Research information only. PrecisePep is an educational library. It is not medical advice and is not intended to assist, encourage or enable self-administration. The compounds documented here are research chemicals — most are not approved for human use. Read the full disclaimer.
PrecisePep/Peptide Library/Ipamorelin
Growth Hormone & Anabolic Support
NNC 26-0161 · Aib-His-D-2-Nal-D-Phe-Lys-NH₂
The first genuinely selective growth hormone secretagogue — a pentapeptide that releases GH without the cortisol, prolactin and hunger surge that made earlier ghrelin mimetics unusable.
Ipamorelin was designed to solve a specific problem. The earlier growth-hormone- releasing peptides — GHRP-6, GHRP-2, hexarelin — released GH effectively but dragged cortisol, ACTH, prolactin and appetite up with it. Raun and colleagues at Novo Nordisk characterised ipamorelin in 1998 as the first pentapeptide with high GH-releasing potency and essentially no effect on those other axes.[1] That selectivity is the entire reason it is still in use nearly thirty years later.
It works at the ghrelin receptor (GHS-R1a), a completely different pituitary receptor from the one GHRH analogues like tesamorelin target. That is the pharmacological basis for combining them: two receptors, two signals, a greater GH pulse than either alone. Ipamorelin also suppresses somatostatin — the brake on GH release — which GHRH analogues do not.
Clinical development was discontinued; ipamorelin was later investigated for postoperative ileus rather than for growth hormone indications, and never reached approval for anything.[2] Human data is therefore thin: good early pharmacology, no long-term outcome trials, and a very large amount of grey-market use.
GHS-R1a agonism. Ipamorelin mimics ghrelin at the growth hormone secretagogue receptor on pituitary somatotrophs, triggering GH release. Unlike ghrelin itself, it does not meaningfully stimulate appetite — the receptor subtype distribution and signalling bias appear to separate the two effects.
Somatostatin suppression. Ghrelin receptor agonism reduces somatostatin tone — the inhibitory brake on GH secretion. This is complementary rather than redundant to GHRH stimulation: one pushes the accelerator, the other releases the brake.
Selectivity. The defining property. Ipamorelin does not produce the ACTH/cortisol or prolactin elevations characteristic of GHRP-6 and hexarelin, which matters because chronically elevated cortisol is catabolic and would work directly against the reason anyone uses a GH secretagogue.
Preserved pulsatility. Like GHRH analogues, ipamorelin stimulates endogenous secretion rather than replacing GH, so the physiological pulse architecture and feedback control remain intact.
Downstream IGF-1. Sustained use raises IGF-1, the practical monitoring marker for total GH exposure.
Effects that have been reported. A study-tier entry means a result was published — not that the effect is established, reproducible, or transferable from a rodent to a person.
Highest confidenceReported in peer-reviewed literature, registered clinical trials, or regulatory filings. Note the model: much peptide literature is in vitro or rodent work, not human trial data.
The foundational pharmacology paper characterised ipamorelin as releasing GH with potency and efficacy comparable to GHRP-6, but without the ACTH and cortisol elevation those compounds produce — the first secretagogue to achieve that separation.
Demonstrated selectivity versus earlier GHRPs. This is the single most cited and best-supported claim about ipamorelin.
Reported in rodent work, consistent with sustained GH axis stimulation.
Ipamorelin was studied in humans for gastrointestinal motility after surgery, exploiting ghrelin-receptor prokinetic effects rather than GH release. It did not reach approval.
Co-stimulation of GHS-R1a and the GHRH receptor produces a greater GH response than either alone — established endocrine pharmacology across the secretagogue class.
Unproven — inference onlyExtrapolated from a known mechanism, receptor profile, or adjacent compound class. Biologically plausible but not directly demonstrated for this compound in this context.
The dominant reason for use. GH raises lipolysis and is nitrogen-sparing; whether pulsatile secretagogue stimulation in a non-GH-deficient adult produces meaningful body-composition change has not been demonstrated in a trial.
GH secretion is coupled to slow-wave sleep, and the relationship is bidirectional. The claim that a secretagogue deepens sleep is plausible and not established for ipamorelin specifically.
Extrapolated from GH-driven collagen synthesis. Inferred, not measured.
The rationale for including ipamorelin in fat-loss stacks. Mechanistically reasonable; untested against incretin-driven weight loss.
Because secretion remains pulsatile and feedback-regulated, receptor downregulation should in principle be less of a problem than with exogenous GH. Not formally characterised over long horizons.
Uncontrolled reportsAggregated from research-community logs, forums, vendor literature and self-reported experience. Uncontrolled, unverified, subject to placebo, polypharmacy and product-purity confounds. Lowest evidentiary weight.
The most consistent community report by a wide margin, typically within the first week of evening dosing.
Widely reported and impossible to separate from the improved sleep that is reported alongside it.
The selectivity claim playing out in practice — users report the GH effects without the ravenous hunger associated with GHRP-6.
Commonly reported in the first minutes, transient.
Reported often enough to be the practical basis for community cycling. Whether this reflects receptor adaptation or simple habituation to a novel sensation is unknown.
Adverse effects, contraindications and unknowns. The grey-market tier is where under-reporting is worst: uncontrolled use produces no systematic safety surveillance at all, so absence of a reported harm is not evidence of safety.
Highest confidenceReported in peer-reviewed literature, registered clinical trials, or regulatory filings. Note the model: much peptide literature is in vitro or rodent work, not human trial data.
Absence of meaningful cortisol and prolactin elevation removes the main endocrine liabilities of earlier secretagogues. This is a demonstrated advantage, not a claim of general safety.
The postoperative ileus programme produced human tolerability data at defined doses over short periods. It says nothing about months or years of use in healthy adults.
Any sustained elevation of GH and IGF-1 carries the class consequences: insulin resistance, fluid retention, arthralgia, carpal tunnel symptoms. These are documented for the GH axis generally, whatever the upstream stimulus.
Development was discontinued. There is no chronic-use safety dataset for ipamorelin in healthy adults.
Unproven — inference onlyExtrapolated from a known mechanism, receptor profile, or adjacent compound class. Biologically plausible but not directly demonstrated for this compound in this context.
The standard concern with sustained GH axis stimulation, and the reason approved GH-axis drugs contraindicate active malignancy. Unmonitored use carries this without the monitoring.
GH is counter-regulatory to insulin. A secretagogue producing meaningful IGF-1 elevation should be expected to affect glucose handling.
The stated rationale for cycling. Preserved pulsatility argues against it; nobody has measured it over a year.
Combining a GH secretagogue with retatrutide stacks two independent pressures on hepatic glucose output.
Uncontrolled reportsAggregated from research-community logs, forums, vendor literature and self-reported experience. Uncontrolled, unverified, subject to placebo, polypharmacy and product-purity confounds. Lowest evidentiary weight.
The most commonly reported effect, dose-related, usually settling within weeks.
Reported at higher doses; the recognisable GH-excess signal.
Transient, common, generally benign.
Reported inconsistently; often attributed to dose being too high.
A counter-report to the selectivity claim: some users describe appetite stimulation at larger doses, suggesting selectivity may be dose-dependent rather than absolute.
Figures below are documented, not recommended. Study ranges come from published protocols in the stated model; grey-market ranges are what the research community reports using and carry no safety validation of any kind.
Highest confidenceReported in peer-reviewed literature, registered clinical trials, or regulatory filings. Note the model: much peptide literature is in vitro or rodent work, not human trial data.
The characterisation work used weight-normalised dosing in animal models and defined intravenous or subcutaneous doses in early human pharmacology, measuring GH response directly rather than clinical outcomes.
Development was discontinued before any therapeutic dose was defined for GH indications. Every figure in circulation is community practice.
Unproven — inference onlyExtrapolated from a known mechanism, receptor profile, or adjacent compound class. Biologically plausible but not directly demonstrated for this compound in this context.
Insulin and elevated blood glucose suppress GH release. Dosing two hours after the last meal is physiologically sound and near-universally practised.
The largest physiological GH pulse occurs in early slow-wave sleep. Timing a secretagogue to reinforce it rather than to create an out-of-phase pulse is the standard argument.
Somatotroph GH stores are finite; above some dose the pulse cannot get larger and only the side-effect burden increases. This is the mechanistic argument against escalation and it is rarely applied in practice.
Some protocols use two or three daily administrations to mimic natural pulse frequency. Reasonable in principle; increases total exposure and therefore IGF-1.
Uncontrolled reportsAggregated from research-community logs, forums, vendor literature and self-reported experience. Uncontrolled, unverified, subject to placebo, polypharmacy and product-purity confounds. Lowest evidentiary weight.
The dominant community range. The Gold Standard protocol specifies 250 mcg nightly, two hours fasted, with sleep immediately after.
The "pulse-mimicking" approach — smaller doses more often. Higher total daily exposure.
Ipamorelin with CJC-1295 no DAC or with tesamorelin, on the two-receptor co-stimulation rationale.
The cycling schedule in the Gold Standard protocol. Not derived from any pharmacological finding.
| Approach | Dose | Frequency | Timing |
|---|---|---|---|
| Gold Standard Protocol | 250 mcg | Nightly | 2 h fasted, sleep after |
| Standard single pulse | 200 – 300 mcg | Nightly | Fasted, pre-sleep |
| Multi-pulse | 100 mcg | 2–3× daily | Fasted windows |
| With CJC-1295 no DAC | 200 – 300 mcg | Nightly | Same syringe, fasted |
Combination effects. Almost no peptide combination has been studied as a combination in humans; stack logic is overwhelmingly mechanistic inference and community practice. Each linked compound has its own page.
Highest confidenceReported in peer-reviewed literature, registered clinical trials, or regulatory filings. Note the model: much peptide literature is in vitro or rodent work, not human trial data.
Simultaneous stimulation of the GHRH receptor and the ghrelin receptor produces a synergistic rather than additive GH response — a well-characterised principle in endocrine pharmacology and the strongest "synergy" claim on this entire site.
Unproven — inference onlyExtrapolated from a known mechanism, receptor profile, or adjacent compound class. Biologically plausible but not directly demonstrated for this compound in this context.
The classic pairing: a modified GRF(1-29) GHRH analogue with a short half-life alongside a selective ghrelin mimetic, producing a single amplified pulse rather than sustained elevation. The "no DAC" specification is the whole point — the DAC version produces a bleed rather than a pulse.
Same principle with an approved GHRH analogue in place of CJC-1295. Better-characterised GHRH side, same untested combination.
GH-driven collagen synthesis alongside BPC-157/TB-500. The BPC-157 literature reporting increased GH receptor expression in tendon fibroblasts is the specific hook for this pairing.
Insulin suppresses GH release. Carbohydrate before an evening dose directly undercuts the mechanism.
Running ipamorelin, a GHRH analogue and an oral secretagogue together does not produce three times the effect — somatotroph capacity is finite — but it does produce three times the IGF-1 exposure risk.
Uncontrolled reportsAggregated from research-community logs, forums, vendor literature and self-reported experience. Uncontrolled, unverified, subject to placebo, polypharmacy and product-purity confounds. Lowest evidentiary weight.
The most common GH-axis combination in circulation, often supplied pre-blended.
The pairing used in the Gold Standard protocol, both dosed nightly two hours fasted.
Common alongside reta/cagri protocols.
Whole schedules — dosing, titration, cycle length, and off-time — as documented in trials, as proposed from mechanism, and as circulated in the research community. Reproduced for study and comparison only.
Highest confidenceReported in peer-reviewed literature, registered clinical trials, or regulatory filings. Note the model: much peptide literature is in vitro or rodent work, not human trial data.
Administer a defined dose, sample GH at fixed intervals, measure peak and area-under-curve, and compare against comparator secretagogues and against cortisol/prolactin as selectivity endpoints.
The only human therapeutic protocol context. Short duration, GI motility endpoints.
Unproven — inference onlyExtrapolated from a known mechanism, receptor profile, or adjacent compound class. Biologically plausible but not directly demonstrated for this compound in this context.
Because the meaningful exposure variable is downstream IGF-1, dosing to a measured IGF-1 within the age-adjusted range is more coherent than dosing to a fixed microgram figure.
Given finite somatotroph capacity and the sleep-coupled physiological pulse, reinforcing one endogenous pulse is the more defensible design.
Uncontrolled reportsAggregated from research-community logs, forums, vendor literature and self-reported experience. Uncontrolled, unverified, subject to placebo, polypharmacy and product-purity confounds. Lowest evidentiary weight.
250 mcg nightly, two hours fasted, sleep after dosing, alongside 1 mg tesamorelin. Run for two vials, then a four-week break before restarting.
Grouped with the GH axis compounds in the structural repair quarter.
Common general cycling pattern outside the specific protocols above.
Ipamorelin is a ghrelin receptor agonist, and that receptor has a real clinical trial history under other molecules. Two of them — anamorelin in cancer cachexia and relamorelin in diabetic gastroparesis — tell you more about what this receptor does in people than anything written about ipamorelin does.
Ipamorelin is not approved anywhere and has no controlled human efficacy trial. The clinical evidence below belongs to other ghrelin receptor agonists. It is included because it is the closest thing to human data this mechanism has, and because what those trials found is not what the marketing implies.
Pathophysiology
Cachexia is inflammation-driven wasting that does not respond to nutrition alone. Loss of function, not loss of mass, is what disables people.
Mechanistic rationale
Anamorelin, an oral ghrelin receptor agonist, was tested in two randomised phase 3 trials in non-small-cell lung cancer with cachexia, against co-primary endpoints of lean body mass and handgrip strength. Lean body mass increased significantly in both trials. Handgrip strength did not differ in either. It is approved in Japan on that basis. This is the single most informative result for anyone evaluating a ghrelin agonist, and it says the mechanism moves mass without moving function.
Community reports
Increased appetite is the most consistently reported effect of ipamorelin, which is exactly what ghrelin agonism should produce and is not usually the effect people are buying it for.
Components carrying the argument: Ghrelin receptor — appetite and GH release
Pathophysiology
Ghrelin is a prokinetic hormone. Delayed gastric emptying in diabetic gastroparesis produces nausea, early satiety, vomiting and unpredictable glycaemic control.
Mechanistic rationale
Relamorelin, a ghrelin agonist developed specifically for this, showed accelerated gastric emptying and symptom improvement in phase 2 work. This is arguably the best-supported clinical application of ghrelin receptor agonism, and it is the one nobody in this space discusses — because it is not a physique application.
Community reports
Essentially absent from community use. Worth knowing in the opposite direction: anyone with delayed gastric emptying from an incretin is taking a compound that opposes this mechanism.
Components carrying the argument: Ghrelin-mediated prokinesis
Pathophysiology
Ghrelin is the principal orexigenic gut hormone, rising before meals and falling after them.
Mechanistic rationale
Ipamorelin is selective for the ghrelin receptor, and appetite stimulation is what that receptor does. In someone trying to lose weight this is working against them, and it is frequently framed as an incidental side effect rather than as the primary pharmacology. In cachexia, poor appetite states, or during aggressive dieting to protect lean mass, it is the point.
Community reports
Marked hunger shortly after dosing is among the most consistently described effects, and is the most common reason people stop.
Components carrying the argument: Ghrelin receptor, hypothalamic appetite circuits
Pathophysiology
Earlier growth hormone secretagogues raised cortisol and prolactin alongside GH, which limited their usefulness.
Mechanistic rationale
Ipamorelin is characterised as selective — releasing GH without meaningfully raising cortisol or prolactin — and that is the genuine argument for choosing it over older secretagogues. It is a claim about what it does not do, which is a modest but real thing to be able to say.
Community reports
Users report fewer of the water retention, mood and libido complaints associated with older secretagogues, consistent with the selectivity claim.
Components carrying the argument: Receptor selectivity
Pathophysiology
The downstream GH and IGF-1 effects are common to the whole axis.
Mechanistic rationale
Sleep, lean mass, visceral fat, bone, glucose and thyroid labs are covered in full on the Ipamorelin + CJC-1295 page, including the point that GH is diabetogenic and that lean mass and function separate.
Community reports
Deeper sleep is commonly reported, and ghrelin signalling does have some independent effects on sleep in animal work.
Components carrying the argument: Downstream GH and IGF-1
| Application | Molecule with the evidence | Result | Read across? |
|---|---|---|---|
| Cancer cachexia | Anamorelin (phase 3) | Mass up, handgrip unchanged | The ceiling for the mechanism |
| Gastroparesis | Relamorelin (phase 2) | Emptying and symptoms improved | Best-supported use of the receptor |
| Appetite | Ghrelin biology | Established | The primary effect, not a side effect |
| Selectivity | Ipamorelin | Preclinical | A claim about what it avoids |
| Strength / function | — | Not demonstrated | See the anamorelin row |
For cachexia: treating the underlying disease is the only thing that reverses it. Multimodal management — nutritional support, resistance exercise where tolerated, treatment of reversible contributors, and specialist palliative input — has more support than any single appetite agent.
For sarcopenia: progressive resistance training with 1.2–1.6 g/kg/day of protein. This improves function, which is the endpoint the ghrelin trials could not move.
For gastroparesis: glycaemic control, dietary modification to small low-fat low-fibre meals, and prokinetics where appropriate. Reviewing medications that delay emptying — opioids, anticholinergics and GLP-1 agonists — comes first.
Physical-chemistry reference for laboratory handling of the lyophilised material. Reproduced so that stability and concentration mathematics can be studied — see the calculator for the arithmetic and the reconstitution guide for sterile technique.
Supplied lyophilised, commonly 2, 5 or 10 mg per vial. At 250 mcg nightly a 5 mg vial is twenty days. Reconstituted with bacteriostatic water; because doses are small, choosing a dilution that puts the dose at a readable syringe mark matters more here than for milligram-dose compounds.
Lyophilised: −20 °C long-term. Reconstituted: 2–8 °C, protected from light.
Commonly 2 mg, 5 mg and 10 mg lyophilised vials; also supplied pre-blended with CJC-1295 no DAC.
Pre-blended ipamorelin/CJC-1295 vials remove the ability to adjust the ratio independently — worth knowing before buying a blend rather than two vials.
Regulatory status changes and differs by country. This is a summary for orientation, not legal advice — check your own jurisdiction.
Not approved for human use. Clinical development was discontinued; ipamorelin has no marketing approval in any jurisdiction. Sold as a research chemical.
The FDA has moved against peptide GH secretagogues in the compounding space, and ipamorelin was among the substances identified as raising significant safety concerns for compounding use.
On 29 October 2024 the FDA's Pharmacy Compounding Advisory Committee voted against including Ipamorelin on the Section 503A Bulks List. The committee cited a lack of evidence for clinical effectiveness and safety in the uses under review.
This was an earlier and separate round from the July 2026 meeting, and it is the part of the story that the coverage of that meeting almost entirely omits. Across two sittings in October and December 2024, PCAC considered seven substances — including ipamorelin, kisspeptin-10, AOD-9604, CJC-1295 and thymosin alpha-1 — and rejected every one of them. In July 2026 the same committee recommended six of the seven it looked at. What changed between the two rounds was the FDA's April 2026 restructuring of the Category 2 list and the set of substances nominated, not the arrival of new efficacy trials for anything on this page.
A negative advisory vote is not a ban and is not binding. It does mean there is no current 503A compounding pathway for this substance, and that a committee reviewing the evidence was not persuaded by it.
Regulatory and trial claims re-checked against primary sources on 16 August 2026. Checked: anamorelin ROMANA co-primary endpoint results. Approvals, trial readouts and compounding decisions move faster than anything else on this page — a date here means someone looked, not that nothing has changed since.
Growth hormone secretagogues, GHRPs and ghrelin-receptor agonists are explicitly named on the WADA Prohibited List under S2. Ipamorelin is prohibited at all times, in and out of competition.
Links resolve to PubMed records, trial registries, publisher pages or primary documents. Where a body of work rather than a single paper is cited, the link opens a PubMed query so the full result set — including newer papers than this page — can be reviewed. Verify every claim against the primary source before relying on it.
For educational and research reference only. Nothing on this site is medical advice, a recommendation, or an instruction to administer any substance to a human being. Every figure on this page is a record of what has been reported, not a recommendation. Full disclaimer.
