Ipamorelin is a synthetic pentapeptide — Aib-His-D-2-Nal-D-Phe-Lys-NH2 — developed at Novo Nordisk in the 1990s as part of a chemistry programme searching for growth hormone secretagogues without the hormonal side effects of earlier compounds in the class. It acts at the growth hormone secretagogue receptor (GHS-R1a), the same receptor the stomach hormone ghrelin uses, and is often described as a ghrelin mimetic.
Its defining property is selectivity. The growth hormone-releasing peptides that preceded it — GHRP-6 and GHRP-2 — released growth hormone effectively but also raised ACTH and cortisol. In the original characterisation study in conscious swine, ipamorelin released GH with potency and efficacy comparable to GHRP-6 while producing no significant rise in ACTH or cortisol, and that selectivity held at doses more than 200-fold above the ED50 for GH release. It also left FSH, LH, prolactin and TSH unchanged. That is the finding the compound is known for, and it is a genuine and well-documented one.
Ipamorelin has been in humans. A dose-escalation pharmacokinetic study in healthy male volunteers was published in 1999, and a Phase 2 randomised placebo-controlled trial in postoperative ileus was published in 2014. It is one of the better-characterised compounds on this site in that narrow sense. What it does not have is a completed development programme: the Phase 2 trial did not separate from placebo on its efficacy endpoints, and ipamorelin has never been approved anywhere for anything.
The route matters. Both published human studies used intravenous administration under clinical supervision — a 15-minute infusion in the pharmacology study, twice-daily intravenous infusions in the ileus trial. Subcutaneous self-administration, which is how ipamorelin circulates informally, has no published human study behind it.
| Weeks | Dosage | Syringe units (U-100) |
|---|---|---|
| Weeks 1–2 | 0.1 mg | 6 units0.06 mL |
| Weeks 3–4 | 0.15 mg | 9 units0.09 mL |
| Weeks 5–8 | 0.2 mg | 12 units0.12 mL |
| Weeks 9–12 | 0.25 mg | 15 units0.15 mL |
FrequencyOnce daily, subcutaneous, 30 to 60 minutes before sleep.
For review — not the route or design of the cited trial. Ipamorelin's human dosing comes from a discontinued hospital programme that infused 0.03 mg/kg intravenously twice a day; the fixed-milligram subcutaneous titration in the chart follows a circulated research protocol. The concentration strip above the chart is calculated from the vial and water volume and is correct.
Unverified — the cited human programme dosed twice daily by intravenous infusion, not once daily under the skin.
The human evidence for ipamorelin is a Phase 2 programme in postoperative ileus that dosed by body weight through an intravenous line under hospital supervision, missed its endpoints and was discontinued — so a fixed subcutaneous amount taken before bed is a different treatment from the one that was studied, and the chart is flagged for review on that basis. The bedtime timing follows from ipamorelin being a growth hormone secretagogue, whose effect is usually measured against the natural overnight pulse, but no trial established it as a schedule. Athena supplies ipamorelin only inside the 1:1 CJC-1295 + ipamorelin blend, whose vial holds 5 mg of it, so 5 mg is the strength charted here. Made up with 3 mL that is about 1.67 mg/mL, so the schedule runs from 6 units at the 0.1 mg first step to 15 units at the 0.25 mg final step, and every row fits inside one 50-unit syringe. Ipamorelin is selective for the ghrelin receptor and does not raise cortisol or prolactin the way earlier secretagogues did, which is a mechanistic distinction rather than evidence for any amount above.
What this evidence establishes. Ipamorelin's human dosing comes from a hospital trial programme in postoperative ileus that did not meet its endpoints and was discontinued. It used intravenous infusion under supervision, not subcutaneous self-administration, and no subcutaneous human dose has been established.
Sources: Phase 2 postoperative ileus trial programme
For educational and laboratory research purposes only. It does not provide medical advice, dosing recommendations, or instructions for human or veterinary use. Syringe units assume a U-100 syringe, on which 1 mL is 100 units and a 50-unit syringe holds 0.5 mL.
Ipamorelin works at a different receptor from the GHRH analogues, which is why the two are so often combined. It is the ghrelin arm of growth hormone regulation rather than the GHRH arm.
Binds the growth hormone secretagogue receptor on pituitary somatotrophs and in the hypothalamus — the ghrelin receptor — triggering a discrete episode of GH release.
Unlike GHRP-6 and GHRP-2, ipamorelin did not raise ACTH or cortisol in the characterisation study, even at doses more than 200-fold above the GH-releasing ED50. FSH, LH, prolactin and TSH were also unaffected.
Identified within a series of compounds lacking the central Ala-Trp dipeptide of GHRP-1. The receptor pharmacology was confirmed with GHRP and GHRH antagonists.
In healthy volunteers the terminal half-life was about 2 hours, with dose-proportional kinetics, clearance of 0.078 L/h/kg and steady-state volume of distribution of 0.22 L/kg.
GH release peaked at roughly 0.67 hours after infusion and declined exponentially to negligible concentrations at every dose tested — one episode of release, not a sustained elevation.
Ghrelin-receptor stimulation has promotility effects in the upper and lower gastrointestinal tract, which is why the one clinical trial of ipamorelin was in postoperative ileus rather than in an endocrine indication.
GHS-R1a agonism and GHRH receptor agonism are separate, complementary inputs to the same pituitary cells. Combining them is a plausible mechanistic rationale for the 1:1 blends in which ipamorelin is usually sold, and it is the reason those blends exist. It is worth being precise about what that rationale is and is not: no published human trial has tested ipamorelin combined with CJC-1295, measured the combination's GH or IGF-1 response, or compared it against either component alone. The pairing is mechanistically coherent and clinically unstudied.
The two human studies answer two narrow questions, and neither of them is the question most people bring to this compound. The 1999 study established that intravenous ipamorelin produces a measurable, dose-proportional GH pulse in healthy men — a pharmacology finding on a surrogate endpoint, over hours, not a clinical outcome. The 2014 trial asked whether ipamorelin shortens postoperative ileus and found that it did not, at that dose, by that route, in that population.
No human trial has measured body composition, lean mass, fat mass, strength, sleep architecture, recovery, injury healing, bone density or any anti-ageing endpoint with ipamorelin. No human trial has used subcutaneous administration. No human trial has run longer than seven days. No human trial has tested it in combination with a GHRH analogue. Long-term safety at any dose is unstudied, and the reassuring selectivity finding — no ACTH or cortisol rise — comes from swine, not from repeated human dosing.
The 2014 trial's negative result deserves to be read on its own terms. It does not show that ipamorelin does nothing; it shows that this dose and route did not improve this endpoint in this population, in a study the authors themselves described as small and enrolling a broad range of underlying conditions. But a negative Phase 2 is what stopped development, and it is the most recent controlled human evidence that exists.
Ipamorelin has no approved label and therefore no regulator-reviewed contraindication list. The entries below are derived from GH-axis pharmacology and from the two published human studies. Tolerability in those studies was good: in the Phase 2 trial, treatment-emergent adverse events occurred in 87.5% of the ipamorelin group and 94.8% of the placebo group — a rate typical of postoperative patients and not higher with active drug.
| Condition / Factor | Risk Level | Rationale |
|---|---|---|
| Active malignancy | CONTRAINDICATED | Raising GH and downstream IGF-1 in the presence of active cancer is contraindicated across the GH-axis class. IGF-1 is mitogenic and anti-apoptotic. |
| Pituitary tumour or hypothalamic-pituitary disease | CONTRAINDICATED | Class contraindication. Ipamorelin acts directly on pituitary somatotrophs. |
| Pregnancy and lactation | NOT ESTABLISHED | No reproductive safety data exist. Both human studies enrolled non-pregnant adults. |
| Diabetes or impaired glucose tolerance | CAUTION | Growth hormone antagonises insulin action. Glucose effects were not a primary endpoint in either published human study. |
| Subcutaneous self-administration | UNSTUDIED ROUTE | Both published human studies used supervised intravenous infusion. No published human study has characterised subcutaneous ipamorelin, and the pharmacokinetics of a subcutaneous depot differ from a 15-minute infusion. |
| Use beyond seven days | UNSTUDIED DURATION | The longest published human exposure is seven days in the postoperative ileus trial. Multi-week and multi-month protocols exceed all published human experience. |
| Expectation of body-composition or recovery benefit | UNSUPPORTED | No human trial has measured any of these endpoints. The only efficacy trial that exists tested gastrointestinal recovery and was negative. |
| Competitive athletes | PROHIBITED | Growth hormone secretagogues, including GHS-R1a agonists such as ipamorelin, are prohibited at all times under WADA Prohibited List section S2. |
FDA: ipamorelin is not approved for any indication in the United States or anywhere else. Its clinical development ended after a Phase 2 proof-of-concept study in postoperative ileus that did not meet its efficacy endpoints. It is not eligible for pharmacy compounding and has been the subject of FDA attention as an unapproved drug marketed as a research chemical.
WADA: prohibited at all times, in and out of competition, under section S2, which covers growth hormone secretagogues, GHRPs and ghrelin receptor agonists.
How to read the selectivity finding: ipamorelin's reputation rests on a real and carefully documented preclinical result — that it releases GH without the ACTH and cortisol response of earlier GHRPs. That is a favourable pharmacological property. It is not evidence that ipamorelin is effective for any purpose, and it does not substitute for the Phase 3 programme that was never run. A cleaner hormone profile in swine and a negative Phase 2 in humans are both true at the same time.
Test your understanding of the selectivity finding, the two human studies, and what the Phase 2 result means.
This profile is for educational and research purposes only. It is not medical advice, and nothing on it is a protocol, a recommendation, or an instruction for use in a person or an animal.
Athena Peptides Education does not prescribe, sell, or recommend any compound. Compounds discussed here are for laboratory research only and are not for human consumption. Always consult a qualified physician before making any decision about your health.