The original synthetic ghrelin-receptor agonist (Bowers, Tulane, 1984) — the molecule that predicted the existence of ghrelin. Its real distinguishing feature among the older GHRPs is a strong central appetite signal, not exceptional cortisol or prolactin elevation.
GHRP-6 is the original synthetic growth-hormone-releasing peptide: His-D-Trp-Ala-Trp-D-Phe-Lys-NH2, six amino acids with a C-terminal amide and two D-amino-acid substitutions (D-Trp at position 2, D-Phe at position 5) that confer protease resistance. Founding paper: Bowers CY, Momany FA, Reynolds GA, Hong A. Endocrinology 1984;114(5):1537-45 (PMID 6714155).
It's the parent scaffold of the family. GHRP-2 (pralmorelin), hexarelin, GHRP-1, and structurally related ghrelin-receptor agonists are all derived from it. The ancestry traces further back to weak GH-releasing Met-enkephalin analogs from the same Bowers lab (Momany & Bowers 1981, PMID 6109621); the final hexapeptide isn't a structural enkephalin, but it descends from those scaffolds via iterative conformational-energy design.
The unusual fact about GHRP-6: it predicted the existence of the natural hormone. The ghrelin receptor (GHS-R1a) was cloned in 1996 (Howard et al., Science, PMID 8688086) specifically because GHRP-6 and the small-molecule MK-677 needed a receptor. The endogenous ligand ghrelin was then discovered three years later (Kojima et al., Nature 1999, PMID 10604470). Few small-molecule pharmacology stories run in this order.
GHRP-6 acts on the Growth Hormone Secretagogue Receptor 1a (GHS-R1a), a class-A G-protein-coupled receptor on anterior-pituitary somatotrophs and hypothalamic neurons (arcuate nucleus, ventromedial and paraventricular nuclei), with lower density on heart, vasculature, immune cells, pancreas, and gut. Signaling runs through Gαq/11 to phospholipase C, generating IP₃ and diacylglycerol, mobilizing intracellular Ca²⁺, and driving calcium-dependent GH exocytosis (Herrington & Hille 1994, PMID 8070352).
This pathway is mechanistically distinct from the GHRH-receptor signaling used by sermorelin, tesamorelin, and CJC-1295 (class-B GPCR, Gαs → cAMP → PKA). Because the two pathways converge on the somatotroph through different second messengers, GHRH + GHRP synergy is robust in human acute provocation studies (Popovic 1994 PMID 8045963; Cordido 1996 PMID 8772550). Pairing GHRP-6 with a GHRH analog produces a larger GH pulse than either alone.
The full GH-release effect involves three components: direct pituitary stimulation on somatotrophs, hypothalamic mediation (GHRP-6-induced GH release is completely blocked in patients with hypothalamic-pituitary disconnection — Popovic 1995 PMID 7883854), and functional release-from-somatostatin-brake inferred from the GHRH+GHRP synergy data.
GHRP-6 binds GHS-R1a in the hypothalamic arcuate nucleus and ventromedial hypothalamus — the same loci where endogenous ghrelin acts on NPY/AgRP feeding circuits. Intranasal GHRP-6 activates appetite-regulating neurons in the mouse hypothalamus and increases GH levels (Poelman 2025, PMID 39813130, the most recent verified primary paper). IP GHRP-6 enhanced high-fat-diet intake in ovariectomized rats, with the effect reversed by estradiol (Yokota-Nakagi 2020, PMID 32224927). Antagonist studies using [D-Lys³]-GHRP-6 consistently show that blocking GHS-R1a at hypothalamic sites reduces ghrelin-driven feeding — confirming the agonist circuit.
This appetite signal is the defensible distinguishing feature for GHRP-6 — real, central, dose-dependent, and peer-reviewed. It's not the "more cortisol than other GHRPs" framing some older content claims. See the comparison section.
Older content circulating online frames GHRP-6 as exceptionally cortisol- and prolactin-elevating compared to GHRP-2. The head-to-head literature doesn't support that.
Start with what the two relevant papers did and did not test, because this is where the claim breaks down.
Arvat et al. Peptides 1997 (PMID 9285939) dosed six young adults with GHRP-2 and hexarelin and compared them against GHRH, TRH and hCRH. GHRP-6 itself was never administered in this study. It describes GHRP-2 and hexarelin as "synthetic, non-natural super-analogs of GHRP-6" with a "slight stimulatory effect on PRL, ACTH and cortisol"; the two super-analogs behaved similarly to each other, and their ACTH/cortisol-releasing activity was comparable to hCRH. So this paper establishes that the class raises ACTH and cortisol. It cannot rank GHRP-6 against GHRP-2, because it never measured GHRP-6.
Raun et al. 1998 (PMID 9849822) — the ipamorelin paper — is the study that did include GHRP-6, in swine. Both GHRP-6 and GHRP-2 raised plasma ACTH and cortisol; ipamorelin did not, even at doses more than 200× the ED50 for GH release. Again the finding is GHRP-6 and GHRP-2 together on one side, ipamorelin on the other. Nothing in it puts GHRP-6 above GHRP-2.
Raun also supplies the potency numbers the vague rankings usually gloss over. In conscious swine: GHRP-6 ED50 3.9 nmol/kg with Emax 74 ng/mL, GHRP-2 ED50 0.6 nmol/kg with Emax 56 ng/mL. GHRP-2 is roughly six times more potent per mole, while GHRP-6 reached the higher peak GH. Ipamorelin matched GHRP-6 closely on both. Cheng 1997 (PMID 9096259) separately confirmed GHRP-2 acts through the same receptor and mechanism as GHRP-6.
The bottom line: no published head-to-head study ranks GHRP-6 above GHRP-2 on cortisol or prolactin. The well-supported contrast is ipamorelin versus the rest.
| Peptide | GH Release | Cortisol / Prolactin / ACTH | Hunger |
|---|---|---|---|
| Ipamorelin | Comparable to GHRP-6 (Raun, swine) | No rise vs GHRH control, even at 200× the GH dose | Minimal |
| GHRP-6 (parent) | Lower potency, highest peak GH of the three in swine | Yes — measured, magnitude not distinguished from GHRP-2 | Highest of the older GHRPs |
| GHRP-2 (super-analog) | ~6× more potent per mole, lower peak | Yes — measured alongside GHRP-6, no head-to-head ranking exists | Moderate |
| Hexarelin (super-analog) | Similar to GHRP-2 in man (Arvat) | Similar to GHRP-2 | Moderate |
What the literature does support as GHRP-6 distinctions: strongest appetite signal among the older GHRPs (PMIDs 39813130, 32224927; antagonist literature confirms the circuit), lower GH potency per mole than GHRP-2 (though not a lower ceiling), the CD36 cytoprotective profile the other GHRPs do not share to the same degree, and historical primacy as the parent of the family.
If appetite is a feature (cachexia recovery, recovering from illness, hard-gainers struggling to eat enough) → GHRP-6. If you want a clean GH pulse without HPA-axis activation → Ipamorelin. If you want maximum GH potency → GHRP-2 or Hexarelin. For GHRH synergy → pair any of the GHRPs with Sermorelin, CJC-1295, or Tesamorelin.
Build your protocol, log every dose, monitor your body's response, and get reminders so you never miss a dose.
Start Tracking FreeGHRP-6 has one published human pharmacokinetic study, and it is worth knowing in detail because it is the firmest human number attached to this compound.
Cabrales and colleagues (Eur J Pharm Sci 2013, PMID 23099431) gave nine healthy men a single intravenous bolus at 100, 200 or 400 mcg/kg and quantified plasma GHRP-6 by a validated LC-MS method. Disposition fitted a two-compartment model with R² above 0.99. Averaged across doses:
| Distribution half-life | 7.6 ± 1.9 minutes |
| Elimination half-life | 2.5 ± 1.1 hours |
| Dose proportionality | AUC trended proportional with dose |
| Subjects | 9 healthy men, single IV bolus |
A distribution half-life of about eight minutes is why the GH pulse is sharp and short rather than sustained, and it is the pharmacological argument for multiple daily injections rather than one. The authors also reported unexplained concentration spikes during the elimination phase in four of the nine subjects.
Two limits to keep in view. This was a single intravenous dose, not repeated subcutaneous dosing, and the doses were 30 to 100 times higher per kilogram than practice doses. It establishes that the molecule has been given to humans and characterised — it does not validate any protocol.
Claims that GHRP-6 has cleared a formal dose-escalation safety trial with no adverse events are widely repeated, but they trace back to review articles rather than to a published primary trial. The Cabrales pharmacokinetic study is the primary human paper.
This is the part of GHRP-6 pharmacology that has nothing to do with growth hormone, and it is genuinely unusual within the class.
GHRP-6 binds a second receptor, CD36, a scavenger receptor found on cardiomyocytes, immune cells, vasculature and wound granulation tissue. Through CD36 it activates PI-3K/AKT1 prosurvival signalling, reduces reactive oxygen species and supports antioxidant defences (review: Berlanga-Acosta 2017, PMID 28469491).
The cardiac evidence. In the most-cited experiment, female Cuban Creole pigs underwent one hour of complete left circumflex occlusion followed by 72 hours of reperfusion, randomised to GHRP-6 at 400 mcg/kg or saline (Berlanga 2007, PMID 16989643). Infarct mass fell by 78% and infarct thickness by 50% versus saline (p < 0.01), more than half the treated pigs showed no pathological Q waves in any ECG lead, and CK-MB and CRP confirmed reduced necrosis. Oxidative-stress markers indicated the mechanism was ROS reduction and preservation of antioxidant defences rather than IGF-I induction — myocardial IGF-I transcription was not amplified beyond what the ischaemic episode alone caused.
The review literature reports that this protection is absent in CD36-null mice and persists in hypophysectomised animals, which is the argument that the effect runs through CD36 directly rather than through growth hormone at all.
The wound evidence. Mendoza Marí 2016 (PMID 27200188) found GHRP-6 accelerated wound closure with differences visible in the first 24 hours, reduced mononuclear inflammatory infiltration, and in a hypertrophic scar model reduced exuberant scarring via PPARγ activation. It did not affect scars that had already formed.
Read this section with the ceiling clearly marked. Every result above is from animals — pigs, rats, mice. No human trial has tested GHRP-6 for cardioprotection, wound healing or organ protection, and the doses used are around 400 mcg/kg, roughly a hundred times the per-kilogram dose anyone injects subcutaneously. None of this is a reason to expect a cardiac or healing benefit from a 100 mcg shot. It is an interesting and well-documented pharmacological property of the molecule, and that is the whole claim.
Pre-filled with a typical GHRP-6 setup. Edit any field — the draw updates live.
Insulin syringe — 100 units = 1 mL
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Not medical advice. These figures describe what is reported in the literature and what practitioners and communities do — not a recommendation, and for most compounds here no human dose-finding study exists. Talk to a qualified healthcare provider.
Human GHRP-6 dosing exists, and it looks nothing like how the compound is used. The only published human pharmacokinetic study gave a single intravenous bolus of 100, 200 or 400 mcg/kg to nine healthy men (Cabrales 2013, PMID 23099431). For an 80 kg adult that is 8–32 mg in one shot — roughly 30 to 100 times the 100–300 mcg subcutaneous dose used in practice, by a different route.
The cardioprotection work sits at the same order of magnitude: the pig infarct study used 400 mcg/kg (PMID 16989643). Nothing in the literature tested a small repeated subcutaneous bolus over weeks, which is the only way anyone actually uses this peptide.
No dose-finding study exists for the protocols below. They are practice patterns and community convention carried over from broader GHRP-class use, not trial-derived regimens.
| Dose | 100–300 mcg per injection |
| Frequency | 2–3 times daily, fasted |
| Timing | Morning, pre-workout and/or ~30 min before sleep |
| Route | Subcutaneous (intranasal is documented to work — Frieboes 1999, PMID 10336729; oral bioavailability is poor) |
| Cycle length | 8–16 weeks, then 4 weeks off |
The most common protocol, and the one with the clearest mechanistic rationale — two receptors, two second messengers, one axis.
| GHRP-6 | 100–200 mcg per injection |
| CJC-1295 without DAC | 100–200 mcg per injection |
| Frequency | 2–3 times daily, fasted |
| Cycle length | 8–12 weeks |
The synergy itself is real and measured in humans as an acute GH response (PMIDs 8045963, 8772550). The combination protocol above has never been tested.
| Body weight | Dose per injection |
|---|---|
| Under 150 lb | 100–150 mcg |
| 150–200 lb | 150–200 mcg |
| Over 200 lb | 200–300 mcg |
This is convention, not pharmacology — the one human study that did dose by body weight used a range 30–100× higher.
The desensitisation evidence is borrowed from hexarelin, not GHRP-6 itself. Rahim and Shalet (PMID 10990150) gave twice-daily subcutaneous hexarelin to 12 healthy elderly subjects for 16 weeks. GH area-under-curve fell from 19.1 at baseline to 13.1 at week 1, 12.3 at week 4 and 10.5 at week 16 (p = 0.0003 across the study) — about a 45% loss, most of it inside the first week. Four weeks after stopping it returned to 19.4, statistically indistinguishable from baseline. The attenuation is partial and fully reversible. That is the basis for the 4-week break, and it is an inference across compounds.
This matters more than most people appreciate. Free fatty acids blunt the GHRP GH response: Peino 1996 (PMID 8772549) showed that suppressing FFAs with acipimox potentiates the GHRP-6 GH response, and Cordido 1996 (PMID 8772550) showed FFA suppression rescues the blunted response in obese subjects. Eating before an injection — fat especially — measurably reduces the on-target effect.
Not medical advice. These figures describe what is reported in the literature and what practitioners and communities do — not a recommendation, and for most compounds here no human dose-finding study exists. Talk to a qualified healthcare provider.
For a 5 mg vial in 2 mL bacteriostatic water: 2.5 mg/mL, so 1 unit on a U-100 insulin syringe = 25 mcg. A 100 mcg dose is 4 units, 200 mcg is 8 units, 300 mcg is 12 units.
Lyophilized vials are stable at room temperature short-term; refrigerate for longer. Reconstituted vials should be refrigerated and used within 28 days. Note that GHRP-6's histidine and tryptophan residues are oxidation-sensitive (Cheng 1995, PMID 8633765) — protect from light and avoid temperature extremes.
For the full reconstitution protocol, see the Bacteriostatic Water guide.
Common acute effects, all anchored in the literature:
Less-cited reports from community use (lower PubMed anchor): water retention and mild fluid shifts, injection-site irritation, tingling or numbness in hands, drowsiness with evening dosing, joint stiffness with chronic use, occasional first-week headache.
The "intense hunger" framing is well-supported. The "high cortisol vs other GHRPs" framing in older content is not (PMID 9285939 — these effects exist for GHRP-6 but match magnitudes of GHRP-2 and hexarelin). No Western pharmacovigilance database entries because the molecule has never been approved.
Ghrelin (the natural hormone). Endogenous 28-residue acylated peptide secreted by gastric P/D1 cells. Same receptor as GHRP-6, structurally unrelated, requires octanoylation at Ser3 for binding. GHRP-6 is the synthetic small-peptide mimetic that predicted ghrelin's existence.
MK-677 (ibutamoren). Non-peptide, orally active GHS-R1a agonist (Patchett 1995, PMID 7624358). Same receptor as GHRP-6 but small-molecule, oral, ~24-hour half-life.
Hexarelin (examorelin). The position-2 D-Trp-methylated GHRP-6 cousin. Higher GH-releasing potency.
Ipamorelin. Pentapeptide (Aib-His-D-2-Nal-D-Phe-Lys-NH2). Different scaffold, designed for GHS-R1a selectivity without HPA-axis activation. The cleanest comparator for what GHRP-6 isn't.
GHRP-2 (pralmorelin / KP-102). N-terminus-modified GHRP-6 derivative with higher GH potency. Reached pharma development in Japan as a GH-deficiency diagnostic.
[D-Lys³]-GHRP-6 (the antagonist). Same parent peptide with position-3 Ala swapped for D-Lys, converting the agonist into a competitive GHS-R1a antagonist. Used as a research tool, never therapeutically. If a vendor lists "D-Lys3-GHRP-6" as a product, that's a different molecule with the opposite effect.
GHRP-6 is a research peptide not approved by the FDA for human use. It is sold only as a research chemical, and StackTrax does not endorse or facilitate personal use.
Quality varies enormously among research-chemical suppliers. At minimum, look for:
Lyvn does not carry GHRP-6. They are the vendor we recommend elsewhere on this site, and they publish the full independent panel per batch — which makes their catalogue a useful yardstick for the criteria above even on a compound they do not stock. We are not recommending a specific supplier for GHRP-6 itself, because we have no basis to.
For research use only. Not for human consumption. 21+.
Build your protocol, log every dose, monitor your body's response, and get reminders so you never miss a dose.
Start Tracking FreeNo. GHRP-6 has never been FDA, EMA, or any other regulatory authority approved. It has been studied in academic research (Frieboes, Popovic, Cordido groups in the 1990s) but no commercial development program advanced it. Sold in the US only as a research chemical.
Community-practice dosing is 100–300 mcg subcutaneously 2–3 times daily, often in 8–16 week cycles. This is community/vendor protocol — there is no Tier-2 chronic-dose RCT in adults supporting it. The cited "~30 minute half-life" is GHRP-class extrapolation (from hexarelin IV PK), not a GHRP-6-specific human PK study.
A typical reconstitution is 5 mg of GHRP-6 + 2 mL of bacteriostatic water, yielding 2.5 mg/mL. A 100 mcg dose draws to 0.04 mL (4 units on a 100-unit insulin syringe), 200 mcg = 0.08 mL (8 units), 300 mcg = 0.12 mL (12 units).
GHRP-6 is a potent ghrelin-receptor (GHSR-1a) agonist. Ghrelin is the body’s hunger hormone — activating its receptor produces the same orexigenic signal. The hunger effect is dose-proportional and is the most distinctive subjective effect of GHRP-6, sometimes used clinically as evidence the molecule is bioactive in the dose taken. For users wanting GH effects without the hunger, ipamorelin (selective for GH, no ghrelin-receptor hunger response) is the alternative.
All three are GHSR-1a agonists. GHRP-6 produces strong hunger and a notable cortisol/prolactin spike. GHRP-2 produces less hunger but still elevates cortisol/prolactin. Ipamorelin is selective for GH release with no cortisol/prolactin response — generally the preferred choice for chronic GH-axis support. GHRP-6 sees use mostly when appetite stimulation is wanted (cachexia, very lean cutting phases) or for short, intense GH-mobilization periods.
Yes. GHRP-6 is prohibited at all times under WADA S2.2 (Growth Hormone Secretagogues). No therapeutic-use exemption is available.
Disclaimer: This guide is for educational and informational purposes only and is not intended as medical advice, diagnosis, or treatment. The compounds discussed are not FDA approved for human use. Always consult a qualified healthcare provider before starting any new supplement or peptide protocol. StackTrax does not sell peptides or supplements directly — purchase links go to third-party vendors. StackTrax is not responsible for the products, quality, or business practices of any third-party vendor.
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StackTrax guides cover peptides and compounds that are not FDA-approved for the uses discussed. The dosing, reconstitution, and safety information is compiled from published research and community protocols for educational purposes only.
Before using any compound mentioned here, consult a qualified healthcare provider. StackTrax does not sell, prescribe, or recommend these substances for personal use.