GHRP-2 vs GHRP-6 vs Ipamorelin: Which One Is Selective, and in Which Species It Was Measured

Three ghrelin-receptor agonists, one selectivity claim. The trade-off this page resolves is side effects against species: GHRP-2's and GHRP-6's cortisol data are human, ipamorelin's absence of it was measured in pigs. The appetite claim has no human trial at all.

That is the whole argument in this class, and it is usually stated backwards. All three sit in the growth hormone peptides category, with individual records in GHRP-2 (pralmorelin): the only growth hormone secretagogue that is an approved drug, GHRP-6: the appetite claim with no human trial behind it and ipamorelin: the selective secretagogue that failed its only published human trial.

Which of the three is actually the clean one, and in which species was that measured?

The clean one is ipamorelin, and the cleanliness was demonstrated in pigs. GHRP-2 and GHRP-6 both raise cortisol and ACTH in humans, measured directly. Ipamorelin produced no rise in conscious swine at more than 200 times its own GH ED₅₀, and no human study measuring cortisol or prolactin after ipamorelin was located. The selectivity ranking everyone quotes therefore compares an animal measurement against two human ones.

The first three rows are the reason anyone runs this comparison, and they are the only rows where the compounds are being judged on evidence of different quality. Everything below them is a like-for-like property.

These are not three variations on one molecule. GHRP-2 and GHRP-6 are hexapeptides; ipamorelin is a pentapeptide, and it is the only member of the group without the Trp-Trp core, using Aib and D-2-naphthylalanine instead. That is a genuinely different chemistry rather than a one-residue tweak, and it is the structural reason the selectivity profile differs at all. GHRP-6 adds a second target the other two do not have — it binds CD36 as well as GHS-R1a, which underpins an entire animal literature on cytoprotection.

One shared position is worth stating up front so it does not have to be repeated. All three are on FDA's Category 2 list of bulk substances that may present significant safety risks, all three were added on 29 September 2023, and all three are prohibited in sport at all times under WADA S2.2.4. Whatever separates these compounds, legality does not. Our FDA peptide regulation timeline tracks how each nomination has moved since.

Does GHRP-6 actually cause hunger?

GHRP-6 is bought for appetite and no human trial of GHRP-6 and appetite exists. The canonical citation, Locke et al. 1995 in Life Sciences, delivered the peptide intracerebroventricularly in rats — directly into the cerebral ventricles. The only human appetite trial for any compound in this class is GHRP-2's: 7 of 10 GH-deficient children reported increased appetite over six months, with no significant BMI change. Ipamorelin has no appetite data at all.

Read the rat paper's own title: Locke et al., "Intracerebroventricular growth-hormone-releasing peptide-6 stimulates eating without affecting plasma growth hormone responses in rats". Rats. Intracerebroventricular. The finding is genuinely interesting on its own terms — the feeding effect is centrally mediated and dissociable from GH release, which is a mechanism result about brain circuitry. It is not evidence that subcutaneous GHRP-6 increases appetite in people, and it was never presented as such.

The GHRP-2 comparison is the closest thing this class has to a human answer, and it is thin. Mericq et al. 2003 dosed 10 prepubertal GH-deficient children orally for 12 months. Seven of ten reported increased appetite during the first six months. BMI standard deviation score moved from 0.21 ± 1.5 to 0.25 ± 1.51, which was not statistically significant. Transient, self-reported, ten children, and no meaningful weight change.

The appetite effect may well be real. Ghrelin biology makes it plausible and community reports are consistent. But "plausible and widely reported" is a different claim from "demonstrated," and the compound with the strongest reputation for it is the compound with the weakest evidence for it. That is the single most useful finding on this page: the reputational ranking and the evidential ranking are inverted.

Which of them raises cortisol, ACTH and prolactin?

GHRP-6's cortisol effect is the best-characterised side effect in the class: cortisol was substantially elevated across a whole night in healthy men, alongside ACTH. GHRP-2 raises prolactin, ACTH and cortisol, measured in humans alongside hexarelin. GHRP-6's prolactin claim has no primary human measurement behind it at all. Ipamorelin's cortisol and prolactin have never been measured in a human being — only in swine.

Frieboes et al., "Growth Hormone-Releasing Peptide-6 Stimulates Sleep, Growth Hormone, ACTH and Cortisol Release in Normal Man" (Neuroendocrinology, 1995) gave healthy male controls repetitive intravenous GHRP-6 boluses versus placebo with EEG and hormone monitoring from 23:00 to 07:00. GH and ACTH rose significantly in the early morning hours, and cortisol was substantially elevated across the whole night, particularly the first half. Stage 2 sleep increased; slow-wave sleep did not change — the opposite of what most sleep-related marketing implies.

That timing matters more than it looks. The cortisol elevation was measured with nocturnal dosing, which is the pattern most community protocols use.

For GHRP-2, Arvat et al. 1997, in Peptides, measured GH, prolactin, ACTH and cortisol after both GHRP-2 and hexarelin in humans, and the paper remains the human reference point for the class. What it establishes is that these compounds are not GH-specific. Marketing that presents GHRP-2 as a clean or selective growth hormone releaser is contradicted by the primary human literature, not merely unsupported by it.

The prolactin gap is specific and worth stating precisely. We found no primary human result quantifying a prolactin rise from GHRP-6. Frieboes measured GH, ACTH and cortisol — not prolactin. Bowers et al. (JCEM, 1990), the first-in-man study, did measure prolactin, as one of four specificity checks alongside LH, TSH and cortisol, and reported specificity at the low intravenous doses used. So the one human dataset that looked found nothing to report, and the study people cite for the claim never measured it. Treat it as unsupported until someone produces the measurement — a narrower statement than "GHRP-6 does not raise prolactin."

There is also a dose-and-pattern tension inside GHRP-6's own file. At 0.1–1.0 µg/kg intravenously in 18 men, the 1990 paper frames GHRP-6 as GH-specific. With repetitive nocturnal dosing five years later, it clearly was not. Dose and pattern probably matter, and nobody has mapped that curve in humans.

FDA names the cortisol issue itself in its Category 2 rationale for GHRP-6:

"Compounded drugs containing GHRP-6 may pose risk for immunogenicity for certain routes of administration due to the potential for aggregation and peptide-related impurities. FDA has identified limited safety-related information, but the available data reveal safety concerns including potential effect on cortisol and increase in blood glucose due to decreases in insulin sensitivity."

Its GHRP-2 rationale is harder still, and contains a signal that appears nowhere in the marketing:

"Compounded drugs containing GHRP-2 for injectable and nasal administration may pose risk for immunogenicity due to the potential for aggregation and peptide-related impurities. GHRP-2 also contains an unnatural amino acid, which adds to the complexity of peptide characterization. FDA is aware of reports of serious adverse advents in patients who received GHRP-2, including increased insulin requirement to maintain the blood glucose level, death of critically ill study subjects, infection and pancreatitis, though causality has not been established."

The typographical error is FDA's and is preserved. The substance is that the agency is aware of deaths among critically ill study subjects and of pancreatitis reports, with causality unestablished.

Is ipamorelin's selectivity real, or is it a pig study?

Both. Ipamorelin's selectivity is a real finding and it was produced in conscious swine. Raun et al. 1998, working at Novo Nordisk, showed that GHRP-6 and GHRP-2 raised ACTH and cortisol while ipamorelin did not, even at doses more than 200-fold above its own GH ED₅₀, with no secretagogue altering FSH, LH, prolactin or TSH. The problem is not the experiment. It is that the comparison built on top of it crosses a species boundary.

The founding paper, "Ipamorelin, the first selective growth hormone secretagogue" in European Journal of Endocrinology, is a good piece of work and it is entirely animal work. In rat pituitary cells, ipamorelin's EC₅₀ was 1.3 ± 0.4 nmol/L against GHRP-6's 2.2 ± 0.3. In anaesthetised rats, ED₅₀ was 80 ± 42 nmol/kg versus GHRP-6's 115 ± 36. The authors concluded that ipamorelin was "the first GHRP-receptor agonist with a selectivity for GH release similar to that displayed by GHRH."

So "cleaner than GHRP-2" is a cross-species inference, not a measured difference, and it is the single most repeated sentence written about this compound. Confirming that a vial holds ipamorelin rather than GHRP-2 confirms the molecule. It does not confirm the selectivity advantage.

There is a second, quieter finding in ipamorelin's human file. In the eight-man study, inter-individual variability in GH response exceeded variability in drug levels, which means the dose is not the main variable in the response. Nothing in the human record identifies what the main variable is.

Which of the three has the strongest human evidence?

GHRP-2, and it is not close: 135 subjects in a diagnostic validation study, plus an approved label with a regulated adverse-reaction table. GHRP-6 has three human studies, one of which — 18 men in 1990 — is widely cited. Ipamorelin has an eight-man pharmacokinetic study, one randomised trial that missed its endpoint at p = 0.15, and a 320-patient Phase 2 that completed in May 2014 and has never posted results.

None of these comparisons is head-to-head. No trial has put any two of these three compounds against each other in humans. The only genuine within-experiment comparison anywhere in the class is Raun's — and it is in pigs. Everything else on this page places different populations, routes, decades and endpoints side by side, and should be read as a map of how much evidence each compound has rather than as a ranking of effect sizes.

Two things about GHRP-2's strong position deserve qualification. Its approval covers a diagnostic reagent, therapeutic category 7223, at ¥6,684 per 100 µg vial from Kaken Pharmaceutical, marketed as GHRP KAKEN 100 Injection under the generic name pralmorelin hydrochloride — and it is licensed to measure the pituitary rather than to drive it. Somebody tried the other thing: Drugs in R&D recorded in 2004 that Kaken sublicensed United States and Canadian rights to Wyeth, and that US development for treating growth hormone deficiency was discontinued. The public record documents the discontinuation, not the reasoning. And the label's adverse-reaction rates describe a single diagnostic dose. A 16.0% rate of heat sensation after one injection tells you nothing about what twice-weekly subcutaneous dosing over a year does.

What dose of each has actually been validated?

One dose, on one compound, for one purpose: GHRP-2 at 100 µg intravenously as a single injection in adults, and 2 µg/kg to a 100 µg maximum in children aged 4 to 17, given slowly and fasting. Nothing else in this comparison has a validated protocol. Every published human dose of GHRP-6 is intravenous and acute, both published ipamorelin exposures were intravenous, and no chronic human dosing study exists for GHRP-6 at any dose.

The route mismatch is the substantive problem rather than a technicality. Every human dose of all three compounds on record was given intravenously, and the route everyone actually uses has never been characterised in a published trial — so bioavailability, timing and the shape of the GH curve after a subcutaneous injection are extrapolations for all three.

Two compound-specific cautions attach. GHRP-6's one human overnight study is the one that found cortisol raised across the night, and nocturnal dosing is precisely the community pattern; reduce or stop if glucose control deteriorates, since insulin sensitivity is the mechanism FDA named. GHRP-2's longest human exposures are paediatric — 18 to 24 months in 15 children and 12 months in 10 children, both uncontrolled — and nothing in that record transfers to adult dosing for body composition.

For per-injection volume, use the peptide dosing calculator for GHRP-2 and GHRP-6 and the CJC-1295 and ipamorelin calculator for ipamorelin, each alongside the reconstitution calculator. Those tools convert a chosen dose into a syringe volume. For two of these three compounds, no published source tells you which dose to choose. See also the peptide dosage guide.

What does each cost, and which is easiest to substitute?

GHRP-6 is the cheapest at a $3.90/mg median and the most exposed to substitution, because it sits 14.0157 daltons from hexarelin and hexarelin sells for $9.20/mg. Ipamorelin is the dearest at $6.00/mg and the easiest to confirm, sitting 106 to 175 daltons below all three neighbours. GHRP-2's median is $4.60/mg, across only 9 shops in stock — the thinnest supply coverage of the three (verified August 2026).

The 14-dalton problem is the only genuine identity trap in this trio. GHRP-6 and hexarelin differ by a single methyl group. Both are hexapeptides with two indole chromophores, near-identical UV absorbance and closely similar chromatographic retention, so an HPLC-UV certificate cannot distinguish them. Mass spectrometry does so trivially. The commercial incentive runs one way: hexarelin sells for more than twice as much per milligram, so the substitution favours hexarelin vials containing GHRP-6. A 14 Da discrepancy on a certificate deserves scrutiny in either direction, since it is also the shift produced by common methylation artefacts. Separately, acetate salt forms add roughly 60 Da per acetate to the weighed material without changing the peptide ion — a routine source of certificate confusion.

Ipamorelin has the opposite problem, which is to say it has none. Nominal masses of 818, 873, 887 and 712 are distinguishable even on a low-resolution instrument, so an ipamorelin certificate with a purity figure and no identity result is a choice rather than a technical limitation. Its realistic risks are underfill and non-peptide bulking, which is exactly what FDA complained about when it called the free base "not well-characterized from the physical and chemical characterization perspective."

A database caution applies to GHRP-6 specifically, because it propagates into vendor listings. PubChem's main GHRP-6 record carries no CAS number, the compound appears under two duplicate CIDs, and the synonym list for CID 4345065 erroneously includes "GHRP-2 Acetate". Verify against formula and mass rather than trusting a name string.

Platform data, all verified August 2026. The Purity Index records GHRP-2 at 99.21 across 35 recency-weighted tests from 10 laboratories, GHRP-6 at 99.35 across 44 recency-weighted tests from 11 laboratories, and ipamorelin at 99.65 across 323 recency-weighted tests from 21 laboratories, against a platform composite of 99.50 across 10,110 tests. The ipamorelin compound page separately shows 407 total tests averaging 99.66% across 229 shops, the difference being recency weighting and exclusions. GHRP-2 price data shows 9 shops in stock, a $4.60/mg median and a $2.80/mg low; GHRP-6 price data shows 13 shops in stock, a $3.90/mg median and a $1.50/mg low; ipamorelin price data shows 63 shops in stock, a $6.00/mg median and a $2.00/mg low on a 10 mg vial. Those figures exclude shipping, taxes and customs, coupon codes, bulk tiers, multi-vial kits and account-gated pricing.

Thirty-five tests on GHRP-2 and forty-four on GHRP-6 are modest evidence bases — enough to be meaningful, thin enough that individual results move the average, and worth stating plainly rather than presenting as settled. Ipamorelin's 323 is an order of magnitude more. Peptigrity tracks 530 shops and 11,852 independent lab tests across 118 peptides, with 1,283 community reviews (verified August 2026), weighting community reviews and independently verified purity equally at 50% each in every trust score. Individual results are searchable in the lab test database, the GHRP-2 compound page and GHRP-6 compound page carry vendor-level detail, and the method reading is mass spectrometry for peptides, how to read peptide lab test results and where to buy ipamorelin: 7 purity and identity checks.

So which should you choose?

For reliable GH release at a dose someone has validated, GHRP-2 — it is the only one with a label. For avoiding a measured cortisol rise, ipamorelin, on animal data alone. For appetite, none of them has human evidence worth the name. For adult body composition, none of them has any evidence at all: no adult efficacy trial exists for GHRP-2, GHRP-6 or ipamorelin, and the one clinical trial any of them completed missed its endpoint.

The honest summary of that table is that this class is chosen on side-effect reputation and the side-effect data is unevenly measured. Two of the three have their side effects documented in humans; the third has its absence of side effects documented in pigs. A compound looks cleaner when nobody has run the measurement.

The trial that would settle this

No head-to-head human trial of these three compounds exists, and one study would resolve most of the page: subcutaneous dosing at community doses, repeated over months, with cortisol, ACTH and prolactin measured in every arm and measured energy intake as a primary endpoint. Every human dose of all three on record is intravenous and acute. Every appetite result is intracerebroventricular and in rats, or self-reported by ten children.

Frequently Asked Questions

Which of the three causes the least cortisol?

Ipamorelin, on the evidence available — but that evidence is porcine. Raun et al. found no ACTH or cortisol rise in conscious swine at more than 200 times the GH-releasing dose. GHRP-2 and GHRP-6 both raise cortisol in humans, measured directly. Nobody has measured cortisol after ipamorelin in a person, so the ranking mixes species.

Does GHRP-6 really make you hungry?

No human trial has tested it. The canonical study injected the peptide directly into rat brains, which established that the effect is centrally mediated and separable from GH release but says nothing about subcutaneous dosing in people. The only human appetite data in this class is GHRP-2's: seven of ten children over six months, with no significant BMI change.

Which one raises prolactin?

GHRP-2 does — prolactin was measured in humans alongside ACTH and cortisol. For GHRP-6 there is no primary human measurement at all: the overnight study measured GH, ACTH and cortisol but not prolactin, and the 1990 first-in-man study that did measure it reported specificity at the low doses used. Ipamorelin's prolactin was unchanged in swine only.

Is any of the three approved anywhere?

GHRP-2 only, in Japan, as pralmorelin hydrochloride marketed by Kaken Pharmaceutical for diagnosing growth hormone deficiency with a single injection. GHRP-6 is approved nowhere. Ipamorelin is approved nowhere, and FDA's advisory committee voted 0 in favour, 12 against, with 1 abstention in October 2024.

Which is easiest to confirm in a vial?

Ipamorelin. At 711.3857 monoisotopic it sits 106 to 175 daltons below GHRP-2, GHRP-6 and hexarelin, so even a low-resolution mass spectrometer separates it. GHRP-6 is the hardest: it is 14.0157 daltons from hexarelin, which no HPLC-UV certificate resolves, and hexarelin sells for more than twice as much per milligram.

Are they all banned in sport?

Yes. GHRP-2 is named at WADA S2.2.4 as "GHRP-2 (pralmorelin)", GHRP-6 is named at the same section under growth hormone-releasing peptides, and ipamorelin is named there under growth hormone secretagogues and their mimetics. All three are prohibited at all times and classified as non-specified. Urine detection methods for pralmorelin and its metabolites have been published.

Where the selectivity argument leaves the three

The selectivity ranking in this class is an artefact of who got measured. GHRP-2 and GHRP-6 were studied in people, and people showed cortisol rises. Ipamorelin was studied in pigs, and the pigs did not. That is not evidence that ipamorelin is cleaner in humans; it is evidence that nobody has looked. Thirty years of marketing has treated an unmeasured quantity as a demonstrated zero.

The appetite argument runs the same way and lands harder, because it is the reason most buyers choose GHRP-6 in the first place. Its canonical study is rats with a hole in the skull. The only human appetite data in the class belongs to a different compound, ran in ten children, and produced no significant BMI change over twelve months.

What is left, when the species are sorted out, is narrow and consistent. All three release growth hormone in humans. GHRP-2 has an approved label, a validated dose and a regulated adverse-reaction table for one injection. GHRP-6 has the best-documented cortisol effect and the least-examined signature property. Ipamorelin has the cleanest pharmacological story and the weakest clinical record, including a randomised trial that missed its endpoint and a 320-patient trial that never reported. None of the three has an adult efficacy trial, and all three are on the same regulatory list.

Browse the growth hormone peptides category, or our complete peptide guide with 118 compounds (verified August 2026). For per-injection volume, use the peptide dosing calculator or the CJC-1295 and ipamorelin calculator alongside the reconstitution calculator. Compare shops through independent lab tests and community-verified shop reviews.

This article is for educational and informational purposes only and does not constitute medical advice. Peptides discussed may be investigational compounds not approved by the FDA (or equivalent regulators in your jurisdiction) for human use. Always consult a qualified healthcare provider before using any peptide or research compound. Peptigrity is an independent review platform and does not sell, endorse, or recommend specific products or vendors.