# Ipamorelin: The Skeletal Evidence on a Selective GH Peptide > Ipamorelin raised longitudinal bone growth dose-dependently in rats; its one human Phase 2 trial missed. A plain-English, cited digest of the literature, led by the bone-skeletal record. A plain-English digest of the bone, growth-hormone, and human-trial evidence on a selective GH-releasing peptide, with every quantitative claim cited and the gaps named. ## Start here, in plain English Ipamorelin is a lab-made peptide (a short chain of amino-acid building blocks) that tells the pituitary gland in the brain to release a pulse of growth hormone — the body's own signal for growth and repair. What makes it stand out is precision: it nudges growth hormone up without meaningfully raising stress hormones like cortisol, which older peptides in its family do [1]. Researchers were most curious about bone. In rats, ipamorelin made long bones grow faster, in step with the dose [4]. But the picture in people is thin: the only proper human trial — for slow bowel recovery after surgery — did not work [3]. So this site does two things at once: it celebrates what the bone and growth-hormone studies actually found, and it stays honest about how little has been tested in humans. What people report — including the downsides — is on [the effects page](/effects), and the [Ipamorelin research](/research) lays out every study. ## What the skeletal studies actually showed The headline finding sits in bone. When adult female rats received ipamorelin under the skin at 18, 90, and 450 micrograms a day for 15 days, the rate their long bones grew lengthwise climbed step by step with the dose — from 42 micrometers a day on placebo to 44, then 50, then 52 micrometers a day [4]. (A micrometer is one-thousandth of a millimeter; these are small, careful measurements of growth-plate activity, not visible changes.) What is striking is the route: blood levels of IGF-1 — the liver-made messenger that carries many growth-hormone effects — did not change [4]. That points to a partly local, pulse-driven skeletal effect rather than a flood of systemic growth factor. A second study delivered ipamorelin continuously by a tiny implanted pump at 0.5 mg/kg per day for 12 weeks. It raised the mineral *content* of the tibia and spine, but the volumetric mineral *density* did not change [8]. Read carefully, that means the bones got bigger rather than denser. A third study tackled steroid-weakened bone: ipamorelin given alongside a glucocorticoid lifted the periosteal bone-formation rate roughly four-fold versus the steroid alone, and improved muscle force [7]. The skeletal signal is real and reproducible — but every datum here is from rodents, and that boundary matters. ## The signature trait: selectivity Ipamorelin's defining feature is what it does *not* do. In its founding 1998 characterization it released growth hormone potently in rat pituitary cells, anaesthetised rats, and conscious pigs (pig ED50 of 2.3 nmol/kg, close to GHRP-6's 3.9 nmol/kg), yet it did not push ACTH or cortisol above the level seen with the body's own releasing hormone — even at doses more than 200 times its growth-hormone threshold [1]. (ACTH and cortisol are the stress-hormone pair; older GH-releasing peptides such as GHRP-6 raise them.) That clean separation is why ipamorelin earned the label "the first selective growth hormone secretagogue," and why a study of the [what is ipamorelin peptide](/what-is-ipamorelin) chemistry keeps coming back to its receptor selectivity. It works through the ghrelin receptor (GHS-R1a), a different doorway than the GHRH analogs, which is the whole rationale for pairing it with one. ## Where the human evidence stops Human data on ipamorelin is sparse and, for the indication tested, negative. The single published Phase 2 randomized trial enrolled 114 adults recovering from bowel surgery and gave 0.03 mg/kg intravenously twice daily for up to seven days. It missed its primary endpoint: the median time to a first tolerated meal was 25.3 hours with ipamorelin versus 32.6 hours with placebo, which was not statistically significant (p=0.15) [3]. A separate human pharmacokinetic study in eight volunteers per dose established a terminal half-life of about two hours and a single growth-hormone pulse peaking near 40 minutes after a dose [2]. There are no completed Phase 3 trials and no approved indication anywhere [3]. The full record — including the dose-by-dose [ipamorelin benefits](/benefits) reported in research and the cautions worth knowing — is laid out across this site, every figure tied back to its study in the [Ipamorelin references](/references). --- An md-desk reading of the ipamorelin record, led by the rat bone-growth data and kept honest about where the human evidence thins — every figure carried back to its study, no clinic behind the name and nothing dispensed.