# Ipamorelin: Half-Life, Clearance, and the GH Pulse It Triggers > Ipamorelin clears the human body with a terminal half-life of about 2 hours and triggers a single GH pulse peaking near 40 minutes. A pharmacokinetics-first literature digest, cited. A telemetry-grade reading of the published record: the half-life, the clearance, the volume of distribution, and the one human trial — every constant cited to source. ## The short version Ipamorelin is a small lab-made peptide — a chain of five amino acids — that tells the pituitary gland (a pea-sized gland under the brain) to release a burst of growth hormone. What makes it stand out is its precision: in animal studies it raised growth hormone without raising the stress hormone cortisol or the hormone prolactin, which the older peptides in its class did [1]. The numbers that matter most are about timing. In the one human study, the peptide left the bloodstream with a half-life (the time for the level in blood to drop by half) of about 2 hours, and the growth-hormone burst it set off peaked roughly 40 minutes after the dose [2]. People in research-use communities report deeper sleep and faster recovery; they also report flushing, hunger, and water retention. What people report — including the downsides — is on [the effects page](/effects). One important fact up front: ipamorelin has never been approved as a medicine anywhere, and the single mid-stage human trial it reached did not work [3]. ## What the ipamorelin record actually measures Ipamorelin is a synthetic pentapeptide (Aib-His-D-2-Nal-D-Phe-Lys-NH2) and a selective agonist of the ghrelin receptor — formally the growth hormone secretagogue receptor type 1a, or GHS-R1a (the docking site on pituitary cells that the hunger hormone ghrelin normally fits). Activating it triggers a pulse of growth hormone. The founding 1998 characterization measured that pulse and, more importantly, measured what it did *not* trigger: in conscious swine ipamorelin released growth hormone with an ED50 of 2.3 nmol/kg, comparable to the older peptide GHRP-6, yet it did not raise ACTH or cortisol above baseline even at doses more than 200-fold above the growth-hormone ED50 [1]. That selectivity — power without the off-target hormones — is the entire reason the molecule was named the first selective growth hormone secretagogue. The pharmacokinetics are where this site leads, because they are unusually well pinned for a research peptide. Human pharmacokinetic-pharmacodynamic modeling in eight healthy male volunteers per dose level, given five 15-minute intravenous infusions ranging from 4.21 to 140.45 nmol/kg, found dose-proportional kinetics: a terminal half-life of approximately 2 hours, a clearance of 0.078 L/h/kg, and a steady-state volume of distribution of 0.22 L/kg [2]. The growth-hormone response was a single discrete pulse peaking at about 0.67 hours — 40 minutes — after dosing [2]. Read [the half-life page](/half-life) for the full elimination profile. ## One human trial, and it missed The defining human anchor is a single Phase 2 randomized controlled trial. Under registration NCT00672074, 114 adults undergoing bowel resection received 0.03 mg/kg of ipamorelin intravenously twice daily for up to seven days [3]. The trial 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 statistical significance (p=0.15) [3]. Treatment-emergent adverse events occurred in 87.5% of the ipamorelin arm versus 94.8% of the placebo arm — no ipamorelin-specific safety signal surfaced in that short window, but efficacy was not demonstrated [3]. No Phase 3 trial followed, and no regulator has ever approved the compound [3]. The contrast between that thin human record and the broad preclinical literature is the honest frame for everything here. Across rodent and large-animal models the selective growth-hormone effect is reproducible; the human outcome data is one negative trial and one pharmacokinetic dataset. This is a research story, not a verdict — but the verdict so far, where verdicts exist, is that efficacy in humans was not shown. ## What the preclinical models added Beyond the founding characterization, the animal literature filled in mechanism and body-composition signals. Subcutaneous ipamorelin at 18, 90, and 450 microg/day (divided three times daily for 15 days) raised the longitudinal bone-growth rate of adult female rats from 42 microm/day on vehicle to 44, 50, and 52 microm/day, with no measurable change in total IGF-1 or bone-turnover markers — a partly local, pulse-driven skeletal effect [4]. The most recent published in-vivo study, a 2024 ferret experiment, found that intraperitoneal ipamorelin (1-3 mg/kg) inhibited cisplatin-induced body-weight loss by roughly 24% during the delayed phase, while having no anti-emetic effect [5]. The metabolism literature is equally specific. In male rats, ipamorelin showed roughly five-fold lower plasma clearance than GHRP-6, with 60-80% of the dose recovered intact in bile and urine and an intranasal bioavailability near 20% [7]. The receptor reach extends past the pituitary, too: ex vivo pancreatic tissue from normal and diabetic rats released insulin directly in response to ipamorelin, a peripheral effect independent of growth hormone [13]. These are the [Ipamorelin research](/research) details that the pharmacokinetics lens is built on — the clearance numbers, the route comparisons, and the single human dataset that ties them together. ## How to read this site This is a research digest, not a clinic and not a store. The word 'doctor' in the domain names a reading posture — examining the evidence closely — not a medical service, and nothing here is medical advice. Three habits run through every page. First, leading with the measurement: the half-life, the clearance, the ED50, the trial endpoint, before any interpretation. Second, keeping community reports separate from clinical findings — anecdotal effects people describe are labeled as such and never carry a dose. Third, citing every quantitative claim to a primary source, listed in full on the references page. The result is a frank account of what the ipamorelin literature shows: a precisely characterized pharmacokinetic profile, a reproducible selective mechanism, one negative human trial, and a long-term human safety record that simply does not yet exist [2][3]. The pages are organized around that pharmacokinetics-first frame. The two dedicated pages answer the timing questions people ask most: [how long does ipamorelin stay in your system](/half-life), which walks through the half-life, clearance, and volume of distribution, and [how long does it take for ipamorelin to work](/how-long-to-work), which separates the roughly 40-minute hormonal onset from the multi-week effects users report. The research page lays out the full mechanism and every key study; the dosage page reports only the doses that appear in published work, never a recommendation. For the honest human-interest layer — what people say they feel, good and bad, plus who has reason to be careful — start with the effects page. --- A telemetry-grade reading of the published ipamorelin record — the half-life, the clearance, and the single growth-hormone pulse logged and cited; no clinic behind the console and nothing here dosed, dispensed, or sold.