# Ipamorelin Dosage Research Context — As the literature records it > Dose ranges as they appear in the published ipamorelin literature: rodent ED50 values, subcutaneous bone-formation studies, the 0.5 mg/kg/day osmotic-minipump protocol, and the 0.03 mg/kg IV human Phase 2 protocol. Research context only. Not dosing guidance. ## What this page is and is not The published ipamorelin literature reports specific doses administered to specific species, by specific routes, for specific durations, to produce specific measured outcomes. Those numbers are quoted here, with each one attributed to the study that produced it. Nothing on this page is dosing guidance, dosing advice, a dosing recommendation, or a dosing protocol for human use. Ipamorelin is not approved by the United States Food and Drug Administration or any major regulatory agency for any human indication. Its presence on the World Anti-Doping Agency Prohibited List (S2.2) is reason enough — apart from the regulatory and safety questions — that no one in WADA-code sport could use it without violating the code. The site does not sell ipamorelin and is not affiliated with any vendor. ## Rodent intravenous: the ED50 anchor (Raun 1998) In the anesthetized rat intravenous bolus model used by Raun and colleagues, the median effective dose for growth hormone release was 80 ± 42 nmol/kg, producing a maximal growth hormone response of 1545 ± 250 ng/ml [1]. In the conscious swine model from the same paper, the median effective dose was 2.3 ± 0.03 nmol/kg intravenous, with a maximal response of 65 ± 0.2 ng/ml [1]. These ED50 figures anchor every subsequent ipamorelin dose discussion in the preclinical literature — they are the reference points other studies titrate around or scale from. ## Rodent subcutaneous: bone-formation protocols (Johansen 1999; Svensson 2000) Two protocols anchor the rodent bone-formation literature. Johansen and colleagues administered 0, 18, 90, and 450 micrograms per day subcutaneously to adult female Sprague-Dawley rats for 15 days, **divided three times daily** [3]. The three-times-daily fractionation is consistent with the approximately 2-hour pharmacokinetic half-life that Gobburu later characterized in humans [2] — pulsatile dosing aligns with pulsatile growth hormone release rather than producing a continuous tonic exposure. The dose-dependent rise in longitudinal bone growth rate (42, 44, 50, 52 micrometres per day) is the principal pharmacodynamic readout from that study. Svensson and colleagues used a contrasting design — continuous subcutaneous infusion via osmotic minipump at 0.5 mg/kg/day for 12 weeks — in 13-week-old female Sprague-Dawley rats [4]. The continuous-infusion design was deliberately chosen to maintain steady-state ipamorelin concentrations and test whether sustained GHS-R1a agonism produced bone mineral content gains. It did, with some parameters comparable to recombinant growth hormone at 3.5 mg/kg/day. The two designs — pulsatile three-times-daily versus continuous infusion — bracket the dose-rhythm question in the rodent bone literature. ## Rodent intravenous: the gastric-motility protocol (Greenwood-Van Meerveld 2012) In the postoperative ileus rodent model from Greenwood-Van Meerveld and colleagues, two intravenous bolus doses were tested: 0.014 micromol/kg and 0.14 micromol/kg [6]. The higher dose accelerated gastric emptying (less than 25% of an orally administered radiolabel retained in the stomach at 15 minutes, versus 78 ± 5% in vehicle) and normalized small-bowel transit. In vitro tissue-bath experiments used 1 micromolar ipamorelin. These doses are an order of magnitude below the growth-hormone-release ED50 in the same species, suggesting that gastric-motility effects can occur at sub-secretagogue exposures — though that observation has not been replicated in human studies. ## Human intravenous: the Beck 2014 protocol The only published human Phase 2 efficacy protocol administered 0.03 mg/kg intravenously twice daily for up to 7 days (or until discharge) to adults undergoing bowel resection [7]. The trial design used scheduled twice-daily dosing tied to the postoperative recovery window. With a 70 kg adult, 0.03 mg/kg works out to 2.1 mg per dose — substantially higher than the chronic doses used in the rodent bone studies on a per-kilogram basis, but limited in duration to seven days. The trial missed its primary endpoint (p = 0.15 for time to first tolerated solid meal) [7]; the protocol has not been repeated in any subsequent Phase 2 or Phase 3 trial in any indication. The Gobburu 1999 pharmacokinetic study used single intravenous bolus doses across a dose range to construct the pharmacokinetic-pharmacodynamic model; the published paper reports the resulting parameters (half-life ~2 h, clearance 0.078 L/h/kg, volume of distribution at steady state 0.22 L/kg) rather than a single recommended dose [2]. ## Half-life, pulsatility, and what the rhythm implies The 2-hour terminal half-life in healthy human volunteers [2] is the single most consequential pharmacokinetic number on this page. It tells the literature several things at once. First, that a single intravenous dose produces a growth hormone pulse lasting two to three hours and then returns the system to baseline. Second, that any chronic-exposure design has to choose between repeated pulsatile dosing (Johansen's three-times-daily approach in rats) or continuous infusion (Svensson's osmotic-minipump approach) — there is no intermediate. Third, that ipamorelin combined with a long-acting growth hormone-releasing hormone analog such as the long-acting CJC-1295 produces a fundamentally different research-axis stimulation pattern than ipamorelin alone, because the GHRH analog provides a tonic background against which ipamorelin's short pulse can ride [17]. The 28-day insulin-like-growth-factor-1 elevation reported with long-acting CJC-1295 in healthy adults [17] is the canonical reference for this asymmetry. None of these observations are dosing recommendations; they are statements about what the published rhythm of doses, in research models, has produced as measured outcomes. ## Routes that have been studied The published literature records ipamorelin administration by intravenous bolus (rat, swine, human pharmacokinetics and the Beck Phase 2 trial), subcutaneous injection (rodent bone studies), continuous subcutaneous infusion via osmotic minipump (rodent bone mineral-content studies), and intranasal (an exploratory pharmacokinetic study in rat and dog reported nasal bioavailability comparable to other small peptidyl growth hormone secretagogues [8]). No oral or sublingual route has been published with usable bioavailability data. The intranasal observation has not been carried forward into a human pharmacokinetic study, and the route is not part of any registered human trial. ## Stability and handling, as the literature notes Ipamorelin is a synthetic pentapeptide whose two non-natural residues (alpha-aminoisobutyric acid and D-2-naphthylalanine) and C-terminal amide together confer increased resistance to peptidase degradation relative to natural ghrelin — a 28-amino-acid peptide that additionally requires octanoylation at serine-3 to bind GHS-R1a [10]. The compound is typically handled in research settings as the acetate salt, soluble in aqueous buffer. Lyophilized peptide is reported stable refrigerated; reconstituted solutions are reported stable for limited durations at 2–8 °C in research-use literature. None of those stability notes constitute a use protocol — they are descriptions of how a research material behaves on a laboratory bench. --- For research purposes only. Not for human consumption. 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