Peptide Secretagogue Analogs · Checked
Ipamorelin
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How we rank
Rows are ordered by price per mg: listed price divided by stated peptide content, excluding shipping and codes, so every vial competes on the same axis. Each row carries its own $/mg figure, so the size of the gap between vendors is visible, not just the order. Sprays follow the vials, unranked.
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Selective ghrelin-receptor agonist pentapeptide
Selective GHRP — stimulates natural growth-hormone release without cortisol or prolactin spikes.
A 5-residue synthetic pentapeptide characterised as a highly selective growth-hormone secretagogue receptor (GHS-R1a) agonist with minimal reported cross-reactivity at cortisol or prolactin pathways in preclinical models. For laboratory characterisation only.
Ipamorelin — clinical & mechanistic profile
Ipamorelin is the first GHRP with GHRH-like selectivity, binding GHSR-1a (ghrelin receptor) to stimulate pulsatile GH release with EC50 = 1.3 nmol/L and Emax = 85% comparable to GHRP-6, but without ACTH/cortisol elevation even at >200-fold above GH ED50. Lower plasma clearance (5-fold slower than GHRP-6) with ~50% nasal bioavailability.
Studied applications
- Exceptional selectivity
- no significant ACTH/cortisol elevation at >200-fold GH ED50, mirroring GHRH selectivity
- GHRP-6 equivalent potency
- EC50 = 1.3 ± 0.4 nmol/L, Emax = 85 ± 5% in rat pituitary; ED50 = 80 nmol/kg in vivo
- Pulsatile GH release
- dose-dependent peaks at 15-60 min, baseline by 180 min; synergistic with GHRH
- Superior pharmacokinetics
- 5-fold lower plasma clearance than GHRP-6, ~50% nasal bioavailability
- GI-independent action
- gastrectomy reduces GHRP-6 GH release 60-70%, suggesting gastric ghrelin component
Research constraints & safety notes
- Not approved for human therapeutic use—research compound only
- Clinical development for postoperative ileus discontinued
- Short half-life (~2 hours) requires multiple daily administrations
- GH elevation may affect glucose metabolism
- Quality and purity of research compounds varies between sources
Full agonist (in vitro)
In-vitro cAMP and Ca²⁺ mobilisation assays report full agonism at GHS-R1a. Selectivity over ACTH/cortisol axes is the defining feature reported in the discovery literature.
In-vitro / preclinical characterisation only — no clinical or therapeutic claim is expressed or implied. Research use only.
Ipamorelin is a synthetic pentapeptide (GH-secretagogue secretagogue). Ipamorelin is the first GHRP with GHRH-like selectivity, binding GHSR-1a (ghrelin receptor) to stimulate pulsatile GH release with EC50 = 1.3 nmol/L and Emax = 85% comparable to GHRP-6, but without ACTH/cortisol elevation even at >200-fold above GH ED50. Lower plasma clearance (5-fold slower than GHRP-6) with ~50% nasal bioavailability. It has a molecular formula C38H49N9O5, mass 711.85 Da. Its published amino-acid sequence is Aib-His-D-2-Nal-D-Phe-Lys-NH2. Common synonyms in the literature include NNC 26-0161, Peptide secretagogue, and GHRP.
What it’s studied for
Investigation of Ipamorelin to date is clinical-investigational, with the majority of citations concentrated in animal models and in-vitro assays rather than randomized controlled human trials. Published work referencing Ipamorelin spans Selectivity studies: Direct comparisons with GHRP-2, GHRP-6, and hexarelin demonstrated ipamorelin's unique selectivity. At GH-equivalent doses, ipamorelin showed no significant increase in cortisol or ACTH, while other GHRPs produced dose-dependent elevations. Prolactin effects were also minimal compared to GHRP-2, Dose-response research: Studies in swine and humans showed linear dose-response relationships for GH release up to plateau doses. The predictable pharmacology distinguishes ipamorelin from GHRPs with more complex dose-response curves, and Postoperative ileus trials: Phase 2 clinical trials evaluated ipamorelin for accelerating GI recovery after surgery. While the compound showed GH-independent effects on GI motility via GHS-R1a in the gut, development was discontinued and the compound did not receive approval. Proposed mechanisms in the literature include GHSR-1a agonism: selectively binds ghrelin receptor, confirmed via GHRP antagonist pharmacology (not GHRH pathway) and Pituitary somatotroph activation: directly stimulates GH-producing cells via Gq-protein/calcium signaling. None of this material describes therapeutic outcomes in humans, and No vendor listed here provides dosing guidance for Ipamorelin outside laboratory research.
Related research
For the full mechanistic profile, published references, and constraint notes on Ipamorelin, see the Ipamorelin research page. All references cited on that page are peer-reviewed primary literature.
For research use only. This summary is a research-scientific overview compiled from peer-reviewed sources. It is not medical advice and is not intended for human or veterinary consumption.
Receptor engagement in the primary literature
Binding and functional-assay data for Ipamorelin, from peer-reviewed in-vitro pharmacology publications. Values are receptor activity parameters — not clinical outcomes.
Investigational context
Study designs referencing this compound in the published literature. Descriptions cover framework only — phase, participant count, duration, and citation — not outcomes. Click a card to review the source directly.
Specifications
| Attribute | Value |
|---|---|
| Molecular Formula | C38H49N9O5 |
| CAS Number | 170851-70-4 |
| Molecular Weight | 711.85 g/mol |
| Sequence | Aib-His-D-2-Nal-D-Phe-Lys-NH2 |
| Sequence length | 5 residues |
| Physical form | Lyophilized powder |
| PubChem CID | 9831659 ↗ |
Chemistry comparison — growth-hormone secretagogue peptides
Two peptide research compounds published as growth-hormone-secretagogue-family molecules with distinct receptor targets. Reference chemistry only.
| Compound | Sequence | MW | Half-life (lit.) | Reference |
|---|---|---|---|---|
| Ipamorelinpeptide | 5 residues | 711.85 g/mol | ~2 hours (lit.) | Raun Eur J Endocrinol 1998 |
| CJC-1295 (no-DAC)peptide | 29 residues | 3367.9 g/mol | ~30 min (lit.) | Alba JCEM 2006 |
Reference chemistry only. Receptor-binding indications are qualitative (compound engages / does not engage the receptor in in-vitro assays as reported in the cited literature). No comparative-effectiveness claim is expressed or implied.