GHRP-6

GHRP-6 was the first synthetic GHS to demonstrate that a receptor other than the GHRH receptor governed GH release, and its discovery led directly to the identification of ghrelin as the endogenous ligand. It stimulates somatotroph GH release and suppresses somatostatin, but it is the least selective of the common GHRPs at the appetite level: it strongly drives arcuate NPY and AgRP neurons, producing hunger that many users describe as overwhelming within 20 minutes of injection. It also has documented cytoprotective effects on gastric mucosa and, in Cuban research, on cardiac and hepatic tissue in injury models. Cortisol and prolactin elevation occur but are generally modest at 100 mcg doses.

Targets: GHS-R1a (ghrelin receptor), Arcuate NPY/AgRP neurons, Pituitary somatotrophs, Gastric mucosa

• · 100 mcg is the saturation dose for GH. Higher doses mainly add hunger and cortisol.
• · Used specifically by people struggling to eat enough. The hunger is the feature here, not the side effect.
• · Standard synergy, with the same hunger caveat.

Work out your exact syringe units →

• very commonIntense hunger— The defining effect. Onset within 20 minutes, lasts about an hour.
• commonWater retention
• commonElevated cortisol and prolactin— Modest at 100 mcg, clearer at higher doses.
• commonHead rush, flushing and tingling
• commonWeight gain from increased food intake— Entirely predictable and the main reason it is unsuitable during a deficit.
• uncommonDrowsiness after injection
• uncommonReduced insulin sensitivity

• Active malignancy.
• Poorly controlled diabetes.
• Any eating disorder involving binge behaviour - the hunger effect is severe and non-negotiable.
• Pregnancy and breastfeeding.

• synergycjc-1295-no-dac — Classic GHRH plus GHRP pairing.
• conflictsemaglutide — Directly opposing appetite signals; running both is self-defeating.
• redundantipamorelin — Same receptor; ipamorelin is the choice if you do not want the hunger.
• redundantmk-677 — Same receptor and the same appetite problem, only MK-677's version lasts all day.

• · IGF-1 at baseline and 8 to 12 weeks.
• · Prolactin and cortisol if dosing above 300 mcg per day.
• · Fasting glucose and bodyweight trend, given the food-intake effect.

Not approved for human use in the US or EU; sold as a research chemical. Prohibited in sport under WADA S2.

• Bowers et al., original characterisation of GHRP-6 as a growth hormone-releasing peptide (preclinical)
• Kojima et al. 1999 Nature, ghrelin identified as the endogenous ligand for the GHRP receptor (preclinical)

GHRP-6 matters historically far more than it matters practically. It was the compound that proved a receptor other than the GHRH receptor governed GH release, and hunting for its endogenous ligand is what led Kojima and Kangawa to ghrelin in 1999 - a Nature paper that reframed the whole field. Pharmacologically it is the least modified member of the family and therefore the shortest-acting and least selective. The defining feature is the appetite response, and the mechanism is worth understanding because it is not a side effect of GH release. GHS-R1a is densely expressed on arcuate NPY/AgRP neurons, which are the primary orexigenic population in the hypothalamus; activating them drives food intake directly and simultaneously inhibits the anorexigenic POMC neurons through GABAergic projections. GHRP-6 engages this circuit strongly - more strongly relative to its GH effect than any other compound in the class - which is why the hunger arrives within twenty minutes and feels categorically different from ordinary appetite. It is also why GHRP-6 is genuinely useful for a specific person: someone who cannot eat enough, whether because of illness, a hard bulk, or appetite suppression from another drug. The gastric cytoprotection literature is a separate strand, mostly Cuban work on gastric mucosa and on cardiac and hepatic injury models, and it is almost entirely rodent. The GHRP-6 that gets sold as a healing peptide is trading on that literature at several removes.

People buy it for GH and get an eating disorder-adjacent experience instead. The hunger is not ordinary appetite - it is fast, physical and hard to reason with, and it arrives on a timescale that makes it feel involuntary. Anyone with a history of binge eating should not go near this compound, and that is not a disclaimer, it is the single most predictable harm it causes. The second failure is bedtime dosing, which is the default for GH secretagogues and which here means lying awake wanting to eat. The third is running it during a cut because a forum post said the hunger was manageable; it usually is not, and the caloric surplus it produces will outrun any GH-mediated fat oxidation by a wide margin. Fourth, the tissue-protection marketing: gastric, cardiac and hepatic cytoprotection are rodent findings, and there is no human evidence that injecting GHRP-6 heals anything.

1. 100 mcgWeek 1 — 100 mcg once daily, and deliberately at a time when eating is convenient rather than at bedtime. The point of week one is finding out how the hunger lands on you - some people find it manageable, some find it genuinely disruptive.
2. 100 mcgWeeks 2 to 8 — Add pulses to a maximum of three daily, each 100 mcg and each fasted. If the goal is eating more, dose 20 minutes before meals; if the goal is GH, dose fasted and at bedtime and accept that you will be hungry at bedtime.
3. 300 mcgNot recommended — Single doses above 200 mcg add hunger, cortisol and prolactin without adding GH. The 300 mcg figure appears in bulking protocols precisely because the hunger is the point there.

• GHS-R1a, pituitary somatotroph — The reference compound for the family; lower potency than GHRP-2 and hexarelin

  Gq/PLC/calcium GH exocytosis. Roughly 100 mcg is the saturating dose.

• GHS-R1a, arcuate NPY/AgRP neurons — Not separately quantified

  The strongest orexigenic response of any injectable in this class. NPY/AgRP activation plus GABAergic inhibition of POMC neurons. Onset within 20 minutes, duration about an hour.

• GHS-R1a, hypothalamic somatostatin neurons — Not separately quantified

  Somatostatin suppression - the basis of GHRH synergy.

• Gastric mucosa and gastrointestinal motility — Not characterised

  Cytoprotective effects documented in rodent models. No human data.

• ACTH, cortisol and prolactin — Not applicable

  Modest at 100 mcg, clearer at higher doses. Less than hexarelin per unit GH.

Hunger within 15 to 20 minutes and lasting roughly an hour - this is the fastest and most reliable subjective effect of any compound in the class. GH peaks by about 30 minutes and is back to baseline within 90 minutes to two hours. Flushing, tingling and sometimes drowsiness come with the injection. Weight gain from increased intake shows in the first fortnight. IGF-1 changes are measurable at 8 to 12 weeks. Desensitisation is intermediate - slower than hexarelin, faster than ipamorelin - and eight to twelve weeks with a four-week break is the usual pattern.

The GHRH pairing works exactly as it does for the rest of the family, and 100 mcg GHRP-6 with 100 mcg Mod GRF 1-29 is a legitimate and cheap stack if the hunger is acceptable to you. Everything else in the stacking conversation is about managing the appetite. GHRP-6 with a GLP-1 agonist is directly self-cancelling and slightly absurd, though people do it. GHRP-6 with MK-677 is the worst combination in this class from an appetite standpoint - the same receptor, the same circuit, one of them lasting all day. If you want GH release without the hunger, ipamorelin is the answer and has been since 1998. The one context where GHRP-6 is the right tool rather than the wrong one is deliberate weight gain in someone who genuinely cannot eat, and there the hunger is the therapeutic effect and the GH is the bonus.

Against ipamorelin: GHRP-6 is the older, cruder version of the same idea. Ipamorelin exists specifically because GHRP-6's appetite and endocrine side effects were unacceptable, and unless you want the hunger there is no reason to choose GHRP-6. Against GHRP-2: comparable or slightly less GH for considerably more hunger. Against hexarelin: hexarelin is roughly twice as potent for GH with less hunger and much faster desensitisation. Against MK-677: same receptor, same appetite circuit, but MK-677's version lasts all day and raises IGF-1 far more - if you want the ghrelin-mimetic experience continuously, that is the compound. Against ghrelin itself: GHRP-6 is a stable synthetic mimic of the natural ligand, which is a fair description of what it is and why it works.

$15–$50/month. Approximate grey-market pricing and the cheapest injectable in this class. A 5 or 10 mg vial commonly runs 20 to 45 USD and lasts one to three months. Figures are observed and approximate.

• ?The 15 to 20 minute half-life has no primary human source resolved here, and no bioavailability, clearance or volume of distribution data exists.
• ?The sequence His-D-Trp-Ala-Trp-D-Phe-Lys-NH2 is universally reported in secondary sources and appears in the Core record's own alias list, but was not resolved from a primary structural reference in this session. The molecular weight of 873.0 was likewise not independently confirmed.
• ?The magnitude of the appetite effect has never been quantified in a controlled human study at the doses people actually inject.
• ?The gastric, cardiac and hepatic cytoprotection literature is almost entirely rodent and much of it is published in venues that are hard to access. None of it was verified here.
• ?No chronic human safety data exists at any subcutaneous dose.

• Ghrelin is a growth-hormone-releasing acylated peptide from stomach Kojima M, Hosoda H, Date Y, Nakazato M, Matsuo H, Kangawa K, Nature, 1999 · PMID 10604470

  The paper GHRP-6 made possible. Identifies ghrelin as the endogenous ligand for the receptor that GHRP-6 was discovered to act on, which is GHRP-6's real place in history.

• GH releasing peptides - structure and kinetics Bowers CY, Journal of Pediatric Endocrinology, 1993 · PMID 8374685

  Bowers on his own compound series. The best available primary account of GHRP structure-activity relationships from the person who built them.

• Growth hormone-releasing peptides: clinical and basic aspects Argente J, García-Segura LM, Pozo J, Chowen JA, Hormone Research, 1996 · PMID 8950613

  Further reading. Contemporary review of where the GHRP field stood before ghrelin was identified.