Ipamorelin
Also known as: NNC 26-0161 · selective GHRP · growth hormone releasing peptide
A selective ghrelin-receptor agonist growth-hormone-releasing peptide, most commonly stacked with CJC-1295 for physiological GH-pulse research — the reference selective GHRP in modern research practice.
Ipamorelin is the reference selective ghrelin-receptor agonist GHRP with substantially reduced off-target effects on cortisol and prolactin; standard CJC-1295 stack partner.
Evidence tier: C — preclinical / mechanistic evidence only
- Category
- Sleep & Recovery
- Half-life
- Approximately 2 hours plasma; pharmacodynamic effects extend beyond exposure
Section 1
Overview
Ipamorelin is a synthetic pentapeptide developed by Novo Nordisk as a selective ghrelin-receptor agonist growth-hormone-releasing peptide (GHRP). Unlike earlier GHRPs (GHRP-2, GHRP-6, hexarelin), Ipamorelin is engineered for greater selectivity — it drives GH release with substantially less effect on cortisol, prolactin, and ACTH release than the earlier compounds. This selectivity is the compound's defining pharmacological property and the reason it has become the reference selective GHRP in modern research practice.
In research-peptide practice, Ipamorelin is most commonly used as a stack component alongside CJC-1295 — Ipamorelin provides the ghrelin-receptor arm signalling while CJC-1295 provides the GHRH-receptor arm signalling, and the combination produces higher-magnitude physiological GH pulses than either arm alone. The CJC-1295 + Ipamorelin stack is the most-common GH-axis research configuration in modern practice.
The cognitive-relevance angle is indirect, operating through sleep-onset GH pulse augmentation and downstream IGF-1 effects on CNS-relevant signalling. Direct cognitive-endpoint clinical trials have not been completed, but the mechanism-of-action framework supports continued research interest in the indirect cognitive-relevance research angle.
Section 2
Discovery & History
- Developed by Novo Nordisk in the 1990s as part of a systematic effort to engineer selective ghrelin-receptor agonists with reduced off-target effects on cortisol, prolactin, and ACTH release.
- Underwent early clinical evaluation for GH-axis restoration in age-related and disease-related GH decline contexts.
- Did not progress to marketing authorisation despite the favourable selectivity profile.
- Widely adopted in research-peptide practice as the reference selective GHRP, particularly in combination with GHRH analogues (CJC-1295) for physiological GH-pulse research.
- Not licensed as a medicine in any major jurisdiction; remains a research chemical.
Section 3
Mechanism of Action
- 1Selective ghrelin-receptor (growth hormone secretagogue receptor, GHSR-1a) agonism on pituitary somatotroph cells, driving GH release from the pituitary in the physiological pulsatile pattern.
- 2Reduced off-target effects on cortisol, prolactin, and ACTH release compared with earlier GHRPs — the compound's defining selectivity property and the mechanism-of-action framework that motivated its development.
- 3Combined pulse-effect with GHRH analogues — Ipamorelin provides the ghrelin-receptor arm that potentiates the GHRH-receptor arm signalling from CJC-1295 or similar compounds, producing higher-magnitude physiological GH pulses than either arm alone.
- 4Systemic GH-mediated effects — increased IGF-1 production by hepatocytes, downstream metabolic effects, tissue-repair effects, and CNS-relevant IGF-1 signalling.
- 5Sleep-onset GH pulse augmentation — the endogenous slow-wave-sleep-associated GH pulse is augmented by Ipamorelin administration, providing the indirect cognitive-relevance mechanism via sleep-mediated memory consolidation.
- 6Reported effects on body composition (lean mass, adiposity) via the systemic GH mechanism, providing the practical research-endpoint framework for body-composition-focused research applications.
- 7Central ghrelin-receptor effects on appetite regulation via hypothalamic ghrelin-receptor engagement — a mechanism-of-action angle relevant to the compound's appetite-stimulating effects.
- 8Reported effects on bone density and calcium metabolism via the systemic GH-IGF-1 mechanism, extending the research applications into bone-metabolism research.
Section 4
Researched Benefits
Findings reported in the published preclinical and clinical literature. Effects in research contexts do not constitute claims of therapeutic benefit in humans.
- 1Selective GHRP mechanism providing GH release with substantially less effect on cortisol, prolactin, and ACTH than earlier GHRPs — the reference selectivity profile in the class.
- 2Effective research-tool combination with CJC-1295 for physiological GH-pulse research — the most-common GH-axis research configuration.
- 3Reported effects on body composition, tissue-repair markers, and metabolic parameters in research applications.
- 4Sleep-onset GH pulse augmentation with indirect cognitive-relevance via sleep-mediated memory consolidation.
- 5Substantial research-community usage providing anecdotal (though not clinically-validated) tolerability data.
- 6Preservation of physiological GH-pulse pattern rather than continuous supraphysiological GH exposure — a mechanistic distinction from direct GH administration.
- 7Well-tolerated in the reported research applications relative to earlier GHRPs owing to the selectivity profile.
Section 5
Theoretical Dosing & Protocols
| Route | Dosage | Frequency | Duration |
|---|---|---|---|
| Subcutaneous injection (research) | 100-300 mcg per dose in most research protocols | 2-3× daily in the standard research configuration | Research protocol dependent; chronic research use continues 8-12+ weeks |
Note: Not approved for any indication. The 2-3× daily dosing frequency reflects the compound's shorter half-life versus DAC-modified GHRH analogues.
Section 6
Administration Routes
- Subcutaneous injection — the primary research route; abdominal-subcutaneous administration in the standard research-community pattern.
- Intramuscular administration in some research contexts.
- Oral administration is not viable — the pentapeptide is degraded by gastrointestinal proteases.
- Sublingual administration has been anecdotally reported in some non-clinical use contexts but not peer-reviewed-characterised.
Section 7
Safety Profile
Commonly reported
- · Injection-site reactions with subcutaneous administration — the most common tolerability signal.
- · Occasional headache during initial dosing.
- · Mild transient effects on appetite (typically increased appetite via the ghrelin-receptor mechanism).
- · Fluid retention and mild peripheral oedema — expected GH-mediated effect, typically clinically insignificant at studied doses.
- · Occasional mild fatigue or drowsiness reported after dosing, consistent with post-GH-pulse physiological effects.
Rare / theoretical
- · Diabetes precipitation or worsening of glycaemic control in susceptible research subjects.
- · GH-mediated effects on cardiac hypertrophy in chronic high-dose research — a theoretical concern extrapolated from the broader GH-therapy literature.
- · Theoretical GH-mediated tumour-growth concerns in active malignancy.
- · Development of anti-drug antibodies during chronic dosing — reported at low frequency.
- · Rare hypersensitivity reactions.
Contraindications
- · Not authorised for human use in the UK.
- · Active malignancy — theoretical contraindication via the GH-axis mechanism.
- · Pregnancy and lactation.
- · Severe uncontrolled diabetes.
Section 8
UK & EU Regulatory Context
United Kingdom
Not a licensed medicine in the UK. Research chemical only.
European Union
Not approved by the EMA.
Section 9
Clinical Studies Summary
Ipamorelin selectivity characterisation
Molecular and clinical pharmacology characterisation of Ipamorelin's selectivity profile — driving GH release with substantially reduced effects on cortisol, prolactin, and ACTH compared with GHRP-2 and GHRP-6. Establishes the compound's defining selectivity property and the mechanism-of-action framework that motivated its development.
Ipamorelin + GHRH combined GH-release research
Research characterising the combined-arm effect of Ipamorelin plus GHRH analogues (CJC-1295, sermorelin) on GH pulse magnitude, providing the mechanistic scaffold for the stack-configuration research practice and demonstrating higher-magnitude physiological GH pulses under combined rather than single-arm stimulation.
Ipamorelin in body-composition research
Research applications of Ipamorelin in body-composition-endpoint studies reporting effects on lean mass, adiposity, and metabolic parameters over 8-12 week research protocols. Reflects the systemic GH-mediated mechanism and provides the practical research-endpoint framework for body-composition-focused research applications.
Ipamorelin sleep-onset GH pulse research
Endocrinology characterisation of Ipamorelin's effects on the endogenous slow-wave-sleep-associated GH pulse, providing the mechanistic scaffold for the indirect sleep-mediated cognitive-relevance research angle. Compared sleep-GH-pulse magnitude under Ipamorelin versus vehicle conditions.
Section 10
Frequently Asked Questions
Section 10a
Practical Research Guidance
Cycle guidance
Reconstitution & storage
UK sourcing notes
Section 11
Sourcing for Laboratory Research
Sourcing Ipamorelin for laboratory research
Researchers in the United Kingdom and elsewhere typically obtain Ipamorelin from specialist research-chemical suppliers. Purity, third-party testing, and supplier transparency are the principal differentiators worth evaluating before placing an order. The two suppliers below are commonly referenced in UK research contexts.
Reminder: research peptides are sold strictly for in vitro and preclinical laboratory purposes. Importation or supply for human consumption is not permitted under UK medicines legislation.