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Ipamorelin

NNC 26-0161

C
Animal replicated
RouteInjectableGray-market only
C
Evidence grade: Animal replicated

Effect demonstrated in multiple animal studies; human data sparse or extrapolated. Grades summarize evidence quality, not whether a compound is appropriate, legal, or risk-free.

At a glance
What it is
NNC 26-0161 — Selective GHS-R1a Agonist — Pentapeptide — WADA S2 — The First Selective GH Secretagogue — GHRP, Growth Hormone Secretagogue, Ghrelin Receptor Agonist, Peptide.
Why people use it
Used primarily for muscle and performance and sleep and recovery.
If you only read one thing

Ipamorelin's identity is defined by its selectivity. The compound produces a clean GH pulse with no cortisol, ACTH, or prolactin elevation — something no previous GHRP could claim. This selectivity drives its community dominance: users seeking body composition, recovery, and sleep benefits from GH elevation without the HPA axis activation of GHRP-6 made ipamorelin the standard. The tension is subtle: ipamorelin produces less appetite stimulation than GHRP-6, which is a 'problem' for users who specifically want the hunger drive for bulking phases. GHRP-6 retains its niche there. For everything else, ipamorelin's cleaner profile makes it the correct choice. The chapter's job is to explain what 'selective' means pharmacologically and why it matters in practice.

Published literature
3human RCTs0human studies0animal0in vitro
Evidence reality check
Human evidence
3 human studies
3 randomized; 0 observational.
Preclinical base
0 lab signals
0 animal; 0 in-vitro/mechanistic.
Risk posture
No major flags listed
Review route-specific cautions before use.
Properties
Active malignancy: cautionWADA S2✓ Human RCTHPTA: stimulatingNot injectable
Half-life
Plasma half-life approximately 2 hours — longer than GHRP-6 (~30 min distribution phase) due to the structural features providing protease resistance
Evidence
CAnimal replicated
The Selectivity Story
Before ipamorelin, every characterized GHRP (GHRP-6, GHRP-2, hexarelin) elevated cortisol and prolactin alongside GH. The cortisol elevation was a consequence of GHS-R1a activation on HPA axis neurons in addition to pituitary somatotrophs. Ipamorelin was designed by Novo Nordisk researchers specifically to maximize GHS-R1a selectivity and eliminate off-target HPA activation. Raun 1998 demonstrated: at doses producing maximal GH release in rats, ipamorelin produced zero ACTH elevation and zero cortisol elevation (GHRP-2 at the same dose produced significant ACTH). The selectivity advantage is dose-independent within the therapeutic range.
Mechanism
GHS-R1a (ghrelin receptor) agonist: Gq-protein coupled → PLC-IP3-Ca²⁺ pathway → GH granule exocytosis from pituitary somatotrophs. Additionally: suppresses hypothalamic somatostatin tone via GHS-R1a on somatostatin neurons (removes the inhibitory brake on GH release). The net result: a discrete pulsatile GH pulse that peaks within 30-60 min post-injection and returns to baseline within 2-3 hours. No direct ACTH, cortisol, or prolactin stimulation at any clinically relevant dose.
The GH Stack Role
Ipamorelin is the GHRP component of the GH Stack (CJC-1295 no-DAC + Ipamorelin). See pbghstack_v4. Paired with CJC-1295 (no-DAC), the GHRH receptor (CJC) + GHS-R1a (ipamorelin) produce a supraadditive GH pulse 3-5x larger than either alone (Bowers 1991 GHRH+GHRP synergy). This chapter provides standalone ipamorelin pharmacology that the GH Stack chapter references.
The Community Position
Ipamorelin has largely replaced GHRP-6 as the default GHRP for most community applications (cutting, body recomposition, recovery, sleep enhancement). GHRP-6 is preferred in bulking contexts specifically for its appetite-stimulating effect — ipamorelin produces essentially no appetite stimulation. For everything else, ipamorelin's clean hormonal profile (GH without cortisol/prolactin) makes it the preferable choice.
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