What it is
Ipamorelin is a synthetic pentapeptide, Aib-His-D-2-Nal-D-Phe-Lys with a C-terminal amide. Two of its five residues are not standard amino acids: aminoisobutyric acid at position one and 2-naphthylalanine at position three. FDA counts those two non-proteinogenic residues as part of why the substance is difficult to characterise.
It is a growth hormone secretagogue, meaning it acts at the ghrelin receptor rather than the GHRH receptor, which is what separates it from sermorelin, tesamorelin and CJC-1295. In the originating work its growth hormone release was blocked by GHRP antagonists and not by a GHRH antagonist, which is how that was established before the receptor was cloned.
It was discovered at Novo Nordisk as NNC 26-0161 and published in 1998 as the first selective growth hormone secretagogue.
How it works, and what the selectivity claim rests on
Ipamorelin agonises the growth hormone secretagogue receptor 1a. In rat pituitary cells its half-maximal effect came at 1.3 nanomolar with a maximum response of 85 percent, against GHRP-6 at 2.2 nanomolar and 100 percent. In conscious swine its half-maximal dose was 2.3 nanomoles per kilogram, against GHRP-6 at 3.9 and GHRP-2 at 0.6.
Read that last figure again. GHRP-2 is more potent than ipamorelin. The compound was never sold on potency. It is sold on selectivity, meaning the claim that it raises growth hormone without raising cortisol, prolactin or ACTH.
That claim rests on one experiment, in pigs, published in 1998. Intravenous dosing in conscious swine, with FSH, LH, prolactin, TSH, ACTH and cortisol measured. None of the secretagogues tested affected FSH, LH, prolactin or TSH. GHRP-6 and GHRP-2 both raised ACTH and cortisol. Ipamorelin did not, and the authors noted the absence held even at doses more than 200 times the growth hormone half-maximal dose.
That is a real, well-designed result. It is also a pig result, and there is no human counterpart. The only published human pharmacology study measured ipamorelin concentrations and growth hormone, and nothing else. There is no published human cortisol, ACTH or prolactin dataset for this compound at any dose by any route. FDA put it plainly: there are insufficient data to conclude that ipamorelin would not raise safety concerns similar to those associated with approved products that stimulate growth hormone release.
One piece of internal evidence does support the selectivity being structurally real rather than an artefact. Novo Nordisk derived a successor compound from ipamorelin, tabimorelin, and that one did raise cortisol, by about 50 percent at every dose tested in the same species.
Research evidence
Three human datasets, and that is all
The phase 1 study, from 1999, gave 15 minute intravenous infusions at five ascending doses to healthy men. Terminal half-life about two hours, clearance 0.078 litres per hour per kilogram. Growth hormone rose in a single episode peaking at 40 minutes and returning to negligible by six hours at every dose. Inter-individual variability was larger for the response than for the pharmacokinetics.
Two things that study did not report: IGF-1 and cortisol. No human IGF-1 value for ipamorelin exists, from that study or any other, at any dose, by any route. The near-universal claim that ipamorelin raises IGF-1 has no human source. In rats, fifteen days of dosing did not change total IGF-1.
Then two phase 2 trials, both in postoperative ileus, both intravenous.
The trial that reported: endpoint missed
NCT00672074 ran from 2008 to 2009 across nineteen US sites, 117 patients, 0.03 milligrams per kilogram intravenously twice daily from the first postoperative day for up to seven days. The primary endpoint was time from first dose to tolerating a standardised solid meal.
Median 25.3 hours on ipamorelin against 32.6 on placebo. A difference of 7.3 hours at p equals 0.15. The authors wrote that there were no significant differences between ipamorelin and placebo in the key and secondary efficacy analyses. No difference in time to bowel movement, readiness for discharge or length of stay. A subgroup of patients having open laparotomy showed shorter recovery, which was exploratory rather than pre-specified.
It was published in 2014, five years after completion.
On safety, treatment-emergent adverse events occurred in 87.5 percent of the ipamorelin arm and 94.8 percent of placebo. FDA Category 2 listing states that a study published in the literature identified serious adverse events including death when ipamorelin was administered intravenously for improving gastric motility. The advisory committee transcript adds the necessary qualifier: those events occurred after completion of therapy, and it is unclear whether the deaths were related to ipamorelin because causality was not provided in the article. Per-arm death counts are not public. Both halves of that belong together.
The trial that never reported, and it was the big one
NCT01280344 ran from 2011 to 2014 across 45 US sites with 320 patients, nearly three times the size of the published trial. Randomised, quadruple-blind, placebo-controlled, dose-finding, with three dose levels: 0.03 milligrams per kilogram twice daily, 0.06 twice daily and 0.06 three times daily, up to triple the daily dose of the earlier trial. It was restricted to open resections with incisions of at least ten centimetres, which is to say it was designed to test whether the open-laparotomy subgroup signal was real.
Primary completion was June 2013. No results have been posted and no publication exists.
That is the single biggest hole in the public record on this compound. Whether the higher doses worked where the lower one did not is unknown, and whether the subgroup signal held is unknown, because the trial designed to answer both questions has never released its data.
How the programme ended
Novo Nordisk discovered ipamorelin and then used it as a starting point to improve on. Within the same publication series the company produced a series of more orally available analogues and moved to tabimorelin, which entered phase 2. Ipamorelin, an injectable, was the abandoned parent of an oral programme.
It was picked up again for postoperative ileus, ran the two trials above, and stopped. Development-tracking databases record its growth-disorder status as discontinued and its gastrointestinal status as no development reported. The company that owned it took a different asset through phase 3 instead.
Two sentences are defensible from that record and both are worth stating. No ipamorelin trial has ever met an efficacy endpoint in a human being. And growth hormone deficiency, the indication ipamorelin is most associated with in consumer writing, was never tested in a single registered trial. FDA states that it has not identified data to support effectiveness for the diagnosis or treatment of growth hormone deficiency in children or adults.
Safety
The longest human exposure ever studied is seven days, by intravenous infusion, in patients recovering from bowel surgery. There is nothing beyond about a week.
There is no human pharmacokinetic data by the subcutaneous route, which is the route essentially everyone uses. FDA found none in any population. Every published human figure comes from a 15 minute intravenous infusion, so bioavailability, peak concentration and growth hormone response after a subcutaneous injection are unmeasured in people.
On toxicology the record is empty: no acute toxicity study, no repeat-dose toxicity, no genotoxicity, no carcinogenicity, and no reproductive or developmental work specific to ipamorelin. Human glucose and insulin sensitivity have never been measured, and tachyphylaxis has never been tested in a human at any duration.
FDA also found the substance not well characterised physically and chemically, noting that the certificates of analysis it reviewed lacked specifications for aggregates, bacterial endotoxins and bioburden, and that the unnatural amino acids add to the difficulty.
Regulatory status
Not approved for any indication in any country, and it has no pharmacopoeial monograph.
The compounding history is more decisive than for most compounds on this site, and it is frequently reported wrongly. Ipamorelin acetate was nominated for the 503A bulk drug substances list and the nomination was withdrawn. FDA then set it for advisory committee evaluation, and on 29 October 2024 the Pharmacy Compounding Advisory Committee voted on it. The vote was zero in favour, twelve against, one abstention, for the free base, and identically for the acetate. Unanimous against, twice.
FDA grounds were that the substance is not well characterised, that there was insufficient information to determine how long it had been used in compounding, that no effectiveness data exists for growth hormone deficiency or for postoperative ileus, and that approved alternatives exist for both.
Separately, ipamorelin acetate remains in Category 2 under the 503B interim policy as of the April 2026 page, which is a live designation rather than a withdrawn one. Several secondary sources collapse these into a single claim that it was removed from Category 2. For ipamorelin that is wrong.
It was not among the substances considered at the July 2026 advisory committee meeting.
WADA names ipamorelin directly in section S2.2.4, among growth hormone secretagogues and their mimetics. Prohibited at all times, in and out of competition, and Sport Integrity Australia states that a therapeutic use exemption would not be granted.