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GHRP-2

Also known as Pralmorelin, Pralmoreline hydrochloride, KP-102, GPA-748, Growth Hormone Releasing Peptide-2

Ghrelin receptor agonist with strong GH release, but also raises cortisol, prolactin and appetite.

early-clinical Growth hormone research chemical

At a glance

Category
Growth hormone
Status
research chemical
Route
subcutaneous; intravenous in the Japanese diagnostic application
Half-life
approximately 30 minutes (human, subcutaneous)
Onset
GH peak within 15-30 minutes; increased appetite often within an hour
Molecular weight
817.99 g/mol
Sequence
D-Ala-D-2-Nal-Ala-Trp-D-Phe-Lys-NH2 (hexapeptide with non-natural amino acids)

Used in Japan as a diagnostic agent (GHRP Kaken 100, pralmorelin) for testing the pituitary's GH secretory capacity: a Japanese review notes that the GHRP-2 test is available there and is recommended as a convenient and safe GH stimulation test, with a peak GH below 9 mcg/L during the test diagnosing severe adult GH deficiency 4. There is no approved GHRP-2 medicine in the US or the EU. In the US it is a compounding bulk substance that the FDA placed in category 2 — substances that may present significant safety risks — for injectable and nasal routes on 29 September 2023, citing immunogenicity risk from aggregation and peptide-related impurities, the characterisation difficulty added by its unnatural amino acid, and reports of serious adverse events in patients who received GHRP-2 including increased insulin requirement, death of critically ill study subjects, infection and pancreatitis, though the FDA states causality has not been established 5. It is otherwise sold as a 'research chemical'.

Doping status: Prohibited at all times (WADA S2, growth hormone secretagogues)

Checked against the WADA 2026 Prohibited List. For a specific product and country, Global DRO is the lookup athletes are expected to use — the List names substances, not brand names.

Mechanism of action

GHRP-2 (pralmorelin) is a synthetic hexapeptide that activates the growth hormone secretagogue receptor type 1a (GHS-R1a) - the ghrelin receptor. On the somatotroph cells of the anterior pituitary this produces a GH pulse via calcium signalling; in the hypothalamus it suppresses somatostatin tone and enhances GHRH release. It thus belongs to the class of ghrelin receptor agonists, together with ipamorelin, hexarelin, GHRP-6 and MK-677.

This class works via a different receptor from the GHRH analogues (sermorelin, tesamorelin, CJC-1295, mod GRF 1-29). Because the two pathways partly relieve each other's inhibition, the combined GH peak on simultaneous administration is greater than the sum of the individual effects. That is the pharmacological reason GHRPs and GHRH analogues are combined in virtually all protocols.

In terms of GH potency GHRP-2 is stronger than GHRP-6 and ipamorelin, but less selective than ipamorelin. In direct comparative research in humans (Arvat et al., Peptides 1997) GHRP-2 and hexarelin raised prolactin, ACTH and cortisol to a comparable degree alongside GH 1. The cortisol rise is usually mild and short-lived, but it is real and dose-dependent - a clear difference from ipamorelin, which at GH-effective doses produces no ACTH or cortisol response above the GHRH level.

As a ghrelin mimetic GHRP-2 also increases food intake. In controlled human research (Laferrère et al., JCEM 2005) infusion of GHRP-2 raised calorie intake in healthy men by about a third compared with placebo 2; a follow-up study showed the same in people with obesity 3. The hunger effect is less pronounced than with GHRP-6, but clearly present - unlike with ipamorelin.

The negative feedback via IGF-1 and somatostatin remains intact, which keeps the GH rise within physiological limits. With daily use partial desensitisation of the receptor occurs, less rapidly than with hexarelin but more than with ipamorelin.

What the research shows

The acute GH, cortisol, prolactin and appetite effects in humans are well documented in small controlled research. The diagnostic application is validated and registered in Japan. There is no controlled evidence that prolonged use in healthy adults leads to more muscle mass, less fat mass or better recovery.

Research in humans

The diagnostic application has been studied and registered in Japan for assessing pituitary GH reserve. Arvat et al. (1997) characterised the simultaneous GH, PRL, ACTH and cortisol response in healthy adults 1. Laferrère et al. (JCEM 2005; Obesity 2006) showed in randomised research that GHRP-2 increases food intake in both healthy and obese subjects 23. There are short-term studies in children with growth retardation and in older people. Randomised long-term studies in healthy adults with functional endpoints are absent.

Animal and lab research

In rats and pigs GHRP-2 produces robust dose-dependent GH release and promotes growth in young animals. The animal models also confirm the appetite-increasing effect.

Caveats. The human studies are small, mostly single-dose studies with hormone levels as the endpoint. The literature dates largely from 1994-2006. There are no long-term safety data, no research on the cumulative effect of repeated cortisol rises, and no study measuring the influence on body composition over months. What is sold as GHRP-2 outside Japan is not subject to regulatory control of identity and purity.

What it is used for

  • Used in Japan: diagnostic test of the pituitary's GH secretory capacity, recommended there as a convenient and safe GH stimulation test 4
  • Studied in growth hormone deficiency and in growth retardation in children
  • Outside research: raising one's own GH release, usually combined with a GHRH analogue (mod GRF 1-29, CJC-1295)
  • Sometimes used for the appetite-increasing effect by people who struggle to eat enough - an application for which no controlled evidence exists

Dosing

Dose
In the Japanese diagnostic test: 100 mcg intravenously as a single bolus. User protocols mention 100-300 mcg subcutaneously per administration (approximately 1 mcg/kg as a 'saturation dose').
Frequency
1-3x daily with at least 3 hours in between
Route
subcutaneous; intravenous in the diagnostic test
Duration
Cycles of 8-12 weeks with a break are described in user protocols; no substantiation from research
  • Only the diagnostic dose of 100 mcg intravenously is an established dose. All other schedules come from user protocols and are not substantiated in controlled research.
  • The widely repeated claim that the GH response plateaus above roughly 100-150 mcg is not supported by the human comparative data available here: in the study that characterised the hormone responses, GH release was dose-related between 1 and 2 mcg/kg intravenously — roughly 70 to 160 mcg for an average adult — with no plateau reported over that range 1. Prolactin, ACTH and cortisol rose alongside GH at every dose tested 1. Treat any specific saturation figure as unverified.
  • Administer on an empty stomach: raised insulin and free fatty acids blunt the GH response.
  • Take the appetite-increasing effect into account: for use aimed at fat loss this works against the goal.
  • Anyone wanting GH stimulation without a cortisol or prolactin rise is better served by ipamorelin.

These figures describe what the literature and published protocols report. They are not advice and not a dosing instruction.

Protocols

GHRP-2, common user schedule

user protocol — not validated

Source: Pattern reported on forums and by vendors

This is not a validated schedule. It is a pattern that circulates among users and sellers, reproduced because it is what people actually follow — not because it has been tested. No trial established these doses, this interval or this duration, and nobody is checking what is in the vial. Treat every number below as an assertion, not a finding.

Before bed, on an empty stomach100 mcg subcutaneously, usually combined with a GHRH analogue in the same syringe
Optional further dosesup to three times daily, at least 3 hours apart
Range cited100-300 mcg per administration; about 100 mcg (1 mcg/kg) is described as the 'saturation dose'
Run length8-12 weeks, then a break

The plateau users cite to justify capping the dose here — that above roughly 100-150 mcg the GH response flattens while cortisol and prolactin keep climbing — is not borne out by the human data (see the dosing section); what is documented is that cortisol, prolactin and appetite rise with the dose, the appetite gain working against the fat-loss goal it is frequently taken for. The only established dose for this compound is 100 mcg intravenously as a diagnostic bolus in Japan — a different route, a single administration, and not this schedule.

Schedules are reproduced as their source states them. Units, IU and milligrams explains why the figures are not interchangeable between products.

Reconstitution

Vial sizes
5 mg, 10 mg
Solvent
bacteriostatic water (0.9% benzyl alcohol)
Storage
Reconstituted 2-8 °C, keeps for approximately 3-4 weeks. Powder in the freezer (-20 °C), protected from light.

Worked example

5 mg vial + 2.5 ml bacteriostatic water = 2 mg/ml. 100 mcg = 0.05 ml = 5 units on a U100 insulin syringe.

Let the water run down the wall of the vial; not directly onto the powder and do not shake. GHRP-2 and a GHRH analogue can be drawn into the same insulin syringe in user protocols.

Work it out for GHRP-2

Safety

Side effects

  • Rise in cortisol and ACTH - documented in healthy young and elderly adults at 1 and 2 mcg/kg intravenously, of a magnitude similar to that produced by hCRH; clearly present unlike with ipamorelin 1
  • Rise in prolactin - documented in the same study, though weaker than the response to TRH 1; with sustained use a theoretical risk of reduced libido, gynaecomastia or menstrual disturbances
  • Increased appetite and food intake - confirmed in controlled research in healthy men 2 and in people with obesity 3
  • Fluid retention and oedema in hands and ankles
  • Tingling and numbness in the hands; carpal tunnel syndrome is a class effect of raised GH
  • Joint and muscle pain
  • Reduced insulin sensitivity and raised fasting glucose
  • Flushing, feeling warm, sweating, headache and light-headedness shortly after injection
  • Drowsiness or fatigue
  • Injection site reactions
  • Partial decline in the GH response with continuous daily use
  • The FDA cites reports of serious adverse events in patients who received GHRP-2 — increased insulin requirement to maintain blood glucose, death of critically ill study subjects, infection and pancreatitis — while noting that causality has not been established 5
  • Immunogenicity risk from aggregation and peptide-related impurities in compounded injectable and nasal preparations, per the FDA 5

Do not use if

  • Active or previously treated malignancy - GH and IGF-1 are growth factors and the concern that they may stimulate existing malignant cells is theoretical but not refuted
  • Hypercortisolism (Cushing's syndrome) or untreated adrenal disorder
  • Hyperprolactinaemia or prolactinoma
  • Diabetes mellitus or impaired glucose tolerance without medical supervision
  • Active diabetic retinopathy
  • Pregnancy and breastfeeding
  • Children and adolescents with open growth plates, outside medical supervision
  • Serious acute illness, after open heart surgery or in acute respiratory failure
  • Eating disorders in which an increase in appetite is undesirable

Interactions

Glucocorticoids suppress the GH response; conversely the cortisol rise caused by GHRP-2 can amplify the effect of glucocorticoid therapy. Somatostatin analogues (octreotide, lanreotide) block GH release. Raised GH and IGF-1 lower insulin sensitivity and may increase the need for insulin or oral antidiabetics. The prolactin rise may be amplified by concurrent use of dopamine antagonists (antipsychotics, metoclopramide). Concurrent use with a GHRH analogue produces a more than additive GH response. Other interactions have not been systematically studied.

Sources