Ipamorelin Canada: Buy 10mg Research Vials

Ipamorelin is a synthetic five-residue peptide, Aib-His-D-2-Nal-D-Phe-Lys-NH₂, developed in a Novo Nordisk chemistry programme and first described in 1998 as a growth hormone (GH) secretagogue that released GH through the GHRP-type receptor while leaving ACTH and cortisol untouched in swine^[2]. That receptor, GHS-R, had been cloned two years earlier^[1], and its natural ligand, ghrelin, was identified from rat stomach a year later^[8] — which is why ipamorelin is described interchangeably as a GH secretagogue, a GHS-R1a agonist and a ghrelin mimetic. Its literature is mostly rat, mouse and swine pharmacology from 1998–2012, a handful of gastrointestinal-motility studies, two human studies (a volunteer pharmacokinetic study and one negative phase 2 trial)^{[6, 19]}, and a growing anti-doping analytical literature. It has no approved drug form. The vial on this page is lyophilized research-grade material for laboratory use only.

Key facts

• Sequence: Aib-His-D-2-Nal-D-Phe-Lys-NH₂ — an α-aminoisobutyric acid, a histidine, a D-2-naphthylalanine, a D-phenylalanine and a lysine amide; the central Ala-Trp of GHRP-1 was deliberately left out^[2]
• Formula and weight: C₃₈H₄₉N₉O₅, 711.9 g/mol (PubChem CID 9831659); ChEMBL lists 711.87 (CHEMBL58547) — the two databases agree to the second decimal
• Identifiers: CAS 170851-70-4; development code NNC 26-0161; INN ipamorelin (PubChem synonyms)
• Receptor: GHS-R1a, the ghrelin receptor^{[1, 8]}; antagonist profiling in 1998 placed it on the GHRP pathway rather than the GHRH pathway^[2]
• Distinguishing pharmacology: in swine it did not raise ACTH or cortisol above the GHRH response, where GHRP-2 and GHRP-6 did — the property that gave the 1998 paper its title^[2]
• Human data: one dose-escalation pharmacokinetic study in healthy men^[6] and one randomised placebo-controlled phase 2 trial in bowel-resection patients that found no significant benefit^[19]; ChEMBL records the highest development phase as 2
• Regulatory and sport status: not approved anywhere; GH-releasing peptides including ipamorelin are on the WADA Prohibited List^[20], and glycine-extended copies have turned up in seized and black-market products^{[21, 22]}
• Format on this site: one 10mg vial, lyophilized powder, laboratory research only

Where does ipamorelin come from?

The story starts with a receptor rather than a peptide. Small synthetic GH secretagogues had been known to act on the pituitary and hypothalamus for years before Howard and colleagues cloned their G-protein-coupled target from swine and human tissue in 1996 and argued that the synthetic molecules must be mimicking an undiscovered hormone^[1]. Novo Nordisk’s medicinal chemists were working through series of GHRP-like peptides at the time; Raun and co-workers reported in 1998 that a pentapeptide lacking GHRP-1’s central Ala-Trp dipeptide, coded NNC 26-0161 and named ipamorelin, released GH from primary rat pituitary cells with potency and efficacy close to GHRP-6 (EC₅₀ 1.3 ± 0.4 nmol/l, E_max 85 ± 5% of the GHRP-6 response)^[2]. The same group then trimmed the molecule further, replacing residues with a 3-(aminomethyl)benzoic acid fragment and N-methylating the backbone to reach smaller derivatives with some oral bioavailability in dogs^[3]. In 1999 Kojima’s laboratory purified the receptor’s endogenous ligand from rat stomach and named it ghrelin^[8], closing the loop the 1996 paper had opened.

Chemical identity

The acetate counter-ion and the water content of a lyophilized lot both add to the mass of “ipamorelin” in a vial without adding peptide, so a certificate of analysis that reports peptide content by mass is the number to read, not the label weight alone.

What has been studied in the laboratory?

Pituitary cells and receptor pharmacology (in vitro)

In primary rat pituitary cell cultures ipamorelin released GH at nanomolar concentrations with a maximum response somewhat below GHRP-6^[2]. Pituitary cells taken from young female rats after three weeks of in-vivo ipamorelin showed a larger volume of secretory granules in somatotrophs, and only in those cells did a four-hour in-vitro challenge with ipamorelin, GHRP-6 or GHRH raise both the proportion of somatotrophs and their GH content^[12]. Those are dish measurements of a hormone-secreting cell; they say nothing about tissue outcomes.

GH release and hormone selectivity (anaesthetised rats, conscious swine)

In anaesthetised rats and in conscious swine, ipamorelin’s GH-releasing potency and maximal effect sat close to GHRP-6, with GHRP-2 more potent but less efficacious. None of the secretagogues changed FSH, LH, prolactin or TSH in swine; GHRP-2 and GHRP-6 raised ACTH and cortisol, whereas ipamorelin did not, even at doses far above those needed for GH release^[2]. Methylprednisolone did not blunt the acute GH response to ipamorelin in rats^[7]. In streptozotocin-diabetic mice the GH surge after an ipamorelin challenge was more than twice that of non-diabetic mice while IGF-I failed to rise — a model of the GH hypersecretion and GH resistance seen in type 1 diabetes rather than a finding about the peptide itself^[13].

Pharmacokinetics (rat, human volunteers)

In male rats, plasma concentrations fell biexponentially after injection; ipamorelin’s clearance was about five-fold lower than GHRP-6’s, it left the body mainly in urine rather than bile, and 60–80% of the material was recovered intact, indicating moderate resistance to metabolism. Nasal bioavailability in rats was about 20%, lower than the 50% seen for GHRP-2 and two NNC analogues^[4]. In healthy men across five escalating dose levels, pharmacokinetics were dose-proportional, the terminal half-life was about 2 hours, and each exposure produced a single GH pulse peaking at roughly 40 minutes before declining to baseline; a population PK/PD model estimated the half-maximal stimulating concentration at 214 nmol/l^[6]. Later in-vivo (rat) and in-vitro (human serum) work mapped the urinary metabolites of the GHRP family, including ipamorelin, for doping-control assays^[18].

Bone growth and bone mass (rat)

Three Scandinavian rat studies make up most of the skeletal literature. Over 15 days in adult female rats, ipamorelin increased the longitudinal growth rate of the proximal tibia dose-dependently, measured by the spacing of tetracycline labels, and increased body-weight gain, without changing total IGF-I, IGF-binding proteins or serum markers of bone turnover^[5]. Twelve weeks of continuous infusion in 13-week-old female rats raised total tibial and vertebral bone mineral content, but the gain disappeared once corrected for the increase in body weight, and cortical volumetric density was unchanged — the extra mineral came from a larger cross-sectional bone area, not denser bone^[9]. In 8-month-old rats given methylprednisolone for three months, adding ipamorelin increased calf-muscle tetanic tension and quadrupled the periosteal bone-formation rate relative to glucocorticoid alone^[11].

Glucocorticoid catabolism and nitrogen balance (rat)

Rats receiving methylprednisolone lost weight after surgery; those also given ipamorelin lost markedly less, with IGF-I rising in parallel^[7]. In prednisolone-treated rats, ipamorelin reduced the liver’s capacity for urea synthesis by a fifth, lowered urea-cycle gene expression and brought nitrogen balance back to neutral — a smaller effect than GH itself produced in the same experiment^[16].

Body fat, leptin and feeding (mouse)

The one result that runs against the “GH-releasing” label: in both GH-deficient (lit/lit) and GH-intact mice, repeated ipamorelin produced a modest body-weight increase that plateaued by two weeks and raised fat-pad weight relative to body weight, while GH itself lowered relative fat mass. GHS treatment, but not GH, also increased serum leptin and food intake in GH-intact mice. The authors concluded that GH secretagogues increase adiposity by GH-independent routes, probably including feeding^[10].

Pancreatic insulin release (rat tissue, in vitro)

Fragments of pancreas from normal and streptozotocin-diabetic rats released more insulin when incubated with ipamorelin across a wide concentration range; the effect was blocked by a calcium-channel blocker and by adrenergic antagonists, pointing to calcium-channel and adrenergic pathways^[14].

Gastrointestinal motility and visceral sensitivity (rat)

Because ghrelin receptors drive gut motility, ipamorelin was tested in rats after laparotomy and intestinal handling. A single dose shortened the time to the first bowel movement; repeated doses over two days increased faecal pellet output, food intake and weight gain^[15]. In the same model, ipamorelin accelerated gastric emptying of a radiolabelled meal and restored the contractile response of isolated gastric fundus strips to acetylcholine and electrical stimulation^[17]. In a non-inflammatory model of colonic hypersensitivity induced by dilute acetic acid, the peripherally restricted agonist ipamorelin and the brain-penetrant agonist HM01 both reduced abdominal contractions to colorectal distension and paw withdrawal to a von Frey filament, and a ghrelin-receptor antagonist abolished the effect^[23].

Ferret and fish models

In ferrets given cisplatin, ipamorelin and anamorelin each reduced the weight loss of the delayed phase by about a quarter but had no effect on acute or delayed emesis; only centrally administered anamorelin reduced acute vomiting^[24]. In the cichlid Oreochromis mossambicus, 21 days of ipamorelin acetate increased food intake dose-dependently, increased spermatocyte and spermatid counts, and raised serum LH and 11-ketotestosterone without changing hypothalamic GnRH fibres^[25].

Humans

Two studies. The 1999 volunteer study described above characterised pharmacokinetics and the GH response^[6]. The 2014 phase 2 trial (NCT00672074) randomised 117 adults undergoing small- or large-bowel resection to ipamorelin or placebo after surgery. The peptide was well tolerated at the dose tested, but median time to tolerating a solid meal (25.3 vs 32.6 hours) did not differ significantly from placebo (p = 0.15), and no secondary efficacy endpoint did either^[19]. No later phase of development is recorded in PubMed or ChEMBL.

Study summary

What the evidence does not show

• No demonstrated clinical benefit. The only randomised controlled trial of ipamorelin — for postoperative ileus — was negative on its primary and secondary endpoints^[19]. There is no human trial of ipamorelin for body composition, growth, recovery, ageing or any other use.
• “Selective” describes hormones in swine, not safety. The 1998 selectivity finding is about ACTH, cortisol, prolactin, TSH, FSH and LH in pigs after single doses^[2]. It is not evidence about long-term effects in any species.
• The rodent fat data cut both ways. In mice the peptide increased relative body fat, leptin and food intake through GH-independent mechanisms^[10]; the rat bone gains were largely explained by higher body weight^[9].
• Bone and muscle findings are rat-only and model-specific. They come from adult female rats, in several cases under glucocorticoid stress^{[5, 9, 11]}, and were not followed by human studies.
• Insulin and glucose effects are unresolved. A rat pancreas preparation released more insulin in vitro^[14]; the 2026 reviews list dysglycaemia among adverse effects reported with GH-axis peptides generally^[26]. Neither settles what ipamorelin does to glucose handling in a living organism.
• Market material is not always what the label says. Analyses of black-market and customs-seized “ipamorelin” found glycine-extended analogues in place of the genuine peptide^{[21, 22]} — a reason to read a batch-specific certificate rather than a product name.
• No regulatory approval anywhere. Ipamorelin is an investigational compound whose development stopped after phase 2; it is not a drug in Canada, the US or the EU, and it is prohibited in sport^{[20, 26, 27]}.

Batch documentation

No batch-specific certificate of analysis for the 10mg vial is posted in the COA library at the time of this review. We have not borrowed another product’s report to stand in for it. When an independent report for an ipamorelin lot is issued, the product page will embed it and this page will quote the measured peptide content and purity. In the meantime the analytical literature is a useful guide to what a good report should show: an HPLC purity figure and a mass-spectrometry identity confirmation whose mass matches C₃₈H₄₉N₉O₅ (711.9), since the glycine-extended analogues found in seized material differ from the genuine peptide by exactly one glycine residue^[22].

Ipamorelin is one of the compounds on the page where you can buy peptides online in Canada; every listing there is sold under the same research-use-only terms.

Handling and storage in the laboratory

• Form: lyophilized powder in a sealed vial; the peptide is a C-terminal amide with two D-amino acids, and the 1998 rat study found it moderately resistant to metabolism^[4], but that is a statement about plasma, not about a solution on a bench.
• Storage: the site’s guidance is −20 °C for the sealed vial over the long term (stated stability up to 24 months) and cool, dry, dark conditions for short holds; avoid repeated freeze–thaw.
• Documentation: log the batch, the receipt date and the opening date; match the batch to its certificate before use.
• Protocols: the researcher’s responsibility. Shop Peptides Online publishes no dosing, reconstitution or administration guidance.

References

All references were retrieved from PubMed (NCBI) on 30 September 2026 and cross-checked against Europe PMC; identity data from PubChem and ChEMBL (EMBL-EBI) on the same date.

1. Howard AD, Feighner SD, Cully DF et al. (1996). A receptor in pituitary and hypothalamus that functions in growth hormone release. Science 273(5277):974-7. PMID 8688086
2. Raun K, Hansen BS, Johansen NL et al. (1998). Ipamorelin, the first selective growth hormone secretagogue. Eur J Endocrinol 139(5):552-61. PMID 9849822
3. Ankersen M, Johansen NL, Madsen K et al. (1998). A new series of highly potent growth hormone-releasing peptides derived from ipamorelin. J Med Chem 41(19):3699-704. PMID 9733495
4. Johansen PB, Hansen KT, Andersen JV et al. (1998). Pharmacokinetic evaluation of ipamorelin and other peptidyl growth hormone secretagogues with emphasis on nasal absorption. Xenobiotica 28(11):1083-92. PMID 9879640
5. Johansen PB, Nowak J, Skjaerbaek C et al. (1999). Ipamorelin, a new growth-hormone-releasing peptide, induces longitudinal bone growth in rats. Growth Horm IGF Res 9(2):106-13. PMID 10373343
6. Gobburu JV, Agersø H, Jusko WJ et al. (1999). Pharmacokinetic-pharmacodynamic modeling of ipamorelin, a growth hormone releasing peptide, in human volunteers. Pharm Res 16(9):1412-6. PMID 10496658
7. Malmlöf K, Johansen PB, Haahr PM et al. (1999). Methylprednisolone does not inhibit the release of growth hormone after intravenous injection of a novel growth hormone secretagogue in rats. Growth Horm IGF Res 9(6):445-50. PMID 10629165
8. Kojima M, Hosoda H, Date Y et al. (1999). Ghrelin is a growth-hormone-releasing acylated peptide from stomach. Nature 402(6762):656-60. PMID 10604470
9. Svensson J, Lall S, Dickson SL et al. (2000). The GH secretagogues ipamorelin and GH-releasing peptide-6 increase bone mineral content in adult female rats. J Endocrinol 165(3):569-77. PMID 10828840
10. Lall S, Tung LY, Ohlsson C et al. (2001). Growth hormone (GH)-independent stimulation of adiposity by GH secretagogues. Biochem Biophys Res Commun 280(1):132-8. PMID 11162489
11. Andersen NB, Malmlöf K, Johansen PB et al. (2001). The growth hormone secretagogue ipamorelin counteracts glucocorticoid-induced decrease in bone formation of adult rats. Growth Horm IGF Res 11(5):266-72. PMID 11735244
12. Jiménez-Reina L, Cañete R, de la Torre MJ et al. (2002). Influence of chronic treatment with the growth hormone secretagogue Ipamorelin, in young female rats: somatotroph response in vitro. Histol Histopathol 17(3):707-14. PMID 12168778
13. Johansen PB, Segev Y, Landau D et al. (2003). Growth hormone (GH) hypersecretion and GH receptor resistance in streptozotocin diabetic mice in response to a GH secretagogue. Exp Diabesity Res 4(2):73-81. PMID 14630569
14. Adeghate E, Ponery AS (2004). Mechanism of ipamorelin-evoked insulin release from the pancreas of normal and diabetic rats. Neuro Endocrinol Lett 25(6):403-6. PMID 15665799
15. Venkova K, Mann W, Nelson R et al. (2009). Efficacy of ipamorelin, a novel ghrelin mimetic, in a rodent model of postoperative ileus. J Pharmacol Exp Ther 329(3):1110-6. PMID 19289567
16. Aagaard NK, Grøfte T, Greisen J et al. (2009). Growth hormone and growth hormone secretagogue effects on nitrogen balance and urea synthesis in steroid treated rats. Growth Horm IGF Res 19(5):426-31. PMID 19231263
17. Greenwood-Van Meerveld B, Tyler K, Mohammadi E et al. (2012). Efficacy of ipamorelin, a ghrelin mimetic, on gastric dysmotility in a rodent model of postoperative ileus. J Exp Pharmacol 4:149-55. PMID 27186127
18. Thomas A, Delahaut P, Krug O et al. (2012). Metabolism of growth hormone releasing peptides. Anal Chem 84(23):10252-9. PMID 23101768
19. Beck DE, Sweeney WB, McCarter MD et al. (2014). Prospective, randomized, controlled, proof-of-concept study of the Ghrelin mimetic ipamorelin for the management of postoperative ileus in bowel resection patients. Int J Colorectal Dis 29(12):1527-34. PMID 25331030
20. Semenistaya E, Zvereva I, Thomas A et al. (2015). Determination of growth hormone releasing peptides metabolites in human urine after nasal administration of GHRP-1, GHRP-2, GHRP-6, Hexarelin, and Ipamorelin. Drug Test Anal 7(10):919-25. PMID 25869809
21. Krug O, Thomas A, Malerød-Fjeld H et al. (2018). Analysis of new growth promoting black market products. Growth Horm IGF Res 41:1-6. PMID 29864719
22. Gajda PM, Holm NB, Hoej LJ et al. (2019). Glycine-modified growth hormone secretagogues identified in seized doping material. Drug Test Anal 11(2):350-354. PMID 30136411
23. N Mohammadi E, Louwies T, Pietra C et al. (2020). Attenuation of Visceral and Somatic Nociception by Ghrelin Mimetics. J Exp Pharmacol 12:267-274. PMID 32801950
24. Lu Z, Ngan MP, Liu JYH et al. (2024). The growth hormone secretagogue receptor 1a agonists, anamorelin and ipamorelin, inhibit cisplatin-induced weight loss in ferrets: Anamorelin also exhibits anti-emetic effects via a central mechanism. Physiol Behav 284:114644. PMID 39043357
25. Gouda M, Ganesh CB (2024). The influence of ghrelin agonist ipamorelin acetate on the hypothalamic-pituitary-testicular axis in a cichlid fish, Oreochromis mossambicus. Anim Reprod Sci 268:107550. PMID 38996787
26. Dominikowski A, Rękoś Z, Olejarz M et al. (2026). The emerging landscape of performance-enhancing peptides modulating GH-IGF1 axis: bridging the gap between clinical evidence and patient self-administration. Front Endocrinol (Lausanne) 17:1822475. PMID 42395176
27. Coutinho LFD, DE Oliveira Neves LF, Camilo RP (2026). A new era of doping? Use of peptide and peptide-analog drugs in recreational and professional sport and bodybuilding: a critical review. J Sports Med Phys Fitness 66(7):880-885. PMID 41880199