Peptides & growth hormone

GHRP-2

Updated · 33 sources · Editorial policy

GHRP-2 (growth hormone-releasing peptide-2), also called pralmorelin or KP-102, is a small synthetic peptide that makes the pituitary gland release a burst of growth hormone (GH). It works by activating the ghrelin receptor, the same target as the “hunger hormone” ghrelin. Cyril Bowers and colleagues at Tulane University developed it in the GHRP series that began with GHRP-6.

The most important fact: GHRP-2 is approved in only one setting. Japan approved pralmorelin in 2004 as a one-time intravenous diagnostic test for growth hormone deficiency. It is not approved as a treatment anywhere, and in the US it is not an approved drug at all. Trials in short children did not show that repeated dosing improves growth, and FDA lists the injectable and nasal forms as a significant safety risk in compounding. Outside medicine it is sold online as a “research peptide,” and WADA bans it at all times.

This page summarizes what clinical studies and regulators report. It is for education only and is not medical advice.

Property Detail
Drug class Synthetic hexapeptide growth hormone secretagogue; ghrelin receptor (GHSR) agonist
Other names Pralmorelin, KP-102, GPA-748; pralmorelin dihydrochloride (salt)
Approval Japan, October 2004, as a diagnostic agent (Kaken Pharmaceutical); not approved in the US or EU
Routes studied Intravenous, subcutaneous, intranasal, oral
Doses used in studies 100 µg IV once (adult diagnostic test validation study); 1 µg/kg IV in children; 1 µg/kg/h subcutaneous infusion in adults
Half-life ≈0.55 h (≈33 min) after a 1 µg/kg IV dose in 10 children; no published adult value found
Main effect Large, short GH pulse; also raises ACTH/cortisol and appetite
FDA status Not approved; Category 2 (significant safety risks) for compounding, injectable and nasal routes, since September 29, 2023
US controlled substance Not on DEA’s controlled substances list
WADA status Prohibited at all times (S2.2.4, named as “GHRP-2 (pralmorelin)”)

What it is

GHRP-2 is a six-amino-acid peptide amide. It contains several D-amino acids (mirror-image forms that resist breakdown by enzymes) and one unnatural amino acid, a naphthyl-substituted D-alanine. The free base has the formula C₄₅H₅₅N₉O₆ and a molecular weight of 818.0 g/mol (PubChem CID 6918245). The approved Japanese product is the dihydrochloride salt (KEGG DRUG D02040).

The first unnatural GH-releasing peptides were discovered in 1976. GHRP-6, GHRP-1 and GHRP-2 were the first three tested in humans, and each was more effective than the one before it (Bowers, J Pediatr Endocrinol 1993). The receptor these peptides act on was cloned in 1996 (Howard et al., Science 1996), and its natural ligand, ghrelin, was identified in 1999 (Kojima et al., Nature 1999). So GHRP-2 was in clinical studies years before anyone knew which natural hormone it was mimicking (Bowers, Methods Enzymol 2012).

Kaken Pharmaceutical acquired worldwide rights and sublicensed it to Wyeth for North America. Wyeth’s US phase II program in GH deficiency appears to have been discontinued (Drugs R D 2004).

How it raises growth hormone

GHRP-2 stimulates GH release at two levels (Doi et al., Arzneimittelforschung 2004; Bowers, Methods Enzymol 2012):

  • Pituitary. It acts directly on GH-producing cells. In cultured rat pituitary cells it released GH on its own.
  • Hypothalamus. Its full effect needs the body’s own growth hormone-releasing hormone (GHRH). In rats with the pituitary removed it had no effect, and in rats with the GHRH-producing region damaged its effect was reduced.

In conscious rats and dogs, GHRP-2 was less affected by somatostatin (the hormone that switches GH release off) than injected GHRH was. Given together with GHRH, it releases far more GH than either alone. This synergy was shown in children of short stature and in older adults (Pihoker et al., JCEM 1995; Bowers et al., JCEM 2004).

GHRP-2 is not fully selective for GH. In rats it raised ACTH and corticosterone but not prolactin (Doi et al., Arzneimittelforschung 2004). In humans it raised cortisol at higher doses and increased hunger (see below). Selectivity is the main way the related compounds differ. In pigs, GHRP-2 and GHRP-6 raised ACTH and cortisol, while ipamorelin did not, even at very high doses. GHRP-2 was the most potent of the three in that model (Raun et al., Eur J Endocrinol 1998). Hexarelin is another hexapeptide in the same family, and ibutamoren (MK-677) is an oral, non-peptide drug that acts on the same receptor.

Pharmacokinetics

The only detailed human pharmacokinetic study gave 10 prepubertal children a single 1 µg/kg IV dose (Pihoker et al., JCEM 1998):

Parameter Value (mean ± SD)
Elimination half-life 0.55 ± 0.14 h (≈33 min)
Peak plasma GHRP-2 7.4 ± 3.8 ng/mL
Clearance 0.66 ± 0.32 L/h per kg
Volume of distribution 0.32 ± 0.14 L/kg
Peak GH 50.7 ± 17.2 ng/mL, at ≈0.42 h (25 min)
GH elimination half-life 0.37 ± 0.15 h

Other routes:

Because each dose produces a short GH pulse, the effect does not last long. In GH-deficient children, injections raised GH early in the night but had little effect later (Mericq et al., JCEM 1998).

The response can also fade with repeated dosing. In 9 healthy young men given 100 µg subcutaneously each day, the peak GH fell from 83 µg/L on day 1 to 51 µg/L on day 5, and IGF-1 (insulin-like growth factor 1, the main hormone GH acts through) did not rise (Nijland et al., Eur J Endocrinol 1998).

Approved medical use: a diagnostic test in Japan

Japan approved pralmorelin dihydrochloride on October 22, 2004, as a diagnostic agent for endocrine function (KEGG DRUG D02040). It is used clinically in Japan to diagnose GH deficiency (Haruta et al., J Cachexia Sarcopenia Muscle 2015). The test is an alternative to the insulin tolerance test, the standard first-line test, which is contraindicated in some patients because of severe adverse events (Chihara et al., Eur J Endocrinol 2007).

The validation study enrolled 77 healthy adults and 58 patients with severe GH deficiency, confirmed by an insulin tolerance test. Each received a single 100 µg IV dose after an overnight fast (Chihara et al., Eur J Endocrinol 2007):

Result Healthy adults GH-deficient patients
Peak GH after GHRP-2 (mean ± SD) 84.6 ± 60.9 µg/L 1.36 ± 2.60 µg/L
Timing of peak Within 60 min in all subjects Within 60 min in all subjects
Diagnostic cut-off Peak GH of 15 µg/L (9 µg/L with the WHO 98/574 standard) Same

Responses were slightly lower in older and heavier subjects but this did not change the diagnosis, and repeat tests gave similar results. In a later comparison in 71 adults with pituitary tumors, the GHRP-2 test had 81.3% sensitivity and 94.5% specificity against the insulin tolerance test for severe GH deficiency (Kinoshita et al., Endocr J 2013). Because GHRP-2 also stimulates ACTH, Japanese clinicians have proposed measuring ACTH and cortisol during the test to screen for secondary adrenal insufficiency (Suzuki et al., J Endocr Soc 2022).

What the research shows

Outside the diagnostic test, GHRP-2 was studied as a possible treatment in small trials, mostly in the 1990s and 2000s. No study has tested it for muscle gain, strength or athletic performance in healthy adults.

Short children and GH deficiency

Early open-label studies looked promising, but the one large placebo-controlled trial was negative:

Study Design Dose Result
Pihoker et al., J Endocrinol 1997 15 children with short stature, open-label, 6–24 months Intranasal 5–15 µg/kg two to three times daily Height velocity rose from 3.7 to 6.1 cm/year at 6 months; IGF-1 and IGFBP-3 did not change
Mericq et al., JCEM 1998 6 GH-deficient children, open-label, 8 months Subcutaneous 0.3, 1.0, then 3.0 µg/kg/day Dose-related rise in overnight GH; IGF-1 and IGFBP-3 did not rise; faster growth than before treatment
Mericq et al., J Pediatr Endocrinol Metab 2003 10 GH-deficient children, open-label, 12 months Oral 900 µg/kg twice daily 7 of 10 reported more appetite in the first 6 months; no significant change in BMI score
Tanaka et al., Clin Pediatr Endocrinol 2014 126 children with GH deficiency, double-blind, placebo-controlled, 48 weeks Intranasal 50–200 µg twice daily (two doses by body weight) No difference in growth: height SD score changed +0.07 (placebo), +0.03 (low dose), +0.02 (high dose); no change in IGF-1

The authors of the controlled trial concluded that brief GH pulses from GHRP-2 were too small to drive growth. This is the most rigorous efficacy test of repeated GHRP-2 dosing in humans.

Older adults

In 17 healthy older men and women, a continuous subcutaneous infusion of 1 µg/kg/h for 30 days raised GH secretion more than 3-fold on day 1 and more than 1.8-fold on days 14 and 30. IGF-1 rose to a stable plateau, and IGFBP-3 and IGFBP-5 also increased. Safety screening tests stayed normal (Bowers et al., JCEM 2004). The study measured hormones only, not body composition, strength or function. A continuous pump infusion is also very different from the once- or twice-daily injections used in other studies, which faded within days (Nijland et al., Eur J Endocrinol 1998).

Prolonged critical illness

A Belgian group studied GHRP-2 infusions in intensive care patients, whose GH, thyroid and reproductive hormone release is suppressed during long illness:

  • GH and IGF-1. Overnight GHRP-2 infusion (1 µg/kg/h) raised mean GH 4- to 6-fold and IGF-1 by 61% within 24 hours, without changing cortisol (Van den Berghe et al., JCEM 1997).
  • With TRH. In 14 patients, 5 days of GHRP-2 plus thyrotropin-releasing hormone (TRH) raised osteocalcin (a bone formation marker) by 19% vs −6% on placebo and lowered markers of protein breakdown (Van den Berghe et al., JCEM 1999).
  • GHRP-2 alone vs combinations. In 33 men randomized to placebo, GHRP-2, GHRP-2 plus TRH, or GHRP-2 plus TRH plus GnRH for 5 days, GHRP-2 alone normalized IGF-1 but did not reduce protein breakdown or raise osteocalcin. Only the combinations did. On day 5, GHRP-2 alone and GHRP-2 plus TRH raised blood lactate and white cell counts (Van den Berghe et al., Clin Endocrinol 2002).

These were short, small studies of hormone markers, not of survival or recovery.

Appetite and food intake

Like ghrelin, GHRP-2 makes people hungry. In 7 lean, healthy men, a 270-minute subcutaneous infusion of 1 µg/kg/h increased food eaten at a buffet meal by 35.9% compared with saline, and every subject ate more (Laferrère et al., JCEM 2005). A randomized, double-blind follow-up in 19 lean and obese adults found a dose-related effect: +10.2% at 0.1 µg/kg/h and +33.5% at 1 µg/kg/h. Obesity did not blunt the response (Laferrère et al., Obesity 2006).

A single case report described a woman with long-standing severe anorexia nervosa who gained 6.7 kg (21.1 to 27.8 kg) over 14 months of intranasal GHRP-2 before meals (Haruta et al., J Cachexia Sarcopenia Muscle 2015). One uncontrolled case cannot show that the drug caused the gain.

About “a mild peptide that just boosts GH.” GHRP-2 is often presented as a clean way to raise growth hormone for muscle and recovery. The human data do not support this. It has never been tested for muscle or performance outcomes in healthy adults. Daily injections lost part of their effect within 5 days and did not raise IGF-1. In the only large controlled trial of repeated use, it did not improve growth in GH-deficient children. And it is not selective: it also raises cortisol and appetite.

Side effects and risks

Published human studies of GHRP-2 were small and short, so the safety record is limited. Most reported it as well tolerated. Long-term safety in adults has not been studied.

Hormonal effects beyond GH

Adverse events in trials

In the 48-week controlled trial in 126 children, adverse events were reported in 60.3% of subjects, mostly unrelated infections such as colds and ear infections. Events judged possibly or probably related to GHRP-2 were bowel sounds (borborygmus) in 3 children, and nosebleed, low blood pressure and raised eosinophils (a type of white blood cell) in one child (Tanaka et al., Clin Pediatr Endocrinol 2014; PMC full text). The adult food-intake infusion studies reported no side effects (Laferrère et al., JCEM 2005; Laferrère et al., Obesity 2006).

FDA safety concerns

FDA placed GHRP-2 for injectable and nasal use in Category 2 of its bulk substances list for outsourcing facilities on September 29, 2023 (FDA Category 2 list). FDA’s stated reasons:

  • risk of immune reactions (immunogenicity) from peptide aggregation and impurities;
  • added difficulty in characterizing the peptide because it contains an unnatural amino acid;
  • reports of serious adverse events in people who received GHRP-2, including a higher insulin requirement to control blood sugar, deaths of critically ill study subjects, infection and pancreatitis. FDA notes that causality has not been established.

Long-term GH and IGF-1 exposure

We found no long-term human data on cancer risk, blood sugar or heart effects of repeated GHRP-2 use. Because its purpose is to raise GH and IGF-1, the known risks of raised GH are plausible but have not been measured for GHRP-2 itself. See growth hormone and ibutamoren for what longer trials of GH-axis stimulation found.

  • US. GHRP-2 is not an FDA-approved drug and is in FDA’s Category 2 for compounding by outsourcing facilities (injectable and nasal routes) (FDA Category 2 list). It is not on DEA’s list of controlled substances (DEA).
  • Japan. Approved only as a diagnostic agent since 2004 (KEGG DRUG D02040).
  • Sport. WADA names “GHRP-2 (pralmorelin)” among the GH-releasing peptides under S2.2.4. It is prohibited in and out of competition (WADA 2026 Prohibited List). Anti-doping labs detect GHRP-2 and its metabolites in urine (Okano et al., Rapid Commun Mass Spectrom 2010). One study found that GHRP-2 can partly mask the blood test for injected recombinant GH, because it raises the body’s own GH forms too (Okano et al., Drug Test Anal 2010).

Key takeaways

  • A ghrelin-mimicking hexapeptide. GHRP-2 activates the ghrelin receptor to trigger a short, large GH pulse. It works best when the body’s own GHRH is present and acts in synergy with GHRH.
  • Approved only as a diagnostic test. Japan approved it in 2004 as a diagnostic agent; the validated test uses a single 100 µg IV dose to diagnose GH deficiency. It is not approved as a treatment anywhere and not approved at all in the US.
  • Short-acting, with fading responses. Its half-life was ≈33 minutes in children. Daily injections in young men lost part of their effect within 5 days and did not raise IGF-1.
  • Repeated use did not improve growth. In a 126-child placebo-controlled trial, 48 weeks of intranasal GHRP-2 had no effect on height or IGF-1. No trials exist for muscle or performance in healthy adults.
  • Not selective for GH. It raises cortisol, ACTH and appetite. FDA lists injectable and nasal GHRP-2 as a significant compounding safety risk, and WADA bans it at all times.

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