What Ipamorelin Is
Ipamorelin (IUPAC designation: Aib-His-D-2-Nal-D-Phe-Lys-NH2; CAS 170851-70-4; molecular weight 711.86 Da; molecular formula C38H49N9O5) is a synthetic pentapeptide that acts as a selective agonist at the growth hormone secretagogue receptor type 1a (GHS-R1a), also known as the ghrelin receptor. It was developed at Novo Nordisk Pharma A/S under the research code NNC 26-0161 and first characterized pharmacologically by Raun et al. in 1998.[1]
The compound was derived from GHRP-1 by removing the central Ala-Trp dipeptide and substituting alpha-aminoisobutyric acid (Aib) at the N-terminus. The Aib modification confers metabolic stability against peptidase cleavage — a design feature confirmed by pharmacokinetic data showing that 60–80% of an administered dose is recovered from bile and urine as intact peptide, with plasma clearance approximately five-fold lower than GHRP-6.[11]
GHS-R1a is expressed on anterior pituitary somatotrophs, hypothalamic appetite-regulatory neurons, and enteric nervous system cells. When ipamorelin binds the pituitary somatotroph GHS-R1a, it triggers intracellular calcium mobilization via Gq/11-protein-coupled signaling, which drives a discrete pulse of growth hormone (GH) release. That GH pulse peaks at approximately 40 minutes post-administration and decays to negligible levels within 2–3 hours, consistent with the compound's terminal half-life of approximately 2 hours in human volunteers.[12]
What distinguishes ipamorelin from earlier GHRP-class compounds is selectivity. GHRP-2 and GHRP-6 both stimulate ACTH/cortisol and prolactin secretion at doses near their GH-releasing thresholds. Ipamorelin does not meaningfully elevate ACTH or cortisol even at doses 200-fold above its GH-releasing ED50 in rats.[1] A 2020 review of GHS pharmacology designated ipamorelin the "prototypical selective GHS" — the compound that established the mechanistic paradigm subsequently advanced by capromorelin and anamorelin.[17]
Schematic of the ipamorelin pentapeptide chain: five residues (Aib-His-D-2-Nal-D-Phe-Lys-NH2). The Aib N-terminal cap (filled node, left) confers metabolic stability.
What the Research Record Shows
Eighteen peer-reviewed citations index this site's research record. The literature spans bone biology, GI motility, body composition, nitrogen balance, pharmacokinetics, and oncology-adjacent cachexia models. The majority of data comes from rodent in vivo studies (primarily rat); one Phase 2 randomized controlled trial in humans was conducted (Beck et al., 2014; NCT00672074; N=114) targeting postoperative ileus after bowel resection.[10]
Bone and body composition
Subcutaneous ipamorelin at 18–450 mcg/day (divided doses) for 15 days increased longitudinal bone growth rate from 42 to 52 mcm/day in adult female rats in a dose-dependent manner.[2] Continuous subcutaneous infusion at 0.5 mg/kg/day for 12 weeks significantly increased tibial and vertebral bone mineral content via periosteal expansion.[4] In glucocorticoid-treated rats, 100 mcg/kg three times daily for three months produced a four-fold increase in periosteal bone formation rate and significant recovery of muscle tetanic tension.[3]
GI motility and postoperative ileus
A single intravenous dose (1 mg/kg) reduced time to first bowel movement in a rodent postoperative ileus model.[8] Intravenous ipamorelin at 0.014 mcmol/kg reduced gastric radioactivity retention from 78% (vehicle, post-surgery) to approximately 52%, approaching non-operated control levels of 44%.[9] The 2014 Phase 2 human trial found the compound well tolerated, with a 7.3-hour numeric reduction in time to first tolerated meal that did not reach statistical significance (p=0.15).[10]
Nitrogen balance
Ipamorelin at 0.5 mg/kg/day counteracted glucocorticoid-induced nitrogen wasting in prednisolone-treated rats, reducing hepatic urea-nitrogen synthesis capacity by 20% and normalizing organ nitrogen contents.[7]
Recent data (2024–2025)
Intraperitoneal ipamorelin inhibited cisplatin-induced weight loss by approximately 24% during the delayed phase (48–72 h post-cisplatin) in a ferret model — via peripheral rather than central mechanism, as the compound showed no significant anti-emetic activity.[15]
The Phase 2 trial did not meet its primary efficacy endpoint; virtually all dose-response data are from rodents; long-term safety of repeated GH pulse stimulation has not been characterized in humans.
Regulatory and Anti-Doping Status
Ipamorelin has no FDA-approved indication for any human therapeutic use. Ipamorelin acetate and free base were nominated for the FDA 503A compounding bulk drug substance list (docket FDA-2024-N-4188) for proposed indications of growth hormone deficiency and postoperative ileus; the nomination was withdrawn by the nominator in September 2024.[16]
Ipamorelin is classified as a prohibited substance under the WADA Prohibited List S2 — Peptide Hormones, Growth Factors, Related Substances and Mimetics, subcategory S2.2.4 Growth Hormone Secretagogues. The prohibition applies both in-competition and out-of-competition. No Therapeutic Use Exemption is available for competitive athletes.[18]
Reagent-Grade Sourcing Standards
Research-grade ipamorelin is characterized by purity of ≥98% by reversed-phase HPLC, with molecular weight confirmed by LC-MS at 711.86 Da. Standard Certificate of Analysis documentation for research-grade material includes lot number, HPLC purity percentage, amino acid analysis, mass spectrometry identity confirmation, and storage specifications. Lyophilized powder is stable long-term at −20°C; reconstituted solution is used at 4°C over short research timescales.[16]
Researchers should request and review third-party COA documentation — ideally from an independent analytical laboratory rather than from the vendor's internal QC function — before use. HPLC chromatograms and LC-MS spectra should be requested alongside purity percentage figures to confirm authentic identity.