# Ipamorelin: Safety Record, Combination Stacks, and the Evidence > Ipamorelin is a selective growth hormone secretagogue most often studied beside GHRH analogs like CJC-1295. A cited digest of what the studies measured, the safety record, and the open questions. A scholarly digest that separates single-agent ipamorelin findings from CJC-1295 combination claims, presents the safety record with its cautions, and cites every quantitative figure. ## The short version Ipamorelin is a small lab-made peptide — five amino acids — that tells the pituitary gland to release a pulse of growth hormone (GH). Its claim to fame is being *selective*: it raises GH while barely touching two other hormones, cortisol (the stress hormone) and prolactin, that older peptides in its class pushed up. People in research-use communities are drawn to it for sleep, recovery, and slow changes in body composition, but those are reports, not proof. The honest state of the evidence is thin: one human trial that tested it (for slow bowel recovery after surgery) did not work, and there is no long-term human safety data. It has never been approved as a medicine anywhere. It is also banned in sport. Most online interest pairs it with another peptide, CJC-1295 — that pairing rests on each drug's separate pharmacology, not on any trial of the two together. What people report, including the downsides, is on [the effects page](/effects). ## What ipamorelin is Ipamorelin (Aib-His-D-2-Nal-D-Phe-Lys-NH2; CAS 170851-70-4) is a synthetic pentapeptide — a chain of five amino acids — and a selective agonist of the ghrelin / growth hormone secretagogue receptor (GHS-R1a), the same receptor the natural "hunger hormone" ghrelin binds. To ask *what is ipamorelin peptide* is to ask about a molecule that Novo Nordisk derived in the 1990s from an earlier compound, GHRP-1, by removing a central dipeptide [1]. Two non-natural building blocks in its sequence — alpha-aminoisobutyric acid (Aib) and D-2-naphthylalanine — make it resist the enzymes that would otherwise chew it up. What sets it apart from the peptides that came before it (GHRP-6, GHRP-2) is **selectivity**. In its founding characterization, ipamorelin released GH potently yet did not raise ACTH or cortisol above the level seen with growth-hormone-releasing hormone (GHRH) — even at doses more than 200-fold above the dose needed for half its maximal GH effect [1]. That clean profile is the entire reason it remains of interest decades later. ## What the studies measured it doing Asking *what does ipamorelin peptide do* has a precise answer in animals and a near-empty one in humans. In its founding swine work, the dose for half-maximal GH release was 2.3 nmol/kg, versus 3.9 nmol/kg for GHRP-6 — more potent, and far cleaner [1]. In adult female rats, 15 days of subcutaneous dosing raised the longitudinal bone-growth rate from 42 to as high as 52 micrometers per day, in a dose-dependent way, with no measurable change in circulating IGF-1 (insulin-like growth factor 1, a hormone made by the liver that carries out many of GH's effects) [4]. The single human pharmacology study found a terminal half-life of about 2 hours, with the GH response arriving as one discrete pulse that peaked roughly 40 minutes after dosing [2]. The most recent in-vivo work, a 2024 ferret study, found that ipamorelin blunted chemotherapy-induced weight loss by about 24% — through a peripheral, non-brain mechanism — while doing nothing for nausea [5]. These are real, cited results. None of them is a human outcome trial. ## Where the 'safe' framing actually stands The word in this site's name names a question, not a verdict. Ipamorelin's selectivity *is* a genuine relative-safety advantage: it spares the cortisol and prolactin elevations that dog less selective GHRPs [1]. But selectivity in one dimension is not a clean bill of health. The only controlled human trial of ipamorelin — a Phase 2 study in 114 bowel-resection patients — missed its primary endpoint, with no ipamorelin-specific safety signal across that short seven-day window but no demonstrated benefit either [3]. There is no Phase 3 trial, no approved indication, and no long-term human safety database of any kind. There is also a class-level caution worth stating plainly: a 28-day study of a *different* GHS-R1a agonist found dose-dependent heart-muscle damage in rats [6]. Ipamorelin was not the compound tested, and no equivalent long-duration study of ipamorelin exists — which is precisely the point. The reported effects, the cautions, and the unknowns are laid out on the [Ipamorelin effects](/effects) page; the full study record is in the [Ipamorelin research](/research) digest. ## Why ipamorelin is almost always studied in a stack Ipamorelin releases GH by a mechanism distinct from GHRH — it works on the ghrelin receptor, not the GHRH receptor — and the two pathways are complementary. A class-wide review documents that growth-hormone-releasing peptides act synergistically with GHRH and are partially resistant to the signals (glucose, free fatty acids, somatostatin) that nearly abolish a GHRH pulse on its own [7]. That pharmacology is the published rationale for pairing a GHRH analog with a GHRP. The most discussed pairing in research-use communities is [ipamorelin cjc-1295](/with-cjc-1295) — CJC-1295 being a long-acting GHRH analog. A separate comparison readers ask about is [ipamorelin vs sermorelin](/vs-sermorelin), sermorelin being a short-acting GHRH analog. Both pages keep one line in view: the *combination itself* has never been tested in a trial for any outcome. The synergy is read off each agent's single-drug pharmacology. --- A Carbon-plain reading of the ipamorelin record: the selective GH pulse and the ~2-hour human half-life logged where the studies confirm them, the failed Phase 2 trial and the blank long-term-safety line set in equal type, and the CJC-1295 stack read as class pharmacology rather than a tested product — the word 'safe' here naming a question we keep open, with no clinic behind the page and nothing dosed, compounded, prescribed, or sold.