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Ipamorelin

Ipamorelin

Synthetic pentapeptide Aib-His-D-2Nal-D-Phe-Lys-NH2, growth hormone secretagogue receptor (GHS-R1a) agonist more info
Ipamorelin is a synthetic pentapeptide (H-Aib-His-D-2Nal-D-Phe-Lys-NH2) designed at Novo Nordisk in the mid-1990s as a structurally simplified, receptor-selective growth hormone secretagogue. The molecule mimics the pituitary GHS-R1a binding of acyl-ghrelin without engaging the corticotroph and lactotroph pathways activated at therapeutic doses by GHRP-2, GHRP-6, and Hexarelin in animal preparations. The single Phase 2 human-efficacy trial in postoperative ileus missed its primary endpoint in 2014; the sponsor discontinued development.

Available for laboratory research use only.

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Biochemical Profile

CAS Number
170851-70-4
Molecular Formula
C38H49N9O5
Molecular Weight
711.86 g/mol
Purity
≥99% (HPLC-UV (220 nm + 280 nm))
PubChem CID
11226745
Amino Acid Sequence
H-Aib-His-D-2Nal-D-Phe-Lys-NH2

Receptor Targets and Signaling Pathway Context

Ipamorelin has been characterized as a selective agonist of the growth hormone secretagogue receptor type 1a (GHS-R1a), the cognate receptor of the endogenous 28-residue peptide acyl-ghrelin[1]. Acyl-ghrelin requires Ser3 octanoylation by the GOAT enzyme to bind GHS-R1a; the un-octanoylated form does not. Ipamorelin mimics the receptor-binding interaction with a designed pentapeptide scaffold that is structurally distinct from ghrelin and was derived through medicinal-chemistry simplification of the earlier GHRP-1 / GHRP-2 / GHRP-6 / Hexarelin series at Novo Nordisk.

The Raun et al. 1998 foundational paper reported GHS-R1a binding affinity in the low-nanomolar range and growth hormone release from primary rat pituitary cells, anesthetized rats, and conscious swine at potencies comparable to GHRP-6[1]. In the same animal preparations, plasma ACTH, cortisol, prolactin, FSH, LH, and TSH were not detectably elevated at ipamorelin doses greater than 200-fold above the GH ED50. This receptor selectivity at the pituitary corticotroph and lactotroph relative to other GHRPs is the central biochemical observation in the foundational literature and was the structural goal that motivated the alpha-aminoisobutyric acid (Aib) N-cap plus deletion of the GHRP-1 central Ala-Trp dipeptide[2].

The selectivity finding has methodological limits that the published evidence does not exit. The cortisol comparator in Raun 1998 was GHRH rather than vehicle, so the published comparison cannot resolve an ipamorelin-specific cortisol signal smaller than the (zero) GHRH-driven signal. Prolactin and ACTH measurements in that work were performed in rat and swine. The most-cited human pharmacokinetic study (Gobburu et al. 1999) reported a plasma half-life of approximately two hours after intravenous administration in healthy male volunteers and characterized growth hormone release as the pharmacodynamic readout, but the study did not measure plasma cortisol, ACTH, or prolactin in humans[3]. The narrow defensible claim in the published evidence is that ipamorelin was more selective than GHRP-6 / GHRP-2 at the pituitary somatotroph in animal preparations. Direct human confirmation of an absolute absence of cortisol or prolactin response has not been published in the peer-reviewed literature.

The combined GHRH-analog plus GHRP-class synergy reported by Bowers and colleagues across the 1980s and 1990s used non-ipamorelin GHRPs and non-CJC-1295 GHRH analogs[4]. The mechanism is biologically supported at the level of pulse-amplitude versus basal-frequency control of pituitary somatotroph GH release. No peer-reviewed randomized controlled trial of CJC-1295 with ipamorelin specifically has been conducted; the existing pairing literature is inferred from non-pairing evidence.

GHS-R1a is expressed beyond the pituitary somatotroph, in the hypothalamus, hippocampus, cardiac tissue, pancreas, immune cells, adipose tissue, and bone. The intra-pituitary selectivity story does not address whether other GHS-R1a-expressing tissues are engaged by chronic exposure. Receptor desensitization and downregulation are canonical features of class-A G-protein-coupled receptors under chronic agonism; native ghrelin signaling is pulsatile and meal-anticipatory, not continuous. Whether sustained subcutaneous ipamorelin exposure at the dosing patterns observed in research-use channels produces GHS-R1a tachyphylaxis, sustained supraphysiological IGF-1 elevation, or any other chronic-administration effect has not been characterized in the peer-reviewed published evidence.

Research Applications

Growth Hormone Secretagogue Pharmacology

The Raun et al. 1998 foundational characterization positioned ipamorelin as a structurally distinct GHS-R1a agonist designed to release growth hormone from pituitary somatotrophs without engaging the corticotroph and lactotroph pathways activated at therapeutic doses by GHRP-2, GHRP-6, and Hexarelin[1]. Across primary rat pituitary cell preparations, anesthetized rats, and conscious swine, the reported growth hormone release was comparable in potency to GHRP-6. Plasma ACTH, cortisol, prolactin, FSH, LH, and TSH were not detectably elevated at ipamorelin doses greater than 200-fold above the GH ED50.

Ankersen et al. 1998 reported the structure-activity relationship work that produced the ipamorelin series, including the alpha-aminoisobutyric acid (Aib) N-cap and the deletion of the GHRP-1 central Ala-Trp dipeptide[2]. These two structural moves were associated with the reported intra-pituitary receptor selectivity. The medicinal-chemistry program also produced peptidomimetic successors with improved oral bioavailability, including a series using isonipecotic acid (Inp) at position 1; the Inp notation that occasionally appears in vendor copy for ipamorelin itself is an error.

The first-in-human pharmacokinetic study (Gobburu et al. 1999) reported a plasma half-life of approximately two hours after intravenous administration in healthy male volunteers, with growth hormone release as the measured pharmacodynamic endpoint[3]. Plasma cortisol, ACTH, and prolactin were not reported in that work. Direct human measurement of the cortisol and prolactin endpoints framed by the selectivity story has not been published in the peer-reviewed literature.

Bone and Skeletal Research

Andersen et al. 2001 reported that ipamorelin administration in a rat model of glucocorticoid-induced cortical bone loss was associated with changes in cortical bone formation rate and mineral apposition markers relative to glucocorticoid-only controls[5]. The work was conducted at the Sahlgrenska Academy and remains the most-cited primary preclinical bone-related study using ipamorelin specifically.

Svensson et al. 2000 examined ipamorelin in normal adult rats and reported changes in body weight gain, lean tissue measurements, and serum IGF-1 concentrations under repeated subcutaneous administration over a multi-week timeframe[6]. The reported findings span what subsequent ghrelin-axis literature would identify as the canonical somatotropic-axis readouts (GH pulse, IGF-1 elevation, anabolic markers in rapidly growing tissue compartments) without exiting the rat preparation.

Independent replication of the bone-related findings outside the Sahlgrenska / Sweden academic axis is thin. The published rat-bone literature on ipamorelin has not been extended into systematic human studies. No osteoporosis or glucocorticoid-bone-loss human clinical trial of ipamorelin has been registered or completed.

Postoperative Ileus and Gastric Motility Research

Greenwood-Van Meerveld et al. and related preclinical work in the early 2010s reported observations on gastric emptying and colonic motility under acute ipamorelin administration in rat preparations of postoperative ileus[7]. The mechanistic rationale for the indication rests on the orexigenic and prokinetic effects of GHS-R1a agonism in the enteric nervous system, which is a downstream consequence of acyl-ghrelin signaling in non-pituitary tissues.

This preclinical rationale was developed clinically by Sapphire Therapeutics and then by Helsinn Therapeutics, the latter through Sapphire's acquisition in January 2009. The Beck et al. 2014 study (NCT00672074) was the first and only registered Phase 2 randomized, double-blind, placebo-controlled human efficacy trial of ipamorelin in any indication[8]. Adults undergoing bowel resection received intravenous ipamorelin acetate at the trial-specified weight-based dose (administered as two separate infusions in each 24-hour postoperative interval) or matching placebo for up to seven postoperative days. The mITT analysis enrolled approximately 114 to 117 participants. The pre-specified primary endpoint, median time to first tolerated meal, was 25.3 hours in the ipamorelin arm versus 32.6 hours in the placebo arm, p=0.15. The trial missed its primary endpoint. Reported secondary endpoints did not meet pre-specified statistical thresholds either. Safety was reported as clean; no safety signal emerged.

Helsinn discontinued ipamorelin development following the Phase 2 readout. A follow-on colonic motility study (NCT01280344) also did not advance the program. No Phase 3 trial of ipamorelin in any indication has ever been attempted by any sponsor.

Comparative Ghrelin Receptor Agonist Pharmacology

The growth hormone secretagogue class includes GHRP-1, GHRP-2 (pralmorelin), GHRP-6, Hexarelin, and ipamorelin among the synthetic peptide agonists of GHS-R1a, plus the oral nonpeptide agonists anamorelin, capromorelin, macimorelin, ibutamoren (MK-677), and relamorelin. Each member of the class has distinct off-target engagement and distinct regulatory trajectories.

In animal preparations, GHRP-2, GHRP-6, and Hexarelin produced cortisol and prolactin elevation at therapeutic doses through non-GHS-R1a engagement of pituitary corticotroph and lactotroph pathways[1]. Hexarelin additionally engages CD36 on cardiomyocytes and has been examined in cardiac literature distinct from the somatotropic-axis readout. Ipamorelin's reported intra-pituitary receptor selectivity was the structural goal that motivated its design and the published differentiator across the class in animals.

The regulatory trajectories diverge sharply. Macimorelin was approved by the FDA in December 2017 as an oral single-dose growth-hormone-stimulation test in adult growth hormone deficiency. Capromorelin holds active FDA veterinary approvals (2016 in dogs; 2020 in cats). Anamorelin (Helsinn's oral nonpeptide successor to ipamorelin) achieved Japan PMDA approval in January 2021 for cancer cachexia in non-small-cell lung, gastric, pancreatic, and colorectal cancers and launched April 2021 via Ono Pharmaceutical; the EMA refused marketing authorization in May 2017 (confirmed on re-examination September 2017), and the FDA issued a Complete Response Letter to Helsinn in 2017 (never resubmitted). Importing anamorelin's clinical dataset to ipamorelin claims is methodologically inappropriate — the molecules differ in chemistry (pentapeptide versus small molecule), route (subcutaneous versus oral), indication (healthy-adult GH release versus cancer cachexia), and sponsor-clinical-development trajectory.

Chiral Purity and Quality Control

Ipamorelin's biological activity depends on the chirality of two non-canonical D-isomer residues at positions 3 and 4 (D-2-naphthylalanine and D-phenylalanine). Diastereomers formed by base-catalyzed inversion of either residue to the L-isomer are biologically inactive but share identical molecular mass with the active D,D-pair and frequently co-elute with the active species on standard achiral reversed-phase HPLC columns.

Standard RP-HPLC at 220 nm and 280 nm plus electrospray-ionization mass spectrometry, the conventional analytical battery applied across the synthetic peptide research-use channel, cannot resolve these diastereomers. The diagnostic chiral-purity assay involves derivatization of the acid hydrolysate with Marfey's reagent (FDAA) followed by RP-HPLC, which converts the underivatized amino acids into diastereomers resolvable on conventional achiral columns; the expected pattern is 100% D-2-naphthylalanine at position 3 and 100% D-phenylalanine at position 4. Any L-contamination at either position indicates D-residue racemization during synthesis, storage, or formulation handling. Chiral HPLC on Chiralpak IA, IB, or IC stationary phases is an alternative.

The N-terminal alpha-aminoisobutyric acid residue (Aib) presents a separate synthesis-stage technical challenge. Aib is alpha,alpha-disubstituted, achiral, sterically hindered, and requires HATU activation with extended coupling times and double couplings at both the Aib coupling step and the subsequent histidine-to-Aib step. Acetic anhydride capping after each Aib cycle is standard to terminate deletion sequences. The C-terminal amide is installed via Rink amide resin. These are well-established solid-phase chemistry operations; competent manufacturers produce the molecule at high purity at reasonable yield.

Replication and Clinical Status

The peer-reviewed ipamorelin corpus is approximately 80 to 120 indexed papers on PubMed, smaller than the BPC-157 corpus (approximately 200) and far smaller than the thymosin beta-4 corpus (approximately 1,500 to 1,800). Publication is front-loaded into the 1998 to 2001 Novo Nordisk discovery window and the 2013 to 2015 Helsinn postoperative-ileus window. Post-2016 output is approximately 3 to 6 papers per year. No personality-driven academic champion picked up the molecule after the Helsinn discontinuation; the citation network is corporate rather than concentrated in a single laboratory.

The central applied-evidence point is the Beck et al. 2014 Phase 2 endpoint miss in postoperative ileus, p=0.15, n=114, no Phase 3 attempted in any indication by any sponsor[8]. The cited animal selectivity work (Raun 1998) and the cited first-in-human pharmacokinetic work (Gobburu 1999) characterize acute single-dose responses and do not address the chronic-administration use pattern of the research-use channel[1][3]. As of May 2026, no active recruiting ipamorelin clinical trial is registered on ClinicalTrials.gov. Hudson Biotech, which is sponsoring Phase 2 trials of BPC-157, TB-500, and GHK-Cu, has not registered an ipamorelin trial.

The regulatory status as of May 2026: the FDA Pharmacy Compounding Advisory Committee (PCAC) voted against 503A bulks-list inclusion on October 29, 2024, for both proposed indications (growth hormone deficiency; postoperative ileus) and for both the acetate and free-base forms; the FDA briefing document itself recommended against inclusion[9]. Ipamorelin is NOT scheduled for the July 23-24, 2026 PCAC docket. The 503A door is closed for ipamorelin. The World Anti-Doping Agency lists ipamorelin explicitly under S2 (Growth Hormone Secretagogues), prohibited at all times in all sports with no Therapeutic Use Exemption pathway[10]. Australia's Therapeutic Goods Administration places ipamorelin on Schedule 4 with Appendix D Item 5, stricter than baseline Schedule 4. Ipamorelin was named explicitly in the 2020 Tailor Made Compounding plea and in the April 1, 2026 federal indictment of Justin Bradley Watkins (USA v. Watkins, 1:26-cr-00015-DBB, D. Utah)[11].

Reconstitution & Storage

Recommended Diluent
Sterile water
Storage (lyophilized)
-20°C, dry, dark, 24+ months
Storage (reconstituted)
2-8°C, use within 30 days
Shelf Life
24 months lyophilized

Research References

  1. [1] Raun K, Hansen BS, Johansen NL, et al. Ipamorelin, the first selective growth hormone secretagogue. Eur J Endocrinol. 1998;139(5):552-561. doi:10.1530/eje.0.1390552PMID:9849822
  2. [2] Ankersen M, Johansen NL, Madsen K, et al. A new series of highly potent growth hormone-releasing peptides derived from ipamorelin. J Med Chem. 1998;41(20):3699-3704. PMID:9733495
  3. [3] Gobburu JV, Agersø H, Jusko WJ, Ynddal L. Pharmacokinetic-pharmacodynamic modeling of ipamorelin, a growth hormone releasing peptide, in human volunteers. Pharm Res. 1999;16(9):1412-1416. PMID:10496658
  4. [4] Bowers CY. Growth hormone-releasing peptide (GHRP). Cell Mol Life Sci. 1998;54(12):1316-1329. PMID:9893707
  5. [5] Andersen NB, Malmlöf K, Johansen PB, Andreassen TT, Ørtoft G, Oxlund H. The growth hormone secretagogue ipamorelin counteracts glucocorticoid-induced loss of cortical bone in rats. Bone. 2001;28(3):288-294. doi:10.1016/s8756-3282(00)00478-9PMID:11248658
  6. [6] Svensson J, Lall S, Dickson SL, et al. The GH secretagogues ipamorelin and GH-releasing peptide-6 increase bone mineral content in adult female rats. J Endocrinol. 2000;165(3):569-577. PMID:10828840
  7. [7] Venkova K, Mann W, Nelson R, Greenwood-Van Meerveld B. Efficacy of ipamorelin, a novel ghrelin mimetic, in a rodent model of postoperative ileus. J Pharmacol Exp Ther. 2009;329(3):1110-1116. PMID:19289569
  8. [8] Beck DE, Sweeney WB, McCarter MD; Ipamorelin 201 Study Group. 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. 2014;29(12):1527-1534. doi:10.1007/s00384-014-2030-8PMID:25331030
  9. [9] U.S. Food and Drug Administration. Pharmacy Compounding Advisory Committee Meeting, October 29, 2024 — vote on ipamorelin acetate and ipamorelin free base for 503A bulks-list inclusion. PCAC voted against inclusion for both indications (growth hormone deficiency; postoperative ileus). FDA briefing document recommended against inclusion (verified 2026-05-19).
  10. [10] World Anti-Doping Agency. 2026 Prohibited List, Section S2 (Peptide Hormones, Growth Factors, Related Substances and Mimetics), subsection 2 (Growth Hormone Secretagogues). Ipamorelin is named explicitly. Prohibited at all times, all sports.
  11. [11] United States v. Justin Bradley Watkins, Case No. 1:26-cr-00015-DBB, U.S. District Court for the District of Utah. Federal indictment filed April 1, 2026. Ipamorelin named explicitly alongside CJC-1295, BPC-157, TB-500, GHK, GHK-Cu, NAD+, and GLP-1 analogs as substances at issue in the misbranding charges.
  12. [12] Johansen PB, Segel E, Christoffersen J, et al. Ipamorelin, a non-peptide growth hormone secretagogue, exhibits a sustained GH-releasing effect during oral and intranasal administration. Xenobiotica. 1998;28(11):1083-1090. PMID:9879640
  13. [13] Lall S, Tung LY, Ohlsson C, Jansson JO, Dickson SL. Growth hormone (GH)-independent stimulation of adiposity by GH secretagogues. Biochem Biophys Res Commun. 2001;280(1):132-138. PMID:11162489
  14. [14] Helsinn Therapeutics. Ipamorelin acetate for postoperative ileus. ClinicalTrials.gov Identifier: NCT00672074. Phase 2 randomized double-blind placebo-controlled, n=114-117 mITT; completed; primary endpoint (median time to first tolerated meal) MISSED, p=0.15 (verified 2026-05-19). Helsinn discontinued ipamorelin development following this readout. No Phase 3 in any indication has been attempted.
  15. [15] Garcia JM, Boccia RV, Graham CD, et al. Anamorelin for patients with cancer cachexia: an integrated analysis of two phase 2, randomised, placebo-controlled, double-blind trials. Lancet Oncol. 2015;16(1):108-116. PMID:25524795
  16. [16] European Medicines Agency. Refusal of the marketing authorisation for Adlumiz (anamorelin hydrochloride). CHMP opinion adopted 18 May 2017; confirmed on re-examination 14 September 2017. Adlumiz subsequently approved by the Japan PMDA on January 22, 2021 for cancer cachexia in NSCLC, gastric, pancreatic, and colorectal cancers; launched April 2021 via Ono Pharmaceutical (verified 2026-05-19).

Scientific Journal Author

Kirsten Raun, PhD

Health Care Discovery, Novo Nordisk A/S (originating medicinal chemistry program, 1990s)

Landmark Publications

  • Raun K, Hansen BS, Johansen NL, Thøgersen H, Madsen K, Ankersen M, Andersen PH. Ipamorelin, the first selective growth hormone secretagogue. Eur J Endocrinol. 1998;139(5):552-561. (PMID 9849822)
  • Ankersen M, Johansen NL, Madsen K, Hansen BS, Raun K, Nielsen KK, Thogersen H, Hansen TK, Peschke B, Lau J, Andersen PH, Lundt BF. A new series of highly potent growth hormone-releasing peptides derived from ipamorelin. J Med Chem. 1998;41(20):3699-3704. (PMID 9733495)
  • Johansen PB, Segel E, Christoffersen J, Raun K. Ipamorelin, a non-peptide growth hormone secretagogue, exhibits a sustained GH-releasing effect during oral and intranasal administration. Xenobiotica. 1998;28(11):1083-1090. (PMID 9879640)

Dr. Raun is independently cited here as the lead author of the foundational ipamorelin characterization at Novo Nordisk in the 1990s. There is no affiliation or commercial relationship between Dr. Raun, Novo Nordisk A/S, or any associated commercial entity, and Peerless Peptides.

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