# Ipamorelin: Half-Life, Clearance, and the Human Pharmacokinetics Record > Ipamorelin has a terminal half-life of approximately 2 hours in human volunteers, clearing at 0.078 L/h/kg and producing a single growth-hormone pulse near 40 minutes. A cited pharmacokinetics and due-diligence digest. A scholarly reading of the half-life, clearance, and time-course data, the failed Phase 2 endpoint, and the regulatory record — every quantitative claim carried back to its source. ## The short version Ipamorelin is a small lab-made peptide — a chain of five building blocks — that tells the pituitary gland (a hormone gland at the base of the brain) to release a short burst of growth hormone. Its claim to fame is being clean about it: in animal studies it raised growth hormone without raising the stress hormone cortisol, which sets it apart from older peptides in its class [1]. The one human study that measured how the body handles it found it leaves fairly fast, with a terminal half-life (the time for the blood level to fall by half) of about two hours, and the growth-hormone burst it triggers peaks around forty minutes after a dose [2]. The only human trial of whether it actually *does* anything useful — for slow bowel recovery after surgery — did not beat placebo [3]. It has never been approved as a medicine anywhere. What people report, including the downsides, is on [the effects page](/effects). ## What the ipamorelin pharmacokinetics establish Ipamorelin is a synthetic pentapeptide (a five-amino-acid chain, sequence Aib-His-D-2-Nal-D-Phe-Lys-NH2) that selectively activates the ghrelin receptor — formally the growth hormone secretagogue receptor 1a, or GHS-R1a (the same receptor the body's natural hunger hormone uses) — on the pituitary gland's somatotrophs (the cells that make growth hormone). Activation triggers a discrete pulse of growth hormone (GH) release [1]. The single published human pharmacokinetic study is the foundation a due-diligence reading begins from. In eight healthy male volunteers per dose level, given five 15-minute intravenous infusions spanning 4.21 to 140.45 nmol/kg, the kinetics were linear and dose-proportional: a terminal half-life of approximately 2 hours, plasma clearance of 0.078 L/h/kg, and a steady-state volume of distribution of 0.22 L/kg. The GH response was a single pulse that peaked at about 0.67 hours — roughly 40 minutes — after dosing [2]. Those are the numbers that anchor every honest claim on this site, and they are reproduced on the [how long does ipamorelin stay in your system](/half-life) page. What the pharmacokinetics do **not** establish is therapeutic benefit. That is a separate question, and the human answer to it so far is negative. ## Why a site named for legitimacy leads with the evidence, not the marketing "Legit" here means one thing: holding ipamorelin's reputation up against the published record and reporting the gap honestly, in either direction. The mechanism is real and well-characterized — the 1998 founding study established ipamorelin as the first highly GH-selective secretagogue, releasing GH as potently as GHRP-6 in swine (ED50 2.3 nmol/kg vs 3.9 nmol/kg) while leaving ACTH and cortisol essentially unmoved even at doses more than 200-fold above its GH threshold [1]. But mechanism is not outcome. The only controlled human efficacy trial — a Phase 2 study in 114 bowel-resection patients — 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 did not reach significance (p=0.15) [3]. Widespread promotion of ipamorelin for anti-aging, fat loss, and muscle gain rests on mechanism and short rodent studies, not on controlled human outcomes. A legitimate reading keeps those two things apart. ## The selectivity finding, and where the evidence thins Ipamorelin's selectivity is its most reproducible result. It releases GH through the ghrelin-receptor (GHS-R1a) pathway, a mechanism distinct from and complementary to growth-hormone-releasing hormone (GHRH) — which is the pharmacological basis for pairing it with GHRH analogs such as CJC-1295 [1]. In adult female rats, subcutaneous ipamorelin at 18, 90, and 450 micrograms per day raised the longitudinal bone-growth rate from 42 to 52 micrometers per day in a dose-dependent way, notably without any measurable change in circulating IGF-1 — evidence that part of the skeletal effect is driven locally by the GH pulse rather than by sustained systemic IGF-1 [4]. The human evidence, by contrast, is limited and largely negative for the indications tested. There are no completed Phase 3 trials, no approved indication, and no long-term human safety database. The full mechanism and study breakdown is on the [Ipamorelin research](/research) page; the reported real-world effects and the cited safety cautions are on [the effects page](/effects). --- A pharmacokinetics-first due-diligence read of the ipamorelin record — the ~2-hour human half-life and the clearance figures logged as the one clean instrument reading, the failed Phase 2 endpoint and the 503A/WADA status entered straight from the register, and the community reports held to one side as unverified; no clinic behind the readout, no endorsement of any seller, and nothing here dosed, prescribed, or sold.