax — the enhanced Semax analogYou've read the Semax research. The BDNF upregulation is compelling. The Russian clinical data on stroke recovery and cognitive enhancement is more substantial than you expected. The intranasal delivery makes practical sense. And then you get to the pharmacokinetics section and find the number that gives you pause: the half-life of Semax after intranasal administration is measured in minutes. The molecule is active, bioavailable via the olfactory route, and then degraded quickly by peptidases in the blood and tissues. Whatever it's doing, it's doing it briefly, and the dosing implications — multiple administrations per day, careful timing around the desired effect window — are a practical constraint on a compound that's already operating outside the mainstream pharmaceutical supply chain.8 min readRecovery and inflammationARA-290 — the erythropoietin fragment that doesn't make red blood cellsThe drug that saves you during a heart attack also, it turns out, does something your bone marrow was never involved in. Doctors have known for decades that erythropoietin — the hormone produced by the kidneys in response to low oxygen — does more than stimulate red blood cell production. When someone has a stroke or a myocardial infarction, tissues that should die don't, sometimes, if EPO levels are high enough. The mechanism for why stayed murky for a long time. The therapeutic question it raised was harder: if EPO can protect tissue, why not use it for that?8 min readRecovery and inflammationBPC-157 and TB-500 in plain English — what tissue-repair peptides actually doYou tweaked your shoulder in December and by February it still hasn't come back. Not dramatically hurt — just not right. Range of motion down maybe fifteen degrees. A specific ache when you reach behind your back. You've done the PT exercises, you've iced it, you've rested it. The body isn't doing what the body is supposed to do, which is heal. And you start to wonder whether "it'll come back" is actually true.9 min readWomen's hormonal healthCetrorelix in IVF — what GnRH antagonism actually controlsYou're on day eight of stimulation. You've been injecting FSH every morning, watching follicles grow on the ultrasound monitor, doing the math on retrieval timing with your reproductive endocrinologist. Everything is on schedule. Then you get a call from the clinic: your LH is starting to move. The nurse's voice is calm but there's urgency underneath it — because a premature LH surge at this point, before the eggs are mature, means the follicles might ovulate on their own before retrieval can happen. It means the cycle could be compromised. It means weeks of preparation and thousands of dollars might not yield the retrieval you were planning on. This is the clinical problem that Cetrorelix was designed to solve, and it solves it by going directly to the source.8 min readWomen's hormonal healthCetrorelix in IVF — the patient experience explainedYou've been doing the stimulation injections for a week. Every morning you pull the Gonal-F or Follistim out of the refrigerator, you've gotten comfortable with the needle, and the monitoring appointments have confirmed the follicles are growing. Then the clinic calls: start the cetrorelix tomorrow. You look at the package in your refrigerator — a small pre-filled syringe, different from what you've been using — and you want to understand what it is and what it's doing before you inject it.8 min readCognitive supportCortexin in plain English — the bovine brain extract used in stroke recoveryYou survive the stroke. That part goes as well as it can — the clot is caught early, the emergency intervention works, you're alive and you go home. What no one prepares you for is the months afterward. The word that used to come in half a second now takes four. You lose the thread of a sentence mid-paragraph. You read the same line three times and it doesn't stay. The neurologist says you should be seeing improvement, that the brain is plastic, that recovery takes time — and all of that is true, and none of it tells you what to do about the fact that your thinking feels like it's running through wet concrete.8 min readCognitive supportDihexa in plain English — the neurogenic peptide and the HGF/c-Met storyYou watch your father search for the word he used every day for forty years. He circles it, describes it, lands somewhere near it. The word itself is gone. That particular loss — not catastrophic, not dramatic, just the slow erosion of a mind that built things — is exactly the gap that a small group of neuropharmacologists in Pullman, Washington spent years trying to understand. Not to write a prescription. To understand what was happening at the level of the synapse, and whether it could be changed.8 min readSleep and recoveryDSIP and the deep-sleep story — what the original peptide research suggestedIt's 1974 in Basel, Switzerland, and a rabbit is asleep. Not naturally asleep — electrically induced into a slow-wave state, its brain oscillating in the long, lazy delta rhythms that characterize the deepest phase of sleep. Marcel Monnier and Guido Schoenenberger are collecting something from the animal: blood drawn from the cerebral venous sinus, the vessel draining the sleeping brain. Their hypothesis is strange by the standards of the time. They believe sleep isn't just a brain state — they believe it might be a circulating signal. Something in the blood of a sleeping animal, they suspect, could make a waking animal sleep.8 min readAnti-aging and cellular healthEpigenetic clocks — Horvath, GrimAge, and what biological age tests actually measureYou spit in a tube, seal it, mail it off, and eight weeks later a number arrives: your biological age. Maybe the report says 38.2. You're 44 chronologically. A minor celebration. Or it says 47.6, and you spend the next week wondering what exactly you've been doing to yourself. The number has a quality of authority that a cholesterol panel carries — it arrives formatted, annotated, compared to a reference range, delivered by a company with a clean website and peer-reviewed citations in the footer. The question worth asking before you do anything with it is what the number actually measures, how confident you should be in it, and what the science behind it can and cannot honestly tell you.12 min readMetabolic healthFrag 176-191 in plain English — the hGH C-terminal fragment for fat metabolismWhen researchers started pulling apart human growth hormone in the 1970s and 80s, they were trying to figure out which parts of the molecule did which jobs. Human growth hormone is a 191-amino-acid protein — a single polypeptide chain folded into a specific three-dimensional shape — and it does several things at once: it stimulates IGF-1 production in the liver, which drives tissue growth and cell proliferation; it promotes lipolysis, the breakdown of stored fat; it supports protein synthesis in muscle. The question was whether these effects were separable. Whether you could take a molecule that did five things and isolate the part responsible for one of them.7 min readGrowth hormone and recoveryGHRP-2 in plain English — the GH releaser with appetite and cortisol bonusYou're three weeks into a recovery protocol and you notice something unexpected: you're hungry in a way you weren't before. Not the ordinary hunger that builds over hours since your last meal. Something more insistent, arriving earlier, harder to dismiss. Your sleep feels deeper. Your morning mood is better. But the hunger is real, and it wasn't on your list of expected effects.8 min readGrowth hormone and recoveryGHRP-6 in plain English — the appetite-stimulating GH releaserYou take the injection and forty-five minutes later you're standing in front of an open refrigerator, not because you're hungry in the ordinary sense but because something in your body has decided, with unusual conviction, that food is necessary right now. You weren't thinking about eating before you injected. You're thinking about nothing but eating now. The sensation is specific enough to be disorienting — not the soft background hum of an appetite building over hours, but something that arrives like a signal.8 min readHormonal and endocrineGonadorelin in plain English — GnRH and the pituitary feedback loopBefore you had a single reproductive hormone in your bloodstream, before your gonads had ever been activated, a handful of neurons in your hypothalamus were already learning to fire in a rhythm. Not continuously — in pulses. A burst of electrical activity every hour or two, releasing a ten-amino-acid peptide into the pituitary portal blood, which carried it the short distance to the pituitary gland, which responded by releasing LH and FSH. This pulse had to be irregular enough to feel like a signal rather than background noise. It had to arrive, be recognized, and then stop — so the pituitary's receptors could reset and be ready for the next one. The hypothalamus spent years calibrating this rhythm before puberty began. That rhythm is what started everything else.4 min readGrowth hormone and recoveryHexarelin — the potent GH secretagogue with cardiac effectsThe Italian cardiologists were studying a peptide they'd initially investigated for growth hormone deficiency, and they kept finding something they hadn't expected in the heart. Not a side effect in the ordinary sense — a therapeutic signal. Animal models with damaged cardiac tissue showed improved contractility. Preclinical data suggested the heart was responding to Hexarelin through a mechanism that wasn't the growth hormone axis at all. A peptide built to stimulate GH was doing something in cardiac muscle that GH itself didn't fully explain.5 min readMitochondrial healthHumanin — the mitochondrial peptide that protects neuronsIn 2001, in a laboratory in Tokyo, a researcher named Yuichi Hashimoto was trying to understand why some neurons survive exposure to amyloid-beta and some don't. Alzheimer's disease research at that point was already deeply invested in the amyloid hypothesis — the idea that the accumulation of amyloid-beta peptide fragments is the initiating event in the disease — but the mechanism of neuronal death was still being worked out. Hashimoto's group was screening a library of expressed sequences from the brain tissue of Alzheimer's patients, looking for something that could explain or counteract the toxicity. What they found was not what they were looking for.8 min readGrowth hormone and recoveryIGF-1 LR3 in plain English — what an engineered IGF-1 actually doesYour doctor tells you your IGF-1 is on the low end of normal. You nod, leave the office, and spend the next hour trying to understand what that actually means. The name is impenetrable — Insulin-like Growth Factor 1 — and every search result either leads to pediatric growth disorders or to bodybuilding forums full of syringe photos. The two contexts seem completely unrelated, and yet they're orbiting the same molecule for overlapping reasons that are worth understanding clearly.8 min readGrowth hormone and recoveryIpamorelin in plain English — the cleanest of the secretagoguesIn the late 1990s, a team of researchers at Novo Nordisk was working through a screening problem. They had growth hormone-releasing peptides — GHRPs — that worked. GHRP-2, GHRP-6, Hexarelin: all of them stimulated pituitary GH release reliably, and some of them did it dramatically. The problem was that "worked" turned out to cover too much territory. The same compounds that elevated GH also elevated cortisol. They elevated prolactin. GHRP-6 in particular produced significant appetite stimulation — not a mild increase but a noticeable, sometimes uncomfortable hunger response. The researchers had tools that did the thing they were designed to do, but they did it while simultaneously pulling levers that nobody had asked them to pull.4 min readHormonal and endocrineKisspeptin-10 — upstream of GnRH and the libido conversationIn 1996, a team of researchers studying cancer metastasis in malignant melanoma identified a gene that, when present in tumor cells, suppressed their ability to spread to other tissues. They named it KiSS-1, after Hershey, Pennsylvania — the birthplace of the study's lead researcher and home of the Hershey Kiss. The gene was interesting as an oncology finding, catalogued alongside other metastasis-suppressor genes, and largely forgotten outside that narrow field for several years. Nobody expected it to turn out to be the master switch for the entire human reproductive system.5 min readImmune modulationKPV in plain English — the α-MSH fragmentIn the early 1990s, a research group at the University of Milan was working through a problem that had occupied melanocyte-stimulating hormone research for years: the parent peptide did interesting things to inflammation, but figuring out which part of the peptide was responsible required taking the molecule apart. Alpha-MSH is thirteen amino acids long. The inflammation work kept pointing toward the tail end of it — the C-terminal sequence. Specifically, the last three amino acids: lysine, proline, valine. What the researchers found when they isolated those three amino acids and tested them was that the fragment retained a surprising amount of the anti-inflammatory activity of the full molecule. It even, in some contexts, exceeded it.4 min readPeptide scienceThe melanocortin system, explained — tanning, libido, appetite, inflammation, all from one receptor familyConsider the question for a moment: how does a single biological signaling family govern the color of your skin, the strength of your sexual drive, your appetite at lunch, and the intensity of an inflammatory response happening somewhere in your knee? It seems like too much to ask of one system. The body tends toward specialization — receptors for this, channels for that. Yet here is the melanocortin system, doing all of it, sometimes simultaneously, with a small family of peptide ligands derived from a single precursor protein and five receptor subtypes distributed across nearly every tissue in the body.8 min readGrowth hormone and recoveryMGF and PEG-MGF — the IGF-1 splice variant that turns on after exerciseTwo days after a particularly hard leg session — the kind where you went heavier than you planned and your form started to slide in the last few sets — the soreness is deep. Not the surface ache of muscles that worked hard, but the dense stiffness of tissue that was genuinely stressed. Your quads feel thick. Your hamstrings are tight in the belly of the muscle. This is not injury, exactly. It's the signature of damage that your body is in the process of repairing, and if the biology goes the way it should, you'll come back slightly stronger for it. The question exercise physiologists have spent decades trying to answer is: how does the muscle know to repair rather than just scar?8 min readPeptide scienceThe myostatin pathway in plain English — why blocking it mattersPicture a Belgian Blue bull standing in a Belgian field. The animal looks wrong in the way a cartoon looks wrong — too much muscle packed into a body that should not be able to hold it. Shoulder muscles that stack like boulders. A rear end so hypertrophied it appears almost architectural. These animals are not the product of selective breeding for strength alone, nor any exotic feeding program. They carry a broken gene. The gene that would have told their muscles to stop growing simply does not work. The result is standing in a field, blinking at you.7 min readCognitive supportPACAP — the neuroprotective peptide also implicated in migraineIn 1989, Akira Arimura and colleagues at Tulane University were extracting ovine hypothalamic tissue — sheep brains, processed in quantity — looking for new signaling peptides. They were using an assay designed to detect compounds that elevated cyclic AMP in pituitary cells, a standard probe for peptides that activate adenylate cyclase. What they isolated was a thirty-eight amino acid neuropeptide, unlike anything previously characterized, that was among the most potent activators of adenylate cyclase in pituitary tissue they had ever encountered. They named it Pituitary Adenylate Cyclase-Activating Polypeptide. PACAP. The name was mechanistic rather than elegant, but it stuck.7 min readCognitive supportPE-22-28 — the short neuropeptide for mood, memory, and cognitive resilienceIt's two in the afternoon and you haven't started the thing you were supposed to start at nine. Not because you've been distracted — you've been sitting at the desk, roughly aimed at the work, just not doing it. The ceiling feels lower than usual. The inside of your head has a particular quality to it: not the sharp absence of sleep deprivation, not the flat numbness of serious depression, just a muted, frictionful kind of gray. You're functional. You're also, clearly, not at your best. And the standard advice — sleep, exercise, get some sunlight — is correct and insufficient.7 min readCompounding and compliancePeptide pulsing and microdose protocols — what they are and what evidence supports themYour prescribing provider suggests starting a GLP-1 at a lower dose than standard. Or the protocol sheet says five days on, two days off. Or the documentation you're reading recommends cycling a growth hormone secretagogue for three months and pausing. You're not sure whether this is standard practice, creative optimization, or something invented by the internet. The honest answer is that it depends on the compound — and that the rationale behind non-daily dosing is more grounded in biology than it might appear, even when the specific protocols outrun the formal evidence.9 min readHormonal and endocrinePost-cycle therapy in plain English — what it is and why it mattersYou've stopped. Whether you made the decision yourself, were advised to by a provider ending a supervised TRT course, or simply reached the point where the consequences outweighed the benefits — you've come off exogenous testosterone or anabolic steroids, and now you're waiting for your body to restart something it stopped doing while the external supply was running. The waiting is not comfortable. Energy is low. Mood is poor in the particular way that insufficient testosterone produces — not quite depression, more like a sustained deflation, a thinning of the world. Libido is absent. The body feels different and not in a good way. You've been told it'll come back on its own, and that's true in principle. In practice, the question of how long, how completely, and what you can do to support the process — these are questions that deserve real answers rather than reassurance.9 min readCognitive supportSemax, Selank, and the calm-focus questionYou've tried the stimulant route. The first week was productive — maybe genuinely productive — and then the jitteriness settled in, the appetite disappeared, and the crash at 4 p.m. made the second half of the day feel like a tax you owed. You've tried the other route too: the SSRI that took the edge off everything, including the part of you that cared about getting things done. Somewhere between wired and flat there's a thing you're looking for, and it doesn't seem to have a name.8 min readAnti-aging and cellular healthSenolytics in plain English — clearing aged cells as an aging strategyYou're sixty-two and your joints ache in ways they didn't at fifty. Not an injury — nothing you can point to. Just a general, ambient stiffness that is worst in the morning and never quite goes away. Your doctor says it's wear and tear, which is medically accurate and explains nothing. What it doesn't explain is the mechanism underneath — why tissues that were working fine for decades are now failing in a way that feels less like breakdown and more like something actively going wrong.9 min readHormonal and endocrineSeractide / ACTH 1-39 — adrenal function testing in plain EnglishYou've been fatigued for two years. Not tired — fatigued. The kind where waking up doesn't end it, where the second half of every day feels like dragging yourself through something thick, where you've stopped scheduling things in the afternoon because you know you'll be useless. The labs your primary care doctor ran came back "normal." But normal relative to what, and for whom, and measured at what time of day — those questions don't usually get asked. If they do get asked, eventually someone orders an ACTH stimulation test, and what that test measures is more specific and more useful than most fatigue workups. Understanding what it's doing requires understanding the gland it's interrogating.7 min readSleep and recoverySermorelin in plain English — what growth-hormone-peptide actually doesYou've heard the phrase "growth hormone peptide" and you've probably pictured something adjacent to performance-enhancing drugs — the territory of professional athletes and extreme biohackers, syringe-and-vial culture, people who are trying to be something they're not. The reality of what sermorelin actually is and how it works is substantially less dramatic, and substantially more interesting, than that image.8 min readMetabolic healthSetmelanotide and genetic obesity — what targeted MC4R activation looks likeThe child eats constantly. Not the way toddlers go through phases of wanting snacks — this is something different, something the parents describe to pediatricians with a kind of desperation, the word "insatiable" appearing and reappearing in every appointment. The weight gain started before age two. The hunger doesn't respond to meals the way hunger is supposed to. Doctors check for behavioral causes. Nutritionists are consulted. Families restructure their entire kitchens and still wake up to find a child crying for food in the middle of the night.8 min readAnti-aging and cellular healthSirtuins — the longevity proteins and what they actually doIn the late 1990s, a yeast cell in Leonard Guarente's lab at MIT quietly upended the assumption that lifespan was a fixed parameter. The gene in question was Sir2 — Silent Information Regulator 2 — and when researchers added extra copies of it to yeast, the cells lived longer. When they deleted it, the cells died sooner. Nobody had expected a single gene to move the lifespan needle in either direction. The question the experiment opened wasn't just "what does Sir2 do" but something more unsettling: if a gene could regulate how long a cell lives, what exactly is the machinery of aging, and how close to the surface is it?12 min readMetabolic healthTesofensine — the triple monoamine reuptake inhibitor that almost happenedIn the early 2000s, a Danish pharmaceutical company called NeuroSearch was looking for a drug to treat Parkinson's and Alzheimer's disease. They had a compound — tesofensine — that blocked the reuptake of serotonin, norepinephrine, and dopamine simultaneously, a triple monoamine reuptake inhibitor with a chemical profile they believed might slow neurodegeneration. The trials didn't go the way they hoped for Parkinson's. But the researchers noticed something. Patients in the neurological trials were losing weight. Consistently, significantly, and in a way that didn't seem explicable by nausea or illness.8 min readImmune modulationThymalin — the original Khavinson thymic immunomodulatorYou get sick more often than you used to. Not dramatically — you're not hospitalized, you don't have a diagnosed immunodeficiency, your doctor nods and says it's normal. But the cold that would have resolved in three days now runs a week, and there's a second cold three weeks later, and the overall texture of your immune system's performance has shifted in ways that feel real but don't generate any flagged labs. The lymphocyte count is in range. The CBC is normal. And yet something has changed in the body's capacity to respond quickly, to clear the infection, to recover and return to baseline. This is not imagined. It is one of the most consistent features of biological aging: the immune system declines, and the instrument driving much of that decline is the thymus.8 min readImmune modulationVIP in plain English — the multi-organ vasoactive peptideThe bronchospasm hits in the third floor stairwell. No obvious trigger — no cold air, no allergen you can name. Your airways tighten, your breath shortens, and somewhere in the back of your mind you're cataloguing how many times this week it's happened. The pulmonologist has ruled out asthma three times. The immunologist says your numbers look fine. And you're standing in a stairwell with your hand on the railing, waiting for your lungs to remember what they're supposed to do.8 min read