GHRP-2 (Pralmorelin): The Complete Guide

GHRP-2 is a synthetic hexapeptide that binds the ghrelin receptor in the pituitary and hypothalamus, prompting the pituitary to release its own growth hormone rather than supplying hormone from outside. Its pharmaceutical name is pralmorelin; in the research literature it also appears as KP-102.

One fact separates it from most compounds in this category: it is approved somewhere. Japan licensed it as a diagnostic agent for growth hormone deficiency — a single-dose test of whether a pituitary can respond, not a treatment. That is a narrow approval, and it is not the same as being approved for the uses it is bought for. But it does mean a regulator has reviewed a dossier on this molecule, which is more than can be said for most of the peptides sold alongside it.

Within the GHRP family it sits in the middle on selectivity. It produces a stronger GH pulse than ipamorelin in some comparisons, but unlike ipamorelin it also nudges cortisol and prolactin. It is cleaner than GHRP-6 and hexarelin on that axis, and less clean than ipamorelin.

GHRP-2 mimics ghrelin, the hormone the stomach releases when empty. Ghrelin does two things: it triggers growth hormone release, and it signals hunger. GHRP-2 does both, and the second effect is not a side effect — it is the same signal.

Because it acts on the pituitary's own machinery rather than replacing the hormone, the feedback loop that limits GH release stays intact. That is the mechanistic argument for secretagogues over synthetic HGH, and it is a reasonable one.

Bowers, who characterised this class, reviewed the pharmacology (Cellular and Molecular Life Sciences 1998, PMID 9893708); Doi et al. described KP-102 specifically (Arzneimittel-Forschung 2004, PMID 15646370). Berlanga-Acosta et al. later published a historical appraisal of the evidence behind synthetic GHRPs as a group (2017, PMID 28469491), which is a useful corrective to how they are usually described.

GHRP-2 has more human data than most compounds in this section. Two studies matter, and one of them is routinely left out of write-ups because it complicates the sales pitch.

It reliably makes people eat more

Laferrère et al. (JCEM 2005, PMID 15699539) infused 7 lean healthy men with GHRP-2 at 1 µg/kg/hour or saline for 270 minutes, then put a buffet in front of them.

• They ate 35.9% more on GHRP-2 than on saline.
• Every single subject increased intake — still true when corrected for body weight (136.0 vs 101.3 kJ/kg, p = 0.008).
• The macronutrient mix of what they chose did not change. They simply ate more of everything.
• GH rose sharply, as expected (AUC 5550 vs 412 µg/L/240 min, p = 0.003).

This is worth sitting with if the goal is body composition. GHRP-2 is a ghrelin mimic, and ghrelin is the hunger hormone — the appetite effect is the mechanism working correctly, not a quirk. A compound that raises growth hormone while reliably increasing how much you eat is a harder tool to use than the marketing suggests, and this is the clearest difference between GHRP-2 and ipamorelin in practice.

The growth study, and its odd result

Pihoker et al. (Journal of Endocrinology 1997, PMID 9390009) gave intranasal GHRP-2 to children with short stature at 5–15 µg/kg twice daily for three months, then three times daily. Fifteen children completed six months; six continued to 18–24 months.

Height velocity rose from 3.7 to 6.1 cm/year at six months, holding at 6.0 cm/year at 18–24 months. It was well tolerated.

The curious part: IGF-1 and IGFBP-3 did not change significantly, and neither did the acute GH response over time. Growth improved without the marker that usually tracks it moving. That dissociation is not explained, and it is a reminder that IGF-1 — the number most people check to decide whether a GH peptide is “working” — is an imperfect proxy for what is actually happening.

Mericq et al. (JCEM 1998, PMID 9661608) followed with eight months of graded doses in GH-deficient children.

What is missing

Every human trial above studied children with growth problems or acute infusion in a metabolic ward. There is no trial of GHRP-2 in healthy adults for body composition, strength, recovery or ageing — the reasons it is actually purchased. The compound has real evidence; it is evidence for other questions.

Arvat et al. (Peptides 1997, PMID 9285939) compared GHRP-2 and hexarelin head to head against GHRH and a combined TRH/hCRH challenge in normal adults, tracking GH, prolactin, ACTH and cortisol together. Both peptides produced a stronger GH response than GHRH. The same study is the source of the prolactin and cortisol comparisons quoted throughout this category.

vs. ipamorelin	Stronger GH pulse in some comparisons, but ipamorelin is the selective one — it leaves cortisol and prolactin alone (Raun 1998, PMID 9849822). GHRP-2 does not, and it raises appetite.
vs. hexarelin	Hexarelin is more potent and desensitises faster, requiring cycling (PMID 10990150). GHRP-2 is the milder of the two.
vs. GHRP-6	Both raise appetite; GHRP-6 is generally described as the hungrier of the two.

If appetite suppression or neutrality matters, this is the wrong compound in the family. That is a mechanistic conclusion, not a preference.

What was actually studied

Human dosing exists here, which is unusual — but none of it matches how the compound is used.

• Intranasal 5–15 µg/kg, twice then three times daily, in children (Pihoker).
• Subcutaneous infusion at 1 µg/kg/hour over 270 minutes, in the food-intake study (Laferrère).
• Graded subcutaneous doses of 0.3, 1.0 and 3.0 µg/kg/day in GH-deficient children (Mericq).
• Intravenous bolus of 1 µg/kg as the diagnostic test dose.

No dose-finding study exists for the subcutaneous bolus protocols below, which are what people actually run. They are practice patterns.

Standard protocol

Dose	100–300 mcg per injection
Frequency	2–3 times daily
Timing	Morning, pre-workout and/or before bed, fasted
Route	Subcutaneous
Cycle	8–12 weeks, then a break

Commonly paired with a GHRH analogue such as CJC-1295, on the same logic as the ipamorelin stack — two different receptors on one axis. That pairing has not been studied for GHRP-2 either.

Increased appetite is the headline, and it is documented rather than anecdotal — see the Laferrère data above. Expect it; it is the mechanism.

• Cortisol and prolactin. GHRP-2 raises both modestly, unlike ipamorelin (PMID 9285939). Relevant if prolactin already runs high.
• Water retention and tingling in hands or feet, as with any compound that raises GH.
• Injection site reactions.
• Blood glucose. Growth hormone opposes insulin. Anyone with diabetes or insulin resistance needs medical supervision here.

The paediatric trials reported it as well tolerated over 18–24 months, which is genuinely reassuring — in children, at intranasal doses, with medical monitoring. Long-term safety in healthy adults at the doses above is unstudied.

Do not use with active cancer or a recent malignancy without oncology clearance — GH and IGF-1 signalling is growth signalling — or in pregnancy or breastfeeding, where there is no data. GHRP-2 is prohibited by WADA and is not approved in the US for any use.