Ipamorelin is a synthetic pentapeptide growth-hormone secretagogue studied through the GHS-R1a, or ghrelin-receptor, research lane. Foundational experiments reported a comparatively selective growth-hormone release profile in specified cell, rat, and swine models, while a later small human study described protocol-specific PK/PD measurements. Those records do not establish an approved use, universal human selectivity, comparative superiority, or combination benefit.
A useful Ipamorelin research guide separates four questions: what the analyte is, which receptor system the evidence supports, what each experimental model measured, and what remains unknown. Pairwise comparison and family-level questions belong to their dedicated pages.
- Ipamorelin is a synthetic five-residue growth-hormone secretagogue with a molecular weight of 711.9 g/mol and CAS Registry Number 170851-70-4.
- The foundational paper placed Ipamorelin in the growth-hormone-secretagogue receptor lane and compared it with GHRP-2 and GHRP-6 in defined preclinical models, where its maximal effect reached 85 ± 5% of the GHRP-6 maximum in primary rat pituitary cells.
- The “selective” label describes the tested hormone-release profile; it is not a universal human-safety or superiority claim.
- A small healthy-volunteer infusion study reported compound-specific PK/PD estimates under its protocol, including a 2-hour terminal half-life. It is not a use protocol.
- The wider record is rodent: dose-dependent bone growth, a 4-fold higher periosteal bone-formation rate under glucocorticoid challenge, faster post-surgical gastric emptying. The one randomized human trial missed its endpoint.
- FDA stated in its 2024 compounding review that Ipamorelin free base and acetate were not components of an FDA-approved drug.
- HPLC, mass spectrometry, and a functional bioassay answer different questions about a research material.
What Is Ipamorelin?
Ipamorelin is a synthetic five-residue growth-hormone secretagogue. Raun and colleagues described the sequence as Aib–His–D-2-Nal–D-Phe–Lys–NH2 and reported the compound’s discovery through a chemistry program that modified earlier growth-hormone-releasing peptide scaffolds.[3] The paper used cell, rat, and swine experiments to characterize the compound. That publication is the primary source for both the pentapeptide identity and the “first selective growth hormone secretagogue” description.
Ipamorelin should not be confused with GHRH analogs such as Sermorelin, Tesamorelin, or literature-defined CJC-1295. Those compounds are studied through the GHRH receptor. Ipamorelin belongs to the GHS-R1a, or ghrelin-receptor, lane. The two receptor systems can influence overlapping pituitary readouts while remaining mechanistically distinct.
It should also not be treated as a class synonym for GHRP-2, GHRP-6, or Hexarelin. Those compounds share a growth-hormone-secretagogue research context but have different structures, model-specific pharmacology, and evidence records. A family label cannot replace compound matching.
Ipamorelin Technical Identity
The FDA Global Substance Registration System records Ipamorelin under UNII Y9M3S784Z6. The public substance record and PubChem identify the free-base formula as C38H49N9O5, molecular weight 711.9 g/mol, and CAS Registry Number 170851-70-4. PubChem also records the sequence notation used in the primary paper.
| Identity field | Ipamorelin free-base record | Interpretation boundary |
|---|---|---|
| Peptide length | Five residues | “Pentapeptide” describes the defined sequence, not a broad GHS class. |
| Sequence | Aib–His–D-2-Nal–D-Phe–Lys–NH2 | Contains noncanonical residues and stereochemical specifications that must be preserved. |
| Molecular formula | C38H49N9O5 | Free-base identity; a salt or counterion requires separate declaration. |
| Molecular weight | 711.9 g/mol (PubChem CID 9831659) | Free-base average mass, 711.87 g/mol computed from the formula; a lot record states the observed result and method. |
| CAS Registry Number | 170851-70-4 | A registry identifier does not establish purity, biological activity, or approval. |
| UNII | Y9M3S784Z6 | FDA substance registration is not FDA approval of a finished drug. |
FDA’s 2024 review considered Ipamorelin free base and Ipamorelin acetate as different bulk drug substances. A source or lot record should name which material it addresses. This page does not assign an acetate counterion to a free-base formula or molecular weight.
How Does Ipamorelin Fit the GHS-R1a Receptor Lane?
The receptor context predates the endogenous ligand. Howard and colleagues cloned a G-protein-coupled receptor from swine and human pituitary and hypothalamic tissue that functions in growth-hormone release, reporting it in 1996.[1] The foundational Ipamorelin paper appeared in 1998 and used growth-hormone-secretagogue and GHRH antagonists to place the compound in a GHRP-like receptor pathway; in primary rat pituitary cells its maximal effect reached 85 ± 5% of the GHRP-6 maximum.[3] Kojima and colleagues then purified the endogenous ligand from rat stomach in 1999: ghrelin, a 28-residue peptide whose n-octanoylation at serine 3 is required for its growth-hormone-releasing activity.[4]
Modern shorthand calls Ipamorelin a GHS-R1a agonist or ghrelin mimetic. That is useful as an evidence lane, not as a complete mechanism claim: a receptor label does not describe every downstream signaling event, tissue, species, concentration, or endpoint.
What Did the Foundational Ipamorelin Selectivity Study Show?
Raun and colleagues evaluated Ipamorelin in primary rat pituitary cells, pentobarbital-anaesthetized rats, and conscious swine.[3] In those systems, Ipamorelin produced growth-hormone release with potency and efficacy close to GHRP-6. The investigators compared it with GHRP-2 and GHRP-6 and used antagonist experiments to distinguish a GHRP-like receptor pathway from the GHRH pathway.
| Experimental system | Ipamorelin | Comparator secretagogue |
|---|---|---|
| Primary rat pituitary cells (in vitro) | EC50 1.3 ± 0.4 nmol/L; Emax 85 ± 5% | GHRP-6: EC50 2.2 ± 0.3 nmol/L; Emax set at 100% |
| Pentobarbital-anaesthetized rats (in vivo) | ED50 80 ± 42 nmol/kg; Emax 1545 ± 250 ng GH/mL | GHRP-6: ED50 115 ± 36 nmol/kg; Emax 1167 ± 120 ng GH/mL |
| Conscious swine (in vivo) | ED50 2.3 ± 0.03 nmol/kg; Emax 65 ± 0.2 ng GH/mL plasma | GHRP-6: ED50 3.9 ± 1.4 nmol/kg, Emax 74 ± 7; GHRP-2: ED50 0.6 nmol/kg, Emax 56 ± 6 ng GH/mL plasma |
The selectivity claim came from the swine hormone profile. Under the tested conditions, GHRP-2 and GHRP-6 increased ACTH and cortisol, while Ipamorelin did not produce statistically different ACTH or cortisol levels from the GHRH comparator — and that dissociation held at doses more than 200-fold above its own ED50 for growth-hormone release in swine. The authors also reported no measured changes in FSH, LH, prolactin, or TSH for the secretagogues under that experiment.
Three qualifications are essential. First, the finding was model-specific. Second, a hormone panel is not a complete safety assessment. Third, “selective for GH release” does not mean selective for every tissue, signaling event, exposure, or human outcome. The paper supports a precise statement about its experiments, not a universal claim that Ipamorelin is safer, cleaner, or better than another compound.
Use “comparatively selective growth-hormone release profile in the specified preclinical models.” Do not shorten that to “no side effects,” “no cortisol effect in humans,” or “the safest secretagogue.” Those stronger statements were not tested.
What Does the Human Ipamorelin PK/PD Study Show?
Gobburu and colleagues published a small pharmacokinetic-pharmacodynamic study in healthy male volunteers in 1999.[2] The dose-escalation design used five intravenous infusion rates — 4.21, 14.02, 42.13, 84.27 and 140.45 nmol/kg delivered over 15 minutes — with eight healthy male subjects at each level, and modeled Ipamorelin exposure alongside measured growth-hormone release.
The reported values were dose-proportional pharmacokinetics across that range, a short terminal half-life of 2 hours, clearance of 0.078 L/h/kg, a steady-state volume of distribution of 0.22 L/kg, and a single modeled growth-hormone release episode peaking at 0.67 hours. An indirect-response model put the concentration for half-maximal growth-hormone stimulation at 214 nmol/L and the maximal production rate at 694 mIU/L/h, with wider between-subject variability in the pharmacodynamic parameters than the pharmacokinetic ones.
Those values belong to their protocol: the healthy-volunteer population, infusion design, analytical method, sampling schedule, and model. A terminal half-life measured after intravenous infusion is not a general handling value and does not create a schedule for a research reagent.
Rodent disposition is a separate record. In male rats given intravenous bolus doses, Ipamorelin’s plasma clearance was 5-fold lower than GHRP-6’s, and Ipamorelin was mainly excreted in the urine (Johansen 1998, PMID 9879640): moderate metabolic resistance in a living animal, not a human exposure value and not a claim about lyophilized storage.
The study also does not create a comparison with CJC-1295, Sermorelin, GHRP-2, GHRP-6, or Hexarelin, because a cross-study ratio would mix compounds, designs, routes, assays, and populations. Ipamorelin has a small compound-specific human record; its selectivity evidence remains preclinical.
Additional Reported Ipamorelin Findings
Beyond the records above, Ipamorelin appears in bone, catabolic-stress, adiposity, pituitary-cell, and gastrointestinal studies, plus one randomized human trial. Each row keeps its figure attached to the system that produced it.
| Dosing model | Species or population | Endpoint | Reported result | Source |
|---|---|---|---|---|
| 18, 90 or 450 µg/day subcutaneously, 3 doses daily, 15 days | Adult female rats | Longitudinal tibial growth rate | 42 µm/day on vehicle versus 44, 50 and 52 µm/day dose-dependently (P<0.0001); IGF-I and bone-turnover markers unchanged | Johansen 1999, PMID 10373343 |
| 0.5 mg/kg per day, continuous minipump, 12 weeks (n=7) | 13-week-old female Sprague-Dawley rats | Bone mineral content (DXA, pQCT, ash weight) | Tibial and vertebral content rose, but weight-corrected content and volumetric density were unchanged; the gain tracked larger bone dimensions | Svensson 2000, PMID 10828840 |
| 100 µg/kg three times daily, 3 months, with methylprednisolone 9 mg/kg per day | 8-month-old female rats | Periosteal bone formation; calf tetanic tension | Periosteal bone-formation rate 4-fold higher than glucocorticoid alone; maximum tetanic tension significantly increased | Andersen 2001, PMID 11735244 |
| 0.4 or 1.6 mg/kg per day intravenously, 10 days, with methylprednisolone 5.0 mg/kg | Catheterized rats after surgery | Body-weight loss; IGF-I | Loss fell from 13.6 ± 2.9 g on steroid alone to 1.6 ± 2.0 g at 0.4 mg/kg and 2.3 ± 2.0 g at 1.6 mg/kg (P<0.05); IGF-I rose in parallel | Malmlöf 1999, PMID 10629165 |
| 0.5 mg/kg per day, 7 days, with prednisolone 4 mg/kg per day | Rats | Hepatic urea-nitrogen synthesis capacity | Reduced 20% versus prednisolone alone (p<0.05), against 33% for growth hormone at 1 mg/kg per day | Aagaard 2009, PMID 19231263 |
| Twice-daily subcutaneous dosing, 2 to 9 weeks | GH-deficient lit/lit and GH-intact mice | Body weight; fat mass (DEXA); leptin; food intake | About 15% weight gain by 2 weeks in GH-intact and GH-deficient mice alike, with higher relative fat mass; GHS treatment (Ipamorelin or GHRP-6) raised leptin and food intake in GH-intact mice | Lall 2001, PMID 11162489 |
| 21 days of dosing, then 10 nM in pituitary cell culture | Young female rats | Somatotroph population; intracellular GH | Secretory-granule volume density increased (P<0.05); in pretreated animals only, 10 nM raised somatotroph percentage and intracellular GH | Jiménez-Reina 2002, PMID 12168778 |
| 0.01–1 mg/kg intravenously, single or four doses daily for 2 days | Fasted male rats after laparotomy and intestinal manipulation | Colonic transit; fecal output; food intake | A single 1 mg/kg dose shortened time to first bowel movement; repeat dosing at 0.1 or 1 mg/kg raised fecal output, food intake and weight gain | Venkova 2009, PMID 19289567 |
| 0.014 µmol/kg intravenously after abdominal surgery | Fasted adult male rats | Gastric emptying, 15 minutes after gavage | 52 ± 11% of the meal remained in the stomach versus 78 ± 5% on vehicle (P<0.05); non-surgical controls retained 44 ± 6% | Greenwood-Van Meerveld 2012, PMID 27186127 |
| Intravenous dosing after colonic sensitisation with 0.6% acetic acid | Rats without colonic inflammation | Visceromotor response to distension; paw withdrawal | Visceral hypersensitivity and somatic allodynia were attenuated; the ghrelin-receptor antagonist H0900 blocked the effect | Mohammadi 2020, PMID 32801950 |
| Intravenous bolus and intranasal administration | Male rats | Clearance; intact-peptide recovery; nasal bioavailability | Clearance 5-fold lower than GHRP-6; 60–80% intact-dose recovery in bile and urine (pooled: Ipamorelin plus two NNC peptides); nasal bioavailability about 20% | Johansen 1998, PMID 9879640 |
| 0.03 mg/kg intravenously twice daily, up to 7 days; randomized, double-blind, placebo-controlled phase 2 | 114 adults after bowel resection | Time to first tolerated solid meal | Median 25.3 hours versus 32.6 hours on placebo (p=0.15); adverse events 87.5% versus 94.8%; no significant difference on key or secondary endpoints | Beck 2014, PMID 25331030 |
Two limits govern the table. Eleven of the twelve records are rodent, and rodent responses do not transfer to humans by default. The one randomized human trial missed its endpoint, so a broad preclinical signal has not become a clinical effect.
Evidence and Regulatory Limits
The record has clear gaps. The primary papers here establish receptor discovery context, preclinical pharmacology in rodents and swine, a small human PK/PD study, ghrelin ligand discovery, and one randomized trial that missed its endpoint. They do not establish an approved indication, long-term safety, comparative superiority, a combination benefit, or equivalence between a reagent and a finished drug.
FDA’s October 29, 2024 Pharmacy Compounding Advisory Committee briefing document evaluated Ipamorelin free base and acetate as nominated bulk drug substances. The agency stated that neither was a component of an FDA-approved drug and described safety and peptide-characterization concerns in the compounding context. That review is not a claim about every in-vitro experiment, but it blocks the common assertion that Ipamorelin is an approved medication or a routine substitute for one.
The position is a global negative, not a jurisdictional gap: no marketing authorization for Ipamorelin has been identified from FDA, EMA, NMPA, MHRA, PMDA, TGA, Health Canada or any other national regulator. Published human research stops at phase 2: the postoperative-ileus trial of 0.03 mg/kg twice daily (117 patients enrolled, 114 analysed) missed its key endpoint (p=0.15), and no approval followed (Beck 2014, PMID 25331030).
Ipamorelin also appears in doping-control analytics: a structure-activity study using a radio-competitive GHS-R1a binding assay confirmed receptor-binding activity in urine collected after nasal administration of Ipamorelin and other growth-hormone-releasing peptides (Ferro 2017, PMID 26811125), though the abstract does not state that study’s population. Supplier status is a separate assertion: Apex Laboratory supplying a research-grade reagent says nothing about approval.
How Does Ipamorelin Differ From CJC-1295 and the Broader GH-Axis Family?
Ipamorelin is a GHS-R1a secretagogue. Literature-defined CJC-1295 is a DAC-bearing GHRH analog. They enter the growth hormone axis through different receptor lanes, and the available human studies used different compounds and protocols. The Ipamorelin vs CJC-1295 comparison owns that pairwise question, including the difference between DAC-bearing CJC-1295 and Modified GRF 1-29.
The growth hormone axis research hub owns the broader taxonomy: GHRH analogs, GHS-R1a secretagogues, downstream IGF-related materials, growth-hormone fragments, and parallel myostatin or activin research. This page does not repeat that entire category map.
No direct Ipamorelin-versus-CJC-1295 head-to-head study or exact-compound combination study was identified in this refresh’s verified source set. Distinct receptor pathways do not prove additive, supra-additive, synergistic, safer, or clinically useful effects. Any combination statement needs compound-matched evidence rather than a pathway diagram.
How Should Ipamorelin Be Verified as a Research Material?
Analytical verification begins with the exact analyte. The record should state Ipamorelin free base or another fully declared form, the sequence or identity specification, the lot identifier, and the methods used. A method result answers only the question it was designed to answer.
| Question | Appropriate evidence lane | What it does not establish |
|---|---|---|
| Does the declared material match the intended analyte? | Specification, source record, sequence and salt/counterion declaration | Purity, receptor activity, safety, or approval |
| Does the measured mass fit the identity? | Mass spectrometry with a stated ion assignment or deconvolution method | Chromatographic purity or biological function |
| What is the chromatographic profile? | HPLC under a stated column, gradient, wavelength, integration, and sample method | Molecular identity, sterility, or receptor function |
| Does the material produce a functional response? | A validated bioassay with positive, negative, and matrix controls | Clinical safety or efficacy |
| Is the material an approved drug? | FDA approval records for an exact finished product | Cannot be inferred from a COA, UNII, CAS number, or literature citation |
The HPLC testing guide, mass-spectrometry guide, and COA interpretation guide provide method-specific reading frameworks. Use the current lot document rather than a generic purity badge or an image that resembles an instrument output.
Ipamorelin Research-Material Record
A product page belongs at the end of the evidence path. It documents the current material, lot record, declared form, and commercial status. It cannot establish receptor pharmacology, clinical safety, an approved indication, or equivalence to a pharmaceutical product.
The supplier-reported specification on the Apex Ipamorelin catalog record is ≥99% purity. A specification is a release threshold, not a measurement of the vial in hand: the lot certificate of analysis carries the observed value, method, and date.
Apex Ipamorelin research reagent
Review the current catalog record and request lot-specific documentation before relying on identity or purity claims. Confirm that the declared analyte and salt form match the intended research plan.
View the Ipamorelin research-material recordFrequently Asked Questions About Ipamorelin
What is Ipamorelin?
Ipamorelin is a synthetic pentapeptide growth-hormone secretagogue. Its sequence is Aib–His–D-2-Nal–D-Phe–Lys–NH2, and its foundational pharmacology was studied in cell, rat, and swine experiments.
Which receptor is associated with Ipamorelin?
Ipamorelin is studied through the GHS-R1a, or ghrelin-receptor, research lane. That receptor context is distinct from the GHRH receptor used to classify Sermorelin, Tesamorelin, and literature-defined CJC-1295.
What are Ipamorelin’s molecular formula and molecular weight?
Public substance records list Ipamorelin free base with molecular formula C38H49N9O5, molecular weight 711.9 g/mol, CAS Registry Number 170851-70-4, and UNII Y9M3S784Z6. An acetate or any other salt form has to be declared separately.
What did the Ipamorelin selectivity paper show?
The 1998 study reported a comparatively selective growth-hormone release profile in specified cell, rat, and swine models, including a different ACTH and cortisol pattern from GHRP-2 and GHRP-6 in swine. It did not establish universal human selectivity or safety.
Has Ipamorelin been studied in humans?
Yes. A small 1999 healthy-volunteer infusion study reported protocol-specific pharmacokinetic and pharmacodynamic measurements. The study does not create an approved use, personal-use instructions, or a direct comparison with another secretagogue.
What has Ipamorelin been reported to do in animal studies?
Rodent studies report dose-dependent tibial growth, higher bone mineral content without a change in volumetric density, a 4-fold higher periosteal bone-formation rate under glucocorticoid challenge, greater fat mass, and faster gastric emptying after surgery. Each result belongs to its own model and species.
Is Ipamorelin FDA-approved?
No. FDA stated in its 2024 compounding review that Ipamorelin free base and Ipamorelin acetate were not components of an FDA-approved drug, and no marketing authorization by any other authority, including EMA, NMPA, MHRA, PMDA, TGA or Health Canada, has been identified. A phase 2 postoperative-ileus trial (117 patients enrolled) did not lead to approval. An FDA substance record or UNII is not a finished-drug approval.
How is Ipamorelin different from CJC-1295?
Ipamorelin is a GHS-R1a secretagogue, while literature-defined CJC-1295 is a DAC-bearing GHRH analog. Their dedicated comparison page covers receptor identity, human evidence, half-life limits, and CJC naming without claiming a universal winner or combination benefit.
What can HPLC and mass spectrometry verify for Ipamorelin?
HPLC can report a chromatographic purity estimate under a stated method, while mass spectrometry can support mass identity. Neither method alone establishes receptor activity, biological effect, sterility, clinical safety, or efficacy.
References
- Howard AD, et al. A receptor in pituitary and hypothalamus that functions in growth hormone release. Science. 1996;273(5277):974-7. PMID: 8688086.
- Gobburu JV, et al. Pharmacokinetic-pharmacodynamic modeling of ipamorelin, a growth hormone releasing peptide, in human volunteers. Pharm Res. 1999;16(9):1412-6. PMID: 10496658.
- Raun K, et al. Ipamorelin, the first selective growth hormone secretagogue. Eur J Endocrinol. 1998;139(5):552-61. PMID: 9849822.
- Kojima M, et al. Ghrelin is a growth-hormone-releasing acylated peptide from stomach. Nature. 1999;402(6762):656-60. PMID: 10604470.
- U.S. Food and Drug Administration. Pharmacy Compounding Advisory Committee briefing document: Ipamorelin-related bulk drug substances. October 29, 2024. Accessed July 23, 2026.
- U.S. Food and Drug Administration. Global Substance Registration System: Ipamorelin, UNII Y9M3S784Z6. Accessed July 23, 2026.
- National Center for Biotechnology Information. PubChem Compound Summary for Ipamorelin, CID 9831659. Accessed July 23, 2026.
