Ipamorelin
GHRP (selective)
Ipamorelin is a growth-hormone secretagogue — a peptide that prompts your own pituitary to release growth hormone — and it earned a reputation as the 'cleanest' of its class. Described in 1998 as the first truly <b>selective</b> GH secretagogue, it stimulates GH without the cortisol, prolactin and appetite spikes of older peptides. This guide covers how ipamorelin works, what the research shows, dosing references, safety and status.
Ipamorelin quick facts
| Reported research dosing (Injectable) | 100mcg-500mcg |
| Route | Subq |
| Cycle length | 3-6 Months |
| Frequency | 1-3x Daily AM/Workout/PM · 5 On 2 Off or Daily |
| Half-life | ~2 hrs |
| Forms | Injectable |
| Evidence level | Human PK on components |
| Other forms available | Oral — dosed differently |
The cleanest GHRP. Synergizes hard with a GHRH like CJC no-DAC.
How ipamorelin works
Ipamorelin is a ghrelin-receptor (GHSR-1a) agonist: it binds the growth-hormone-secretagogue receptor in the pituitary and triggers a pulse of natural growth-hormone release. Crucially, it works with your physiology rather than overriding it — it preserves the natural pulsatile rhythm of GH and keeps normal feedback regulation intact, unlike exogenous HGH, which replaces your own GH and suppresses the axis.
Why ipamorelin is called 'selective'
The reason ipamorelin is so popular is selectivity. Earlier GHRPs like GHRP-2 and GHRP-6 raised GH but also bumped cortisol, prolactin and appetite. Ipamorelin stimulates GH at levels comparable to GHRP-6 while producing no statistically significant rise in cortisol or ACTH at research doses, and — unlike other ghrelin agonists — it doesn't significantly spike hunger. That cleaner profile is why it's a go-to in GH-support research and is often paired with a GHRH.
What the research shows
Ipamorelin was originally developed by Novo Nordisk and studied in Phase I/II trials. The published research spans body-composition changes in animal models, bone-density research, and gut-motility studies (GH secretagogues can promote GI motility). As with most peptides in this space, the enthusiasm is built on a mix of mechanism, early clinical work and anecdote rather than large long-term human outcome trials.
Ipamorelin dosing (research reference)
The literature commonly references ipamorelin in the low-hundreds-of-micrograms range per dose, often once to a few times daily and frequently timed around sleep or fasting to align with natural GH pulses, reconstituted with bacteriostatic water. The calculator above converts a research amount into syringe units. It's frequently referenced stacked with a GHRH such as CJC-1295 for a stronger, more synergistic pulse. This summarizes existing references for education only, not dosing advice.
Safety & side effects
Ipamorelin's selectivity is exactly why it's considered one of the better-tolerated secretagogues — minimal cortisol/prolactin effect and little appetite change at research doses. That said, GH-axis stimulation still warrants care (water retention, effects on insulin sensitivity and blood sugar are worth understanding), long-term human safety data is limited, and research-market purity varies. This is educational information, not medical advice.
Related compounds & stacking
Ipamorelin (a GH-releasing peptide) is classically paired with a GHRH like CJC-1295 — the two hit the GH axis through different receptors, producing a bigger combined pulse than either alone. It sits in the same GH-support family as MK-677, Sermorelin and Tesamorelin.
Legal & regulatory status
Ipamorelin is not FDA-approved and is sold as a research compound (research use only). GH secretagogues are also prohibited in competitive sport under WADA. Its compounding status is subject to ongoing FDA review. Follow the laws and any sport rules that apply to you.
Where to get Ipamorelin
Ipamorelin is sold in 2 forms. They are not interchangeable — the dose and the route differ, so pick the one this page describes unless you know why you want another.
Ipamorelin reconstitution calculator
Research reconstitution calculator
Bacteriostatic water is the diluent — sterile water with 0.9% benzyl alcohol, which is what lets a vial be drawn from more than once. It does not come with the vial, and unlike the compound it is bought again every time.
Need bacteriostatic water? Get it at AminoWell USA (my company) → Code CAMERON.
The evidence for Ipamorelin
Graded by what exists behind each claim.
✅ Clinically validated
- Human pharmacokinetic and tolerability data exist from its development as a treatment for post-operative ileus — it reached phase 2 and did not meet that endpoint, so the indication was dropped.
- Note what was being asked. The endpoint was return of gut motility after abdominal surgery, not growth hormone release — and ipamorelin's GH activity was never in question in that program; it was demonstrated in the same trials as a pharmacodynamic marker. A failure to speed up post-surgical bowel function says nothing about whether it raises GH, which it measurably does. The dosing and safety characterization from that program is why its human profile is better described than most peptides here.
📊 Correlative data
- The most widely used GH secretagogue in practice, usually paired with a GHRH analog. What clinicians and users consistently report is the thing the receptor selectivity predicts: a GH pulse without the hunger, cortisol rise or prolactin rise that the older secretagogues cause.
🧪 Theoretical / extrapolated
- A selective ghrelin-receptor (GHS-R1a) agonist. Selectivity is the entire point — GHRP-6 and GHRP-2 hit the same receptor but also drive ACTH, cortisol and prolactin, and ipamorelin largely does not.
- Because it works through a different receptor from the GHRH analogs, the two are predicted to be additive rather than redundant, which is exactly why the CJC/ipamorelin pairing became standard.
How to read these tiers: they say how much human evidence exists, not how well something works — and ✗ flags harm, never a disappointing trial. How the evidence tiers work →
What Ipamorelin actually does
Write the sequence properly first, because the usual way of writing it deletes the two features that make the molecule selective. Ipamorelin is five residues: Aib–His–D-2-Nal–D-Phe–Lys-NH2. This site's verified sequence record stores it as {Aib}H{2Nal}FK with a C-terminal amide, cross-checked against the PubChem formula C38H49N9O5 at 711.9 Da; flattened into the twenty-letter alphabet that becomes XHXFK, where each X marks a residue the standard code has no symbol for. Written as the tidy three-letter form it looks like an ordinary pentapeptide, and it is not.
What each unusual residue is doing, mechanistically. Position 1 is Aib, alpha-aminoisobutyric acid — a non-natural amino acid with two methyl groups on the alpha carbon. It is not a peptidase substrate, so it blocks aminopeptidase attack at the N-terminus, and its steric bulk forces a helical turn in the backbone that holds the rest of the molecule in the shape the receptor recognizes. Position 3 is D-2-naphthylalanine, a two-ring aromatic side chain larger and more hydrophobic than the tryptophan occupying the equivalent position in GHRP-6, and position 4 is D-phenylalanine. Peptidases are stereospecific and cannot process D-residues in the backbone, so those two both raise receptor affinity and block internal cleavage. The C-terminal amide removes the terminal carboxylate — one fewer negative charge, and no carboxypeptidase substrate. Four edits, and every one of them is doing two jobs.
The receptor is GHS-R1a, the ghrelin receptor. Its natural ligand is ghrelin, a 28-residue stomach peptide bearing an unusual octanoyl fatty acid on serine 3 that is required for activity Kojima 1999. GHS-R1a couples to Gq, raising IP3 and intracellular calcium in the somatotrope — a different second messenger from the cAMP that GHRH generates, which is the mechanistic basis for the synergy between the two classes.
And the selectivity, which is what the name of the paper claims. Raun 1998 measured it directly. In rat pituitary cells ipamorelin released GH with an EC50 of 1.3 ± 0.4 nmol/L, comparable to GHRP-6. In anesthetized rats the ED50 was 80 ± 42 nmol/kg with an Emax of 1545 ± 250 ng/mL GH; in conscious swine the ED50 was 2.3 ± 0.03 nmol/kg. The critical result: unlike GHRP-6 and GHRP-2, ipamorelin did not raise ACTH or cortisol even at doses 200-fold above its GH ED50. That is the entire clinical argument for this peptide over its predecessors, and it is a measured number rather than a claim.
One more receptor fact with a practical edge. GHS-R1a has an endogenous antagonist, LEAP2, discovered in 2018 Ge 2018. LEAP2 rises with feeding and with obesity and falls with fasting. So the receptor this peptide targets is under opposing endogenous control that varies with nutritional state, which is a better explanation for why the same dose behaves differently fasted than any of the usual ones.
Cell, rodent, human — and where it stops
Step one, in cells and animals: precise and reproducible. The full dose-response set above Raun 1998, across rat pituitary cells, anesthetized rats and conscious pigs, with the ACTH and cortisol null result at 200-fold excess. This is thorough preclinical pharmacology by any standard.
Step two, in humans, and this is the part the page has to be honest about: the one randomized controlled trial failed its endpoint. Beck 2014 enrolled 117 patients (114 analyzed) undergoing small or large bowel resection and randomized them to intravenous ipamorelin 0.03 mg/kg twice daily on postoperative days 1 to 7 or placebo. Median time to first tolerated meal was 25.3 hours on ipamorelin against 32.6 hours on placebo, P=0.15. Not significant. Adverse events occurred in 87.5% of the ipamorelin group and 94.8% of placebo. The authors' conclusion is that the drug was well tolerated and that there were no significant differences in the key or secondary efficacy analyses.
What that trial does and does not tell you, stated carefully. It was asking whether a ghrelin mimetic speeds the return of bowel motility after abdominal surgery. It was not asking whether ipamorelin raises GH. So the failure is a failure of the prokinetic hypothesis, not of the secretagogue pharmacology — and it remains the case that this compound's only randomized human efficacy trial was negative, and that a page which does not say so is not telling the reader what happened. What the trial contributes that is genuinely valuable is seven days of twice-daily intravenous dosing in 57 people with systematic adverse event capture — the best human tolerability data this peptide has.
Step three, the class in humans. Su 2016 pooled the randomized evidence for two ghrelin receptor agonists in adults with malnutrition. And Sigalos 2017 followed 14 men on testosterone therapy taking 100 mcg of GHRP-6, GHRP-2 and a SERM three times daily for a mean of 134 days: serum IGF-1 rose from 159.5 to 239.0 ng/mL, P<0.0001. Note precisely what that study used — GHRP-6 and GHRP-2, not ipamorelin — and note the schedule, three times daily with strict compliance, which the authors identify as the condition for the effect. It is class evidence, and the class is the right one, and it is not this molecule.
The obstacles, named one at a time. (1) No randomized trial of ipamorelin with a GH, IGF-1 or body-composition endpoint in healthy adults exists. (2) The human dose that has been studied is 0.03 mg/kg intravenously Beck 2014 — about 2.4 mg in an 80 kg person, roughly ten times the 100–500 mcg subcutaneous doses in community use, by a different route. (3) Continuous GHS-R1a stimulation causes receptor desensitization, and the LEAP2 system Ge 2018 adds endogenous opposition that varies with feeding — neither has been characterized on a chronic protocol. (4) The selectivity result is from rats and pigs Raun 1998; the equivalent human ACTH and cortisol measurement has not been published.
What would have to be true, and how you would know it was not
Three predictions, and the second is the one that would settle the single claim this peptide is bought for.
1. IGF-1 is the endpoint; a random growth hormone level is noise. GH is pulsatile and a single growth hormone draw tells you almost nothing. IGF-1 integrates GH exposure over days and is the number the one comparable human study moved — 159.5 to 239.0 ng/mL over 134 days Sigalos 2017. Draw IGF-1 at baseline and 12 weeks at the same laboratory. That study also identifies the variable people get wrong: frequency. Its effect required thrice-daily dosing.
2. The selectivity claim is testable in a person and has never been tested. The entire argument for ipamorelin over GHRP-2 or GHRP-6 is that it does not raise ACTH or cortisol — measured in rats and pigs Raun 1998, never published in humans. A cortisol and a prolactin drawn at baseline and 60 minutes after a dose, on a few people, would produce the first human evidence for or against the selling point. If cortisol or prolactin rises, the reason to pay more for this peptide disappears.
3. The prediction that cuts against the product: GH opposes insulin, so a real effect should show in glucose handling. Growth hormone reduces peripheral glucose uptake and promotes lipolysis. A genuine sustained rise in GH exposure predicts a small rise in fasting insulin and possibly in HbA1c. A person reporting dramatic body-composition change with entirely unchanged insulin, IGF-1 and glucose is describing an effect the GH axis is not producing.
What nobody has tested yet
Four experiments that would answer the questions this compound actually raises.
Nobody has published human ACTH and cortisol data. The selectivity that defines the molecule is a rat and pig result Raun 1998. Six volunteers and a morning of serial draws would convert the compound's core claim from preclinical to human, and twenty-seven years after the original paper it has not been done.
Nobody has run a subcutaneous dose-response for IGF-1. The studied human dose is intravenous and roughly ten times what people inject Beck 2014. What 100, 300 and 500 mcg subcutaneously do to IGF-1 over 12 weeks is unmeasured, and it is the number every user is implicitly guessing at.
Nobody has characterized desensitization. GHS-R1a downregulates under continuous stimulation and the endogenous antagonist LEAP2 varies with feeding and body weight Ge 2018. Whether a daily protocol loses effect at 4 weeks, at 12, or not at all is the single most practically important unknown, and a repeated IGF-1 time course would answer it.
Nobody has measured LEAP2 alongside a secretagogue. The assay exists. Whether a person's LEAP2 level predicts their response is a straightforward correlation study and would be the first attempt at explaining why responses to this class vary so widely between people.
Ipamorelin — its own safety story, not its class's
The class block above is generic to GH secretagogues. Four things belong to this one.
The best tolerability data comes from the trial that failed. Seven days of twice-daily intravenous dosing at 0.03 mg/kg in postoperative patients, with adverse events actually occurring less often than on placebo — 87.5% against 94.8% Beck 2014. In surgical patients everything is recorded, so that is systematic capture rather than absence of looking, and it is far better evidence than community reports.
The selectivity is the safety argument and it is unverified in humans. GHRP-2 and GHRP-6 raise cortisol and prolactin; ipamorelin did not in animals, at 200-fold excess Raun 1998. If that holds in people it removes the main objection to chronic use of this class. Nobody has checked. Treating an unmeasured animal result as an established human property is the most common error made about this peptide.
The hunger effect is the mechanism, not a side effect. GHS-R1a is the ghrelin receptor and ghrelin is the hunger signal Kojima 1999; GHRP-2 measurably increases food intake in healthy men Laferrere 2005. Ipamorelin is reported to do this less, and "less" is not "not at all". Anyone using this while trying to reduce body fat is taking an agonist at the hunger receptor for a body-composition purpose, which is a tension worth naming.
The GH-axis cautions apply as they do to the whole class. Fluid retention, carpal tunnel symptoms and joint aches are dose-related consequences of raised GH; insulin resistance is the metabolic one and is the reason for the marker above. And the standing caution for anything that raises IGF-1 — active or recent malignancy — is reasoning from the growth axis, not from a study of this peptide, because no such study exists.
Sources read for this page
- Raun K, et al. Ipamorelin, the first selective growth hormone secretagogue. European Journal of Endocrinology 1998 · PMID 9849822
- Beck DE, et al. Prospective, randomized, controlled, proof-of-concept study of the Ghrelin mimetic ipamorelin for the management of postoperative ileus in bowel resection patients. International Journal of Colorectal Disease 2014 · PMID 25331030
- Su J, et al. Two ghrelin receptor agonists for adults with malnutrition: a systematic review and meta-analysis. Nutrition Journal 2016 · PMID 27852245
- Sigalos JT, et al. Growth Hormone Secretagogue Treatment in Hypogonadal Men Raises Serum Insulin-Like Growth Factor-1 Levels. American Journal of Men's Health 2017 · PMID 28830317
Ipamorelin — safety, predicted from mechanism
Predicted from mechanism, not from a human safety trial. How that reasoning works →
What the mechanism predicts
Derived from the molecule, not a trial.
- Everything here follows from one fact: these raise GH and therefore IGF-1. The predicted problems are the known consequences of elevated GH/IGF-1, drawn from acromegaly and clinical GH therapy where it HAS been studied — insulin resistance and rising fasting glucose, fluid retention (puffy hands and face, and the ring that stops fitting), carpal tunnel symptoms from that same fluid pressing on the median nerve, and joint aches.
- The proliferation question is the serious one. IGF-1 is a growth signal, and growth signals do not distinguish between tissue you want to grow and tissue you do not. There is no evidence these compounds cause cancer. There is also a clear mechanistic reason not to run them with an active or recent malignancy, and that reasoning does not require a trial to be sound.
What has actually been reported
- Injection-site reactions, transient flushing, tingling and head-rush on dosing — most commonly with the GHRPs, which also release cortisol and prolactin at higher doses.
- Increased hunger is near-universal with the ghrelin-mimetic ones (GHRP-6, MK-677, Hexarelin). That is the mechanism working, not a side effect — the same receptor drives GH release and appetite.
How to reduce the risk
Same mechanism as the prediction.
- Draw an IGF-1 baseline BEFORE you start. Once you are on, that number is the drug and you have permanently lost the comparison. This is the single highest-value thing on this list and it costs one blood draw.
- Watch fasting glucose and HbA1c, not the scale. Insulin resistance is the most likely thing to move and the one you cannot feel. Re-test at 8–12 weeks. If fasting glucose is climbing, that is your signal to cut the dose or come off — long before anything shows up symptomatically.
- Dose at night, on an empty stomach. GH release is pulsatile and largest during early sleep; food, and carbohydrate in particular, blunts the pulse through insulin. This is not a ritual — it is the same mechanism working with you rather than against you.
- Don't run a secretagogue through a high-carbohydrate surplus. The predicted problem is insulin resistance; adding a large carb load is pushing the same lever from the other end.
- Cycle rather than run continuously. Most of the predicted problems — fluid retention, carpal tunnel, glucose drift — are dose-and-duration dependent and reverse on cessation. Time off is the cheapest safety intervention available.
- If fluid retention is the issue, it usually resolves on a dose reduction long before it needs anything else. Reach for the dose before you reach for a diuretic.
What it does to your bloodwork
A fact about the assay.
- IGF-1 drawn on-cycle is not your baseline — it is the drug working, and it will read high. If you want a real baseline, draw before starting or after a proper washout.
- Watch fasting glucose and HbA1c, because insulin resistance is the most likely thing to move and the one you will not feel.
- GHRP-6 and Hexarelin can raise prolactin and cortisol; if you are chasing an unexplained prolactin result, this is a candidate.
What it overlaps with
- Stacking two secretagogues that work by the same route is redundancy, not synergy. A GHRH analog (CJC-1295, Sermorelin, Tesamorelin) plus a ghrelin mimetic (Ipamorelin, GHRP-2, GHRP-6) is the deliberate pairing — two different levers on the same axis. Two GHRH analogs together is paying twice for one lever.
Don't run this if
- Active or recent malignancy — the IGF-1 reasoning above.
- Diabetes or poor glycemic control, unless you are monitoring fasting glucose and HbA1c and know what you are looking at.
- Untreated diabetic retinopathy.
The honest unknown
- Nobody has run long-term studies of intermittent secretagogue use in healthy adults. The specific unmeasured thing is what years of repeatedly pushing IGF-1 above your natural set point does — not whether a single cycle is tolerable, which it evidently is.
Not medical advice. If you take prescription medication or have a diagnosed condition, check this with a pharmacist or doctor.
Fasted — and pre-bed is the best of the windows
Food is the problem here, and specifically carbohydrate and fat. Both trigger somatostatin release, and somatostatin is the brake on growth hormone — eating before the injection pharmacologically cancels it. Two clear hours either side.
Pre-bed is the strongest window because the largest natural GH pulse happens in the first hours of deep sleep, so you are stacking with it rather than asking the pituitary for something it is not primed for. Fasted pre-training is the second-best, for the same reason in a different rhythm.
From half-life and route, not a dosing trial.
Ipamorelin — interference & stacking
Predicted from mechanism, not from an interaction study. How mechanism-predicted claims are made →
What Ipamorelin moves on your bloodwork
Expected direction, not a measured one.
- IGF-1 (Insulin-like Growth Factor 1) — ↑ expected to rise
This is the point. IGF-1 rising is the compound doing its job — it is the stable downstream readout of a GH pulse.
What to do: Test it before you start and again at 6–8 weeks. It is the only number that tells you whether the product was real and the dose was enough. - Growth Hormone, Serum — ✕ unreliable here
A random GH level is close to meaningless here. GH is secreted in pulses during deep sleep and sits undetectable between them, so a daytime draw catches a trough almost every time — including when the compound is working perfectly.
What to do: Do not use GH to judge a secretagogue. Read IGF-1 instead. - Fasting Insulin — ↑ expected to rise
GH is a counter-regulatory hormone: it opposes insulin. Fasting insulin and glucose drifting up is the predicted trade-off, not a surprise.
What to do: Check fasting insulin and HbA1c at baseline and again at 8–12 weeks. This is the marker that decides whether you keep running it. - HbA1c (Hemoglobin A1c) — ↑ expected to rise
Same mechanism, longer window — a slow drift rather than a jump.
What to do: Pair it with fasting insulin; either alone can mislead. - Free T4 (Thyroxine) — ↓ expected to fall
GH accelerates the peripheral conversion of T4 to T3, so free T4 can fall while free T3 holds or rises. Read alone it looks like new hypothyroidism, and it usually isn't.
What to do: Run a full thyroid panel rather than TSH alone before concluding anything.
Everything above follows from one fact: these raise GH and therefore IGF-1. Nothing here needs a trial of the specific molecule.
Everything on this page, in an order
This one is free and stays free. What Skool adds is the rest of the shelf — 278 compounds and 371 supplements with the protocol, the stack order and the bloodwork to run beside it.
Join Skool — $10/mo →Bloodwork to run alongside Ipamorelin
Baseline first, then again at 8–12 weeks.
| Marker | What it’s watching for |
|---|---|
| IGF-1 (Insulin-like Growth Factor 1) | What you dose against — feel is not a measurement |
| Fasting Insulin | The trade that comes with every GH secretagogue |
| HbA1c (Hemoglobin A1c) | Three-month confirmation |
| Comprehensive Metabolic Panel (CMP) | Fasting glucose and organ baseline |
The “Running GH Peptides or MK-677” panel covers these in one order — 9 markers, $132.30 with the discount applied.
Check results you already have → · All 103 markers A–Z
Ipamorelin — frequently asked questions
What is ipamorelin?
Ipamorelin is a selective growth-hormone secretagogue — a peptide that binds the ghrelin receptor to prompt your own pituitary to release a pulse of growth hormone, without the cortisol and appetite spikes of older GHRPs.
How does ipamorelin work?
It's a ghrelin-receptor (GHSR-1a) agonist that triggers a natural, pulsatile release of growth hormone while preserving normal feedback regulation, rather than replacing your own GH the way injected HGH does.
Why is ipamorelin considered 'clean'?
It stimulates GH comparably to older GHRPs but without a significant rise in cortisol, prolactin or ACTH, and without much appetite increase — a more selective profile than GHRP-2 or GHRP-6.
How is ipamorelin dosed?
The literature references low-hundreds-of-micrograms per dose, often around sleep or fasting to match natural GH pulses, reconstituted with bacteriostatic water (see calculator). It's frequently referenced stacked with a GHRH. This is educational, not dosing advice.
What does ipamorelin stack well with?
It's classically paired with a GHRH like CJC-1295 — the two act on different receptors to produce a larger combined GH pulse than either alone.
Is ipamorelin FDA-approved?
No. Ipamorelin is not FDA-approved and is sold as a research compound. GH secretagogues are also banned in competitive sport under WADA.
References & further reading
- Ipamorelin — the first selective growth-hormone secretagogue (1998 paper)
- The growth-hormone secretagogue receptor — signaling & regulation (PMC)
Ipamorelin inside a finished plan
One arm of 1 Protocol Blueprint, free to read in full.
What Ipamorelin is used for
Ipamorelin appears under 3 goals in the goal router.
Related GH & Growth compounds
Where this goes next
Ipamorelin is the depth arm of this plan. The page above is the free breakdown of one compound; the plan it belongs to — the dosing, the order to correct things in, the week-by-week schedule and what to retest — is a lesson inside Skool.