The short version

Plain English first. Everything below this section is the same material with the sources, the numbers and the caveats attached.

What GHRP-6 is

The original growth-hormone-releasing peptide, and the reference compound of the class. A synthetic hexapeptide, C-terminally amidated. We do not sell it; this is a reference entry.

How it relates to the other two

GHRP-2 and Hexarelin are both derived from this molecule. Hexarelin is GHRP-6 with a single methyl group added to the D-tryptophan; GHRP-2 replaces the opening pair entirely and, uniquely among the three, has no histidine at all. One 1997 paper calls the other two “synthetic, non-natural super-analogs of GHRP-6.”

1 mg of GHRP-6 contains 1.61% more molecules than 1 mg of hexarelin and 6.73% fewer than 1 mg of GHRP-2. House arithmetic. Small differences — they matter only because microgram doses get copied across the three as though the compounds were interchangeable.

What the salt costs, and why it costs more than it does on GHRP-2

GHRP-6 has three basic sites, not two: the N-terminal amine, the lysine side chain, and — unlike GHRP-2 — the histidine imidazole. So a third counterion is chemically available, and the plausible spread is wider. House arithmetic:

A vial labelled “10 mg” holds 7.19 to 10.00 mg of GHRP-6 on salt form alone — a 28.2% spread, against 21.8% for GHRP-2, which cannot take a third counterion. That is before purity, residual water or fill accuracy. Imidazole is weakly basic and will not always be protonated, so the three-counterion case is the outside one rather than the likely one — but it is chemically available here and it is not available on GHRP-2.

Where it actually acts

This is the cleanest mechanistic human study in the whole class, and it explains why the compound is unpredictable.

GHRP-6 is a ghrelin receptor agonist — GHS-R1a — not a GHRH analogue. The receptor, the appetite consequence, the cortisol and prolactin consequence, and the reason regulators keep the two classes apart are all set out on the GHRP-2 page and apply here unchanged. What follows is specific to GHRP-6.

What that establishes is unusually clean. GHRP-6's effect on growth hormone requires an intact hypothalamic connection. The pituitary on its own barely responds. This is not a drug that acts on the pituitary and happens to involve the hypothalamus — the hypothalamus is where the work is done.

The five human studies

That is the whole adult and paediatric evidence base we could find. Every one is small, every one is acute or short, and every one measures hormones.

1. The dose-response study, and the one genuinely good news in it

Eighteen normal men, single intravenous bolus, three doses. Peak growth hormone:

House arithmetic: peak GH at the top dose is 57 times placebo, and the curve is supra-proportional — a 3.3× step from 0.3 to 1.0 µg/kg produced a 4.2× rise.

Two limits. It is a single bolus in eighteen men and says nothing about repeated dosing. And it is not the missing source for the “GHRP-6 raises cortisol least” ranking that circulates — it is a comparison of doses within one compound, not a comparison between compounds. That study still does not exist as far as we can find.

2. The hypothalamic-disconnection study

Set out above. Twelve patients, the mechanistic backbone of the page.

3. Oral GHRP-6, in children

Thirteen prepubertal children of normal short stature — not growth hormone deficient — given 300 µg/kg orally. Peak GH 18.8 µg/L, against 20.8 for intravenous GHRH. The authors' conclusion: “oral administration of GHRP-6 is able to increase GH secretion.”

House arithmetic, and it is the honest way to say “orally active”: that is 300 µg/kg by mouth against 1 µg/kg intravenously for a comparable growth hormone peak — a 300-fold ratio. Single dose, thirteen children, hormonal endpoint only. No growth outcome was measured and none should be implied.

4. Thirty-four hours of continuous infusion — the longest exposure that exists

Nine healthy young men, a loading bolus then 1 µg/kg/h for 34 hours.

On desensitisation: this is the closest thing to a GHRP-6 repeat-dosing study and its answer is negative — no attenuation over 34 hours of infusion. That is a narrow answer. It is not 16 weeks, not subcutaneous, and not repeated bolus dosing. The correct statement is that GHRP-6 has no published repeat-dosing desensitisation study at all. An earlier 1991 paper reportedly found partial attenuation on shorter infusion; we could not open it and will not characterise it.

5. The only study with a non-hormonal endpoint — and it cuts both ways

A placebo-controlled within-subject crossover, four intravenous boluses of 50 µg each across the evening, with sleep EEG and overnight hormones.

What has never been measured

Across all five: no body composition, no lean mass, no strength, no fat mass, no recovery, no injury healing, no appetite, and no clinical event of any kind. The endpoints are growth hormone, ACTH, cortisol, prolactin, TSH, IGF-1 and one sleep EEG.

A footnote that is not nothing: there was a real development programme

GHRP-6 is unusual among research peptides in having had state biotech development — a Cuban institute files it as CIGB-500. A published phase I ran 18 healthy men, three per level, at intravenous doses escalating “1-10-50-100-200-400 µg/kg”. It reported 23 adverse events across 12 of the 18 participants, with no serious adverse events, and concluded the compound was “safe and tolerable under the conditions studied.”

House arithmetic: that top dose of 400 µg/kg is 400 times the top dose in the dose-response study above, and at 80 kg it is 32 mg — more than three 10 mg vials in a single intravenous dose. And 67% of participants had at least one adverse event, 1.28 events each. That is a normal phase I profile, and it is also the real number: it is not “no side effects.” The abstract does not enumerate the event types and we did not obtain the full text. There is also one registered trial in acute myocardial infarction patients — safety-led, with ventricular function secondary. The registry would not render its size, status or sponsor to us and we found no published results, so nothing about its outcome should be asserted.

The cardioprotection claim, with the boundary drawn hard

There is a real preclinical literature here. There is no human efficacy result. Those two sentences have to stay in the same paragraph.

All three reached us through review articles written by the same group that produced the primary work. We could not open any of the three primary papers. The “over 70% of the area at risk” figure is the most quotable number in this story and the one we are least able to stand behind — we have not seen the design, the sample size, the blinding, or the infarct-sizing method. It appears here with the species attached and that admission attached, or it should not appear at all.

CD36, the second receptor

The reviews attribute a second target: CD36, a scavenger receptor, with activation in perfused hearts increasing coronary perfusion pressure dose-dependently, and the response absent in “CD36-null mice and hearts from spontaneous hypertensive rats genetically deficient in CD36.” Three things a page has to get right about it:

• The demonstrated experiments used hexarelin, not GHRP-6. The reviews describe CD36 activation “by hexarelin” in perfused hearts. The GHRP-6 attribution is a class statement, not a compound-specific demonstration. We could not open either primary paper, so we cannot close the gap between “GHRP-6 has a second receptor” and “a related peptide does.”
• CD36 is not a growth-hormone receptor. Its ordinary jobs are fatty-acid uptake and oxidised-LDL scavenging in macrophages, endothelium and heart. A ligand binding it is acting outside the growth hormone axis entirely.
• A second receptor is not automatically a second benefit. This is a receptor central to lipid handling and inflammation, engaged at doses and in tissues no human study has characterised. It is the most interesting unexplored thing about this class and equally the most plausible route to an unpredicted effect. “It also works through CD36” asserts the upside of an uncharacterised off-axis interaction, which is the opposite of a safety argument.

The hunger question, and a clean negative

GHRP-6's reputation is that it is the hunger peptide. We went looking for the number behind that and it is not there.

The honest statement: the appetite effect is real in animals, it is the compound's best-known property, and as far as we can find it has never been quantified in a human being in the published literature.

Which makes an interesting comparison with GHRP-2, where it has been measured — seven out of seven men ate about 36% more at a buffet meal, and hunger is a labelled adverse reaction of the licensed Japanese product. So the class effect is documented. It is documented for the other compound.

And a vendor claim worth answering directly: “the hunger spike is how you know it's working.” Whatever is felt is not a documented pharmacological quantity for this compound and is certainly not a potency assay.

The class problems

Everything in this section applies to GHRP-2 and Hexarelin too, and is set out at length on the GHRP-2 page. The short version:

• Cortisol and prolactin. All three compounds raise both. The ordering everyone repeats — hexarelin > GHRP-6 > GHRP-2 — could not be sourced to any head-to-head human comparison; the searches returned vendor blogs exclusively. What GHRP-6 does have is the dose separation above, which is a within-compound finding and a genuinely good one. And its own sleep study more than doubled overnight cortisol at 200 µg.
• Glucose. The best-corroborated metabolic concern in the class, and FDA names it in the GHRP-6 listing specifically. We could not open a GHRP-6-specific human glucose study — the most conspicuous remaining hole on this page, precisely because the regulator cites it by name.
• Desensitisation. No repeat-dosing study for GHRP-6 exists. GHRP-2 lost 46.7% of its GH response in five days; hexarelin lost 45.0% over sixteen weeks and recovered fully four weeks after stopping.
• IGF-1 as a surrogate. Flat on every subcutaneous or repeated-bolus regimen ever tested. It moved on the 34-hour infusion above. And a raised IGF-1 would not have proved benefit anyway — it is a surrogate, and nothing ties an adult IGF-1 number to lean mass, strength or any clinical event.

One thing we could not find a half-life for

A single pharmacokinetic study of GHRP-6 in nine healthy volunteers exists. We could not open it — three separate routes refused. So no half-life for GHRP-6 appears on this page. The figures circulating on vendor sites are unsourced, and the published pharmacokinetics on the GHRP-2 page belong to pralmorelin and do not transfer.

The one shape we can source, from the phase I abstract, is a “bi-phasic concentration profile … with a rapid distribution phase and a second phase that is slower.” That is a shape, not a number, and we are not going to turn it into one.

Reconstitution

A microgram-scale compound in a milligram-scale vial, and the arithmetic runs against the intuition.

House arithmetic. 10 mg vial, U-100 syringe, 1 unit = 0.01 mL.

A 100 µg dose from this vial in 1 mL is one single unit on the syringe, where no meaningful precision is available. The fix is more diluent, not less.

What the published doses actually were

Every human dose above is per kilogram, and every one was given intravenously in a clinical setting. At 80 kg, for scale only — these are study doses, not a protocol:

Two of those land on a fraction of a unit a U-100 barrel cannot resolve. That is arithmetic, not opinion — and it is why the published doses and the circulating protocols do not describe the same thing.

What the 28-day clock costs

House arithmetic. Under our 28-day in-use convention, a 10 mg vial used at 100 µg/day delivers 2.8 mg and discards 7.2 mg — 72% of the vial. For a microgram-scale compound in a milligram-scale vial, the calendar rather than the protocol decides how much is ever used.

Storage

Lyophilised: cool, sealed, dark, desiccated. Reconstituted: 2–8 °C, in the dark, under our 28-day convention — which we publish as “a handling convention that has become repeated as though it were data.”

We found no published stability study of reconstituted GHRP-6 in any diluent at any temperature. The nearest regulator-approved handling statement in this class belongs to the licensed pralmorelin product, which grants no in-use period at all — but that is a different molecule in a different formulation by a different route, and it neither supports nor contradicts our 28 days. See the GHRP-2 page for why.

Regulatory status

GHRP-6 is on FDA's Category 2 list — the actual do-not-compound list — and what it says there is unusually worth reading.

Category 2 is FDA's own assessment. It is a different table from the “nominated but withdrawn” list where most of this catalogue sits — that one records only that the person who filed the nomination withdrew it, which says nothing about the substance. The two get confused constantly; the GHRP-2 page sets the distinction out as a table.

Four things specific to this listing

• 503B only, not 503A. “Banned from compounding” without that qualifier overstates it.
• Not route-scoped the way GHRP-2's is. GHRP-2's entry names “injectable and nasal routes” in the substance name itself. GHRP-6's substance name carries no route qualifier at all, while its risk text says “for certain routes of administration” without naming them. The asymmetry is in the source. Whether it is deliberate is not stated anywhere we found.
• The stated reasons are different from GHRP-2's, and this is the interesting part. GHRP-2's entry cites reported serious adverse events. GHRP-6's cites no adverse events at all — only “limited safety-related information” plus cortisol and blood glucose. Those two map exactly onto what the published human pharmacology shows. A regulator's stated concern and the literature agreeing with each other is rare, and it is worth saying plainly rather than treating the listing as bureaucratic.
• Not a Canadian legal statement. FDA's compounding lists govern US compounding pharmacies.

Canada, and sport

GHRP-6 is named on Health Canada's 1 August 2025 seizure advisory, along with GHRP-2 and hexarelin. It is not named on the 9 April 2026 research-use-only advisory — we checked both directly rather than assuming either. It is named on the College of Physicians & Surgeons of Alberta notice of the same date, which matters because that is our own province.

The general rule reaches it regardless of naming: “In Canada, peptides are generally regulated as prescription drugs,” and research-use-only labelling “does not make these products legal or exempt from regulatory requirements.”

In sport, GHRP-6 is prohibited at all times, in and out of competition, listed by name in the growth-hormone-releasing peptides group alongside GHRP-2 and examorelin. Everything in that class is a non-Specified substance, which attracts the standard sanction.

Sentient Biogenix does not sell GHRP-6.

Questions we actually get

Is GHRP-6 the original one?

Yes. GHRP-2 and hexarelin are both derived from it — hexarelin is this molecule plus a single methyl group. The better vendor pages get this right, and get right that it is not a GHRH analogue. It is where they go next that we disagree with.

Does it work?

It releases growth hormone, clearly and dose-dependently — 57 times placebo at the top of the tested range. Whether anything happens to the person is a different question, and nothing in the published human record answers it: no study measured body composition, strength, recovery or any clinical outcome.

Will it make me hungry?

Probably — but we are not going to pretend that is documented. No human study of GHRP-6 has ever measured appetite. It is the compound's best-known property and the number does not exist. For what it is worth, it has been measured for GHRP-2: about 36% more food at a buffet, in seven out of seven men.

Is it good for sleep?

The only sleep study we could find says the opposite of the marketing. It added about 25 minutes of light sleep and left deep sleep completely unchanged — while more than doubling overnight cortisol.

What's its half-life?

We do not know, and we are not going to print one. A single pharmacokinetic study exists and we could not open it, three ways. Anything you see quoted is unsourced.

Doesn't it protect the heart?

In pigs, rats and hamsters, as reported by review articles written by the group that did the work. There is no human cardiac efficacy result for GHRP-6. Hexarelin — a different molecule — does have human cardiac data, and merging the two is the commonest error made about this class.

Is it on FDA's do-not-compound list?

Yes, Category 2, added 29 September 2023, under the 503B pathway. And what FDA says there is cortisol and blood glucose — which is what the published pharmacology says too.

Why does searching for it in drug databases turn up nothing?

Because it is registered as “Hexapeptide-2,” a cosmetic-ingredient name. Search that instead.

References

1. Bowers CY, et al. Growth hormone (GH)-releasing peptide stimulates GH release in normal men and acts synergistically with GH-releasing hormone. Journal of Clinical Endocrinology and Metabolism 1990;70(4):975 — the dose-response study and the tenfold dose separation.
2. Popovic V, Damjanovic S, Micic D, et al. Blocked growth hormone-releasing peptide (GHRP-6)-induced GH secretion and absence of the synergic action of GHRP-6 plus GH-releasing hormone in patients with hypothalamopituitary disconnection. Journal of Clinical Endocrinology and Metabolism 1995;80(3):942–947. DOI 10.1210/jcem.80.3.7883854 — the 6.8% finding.
3. Bellone J, Ghizzoni L, Aimaretti G, et al. Growth hormone-releasing effect of oral growth hormone -releasing peptide 6 (GHRP-6) administration in children with short stature. European Journal of Endocrinology 1995;133(4):425–429 — the 300 µg/kg oral dose.
4. Jaffe CA, Ho PJ, Demott-Friberg R, Bowers CY, Barkan AL. Effects of a prolonged growth hormone (GH)-releasing peptide infusion on pulsatile GH secretion in normal men. Journal of Clinical Endocrinology and Metabolism 1993;77(6):1641–1647. DOI 10.1210/jcem.77.6.7903313 — 34 hours, no desensitisation, and the one regimen in which IGF-1 rose.
5. Frieboes R-M, et al. Growth hormone-releasing peptide-6 stimulates sleep, growth hormone, ACTH and cortisol release in normal man. Neuroendocrinology 1995;61(5):584–589. DOI 10.1159/000126883 — the sleep study.
6. US Food and Drug Administration. Certain bulk drug substances for use in compounding that may present significant safety risks — content current 22 April 2026. fda.gov — the Category 2 entry, read directly and verified word-for-word on a second read.
7. Selman-Housein-Bernal KH, Hernández-Bernal F, Abreu-Cruz AA, et al. Clinical safety of growth hormone-releasing peptide 6 (GHRP-6) in healthy volunteers. Investigaciones Medicoquirúrgicas 2014;6(1):81–91 — the phase I, and the 23-events-in-12-of-18 figure. Abstract only.
8. Registro Público Cubano de Ensayos Clínicos, RPCEC00000177 — CIGB-500 in acute myocardial infarction (AMIGOS study). Outcome measures read; the registry would not render phase, size, status or sponsor, and no results were found.
9. Berlanga-Acosta J, et al. Growth hormone releasing peptide-6 (GHRP-6) and other related secretagogue synthetic peptides. Integrative Molecular Medicine 2016;3(2):616–623; and Synthetic growth hormone-releasing peptides (GHRPs): a historical appraisal. Clinical Medicine Insights: Cardiology 2017. DOI 10.1177/1179546817694558 — the carriers of the preclinical cardiac results. Both are reviews by the group that produced the primary work, and we could not open any of the primary papers.
10. Health Canada. Unauthorized injectable peptide drugs seized and sold by Canada Peptide, 1 August 2025 — GHRP-6 named. And: Think twice before injecting peptides bought online, 9 April 2026 — not named, checked by direct read. College of Physicians & Surgeons of Alberta, 9 April 2026 — named.
11. The 2026 Prohibited List, World Anti-Doping Code, growth hormone releasing factors subsection — read through a national anti-doping organisation's verbatim reproduction.

What we could not check, listed rather than hidden. The single pharmacokinetic study of GHRP-6 would not open by any of three routes, so this page prints no half-life. We could not open any of the three primary preclinical cardiac papers, nor either of the two primary CD36 papers — which is why we cannot say whether CD36 binds GHRP-6 or only hexarelin. We could not open a 1991 infusion study that reportedly found the partial desensitisation the 34-hour study contradicts, a 1998 paper on GHRP-6's dependence on endogenous GHRH, or the phase I full text. The AMIGOS registry page would not render its header fields. And we could not open a GHRP-6-specific human glucose study — the most conspicuous hole on this page, because it is the concern FDA names by name. Three named searches for a human appetite measurement returned vendor pages, rodents and one study in goldfish.