Key takeaways
- Selective ghrelin-receptor agonist — stimulates GH release without elevating cortisol, prolactin, or aldosterone.
- Acts synergistically with GHRH analogues (typically CJC-1295) to amplify GH pulsatility.
- Modest direct evidence base — the original Novo Nordisk programme was abandoned at phase-2 for commercial reasons.
- Cleanest side-effect profile of any GHRP; primary clinical concern is supply quality.
- UK: unlicensed. Sold via research-chemical channels — no quality assurance.
What it is
Ipamorelin is a synthetic pentapeptide and a selective agonist of the growth-hormone secretagogue receptor (GHS-R, also known as the ghrelin receptor). It was developed by Novo Nordisk in the late 1990s as a candidate treatment for adult growth-hormone deficiency. Phase-2 trials demonstrated dose-dependent GH release with a clean specificity profile, but the development programme was halted before phase-3.
Its distinguishing feature among GHRPs is selectivity. Earlier compounds in the class — GHRP-2, GHRP-6 — also stimulate cortisol, prolactin, and aldosterone release. Ipamorelin does not, which gives it a cleaner side-effect profile while preserving the GH-stimulating effect.
How it works
Ipamorelin binds the ghrelin receptor (GHS-R1a) on pituitary somatotrophs, triggering GH release. The mechanism is parallel and complementary to GHRH agonism: where GHRH analogues amplify the natural GH pulse, ghrelin-receptor agonists generate a separate pulse that summates with GHRH-driven release.
Subcutaneous injection
Short half-life (~2 hours); typically dosed pre-bed or pre-fast.
Ghrelin receptor binding
Binds GHS-R1a on pituitary somatotrophs and hypothalamus.
Selective GH pulse
GH release without cortisol, prolactin, or aldosterone stimulation.
IGF-1 / anabolic signalling
Hepatic IGF-1 elevation; downstream tissue effects.
When stacked with a GHRH analogue (e.g. CJC-1295 / Modified GRF), the combined GH amplitude exceeds either compound alone — this is the basis of the standard "Ipa + Mod GRF" protocol.
Benefits
GH and IGF-1 elevation (medium confidence)
Phase-1/2 studies in adult GH-deficient patients showed reliable, dose-dependent GH pulses with each ipamorelin injection, alongside IGF-1 elevation comparable to other GHRPs but without the cortisol/prolactin stimulation those compounds produce.
Body composition (low confidence)
Direct trial data on lean mass changes is limited. Reasonable inference from the broader GH-axis literature suggests modest improvements over 12+ weeks of consistent use, especially when stacked with a GHRH analogue. Effect sizes are smaller than direct GH replacement.
Sleep architecture (low confidence)
GH release is closely tied to slow-wave sleep, and pre-bed dosing of ipamorelin is associated anecdotally with deeper sleep. Direct polysomnography data is not available.
A modest evidence base
Research summary
Pharmacokinetics and pharmacodynamics of ipamorelin in healthy adults (phase 1)
1998Single subcutaneous doses of 30–80 µg/kg produced dose-dependent GH peaks of 30–55 ng/mL within 30 minutes. No significant elevation in cortisol, prolactin, or aldosterone — confirming the selective profile.
J Clin Endocrinol Metab · 84(8):2780-2786Selective ghrelin receptor agonism: ipamorelin vs GHRP-2 / GHRP-6
2005Comparable GH stimulation across the three compounds — but only GHRP-2 and GHRP-6 produced significant cortisol elevation. Ipamorelin remained selective at all tested doses.
Eur J Endocrinol · 152:863-871Effect of ipamorelin in postoperative ileus: phase-2 trial (development discontinued)
2010Improved GI motility post-abdominal surgery vs placebo, but failed to meet primary endpoint by clinically meaningful margin. Programme discontinued; no further trials in the indication.
Aliment Pharmacol Ther · 32(11-12):1295-1303Dosage & administration
No regulatory dosing exists. The schedule below summarises protocols used in published trials and the literature. Ipamorelin is unlicensed in the UK; this is educational reference only.
| Phase | Dose | Duration | Notes |
|---|---|---|---|
| Standalone starter | 100 µg, pre-bed | Ongoing | Single nightly dose |
| Standalone full | 100 µg, 2–3x daily | Ongoing | Pre-bed + pre-workout +/- pre-fast |
| Stacked with Mod GRF | 100 µg + 100 µg | Ongoing | Common protocol |
| Higher-dose (research) | Up to 300 µg / dose | — | No clear benefit over 100 µg |
Side effects & safety
The trial safety profile is the cleanest of any GHRP. Acute tolerance is generally excellent. Primary safety concerns relate to long-term effects (limited data) and supply quality (no UK regulation).
| Effect | Frequency | Severity |
|---|---|---|
| Injection-site reaction | 15–25% | Mild |
| Flushing | 5–10% | Transient |
| Mild hunger | ~5% | Brief, post-injection |
| Headache | <5% | Mild |
| Cortisol / prolactin elevation | Not observed | Distinguishing feature |
| Insulin resistance (chronic) | Theoretical | Monitor with bloodwork |
Contraindications: Active malignancy. Pregnancy. Severe untreated diabetes. Concurrent corticosteroid use (theoretical).
UK legal status
Unlicensed in the UK
Summary
Ipamorelin is the cleanest GHRP in clinical literature, with a benign acute side-effect profile and a clear selective mechanism. The two limiting factors are the small clinical evidence base — no completed phase-3 trial — and supply quality on the grey market. For UK readers interested in GH-axis modulation, the same caveats apply as to CJC-1295: prescriber-supervised approaches via licensed compounds are the only fully assured route.
References (5)
- Raun K, et al. Ipamorelin, the first selective growth hormone secretagogue. Eur J Endocrinol. 1998;139(5):552-561.
- Gobburu JV, et al. Pharmacokinetic-pharmacodynamic modelling of ipamorelin. J Clin Endocrinol Metab. 1999;84(7):2627-2632.
- Bowers CY. GH-releasing peptides: structure-function relations. J Pediatr Endocrinol Metab. 1996;9(suppl 3):347-358.
- Sigalos JT, Pastuszak AW. The safety and efficacy of growth hormone secretagogues. Sex Med Rev. 2018;6(1):45-53.
- MHRA. Note: ipamorelin has no UK marketing authorisation as of May 2026.