GHRP-2

Pralmorelin

GHRP-2 (Pralmorelin) is a gh & growth research compound. Potent GHRP/ghrelin agonist — strong GH pulse; more prolactin/cortisol bump and appetite than Ipamorelin.

How GHRP-2 works

Potent GHRP/ghrelin agonist — strong GH pulse; more prolactin/cortisol bump and appetite than Ipamorelin.

Proposed benefits

Researched for lean-mass support, recovery, sleep depth, connective-tissue repair and improved body composition via the GH/IGF-1 axis.

Where to get GHRP-2

The evidence for GHRP-2

Graded by what exists behind each claim.

✅ Clinically validated

• Human data exists from its use as a diagnostic agent for growth-hormone deficiency — it reliably and measurably provokes GH release in humans, which is exactly what a provocation test requires. Published PK and dose-response work follows from that use.
• No efficacy trial for body composition or recovery.

📊 Correlative data

• Superseded in practice by ipamorelin, and the reason is well documented in the same human studies: it raises cortisol and prolactin alongside GH. Reported experience matches — strong GH release, hunger, and in some people the prolactin symptoms.

🧪 Theoretical / extrapolated

• A ghrelin-receptor agonist, like ipamorelin, but non-selective — it also drives ACTH and prolactin from the pituitary.
• That lack of selectivity is the whole story. It is a more potent GH releaser than ipamorelin and carries hormonal noise that ipamorelin does not, which is why it persists where raw GH release is the goal and disappeared everywhere else.

How to read these tiers: they say how much human evidence exists, not how well something works — and ✗ flags harm, never a disappointing trial. How the evidence tiers work →

What GHRP-2 actually does

The sequence first, written properly, because the usual way of writing it is wrong in three places. NCBI's own record for this molecule under its development code KP-102 spells it out as a chemical name: D-alanyl-3-(2-naphthyl)-D-alanyl-L-alanyl-L-tryptophyl-D-phenylalanyl-L-lysinamide Doi 2004. Unpack that and you have six residues — D-Ala – D-2-Nal – L-Ala – L-Trp – D-Phe – L-Lys-NH₂.

Now look at what a database does to it. This site's own verified sequence record stores GHRP-2 as A{2Nal}AWFK with a C-terminal amide, cross-checked against the PubChem formula C45H55N9O6 at 818 Da; flattened into the one-letter alphabet that string becomes AXAWFK, where the X marks a residue the twenty-letter code has no symbol for. Write it as the tidy three-letter form Ala-2Nal-Ala-Trp-Phe-Lys and you have silently deleted the D-configuration at residues 1, 2 and 5 and the C-terminal amide. Those are not notation. They are the molecule.

Why each one is there, mechanistically. Peptidases are stereospecific enzymes: they recognize L-amino acids and cannot process a D-residue in the backbone. Putting D-alanine at position 1 blocks aminopeptidase attack at the N-terminus, and the D-residues further in break the recognition of internal cleavage sites. Capping the C-terminus as an amide removes the terminal carboxylate — one fewer negative charge, and no substrate for carboxypeptidase. And position 2 is not a natural amino acid at all: 3-(2-naphthyl)alanine is a two-ring aromatic side chain, larger and more hydrophobic than the tryptophan that occupies the equivalent position in GHRP-6. A six-residue peptide that survives in plasma long enough to reach the pituitary does so because of these three edits, and a synthesis that gets the stereochemistry wrong produces a molecule with the right mass and no activity.

The receptor and the two places it works. GHRP-2 is an agonist at the growth hormone secretagogue receptor GHS-R1a — the ghrelin receptor — which sits both on pituitary somatotrophs and in the hypothalamus. Doi 2004 took that apart with three preparations. In hypophysectomized rats the GH response was completely absent, so the pituitary is required. In median-eminence-lesioned rats it was present but significantly reduced, so endogenous GHRH is required for the full effect. And on cultured rat anterior pituitary cells it worked directly, though less potently than GHRH. Direct action plus hypothalamic amplification — that is why a GHRP and a GHRH stack synergistically rather than additively.

The somatostatin point, which is the real reason it outperforms GHRH in an intact animal. In conscious rats KP-102 released more GH than injected GHRH. Under pentobarbital, which suppresses endogenous somatostatin, GHRH caught up and the two were roughly equivalent Doi 2004. So the advantage is not raw potency at the somatotroph — it is that this class is less sensitive to somatostatin brake. That is the mechanism behind “bigger pop”.

Cell, rodent, human — and where it stops

In cells. Cultured rat anterior pituitary cells, GHRP-2 added to the medium: direct GH secretion, weaker than GHRH in the same dish Doi 2004.

In rodents and dogs. Conscious rats, injected: more potent than exogenous GHRH. Conscious dogs, injected: active where GHRH failed to raise serum GH at all. Three weeks of dosing in normal and monosodium-glutamate-treated rats produced growth acceleration and a slight increase in body weight and in the wet weight of some organs Doi 2004. Note one species difference that matters later: in conscious rats KP-102 raised ACTH and corticosterone but not prolactin.

In humans, acutely, by vein. Arvat 1997 gave 1 and 2 µg/kg intravenously to six young adults aged 22–27 and compared it against GHRH 1 µg/kg, TRH 400 µg and hCRH 2 µg/kg, with a second arm in six subjects aged 66–73. The GH response beat GHRH at both doses and rose with dose. It also did the thing the rat did not: prolactin, ACTH and cortisol all rose, and the paper's own conclusion is that the ACTH/cortisol-releasing activity of these peptides is similar to that of hCRH — the corticotropin-releasing hormone itself — while the prolactin effect is smaller than TRH's. In humans this compound is not selective, and the rat study would not have told you that.

In humans, pharmacokinetically. Pihoker 1998 gave ten prepubertal children a single 1 µg/kg intravenous dose over 1 minute and sampled nine times over two hours. Full numbers are in the pharmacokinetics section; the important structural result is that GH concentration peaked at 50.7 ± 17.2 ng/mL at about 25 minutes, from a half-EC50 of roughly 1 ng/mL of peptide.

In humans, subcutaneously, with a behavioral endpoint. Laferrere 2005 infused seven lean healthy men with 1 µg/kg/h subcutaneously for 270 minutes and then fed them a buffet. They ate 35.9 ± 10.9% more than on saline — every single subject increased — 136.0 versus 101.3 kJ/kg, p = 0.008, with GH area under the curve of 5,550 versus 412 µg/L over 240 min, p = 0.003. That is the most reproducible human effect of this compound and it is an appetite effect.

The obstacle. Every human study of GHRP-2 is acute — minutes to hours — and every human endpoint is a hormone concentration. That is not an accident: the molecule was developed as a diagnostic provocation agent, and a provocation test is designed around a single stimulated pulse. No trial has ever measured lean mass, fat mass, strength, tendon healing or sleep architecture on this compound in humans. The step from ‘GH rises fiftyfold for two hours’ to ‘you recover better’ has never been taken by anyone, in either direction.

GHRP-2 pharmacokinetics — how much of it actually gets in

Route: subcutaneous, and the numbers come from an intravenous study. Pihoker 1998 fitted a biexponential model to plasma concentrations after 1 µg/kg IV in children: terminal half-life 0.55 ± 0.14 h — about 33 minutes — plasma clearance 0.66 ± 0.32 L/h per kg, apparent volume of distribution 0.32 ± 0.14 L/kg, Cmax 7.4 ± 3.8 ng/mL and AUC 2.02 ± 1.37 ng/mL·h.

Read the volume of distribution, because it settles an argument. 0.32 L/kg is roughly extracellular fluid. This peptide does not partition into tissue and does not accumulate anywhere; it sits in water, hits a receptor, and is cleared. There is no depot, no reservoir and no reason to expect anything from yesterday's injection to still be present today.

What degrades it. Plasma and tissue peptidases — aminopeptidase attack from the N-terminus, endopeptidase cleavage internally, carboxypeptidase from the C-terminus — plus renal clearance of a small peptide by glomerular filtration and tubular proteolysis. Every structural oddity in the molecule exists to slow that: D-residues at three positions and an amidated C-terminus Doi 2004. Thirty-three minutes is what those modifications buy; an all-L, free-acid hexapeptide would be gone in a fraction of that.

The oral barrier, with an arithmetic bound. There is no published oral bioavailability figure for GHRP-2 itself. There is one for the parent hexapeptide GHRP-6, and it is instructive: Hartman 1992 gave ten normal men 30, 100 and 300 µg/kg by mouth alongside 1 µg/kg intravenously. Peak GH reached 18–26 µg/L at the highest oral doses against 4.0 µg/L on placebo — real activity, but requiring roughly 100 to 300 times the intravenous dose to get there. That implies a first-pass and gastrointestinal survival penalty leaving something on the order of 1% or less of an oral dose functionally available. The same paper found the extra GH came entirely from larger secretory amplitude, not more frequent pulses, and that the response lasted 120–150 minutes whatever the route.

Why the effect outlives the drug. Peptide half-life 33 min; GH peak at 25 min; GH's own elimination half-life 0.37 ± 0.15 h Pihoker 1998. A one-minute injection therefore produces a hormone excursion lasting about two hours. That mismatch is the reason dosing frequency is argued about endlessly and the reason it mostly does not matter: what you are timing is the GH pulse, not the peptide.

What would have to be true, and how you would know it was not

1. IGF-1 is the only marker that integrates the pulses, and the prediction is smaller than people expect. A GH excursion lasting two hours from one injection is a real event, but against a full day of endogenous pulsatile secretion it is a modest addition. Draw IGF-1 before starting and again at 6 weeks, fasted, same lab. Prediction: a measurable but modest rise at 100–300 mcg once daily, and a clearly larger one on multiple daily doses. If IGF-1 has not moved at 6 weeks, the GH pulses either are not happening or are too small to integrate — and that is a product question as much as a dose question.

2. The prediction that cuts against it: cortisol and prolactin should rise too, and that is not a rumor. Arvat 1997 measured an ACTH and cortisol response in humans similar in size to hCRH — the hormone whose entire job is driving the adrenal axis — alongside a real prolactin response. So draw a morning cortisol and a prolactin at baseline and at 4 weeks, timed identically. If they climb, the compound is doing exactly what the human literature says it does, and the cost side of the ledger is real. Note the rat study saw ACTH and corticosterone but no prolactin Doi 2004 — so anyone reassuring you with rodent selectivity data is citing the wrong species.

3. Glucose handling should drift the wrong way. GH is counter-regulatory to insulin. Fasting insulin and HbA1c at baseline and 12 weeks; fasting insulin will move first, because HbA1c lags by roughly 90 days. A rise in fasting insulin with an unchanged HbA1c at 12 weeks is the expected pattern, not a reassurance.

4. Appetite is the effect most likely to decide the outcome, and it has a number. A 270-minute subcutaneous infusion raised ad libitum intake by 35.9% in every one of seven men Laferrere 2005. So the falsification test for anyone using this for body composition is not a hormone at all — it is a weighed food log for 7 days before and 7 days during. If intake is up 15% and nobody counted, the DEXA at 12 weeks will be blamed on the wrong thing.

What nobody has tested yet

Nobody has run a controlled trial of GHRP-2 with a body composition endpoint. Not one. The compound has existed since the late 1980s, has a published human pharmacokinetic profile, a published human dose-response and a published human appetite effect, and there is no randomized study in which anyone was weighed, scanned or strength-tested after a course of it. Forty people, twelve weeks, DEXA and a handgrip dynamometer, against a GHRH comparator, would be the first real efficacy data this molecule has ever had.

Nobody has measured a 24-hour GH profile under a chronic self-administered schedule. Every human GH curve for this compound comes from a single provoked dose Arvat 1997 Pihoker 1998. Whether nightly dosing for weeks raises integrated 24-hour GH output, leaves it unchanged by shifting pulses around, or blunts it through receptor desensitization is unmeasured — and those three possibilities predict completely different IGF-1 trajectories.

Nobody has checked the stereochemistry of what is being sold. Three D-residues and a C-terminal amide are the entire reason this peptide survives in plasma, and a mass spectrometer cannot see any of them: D-alanine and L-alanine have identical mass, and so does a mis-ordered sequence. A certificate of analysis quoting 818 Da is consistent with the real molecule and with several inactive ones. Chiral chromatography or Marfey-type derivatization on a handful of market vials is a routine analytical experiment that has never been published for this compound.

Nobody has quantified the appetite effect beyond four and a half hours. Laferrere 2005 is a single meal. Whether the hyperphagia persists, adapts or intensifies over weeks decides whether this compound is usable for a body composition goal at all, and it would take a metabolic ward and two weeks to find out.

GHRP-2 — its own safety story, not its class's

This compound's own risk is that it is not selective, and the evidence for that is human rather than theoretical. Arvat 1997 measured ACTH and cortisol responses to intravenous GHRP-2 in healthy adults that were similar in magnitude to those produced by hCRH, plus a real prolactin response. Every stated advantage over ipamorelin comes from the same non-selectivity that produces those two numbers; they are one property, not a benefit with an unrelated side effect.

What chronic cortisol elevation costs, specifically. If morning cortisol runs high across weeks, the effects run directly against the reasons people take a GH secretagogue: impaired collagen synthesis, blunted recovery, central fat retention, and worse glucose handling on top of GH's own counter-regulatory effect. That is the coherent case against using this one for recovery, and it is built out of its own human data rather than out of caution.

The appetite effect is a dose-limiting adverse effect for most goals. Plus 35.9% ad libitum intake in seven of seven men after a single infusion Laferrere 2005. On a fat-loss protocol that is not a side note, it is the primary reason the protocol fails, and it is invisible unless food is being weighed.

The safety database is single doses in a diagnostic setting. This molecule reached humans as a provocation agent for growth hormone testing — give one dose, draw the samples, go home. The 3-week rodent study Doi 2004 is the longest published exposure anywhere near a therapeutic frame, and it reported organ-weight increases. Chronic human safety is not reassuring or unreassuring; it is absent.

And the practical one: you cannot verify the molecule. The D-configuration at three residues and the C-terminal amide Doi 2004 are invisible to the mass check a vendor certificate reports. A vial with the correct 818 Da mass and the wrong stereochemistry would be inert, and the only thing the user would notice is that nothing happened — which is indistinguishable from an underdose, and is why anecdotal potency reports in this corner of the market are so contradictory.

Sources read for this page

• Doi N. Pharmacological characteristics of KP-102 (GHRP-2), a potent growth hormone-releasing peptide.. Arzneimittelforschung 2004 · PMID 15646370
• Arvat E. Effects of GHRP-2 and hexarelin, two synthetic GH-releasing peptides, on GH, prolactin, ACTH and cortisol levels in man. Comparison with the effects of GHRH, TRH and hCRH.. Peptides 1997 · PMID 9285939
• Pihoker C, Kearns GL, French D, Bowers CY. Pharmacokinetics and pharmacodynamics of growth hormone-releasing peptide-2: a phase I study in children.. J Clin Endocrinol Metab 1998 · PMID 9543135
• Laferrere B, Abraham C, Russell CD, Bowers CY. Growth hormone releasing peptide-2 (GHRP-2), like ghrelin, increases food intake in healthy men.. J Clin Endocrinol Metab 2005 · PMID 15699539
• Hartman ML. Oral administration of growth hormone (GH)-releasing peptide stimulates GH secretion in normal men.. J Clin Endocrinol Metab 1992 · PMID 1592884

GHRP-2 — safety, predicted from mechanism

GHRP-2 — interference & stacking

Bloodwork to run alongside GHRP-2

Baseline first, then again at 8–12 weeks.

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GHRP-2 — frequently asked questions

GHRP-2 inside a finished plan

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What GHRP-2 is used for

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