# Ipamorelin: The First Selective Growth Hormone Secretagogue > Ipamorelin raises growth hormone cleanly — minimal cortisol, minimal prolactin. A plain-English digest of the published research, with every quantitative claim cited. A forward-looking digest of the published literature — the selectivity data, the human pharmacokinetics, the one trial that failed, and what people report — with every figure carried back to the study that measured it. ## The short version Ipamorelin is a tiny lab-made peptide — a chain of just five amino acids. Its one job is to tap a single receptor in the brain's master gland (the pituitary) and make it release a quick pulse of growth hormone, the body's signal for repair and rebuilding. What made ipamorelin a landmark when it was first described is that it does this *cleanly*. Older peptides that release growth hormone also spiked stress hormones like cortisol and prolactin; ipamorelin mostly does not [1]. That clean, on-target pulse is the whole story here. What do people use it for? In research-use circles, the most common reasons are better sleep, faster recovery, and a slow shift toward leaner body composition. The honest state of the evidence: animal data is strong on the selectivity itself, but human data is thin — and the one real human trial, for a gut-recovery condition, did not work [3]. Ipamorelin is **not an approved medicine** anywhere, and nothing here is sold, prescribed, or dosed. The downsides people report — a warm facial flush, more hunger, mild puffiness — and who should be careful are laid out on [Ipamorelin effects](/effects). ## One receptor, one clean pulse Ipamorelin (sequence Aib-His-D-2-Nal-D-Phe-Lys-NH2) is a selective agonist of the ghrelin receptor, formally the growth hormone secretagogue receptor type 1a, or GHS-R1a (the docking site that the body's own "hunger hormone" ghrelin normally uses). When ipamorelin binds it, pituitary somatotrophs — the cells that make growth hormone — fire off a discrete GH pulse [1]. The defining result, from the 1998 founding paper, is what *didn't* move. In rats and conscious swine, ipamorelin released GH about as potently as the older peptide GHRP-6 (swine ED50 of 2.3 nmol/kg versus 3.9 nmol/kg for GHRP-6) — yet it did **not** raise ACTH or cortisol above baseline even at doses more than 200-fold above its GH threshold [1]. That is the selectivity that gives this site its name: a strong signal with almost no off-target noise. Want the mechanism in plain language first? Start with [what does ipamorelin peptide do](/how-it-works). Want the molecule itself? See [what is ipamorelin peptide](/what-is-ipamorelin). ## What the human data actually says Human evidence is limited, and it is honest to say so. The cleanest human dataset is a pharmacokinetic study in eight healthy male volunteers per dose level: single intravenous infusions produced dose-proportional kinetics, a terminal half-life of roughly 2 hours, and a single GH pulse peaking about 40 minutes after dosing [2]. That tells you how the drug behaves in the body — fast in, fast out, one clean pulse. What it doesn't tell you is whether ipamorelin treats anything. The only published Phase 2 trial put that to the test: 114 adults recovering from bowel surgery received ipamorelin intravenously, and the study **missed its primary endpoint** — median time to first tolerated meal was 25.3 hours with ipamorelin versus 32.6 hours with placebo, a difference that was not statistically significant (p=0.15) [3]. No further clinical development followed. The honest read: the mechanism is real and elegant; the human outcome record is thin and, where tested, negative. ## Signals from the animal record The preclinical literature is where ipamorelin's profile is fleshed out. Subcutaneous ipamorelin dose-dependently increased the longitudinal bone-growth rate of adult rats — from 42 micrometers per day on vehicle up to 52 micrometers per day at the top dose — without measurably changing circulating IGF-1, suggesting part of the skeletal effect is driven locally by the GH pulse rather than by a sustained rise in IGF-1 [4]. (IGF-1, insulin-like growth factor 1, is the liver-made messenger that carries out many of growth hormone's downstream effects.) The most recent in-vivo study, from 2024, found that ipamorelin blunted chemotherapy-driven weight loss in ferrets by about 24% during the delayed phase — a peripheral, body-composition effect — while having no anti-nausea action [5]. The throughline across three decades: a selective GH-pulse machine with real, reproducible effects on growth and body composition in animals, still awaiting a positive human outcome trial. The full breakdown lives in the [Ipamorelin research](/research) digest. --- A forward-looking read of the ipamorelin literature, led by the one trait the molecule does cleanly — a selective GH pulse with the cortisol and prolactin left out — and honest about where the human evidence still runs thin; a reading instrument, not a clinic, a prescription, or a store.