RESEARCH DIGEST // GHS-R1a
Ipamorelin releases growth hormone and leaves cortisol alone. That is the whole point of the molecule.
A terminal-plain reading of the receptor: one clean GH pulse, two off-target pathways left dark. Every figure logged to the study that measured it.
The short version
Ipamorelin is a small lab-made peptide — a chain of five amino acids. Its job is narrow. It tells one switch on the pituitary gland (a receptor called GHS-R1a, the same switch the hunger hormone ghrelin uses) to release a short burst of growth hormone, then it lets go.
What makes it stand out is what it does not do. Older peptides in its class also pushed up stress hormones like cortisol, and prolactin. Ipamorelin, in the founding study, raised growth hormone strongly but left cortisol and prolactin flat — even at doses far above the level needed for the growth-hormone effect [1]. That clean, single-signal behavior is why people call it "selective."
What is it used for? In labs, to study growth hormone. Outside labs, it is promoted for sleep, recovery, and body composition — claims that rest on mechanism and short animal studies, not on finished human trials. The one human efficacy trial that was run failed [3]. What people report — including the downsides — is on the effects page. It has never been approved as a medicine.
One receptor. One pulse. The rest left dark.
Ipamorelin (sequence Aib-His-D-2-Nal-D-Phe-Lys-NH2) is a synthetic pentapeptide. It binds the ghrelin receptor, GHS-R1a, on pituitary somatotrophs and fires a pulse of growth hormone (GH) [1]. That much it shares with the older growth-hormone-releasing peptides, GHRP-6 and GHRP-2.
The difference is selectivity. In the 1998 characterization, ipamorelin released GH about as potently as GHRP-6 in conscious swine (ED50 2.3 nmol/kg vs 3.9 nmol/kg), yet it did not raise ACTH or cortisol above the level seen with growth-hormone-releasing hormone — not even at doses more than 200-fold above its GH threshold [1]. Prolactin stayed flat too. That is the defining result. Read it in full on the how-it-works page.
This is the lens this site leads with: ipamorelin as an exercise in restraint at the receptor. One pathway lit. The stress-hormone pathways left dark.
What the studies actually measured
Human pharmacokinetics: a terminal half-life of about 2 hours in healthy male volunteers (IV), with the GH response arriving as a single discrete pulse peaking near 40 minutes [2]. That is one of the only human datasets that exists.
Human efficacy: thin, and negative. The only published Phase 2 randomized trial (NCT00672074, 114 bowel-resection patients) missed its primary endpoint — time to first tolerated meal was 25.3 h on ipamorelin vs 32.6 h on placebo, p=0.15 [3]. No Phase 3 followed. No indication was approved.
Animal data: dose-dependent. In adult rats, subcutaneous ipamorelin raised longitudinal bone-growth rate from 42 to 52 micrometers/day across an 18-to-450 microgram/day ladder, with no change in systemic IGF-1 [4]. In a 2024 ferret study, ipamorelin cut chemotherapy-driven weight loss by about 24% — the most recent in-vivo finding on the compound [5]. Numbers, sources, and the full reference list sit on the Ipamorelin research page and the Ipamorelin references page.
Status: never approved
Ipamorelin has never been approved as a drug, anywhere [3]. Novo Nordisk discovered it in the 1990s; development reached Phase 2 for postoperative ileus and stopped when that trial failed [3]. It is sold today only as a research chemical of variable purity.
It is banned in sport at all times under the World Anti-Doping Agency list, category S2, and is detectable in urine. A 2026 critical review flagged it among the GH-axis peptides driving an expanding anti-doping detection framework.
This site sells nothing and supplies nothing. It is a reading of the published record. The community angle — what people report, labeled plainly as anecdote — is kept on its own page and pinned to one side, never mixed with the cited data.