GHRP-2

GHRP-2 binds GHS-R1a with higher efficacy than GHRP-6 at equivalent doses and produces GH release both by direct somatotroph stimulation and by reducing hypothalamic somatostatin output. Its selectivity is imperfect: at GH-releasing doses it produces a modest rise in ACTH and cortisol and a measurable prolactin bump, roughly intermediate between GHRP-6 and hexarelin. Appetite stimulation is real but noticeably milder than GHRP-6. It is approved in Japan under the name pralmorelin as a single-injection diagnostic test of pituitary GH reserve, which gives it a level of regulatory validation the rest of the grey-market GHRPs lack.

Targets: GHS-R1a (ghrelin receptor), Hypothalamic somatostatin neurons, Pituitary somatotrophs, ACTH/prolactin axis

• · 100 mcg is roughly the saturation dose (about 1 mcg/kg). Doses of 300 mcg and above mostly add cortisol and prolactin.
• · A stronger but dirtier alternative to the ipamorelin version of the classic stack.
• · Dosed as a single fixed 100 mcg intravenous bolus - the same absolute amount as a routine subcutaneous dose, not a larger one. It is a provocation test, not a treatment protocol, and it is not evidence that higher doses are safe.

Work out your exact syringe units →

• commonIncreased appetite— Moderate - much less than GHRP-6 but enough to derail a cut for some people.
• commonElevated prolactin— Dose-dependent; the most commonly reported reason people switch to ipamorelin.
• commonElevated cortisol and ACTH— Modest at 100 mcg, clearer above 300 mcg.
• commonWater retention
• commonFlushing and head rush
• uncommonTingling or numbness in extremities— GH-driven fluid retention.
• uncommonReduced insulin sensitivity

• Active malignancy.
• Prolactinoma or existing hyperprolactinaemia.
• Poorly controlled diabetes.
• Pregnancy and breastfeeding.

• synergycjc-1295-no-dac — Standard GHRH plus GHRP pairing with a larger pulse than the ipamorelin version.
• redundantipamorelin — Same receptor. Choose based on whether you want maximum GH or minimum prolactin.
• redundantmk-677 — Same receptor, overlapping side effects.
• cautionCabergoline — Frequently co-used to blunt prolactin elevation; treating a side effect with a second drug is a signal to reconsider the dose.

• · Prolactin at baseline and at six to eight weeks if dosing above 200 mcg per day.
• · Morning cortisol on longer runs.
• · IGF-1 at baseline and 8 to 12 weeks.
• · Fasting glucose.

Approved in Japan as a diagnostic agent (pralmorelin); not approved for any therapeutic use in the US or EU, where it is sold as a research chemical. Prohibited in sport under WADA S2.

• Japanese regulatory approval of pralmorelin (GHRP Kaken 100) as a GH-deficiency provocation test (label)
• Bowers, discovery and characterisation of the growth hormone-releasing peptides (review)

GHRP-2 sits in the middle of the classical GHRP family on every axis that matters: more GH than ipamorelin, less than hexarelin; more prolactin and cortisol than ipamorelin, less than hexarelin; more hunger than ipamorelin, much less than GHRP-6. The signalling is the standard GHS-R1a Gq/PLC/calcium route at the somatotroph plus hypothalamic somatostatin suppression, and the dual site of action is why GHRP-2 combines so effectively with a GHRH analogue - Bowers and Granda-Ayala studied exactly this, acute and chronic GHRP-2, GHRH(1-44)NH2 and the combination in older men and women with decreased GH secretion, and the combination is where the interesting numbers are. What gives GHRP-2 a different standing from the rest of the grey-market GHRPs is regulatory. It is approved in Japan as pralmorelin for diagnostic GH-reserve testing, which means its human dose-response and safety at a single 100 mcg intravenous dose have been through an actual regulatory review. That is a real and unusual credential in this class, and it is also routinely overstated: a validated single-dose provocation test says nothing about the safety of 300 mcg subcutaneously three times a day for twelve weeks. The chronic-use data that does exist is instructive in an unflattering way. Mericq et al. gave oral GHRP-2 long-term to GH-deficient children and reported changes in appetite and body weight - the appetite effect is not a footnote on chronic dosing, it accumulates. The prolactin drift is the other chronic finding and is the usual reason people move to ipamorelin.

The dose-response confusion is the big one. People read that 100 mcg is the saturating dose, do not feel much, and go to 300 or 500 mcg - which does very little for GH because the pituitary is already maximally stimulated, and a great deal for prolactin, cortisol and hunger. More pulses of 100 mcg beats bigger pulses, every time. The second problem is the Japanese approval being used as a safety argument. A single 100 mcg intravenous bolus under supervision as a diagnostic test is not evidence that chronic subcutaneous dosing is safe, and the Core record is right to flag that. Third, the prolactin effect is insidious - it builds over weeks, the symptoms are vague (flat libido, softer erections, mild breast tenderness), and people attribute them to everything except the peptide. Baseline prolactin before starting is cheap and makes the six-week number interpretable. Fourth, appetite: it is much milder than GHRP-6 acutely, which lulls people into running it during a cut, and then the chronic effect that Mericq documented shows up as a stalled deficit.

1. 100 mcgWeeks 1 to 2 — 100 mcg once daily at bedtime, fasted. This is already the saturating dose for GH release; the titration here is about learning your hunger and cortisol response, not about finding an effective dose.
2. 100 mcgWeeks 3 to 8 — Add a second 100 mcg pulse on waking if the first fortnight was uneventful. Two pulses of 100 mcg is a better protocol than one of 200 mcg, because you are limited by granule pool refill rather than by receptor occupancy.
3. 100 mcgWeek 9 onward, optional — A third mid-afternoon pulse, again fasted. Three pulses of 100 mcg daily is the practical ceiling. Check prolactin before going here and again six weeks later.
4. 300 mcgNot recommended — Single doses of 300 mcg and above buy cortisol and prolactin rather than growth hormone. If 100 mcg per pulse is not producing an IGF-1 response, the answer is not a bigger pulse.

• GHS-R1a (ghrelin receptor), pituitary somatotroph — Higher efficacy than GHRP-6 at equivalent doses; no specific Ki resolved here

  Gq/PLC/calcium-driven GH exocytosis. Roughly 100 mcg, about 1 mcg/kg, is the saturating subcutaneous dose.

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

  Suppresses somatostatin output, which is what makes the GHRH pairing more than additive.

• ACTH and cortisol axis — Not applicable

  Modest elevation at 100 mcg, clearer above 300 mcg. Intermediate between GHRP-6 and hexarelin.

• Prolactin release — Not applicable

  Dose-dependent prolactin elevation. The most commonly cited practical reason people switch away from GHRP-2.

• Arcuate NPY/AgRP neurons — Not applicable

  Moderate appetite stimulation - real, noticeably milder than GHRP-6, and cumulative on chronic dosing.

• Pihoker et al., diagnostic studies with intravenous and intranasal GHRP-2 in children of short stature diagnostic · 1995

  Established GHRP-2 as a reproducible GH provocation agent in children by both intravenous and intranasal routes. Part of the evidence base underlying the eventual Japanese diagnostic approval.

• Mericq et al., long-term oral GHRP-2 in growth hormone deficient children - appetite and body weight 2 · 2003

  Changes in appetite and body weight with long-term oral administration. The most direct human evidence that the appetite effect is a chronic-dosing phenomenon rather than an acute one.

• Bowers and Granda-Ayala, GH/IGF-1 response to acute and chronic GHRP-2, GHRH(1-44)NH2 and the combination in older men and women with decreased GH secretion 1/2 · 2001

  Characterised the acute and chronic GH and IGF-1 response to GHRP-2 alone, GHRH alone and the combination in an older population with reduced GH secretion. This is the closest thing to direct human evidence for the GHRH-plus-GHRP stacking logic.

GH begins rising within 10 minutes and peaks at 15 to 30 minutes, back to baseline within about two hours. Flushing and head rush are immediate. Hunger appears within 20 to 30 minutes and lasts about an hour. Prolactin and cortisol responses follow the GH pulse. Subjectively, sleep changes appear in the first week and appetite changes within days. IGF-1 is worth measuring at week 8 to 12. Desensitisation is slower than hexarelin and faster than ipamorelin - most people run eight to twelve weeks before the response is noticeably blunted, with prolactin creep usually arriving first as the reason to stop.

GHRP-2 with 100 mcg of a GHRH analogue is the strongest version of the classic stack that most people will actually tolerate - hexarelin gives more GH but stops working in a fortnight, ipamorelin gives less but stays clean. Bowers and Granda-Ayala studied the GHRP-2 plus GHRH combination directly in older adults, which is more human evidence than most stacking claims in this field can point to. Do not combine with any other GHS-R1a agonist. The cabergoline question comes up constantly and deserves a straight answer: yes, it will suppress the prolactin, and yes, adding a dopamine agonist to manage a side effect of a research chemical you are taking for cosmetic reasons is a bad trade. Cabergoline has its own problems, including valvular concerns at higher cumulative doses in other indications. If prolactin is the issue, ipamorelin exists. With semaglutide or tirzepatide the appetite signals oppose each other; some people run the combination deliberately to get the GH arm without the hunger, and that works, but you are paying for two drugs to partially cancel each other.

Against ipamorelin: bigger pulse, dirtier profile. If you have run ipamorelin and genuinely felt nothing and your IGF-1 did not move, GHRP-2 is the reasonable next step. If you are running something for six months, it is not. Against hexarelin: GHRP-2 is less potent and desensitises far more slowly, which makes it the better choice for anything longer than three weeks. Against GHRP-6: substantially less hunger for a comparable or slightly better GH response, which is why GHRP-2 largely replaced it except among people who want the hunger. Against MK-677: MK-677 raises 24-hour GH and IGF-1 far more and is oral, at the cost of persistent appetite, water retention and measurably worse insulin sensitivity. Against ghrelin itself: GHRP-2 is what ghrelin would be if ghrelin were practical - same receptor, thirty minutes instead of ten, no labile acyl group.

$20–$60/month. Approximate grey-market pricing. A 10 mg vial commonly runs 30 to 60 USD and lasts one to three months depending on how many pulses a day you run. Note the reconstitution hazard: a 10 mg vial in 2 mL gives 5000 mcg/mL, so 100 mcg is 2 units on a U-100 syringe - a volume small enough that measurement error is a real dosing problem. Dilute further. Prices are observed and approximate.

• ?The 30-minute half-life has no primary human source resolved in this session, and no bioavailability, clearance or volume of distribution values exist.
• ?The sequence D-Ala-D-2-Nal-Ala-Trp-D-Phe-Lys-NH2 is consistent with the confirmed formula C45H55N9O6 and MW 818.0 but was not independently resolved residue by residue.
• ?The magnitude of prolactin and cortisol elevation at specific subcutaneous doses is described qualitatively in secondary sources but no quantitative dose-response for those hormones was resolved.
• ?The 100 mcg saturation figure is widely repeated and consistent with the Japanese diagnostic dose but its primary dose-finding source was not located.
• ?There is no chronic safety data for subcutaneous GHRP-2 in healthy adults at any dose. The Japanese approval covers a single diagnostic bolus only.
• ?The Western phase 2 programme in paediatric GH deficiency referenced in the Core record was not independently verified in this session.

• Diagnostic studies with intravenous and intranasal growth hormone-releasing peptide-2 in children of short stature Pihoker C, Middleton R, Reynolds GA, Bowers CY, Badger TM, Journal of Clinical Endocrinology and Metabolism, 1995 · PMID 7559885

  Establishes the diagnostic GH response by both IV and intranasal routes.

• Changes in appetite and body weight in response to long-term oral administration of the ghrelin agonist GHRP-2 in growth hormone deficient children Mericq V, Cassorla F, Bowers CY, Avila A, Gonen B, Merriam GR, Journal of Pediatric Endocrinology and Metabolism, 2003 · PMID 14513874

  Direct human data on the chronic appetite and weight effect, which vendor material tends to describe as negligible.

• Growth hormone/insulin-like growth factor-1 response to acute and chronic growth hormone-releasing peptide-2, growth hormone-releasing hormone 1-44NH2 and in combination in older men and women with decreased growth hormone secretion Bowers CY, Granda-Ayala R, Endocrine, 2001 · PMID 11322505

  The human basis for GHRH plus GHRP stacking, in the population that actually uses these compounds.

• Growth hormone response to GH-releasing peptide-2 in children Asakura Y, Toyota Y, Muroya K, Adachi M, Journal of Pediatric Endocrinology and Metabolism, 2010 · PMID 20662346

  Clinical use of the approved Japanese diagnostic test, showing what a validated GHRP-2 provocation looks like in practice.

• Treatment effects of intranasal growth hormone releasing peptide-2 in children with short stature Pihoker C, Badger TM, Reynolds GA, Bowers CY, Journal of Endocrinology, 1997 · PMID 9390009

  Further reading. One of very few studies of repeated rather than single-dose GHRP-2 administration.

• Pralmorelin, PubChem compound record CID 6918245 PubChem

  Confirms molecular formula C45H55N9O6 and molecular weight 818.0, matching the Core record.