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GHRP-2: what the studies show, status and safety

Status at a glance

MarketStatusDate
United StatesNot approved2023-09-29
European UnionNot approved2026-09-10
GermanyNot approved2026-09-10
United KingdomNot approved2026-09-10
AustraliaScheduled substance2026-05-28
CanadaNot approved2026-09-10
SwitzerlandNot approved2026-09-10
Development stage
Approved
Strongest evidence
Phase 2 randomised trial
WADA status
Prohibited (S2.2.4, 2026)
Last verified
2026-09-10
Version
1.0

This page lists no doses.

GHRP-2: what the studies show, status and safety

Summary

GHRP-2 is a lab-made peptide that makes the pituitary gland release growth hormone. Japan licensed it in 2004, the only licence this family of peptides has, and it covers one injection used to test for a deficiency, not a treatment. The attempt to make a treatment of it stopped in phase 2. It is named on the world anti-doping list.

Key findings at a glance

  • One licence worldwide, and it is a narrow one. Japan approved GHRP-2 on 22 October 2004 as a prescription diagnostic for growth hormone deficiency. It is given once into a vein under medical supervision [1], [2].
  • Not a single registered study. ClinicalTrials.gov returned nothing on 10 September 2026 for GHRP-2, for pralmorelin and for KP-102. Control searches in the same run worked: 24 studies for tesamorelin and one for GHRP-1 [3].
  • It makes people eat more. Seven lean healthy men ate 35.9 ± 10.9 percent more than on placebo, and every one of them ate more (p = 0.008) [4]. A double-blind study in 19 people confirmed it [5].
  • It is not selective. In six young adults the rise in the trigger hormone ACTH and in cortisol matched what hCRH produces. That is the natural hormone used in hospital to test the adrenal glands [6].
  • As a treatment it changed nothing downstream. Over eight months in six children with growth hormone deficiency, night-time growth hormone rose but IGF-1 and IGFBP-3 did not [7]. Over 6 to 24 months through the nose, growth speed rose from 3.7 ± 0.2 to 6.1 ± 0.3 centimetres a year while IGF-1 stayed flat [8].
  • The commonest side effect of the licensed test is a feeling of heat, in 16.0 percent. It is the only side effect the Japanese product information gives a figure for [1].
  • Named on every relevant list. The 2026 Prohibited List prints "GHRP-2 (pralmorelin)" [9], and Australia makes possession without authority illegal [10]. The FDA has listed it since 29 September 2023 among bulk substances that may present significant safety risks [11].

What it is

GHRP-2 is a synthetic hexapeptide, a chain of six amino acid building blocks with a capped tail. Three of them are mirror-image forms and one, 2-naphthylalanine, does not occur in proteins at all. The FDA notes that this unnatural building block makes the substance harder to characterise [11].

It comes from the series of growth hormone releasing peptides built by Cyril Bowers and colleagues at Tulane University, where it carried the code KP 102 [12]. Its official generic name is pralmorelin.

Kaken Pharmaceutical developed it in Japan, and the Japanese product is GHRP KAKEN 100 Injection [1]. The American and Canadian rights went to Wyeth, whose code was GPA-748 [12].

Quick facts

FieldValueRef
NameGHRP-2; international non-proprietary name pralmorelin[13]
CodesKP-102, with KP-102 D for the diagnostic and KP-102 LN for the abandoned treatment; GPA-748 at Wyeth[12]
ClassSynthetic growth hormone releasing peptide, agonist at the ghrelin receptor GHS-R1a[1], [14]
StructureD-Ala-D-2-Nal-Ala-Trp-D-Phe-Lys-NH2, six building blocks, capped tail[1]
Formula and massC45H55N9O6, 818.0 g/mol as the free base; 890.89 g/mol as the dihydrochloride in the Japanese medicine[13], [14]
Half-life0.42 to 0.69 hours in healthy adult men; 0.55 ± 0.14 hours in children[1], [15]
Binding to plasma proteins83.1 to 86.0 percent, measured in the laboratory[1]
StatusPrescription diagnostic in Japan since 22 October 2004; licensed nowhere else[2], [16]
Developed byCyril Bowers and colleagues, Tulane University; developed by Kaken Pharmaceutical[12]
ATC groupNone assigned; Japan files it under national class 7223, diagnostic reagents for endocrine function[14]
CAS registry numbers158861-67-7 free base; 158827-34-0 dihydrochloride[13], [14]
PubChem CID6918245[13]
UNIIE6S6E1F19M[13]
InChIKeyHRNLPPBUBKMZMT-RDRUQFPZSA-N[13]

One warning about the structure. Some papers print a shortened form with only five building blocks, leaving out the alanine in third position. That sequence does not exist; the chemical name in the Japanese product information has six [6], [1].

GHRP-2: what the studies show, status and safety

How it works

GHRP-2 docks onto the receptor for the hunger hormone ghrelin, called GHS-R, and sets off a burst of growth hormone from the pituitary gland. The route it takes runs mainly through the hypothalamus, and it is not the route the body's own releasing hormone GHRH uses [1].

  • The pituitary is essential, the hypothalamus makes the effect full. In rats whose pituitary had been removed, the peptide did nothing at all. In rats with a damaged median eminence the effect survived but was much weaker [17].
  • It is less easily switched off than GHRH. In conscious rats it released more growth hormone than injected GHRH did, and in conscious dogs it worked where GHRH failed. The authors read this as lower sensitivity to the body's own brake hormone, somatostatin [17].
  • It works even when the GHRH receptor is broken. In eleven people carrying a disabling mutation of that receptor, growth hormone still rose to 4.5 times the starting level. That was 0.11 ± 0.11 to 0.49 ± 0.41 µg/l (p = 0.002), against a 79-fold rise in eight controls (p = 0.008) [18].
  • The target region has been located in animals. In rats with both arcuate nuclei destroyed, the response fell to about one sixth. The 95 percent confidence interval ran from one twelfth to one third (p < 0.01). Injected straight into that nucleus, the peptide worked in a dose-dependent way [19].
  • At cell level it closes a potassium channel. In sheep pituitary cells the inward rectifying potassium current fell reversibly. Blocking protein kinase A abolished the effect; blocking protein kinase C did not [20].
  • It releases more than growth hormone. In people, ACTH and cortisol rise as much as after hCRH, and prolactin rises too, less than after TRH (p < 0.01). Arvat and colleagues concluded that the effect is "not fully specific" [6]. In pigs, GHRP-2 and GHRP-6 raised ACTH and cortisol while ipamorelin did not [21].

Two limits apply to all of this. The experiments that located the site of action were done in rats and dogs, not in people [17], [19]. And no binding strength at the human receptor has ever been published; the Japanese product information cites an unpublished company file for it [1].

What the trials found

The human record is unusually broad for a peptide of this family and unusually shallow at the same time. It covers children, healthy young and older adults, people with obesity and intensive care patients. Almost every study is small, and almost every one measures a hormone level rather than an outcome someone would notice [1], [22].

The largest study has 135 participants. Only three studies treated anyone for months, all in children with growth hormone deficiency, all without a control group, and all found that IGF-1 did not move [7], [8], [23].

The diagnostic test, the one licensed use

Diagnostic accuracy study The study covered 77 healthy people and 58 patients whose growth hormone peak in the insulin tolerance test was below 3 µg/l. The peak after GHRP-2 came within 60 minutes in everyone. Patients peaked at 1.36 ± 2.60 µg/l against 84.6 ± 60.9 µg/l in healthy people (p < 0.001) [22].

Sensitivity and specificity crossed between 15 and 20 µg/l. A cut-off of 15 µg/l matches the 3 µg/l mark of the insulin tolerance test, or 9 µg/l when calibrated against the recombinant standard 98/574. The cause of the deficiency, whether in the hypothalamus or in the pituitary, made no difference [22].

Growth hormone peak in the test that Japan licensed
Healthy people, independent study± 60.9, n = 77
84.6µg/l
Healthy people, registration studyn = 89
84.6µg/l
Severe deficiency, independent study± 2.60, n = 58
1.36µg/l
Severe deficiency, registration studyn = 60
1.37µg/l

Average peak concentration after a single injection into a vein. The independent study and the Japanese registration studies were run separately and agree closely. Sources [22], [1].

Registration studies Japan's approval rests on two national studies summarised in the product information. In 89 assessments of healthy people and short children with normal findings, the peak ranged from 15.88 to 345.06 ng/ml, averaging 84.60 ng/ml [1].

In 60 patients with severe deficiency the peak ranged from below 0.05 to 14.79 ng/ml, averaging 1.37 ng/ml. It arrived after 25.78 minutes on average [1].

Both studies cite unpublished company files as their source. Neither has ever been published in the literature, which is why the independent 2007 study matters so much [1], [22].

Appetite and food intake

Controlled cross-over Seven lean healthy men received an infusion under the skin or saline for 270 minutes and were then let loose on a buffet. They ate 35.9 ± 10.9 percent more after GHRP-2, and every single participant ate more [4].

Relative to body weight that was 136.0 ± 13.0 against 101.3 ± 10.5 kJ/kg, or 32.5 ± 3.1 against 24.2 ± 2.5 kcal/kg (p = 0.008). What they chose to eat did not change [4].

Double-blind randomised The same group repeated it in 19 people, ten lean and nine with obesity, at two levels against placebo. Food intake rose by 10.2 ± 3.9 percent at the lower level (p = 0.011). At the higher level it rose by 33.5 ± 5.8 percent (p = 0.000, meaning below 0.001).

Obesity made no difference to the size of the effect [5].

How much more people ate under GHRP-2
Lower level, mixed group± 3.9, p = 0.011, n = 19
10.2% above placebo
Higher level, mixed group± 5.8, n = 19
33.5% above placebo
Higher level, lean men± 10.9, p = 0.008, n = 7
35.9% above placebo

Two studies by the same group, both using an infusion under the skin followed by a free-choice meal. Sources [4], [5].

Open, uncontrolled Ten children with growth hormone deficiency took GHRP-2 by mouth for twelve months. Seven of them reported a markedly bigger appetite during the first six months, but the body mass index score did not shift significantly (0.21 ± 1.5 against 0.25 ± 1.5). The authors called the appetite effect temporary [23].

Growth in children

Open, uncontrolled Six children with growth hormone deficiency were treated under the skin for eight months at rising levels. Night-time growth hormone secretion rose step by step, but IGF-1 and IGFBP-3 did not move at all. Growth speed was higher during treatment than before or after [7].

The authors give the reason the treatment idea failed. The effect of each injection was too short to lift the axis for long, and they called for formulations with a longer duration of action [7].

Open, uncontrolled Fifteen short children were treated through the nose, six of them for 18 to 24 months. Growth speed rose from 3.7 ± 0.2 to 6.1 ± 0.3 centimetres a year at six months and stood at 6.0 ± 0.4 at the end [8].

IGF-1 and IGFBP-3 again did not change significantly, while growth hormone binding protein rose from 439 ± 63 to 688 ± 48 pmol/l. Half the children had no deficiency to begin with [8].

Older adults over 30 days

Controlled infusion study Seventeen healthy older women and men received a continuous infusion under the skin for 30 days. Pulsatile growth hormone secretion more than tripled on day 1 and was still more than 1.8-fold higher on days 14 and 30 (p < 0.001 throughout) [24].

IGF-1 reached a raised plateau (p < 0.025), and IGFBP-3 (p < 0.01) and IGFBP-5 (p < 0.025) rose as well. Safety laboratory values stayed normal [24].

This is the only study in which the growth factor stayed up. It also shows the response fading partly between day 1 and day 14. Nothing about body composition, muscle strength or physical function was measured [24].

Critical illness

Randomised cross-over In adults who had been critically ill for weeks, GHRP-2 produced a strong growth hormone response. The peak was 51 ± 9 µg/l in older and 102 ± 26 µg/l in younger patients (p = 0.005 against placebo). That is more than four times the response to GHRH (p = 0.007) [25].

Over 21 hours of infusion, IGF-1 rose by 61 ± 13 percent within a day (p = 0.02) [26].

Randomised cross-over The largest of these studies is also the most sobering. Urea production fell under GHRP-2 combined with TRH and GnRH (p = 0.01) and under GHRP-2 with TRH (p = 0.009). Under GHRP-2 on its own it did not, and osteocalcin did not rise either [27].

By day 5, lactate and white cell counts were raised under GHRP-2 alone [27].

None of these studies looked at survival, ventilation time or recovery. They are short mechanistic experiments with biochemical markers [26], [27].

Exercise

Controlled cross-over Eight healthy men pedalled to exhaustion on an exercise bike, alone and combined with GHRH, with GHRP-2 or with both [28].

The area under the growth hormone curve over 120 minutes was 2324 ± 312 µg/l for exercise alone and 6952 ± 1083 with GHRH. With GHRP-2 it was 14 674 ± 2210, and with both peptides 17 673 ± 1670 (p < 0.003) [28].

The combinations did not beat the arithmetic sum of the separate stimuli. The two mechanisms work alongside each other, not together. No performance or training outcome was measured [28].

Masking the growth hormone doping test

Analytical study In Japanese men, recombinant growth hormone alone pushed the isoform ratio above the national reference limit (p < 0.001). GHRP-2 alone raised both isoforms and therefore left the ratio unchanged (p > 0.05). Given together, the raised ratio fell back to 39.9 to 43.9 percent [29].

That is the practically most important finding about this substance. GHRP-2 can hide growth hormone doping from the established test, which is why laboratories test for the peptide itself [29], [30].

What is still unknown

  • Everything the grey market is interested in. No study has measured muscle mass, body composition, strength, recovery or sleep. The only exercise study measured a hormone level [28].
  • What repeated use does to healthy adults. The longest exposures with safety laboratory work are 30 days in 17 older adults and 12 months in ten children [24], [23].
  • Whether the effect in critical illness helps anyone. Survival, ventilation time and recovery were never endpoints [27].
  • How tightly it binds the human receptor. No binding figure has been published [1].
  • What it does to blood sugar in people. The FDA lists an increased insulin requirement among reported serious events, and no human study settles the question [11].

Side effects and safety

The one authorised side effect profile describes something very specific: a single injection into a vein, in a fasted person lying down, watched by a doctor. It says nothing about repeated use in healthy adults [1].

  • A feeling of heat, 16.0 percent. The only side effect the Japanese product information puts a number on, and the only one in its "5 percent and above" bracket [1].
  • Between 0.1 and 5 percent: low blood pressure, a rise in the liver enzyme ALT, audible bowel sounds, drowsiness, a runny nose, a raised white cell count, sweating, thirst, light-headedness, cold sweat, hunger, tiredness and unsteadiness [1].
  • Frequency not known: nausea, stomach pressure, retching, fullness, abdominal pain, dizziness, shifts in the white cell differential, a bitter taste, back pain, headache and facial flushing [1].
  • Pregnancy is a contraindication. The Japanese product information rules out use in pregnancy or possible pregnancy without qualification. In breastfeeding, passage into milk was reported in rats [1].
  • Pituitary apoplexy in people with a pituitary adenoma. Reported for related substances, with visual disturbance, field loss, headache and vomiting. It can be life-threatening [1].
  • The hormonal effects are side effects too. ACTH and cortisol rise as much as after hCRH, and prolactin rises as well [6].

The FDA's own wording is the sharpest thing on record. It states that compounded GHRP-2 for injection or nasal use "may pose risk for immunogenicity due to the potential for aggregation and peptide-related impurities" [11].

The same entry adds that the agency is aware of reports of serious adverse events. It names increased insulin requirement, death of critically ill study subjects, infection and pancreatitis, "though causality has not been established" [11].

That sentence deserves reading exactly as written. The agency links it to a 1999 intensive care study whose abstract reports neither deaths nor pancreatitis, so the underlying source is not visible from the page. It is a regulator's summary with its own caveat, not a study finding [11], [26].

Two gaps remain wide. Nothing is known about immune reactions or antibody formation, which is the very risk the FDA names [11]. And grey-market material is not quality controlled: GHRP-2 has been identified and quantified in tablets sold openly as a food supplement, where it was not declared [31].

Why this page lists no doses

One country licenses a medicine containing this peptide, with official product information and an approved schedule behind it. Where a medicine is approved, the amounts belong to that label and to the doctor who administers it, not to a reference page [1].

Everywhere else there is no approved product to reason from, and the published studies used four different routes in populations ranging from small children to intensive care patients. This page therefore gives no amounts, strengths or treatment lengths, in either direction [11], [3].

Development and approval status

From a Tulane laboratory to a named prohibition

  1. 1990sBuilt in the Bowers series at Tulane UniversityCarries the code KP 102 in the early comparative studies, ref [12]
  2. 1995 to 1998First human studies in childrenDiagnostic use, pharmacokinetics, and eight months of treatment in which IGF-1 did not rise, refs [32], [15], [7]
  3. 2004Japan approves it on 22 OctoberPrescription diagnostic for growth hormone deficiency, Kaken Pharmaceutical, ref [2]
  4. 2004The treatment track stallsUS development at Wyeth is discontinued; the planned Japanese launch for short stature never happens, ref [12]
  5. 2007Independent validation of the test135 people; the cut-off is confirmed against the insulin tolerance test, ref [22]
  6. 2010It is shown to mask growth hormone dopingLaboratories switch to testing for the peptide itself, refs [29], [30]
  7. 2023FDA lists it on 29 SeptemberCategory 2 bulk substance under section 503B, for injectable and nasal routes, ref [11]
  8. 2026Named on the anti-doping list and in the Australian Poisons StandardBanned at all times; possession without authority is illegal, refs [9], [10]
MarketStatusSince or note
JapanApproved2004, diagnostic
United StatesUnapprovedSafety-risk list
European UnionUnapprovedNo record found
GermanyUnapprovedNamed in doping law
United KingdomUnapprovedUnlicensed
AustraliaUnregisteredPossession restricted
CanadaUnapprovedNo product number
SwitzerlandUnapprovedNone found
RussiaUnapprovedRegister unreadable

The register checks were made on 10 September 2026. Japan, the United States, Australia, Germany and Canada rest on primary documents read in full. The two database queries were each validated by searching the same source for somatropin [1], [33], [34], [10], [35].

Four entries are weaker. The European, British, Swiss and Russian registers returned no readable result, so the status there follows from the absence of any approval record anywhere else [36], [16].

Two things should be said plainly about the Japanese approval. It covers a diagnostic reagent, filed under a national class for products that do not primarily serve treatment [14]. And a 2016 review states that apart from that one approval for diagnostic purposes, no ligand of this receptor has been successfully brought to market [16].

The wider legal picture is under are peptides legal and FDA-approved peptides.

Anti-doping

GHRP-2 is banned in sport at all times, in and out of competition, and it is printed on the list by name rather than caught by a general clause [9].

Section S2.2.4 of the 2026 Prohibited List reads: "GH-releasing peptides (GHRPs) e.g. alexamorelin, examorelin (hexarelin), GHRP-1, GHRP-2 (pralmorelin), GHRP-3, GHRP-4, GHRP-5 and GHRP-6" [9]. It is the only member of the family whose generic name is printed alongside its code, so a search for just one of the two names can come back empty.

German law names it as well. The annex to the anti-doping act lists "GHRP-2, also known as pralmorelin" as the first example under its heading for these peptides, followed by GHRP-2-Gly, GHRP-6, GHRP-6-Gly and hexarelin [35].

Testing is well established. After injection into a vein, both the unchanged peptide and its marker fragment AA-3 turned up in the urine of all ten volunteers. The limits of quantification lay between 0.5 and 10 ng/ml [30].

After nasal use it stayed detectable for 47 hours, the longest window of the five peptides tested in that work [37]. Routine screens reach 2 to 10 pg/ml [38]. The wider picture is at peptides banned in sport.

Compared with related peptides

PeptideClassApprovalAnti-dopingDistinguishing finding
GHRP-2Growth hormone releasing peptide, six building blocksJapan only, as a diagnostic [2]Named with its generic name, S2.2.4 [9]The only one of the family with published human pharmacokinetics [1], [15]
GHRP-1Growth hormone releasing peptide, seven building blocksNone; the 2016 review names Japan's as the only one in the class [16]Named, S2.2.4 [9]No published human pharmacokinetics and no approval [37]
GHRP-6The starting point of the seriesNone [16]Named, S2.2.4 [9]In pigs it was less potent but more effective than GHRP-2 (ED50 3.9 ± 1.4 against 0.6 nmol/kg) [21]
HexarelinGrowth hormone releasing peptide, six building blocksNone [16]Named under both its names, S2.2.4 [9]Matched GHRP-2 on every hormone measured in six young adults [6]
IpamorelinGrowth hormone secretagogue, five building blocksNone [16]Named, S2.2.4 [9]Left ACTH and cortisol untouched in pigs where GHRP-2 raised both [21]
SermorelinCopy of the natural releasing hormone GHRHNot assessed on this pageNamed, S2.2.4, among the GHRH analogues [9]The list separates the GHRH analogues from the ghrelin-receptor peptides [9]

Two lines run through this table. The first separates the peptides that copy GHRH from those that act on the ghrelin receptor, and the anti-doping list draws it explicitly [9].

The second runs through the ghrelin group and it is about selectivity. Ipamorelin was built to leave the stress hormones alone, and the paper that introduced it calls it "the first selective growth hormone secretagogue" [21]. GHRP-2 is the substance that effect was measured against, in the opposite direction [6], [21].

What sets GHRP-2 apart from all of them is paperwork, not pharmacology. It is the one member of the family a regulator has assessed, and that assessment covers a single diagnostic injection [2], [16].

Common misconceptions

  • "GHRP-2 does not cause hunger, GHRP-6 does." Two controlled studies say otherwise. Lean men ate 35.9 ± 10.9 percent more (p = 0.008), and a double-blind study found a step-wise rise of 10.2 ± 3.9 and 33.5 ± 5.8 percent against placebo [4], [5].
  • "GHRP-2 is as selective as ipamorelin." The opposite is the case. Ipamorelin was developed as the counter-example to GHRP-2, and in pigs it left ACTH and cortisol flat where GHRP-2 raised them [21], [6].
  • "Approved in Japan means approved as a treatment." The Japanese indication is the diagnosis of growth hormone deficiency, given as a single injection under medical supervision with blood drawn over an hour. The treatment track never got past phase 2 [1], [12].
  • "Pralmorelin, KP-102, GPA-748 and GHRP-2 are different substances." They are one substance with four names: a laboratory name, a generic name, a Japanese development code and an American one. All lead to the same PubChem and KEGG records [13], [14], [12].
  • "It works like GHRH or sermorelin." Two receptors, two pathways. In people whose GHRH receptor is disabled by mutation, GHRP-2 still raised growth hormone 4.5-fold (p = 0.002), and unlike GHRH it releases ACTH and cortisol [18], [6].
  • "The Japanese side effect list describes what grey-market use does." It describes one injection in a fasted person lying down under medical supervision. What is documented for other use sits on the FDA's side of the ledger, with its own caveat [1], [11].
  • "GHRP-2 is hard to detect." It is the best detectable of the family, with a 47-hour window after nasal use and screening limits of 2 to 10 pg/ml. What is true is something else: it hides growth hormone doping from the isoform test [37], [38], [29].

Frequently asked questions

Is GHRP-2 approved anywhere?

In Japan only. It has been a prescription medicine there since 22 October 2004, licensed to diagnose growth hormone deficiency and given as a single injection into a vein under medical supervision. There is no approval in the United States, the European Union, Germany, the United Kingdom, Australia, Canada, Switzerland or Russia.

Are GHRP-2, pralmorelin and KP-102 the same substance?

Yes, along with GPA-748. GHRP-2 is the laboratory name from the Tulane series, pralmorelin is the official generic name, KP-102 is the Japanese development code and GPA-748 was the American one. All four lead to the same chemical records.

Does GHRP-2 increase appetite?

Yes, and this is the best-tested effect it has. Seven lean healthy men ate 35.9 ± 10.9 percent more than on placebo, and every one of them ate more. A double-blind study in 19 people found the effect rising step-wise, by 10.2 ± 3.9 and then 33.5 ± 5.8 percent.

Is GHRP-2 selective for growth hormone?

No. In six young adults the rise in ACTH and cortisol matched what hCRH produces, and prolactin rose too. The authors described the effect as not fully specific. Ipamorelin was developed later precisely to avoid this, and in pigs it left both stress hormones untouched.

Did GHRP-2 work as a treatment in children with growth hormone deficiency?

Not in the way it needed to. Night-time growth hormone rose over eight months, but IGF-1 and IGFBP-3 did not, and the same held for 6 to 24 months of nasal use. The researchers concluded that the effect of each injection was too short and asked for longer-acting formulations.

What are the known side effects of GHRP-2?

The licensed profile covers a single diagnostic injection. A feeling of heat occurred in 16.0 percent. Low blood pressure, a rise in the liver enzyme ALT, drowsiness and a raised white cell count each occurred in between 0.1 and 5 percent. Pregnancy is a contraindication. The FDA separately lists reported serious events with an explicit caveat about causality.

Is GHRP-2 banned in sport?

Yes, at all times, in and out of competition. Section S2.2.4 of the 2026 Prohibited List prints it as "GHRP-2 (pralmorelin)". German anti-doping law names it as well, and in Australia possessing it without authority is illegal.

Can a doping test detect GHRP-2?

Yes, better than any other peptide of its family. Both the unchanged substance and its marker fragment appear in urine after injection, the window after nasal use runs to 47 hours, and routine screens reach 2 to 10 pg/ml. The complication is the reverse one: GHRP-2 masks the isoform test for growth hormone doping.

How long does GHRP-2 stay in the body?

About half an hour. The Japanese product information gives an elimination half-life of 0.42 to 0.69 hours in healthy adult men, and an independent study in children found 0.55 ± 0.14 hours. That short duration is what makes it usable as a test and useless as a treatment.

Are there registered clinical trials of GHRP-2?

None at all. On 10 September 2026 ClinicalTrials.gov returned nothing for GHRP-2, pralmorelin or KP-102, while control searches in the same run returned 24 studies for tesamorelin and one for GHRP-1. The registration studies ran in Japan before trial registration became routine.

Sources

  1. Japanese prescribing information for GHRP KAKEN 100 Injection (注射用GHRP科研100), Kaken Pharmaceutical Co., Ltd., revision of July 2022, read in full on 10 September 2026 through KEGG MEDICUS, japic_code 00050479. Sections used: indication (4), administration (6, 7.1), contraindications (2.1, 9.5 to 9.7), side effects with frequencies (11.2), handling (14.1), other precautions (15.1), pharmacokinetics (16.1 to 16.5), clinical results (17.1.1, 17.1.2), pharmacology (18), physicochemical data (19.1) and storage (20). https://www.kegg.jp/medicus-bin/japic_med?japic_code=00050479
  2. KEGG BRITE br08318, New drug approvals in Japan, retrieved 10 September 2026. The row "2004/10/22 | D02040 | 7223 | Pralmorelin dihydrochloride | GHRP | Kaken Pharmaceutical" stands under drugs with new active ingredients, which fixes both the approval date and the licence holder.
  3. ClinicalTrials.gov API version 2, queried 10 September 2026. "GHRP-2", "pralmorelin" and "KP-102" each returned a total count of zero. Control searches in the same run returned 24 studies for tesamorelin and one for GHRP-1, NCT00381602. https://clinicaltrials.gov/
  4. Laferrère B, Abraham C, Russell CD, Bowers CY (2005). Growth hormone releasing peptide-2 (GHRP-2), like ghrelin, increases food intake in healthy men. Journal of Clinical Endocrinology and Metabolism 90(2):611-614. PMID 15699539. DOI 10.1210/jc.2004-1719. Seven lean men, infusion under the skin against saline, free-choice meal.
  5. Laferrère B, Hart AB, Bowers CY (2006). Obese subjects respond to the stimulatory effect of the ghrelin agonist growth hormone-releasing peptide-2 on food intake. Obesity (Silver Spring) 14(6):1056-1063. PMID 16861611. DOI 10.1038/oby.2006.121. Nineteen people, double-blind, randomised, two levels against placebo.
  6. Arvat E, di Vito L, Maccagno B, Broglio F, Boghen MF, Deghenghi R, Camanni F, Ghigo E (1997). 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 18(6):885-891. PMID 9285939. DOI 10.1016/s0196-9781(97)00016-8. The source of the phrase "not fully specific". The abstract carries several typesetting errors in which half-sentences are missing, so individual figures cannot be taken from it with confidence; it also prints a shortened five-part sequence.
  7. Mericq V, Cassorla F, Salazar T, Avila A, Iñiguez G, Bowers CY, Merriam GR (1998). Effects of eight months treatment with graded doses of a growth hormone (GH)-releasing peptide in GH-deficient children. Journal of Clinical Endocrinology and Metabolism 83(7):2355-2360. PMID 9661608. DOI 10.1210/jcem.83.7.4969. Six children, no control group; contains the authors' call for longer-acting formulations.
  8. Pihoker C, Badger TM, Reynolds GA, Bowers CY (1997). Treatment effects of intranasal growth hormone releasing peptide-2 in children with short stature. Journal of Endocrinology 155(1):79-86. PMID 9390009. DOI 10.1677/joe.0.1550079. Fifteen children, open and uncontrolled, half of them without a deficiency.
  9. World Anti-Doping Agency, The 2026 Prohibited List, section S2.2.4. Full text read on 10 September 2026. The entry names the growth hormone releasing peptides individually, including "GHRP-2 (pralmorelin)", and lists the GHRH analogues separately in the same section. The 2025 list was checked in the same run and carries the same entry. https://www.wada-ama.org/en/prohibited-list
  10. Therapeutic Goods (Poisons Standard—June 2026) Instrument 2026, F2026L00633, registered 28 May 2026, full text read on 10 September 2026. Schedule 4 carries "# PRALMORELIN (GROWTH HORMONE RELEASING PEPTIDE-2 (GHRP-2))." and the class entry for the growth hormone releasing peptides. Appendix D, clause 5, headed "Poisons for which possession without authority is illegal", lists pralmorelin at item 30 and the class at item 19.
  11. US Food and Drug Administration. Certain bulk drug substances for use in compounding that may present significant safety risks. Entry "Growth hormone releasing peptide-2 (GHRP-2) (for injectable and nasal routes of administration)", category 2, column 503B, dated 29 September 2023. Page content current as of 22 April 2026, read on 10 September 2026; the column was checked in the HTML source of the table row. Section 503B covers outsourcing facilities, not pharmacy compounding under 503A. https://www.fda.gov/drugs/human-drug-compounding/certain-bulk-drug-substances-use-compounding-may-present-significant-safety-risks
  12. Pralmorelin: GHRP 2, GPA 748, growth hormone-releasing peptide 2, KP-102 D, KP-102 LN (2004). Drugs in R&D 5(4):236-239. PMID 15230633. DOI 10.2165/00126839-200405040-00011. Company history, code assignment, the licence chain from Kaken to Wyeth and the discontinuation of the American development. The same entry names a German company as a co-developer and describes the series as three to five building blocks long, neither of which could be confirmed independently.
  13. PubChem PUG-REST, compound CID 6918245 (pralmorelin), property and synonym query of 10 September 2026. Source of the formula, mass, InChIKey, UNII E6S6E1F19M, the free-base registry number, and the entries "Pralmorelin INN" and "PRALMORELIN WHO-DD". https://pubchem.ncbi.nlm.nih.gov/compound/6918245
  14. KEGG DRUG D02040 (pralmorelin dihydrochloride), REST query of 10 September 2026, with the Japanese and English web records. Source of the target receptor GHSR, the registry number of the dihydrochloride, the mass of the salt form and the Japanese therapeutic class 7223, diagnostic reagents for endocrine function, within the group of agents not primarily for therapeutic purposes. No ATC code is assigned. https://rest.kegg.jp/get/D02040
  15. Pihoker C, Kearns GL, French D, Bowers CY (1998). Pharmacokinetics and pharmacodynamics of growth hormone-releasing peptide-2: a phase I study in children. Journal of Clinical Endocrinology and Metabolism 83(4):1168-1172. PMID 9543135. DOI 10.1210/jcem.83.4.4744. Ten prepubertal children; the only published human pharmacokinetic study of the substance outside the Japanese file.
  16. Vodnik M, Štrukelj B, Lunder M (2016). Ghrelin receptor ligands reaching clinical trials: from peptides to peptidomimetics; from agonists to antagonists. Hormone and Metabolic Research 48(1):1-15. PMID 26551992. DOI 10.1055/s-0035-1564149. Contains the finding that apart from the approval of GHRP-2 for diagnostic purposes in Japan, none of the candidates of this class have been successfully introduced into the market.
  17. Doi N, Hirotani C, Ukai K, Shimada O, Okuno T, Kurasaki S, Kiyofuji T, Ikegami R, Futamata M, Nakagawa T, Ase K, Chihara K (2004). Pharmacological characteristics of KP-102 (GHRP-2), a potent growth hormone-releasing peptide. Arzneimittelforschung 54(12):857-867. PMID 15646370. DOI 10.1055/s-0031-1297041. Conscious and anaesthetised rats, conscious dogs, cultured pituitary cells, and rats after removal of the pituitary or damage to the median eminence.
  18. Gondo RG, Aguiar-Oliveira MH, Hayashida CY, Toledo SP, Abelin N, Levine MA, Bowers CY, Souza AH, Pereira RM, Santos NL, Salvatori R (2001). Growth hormone-releasing peptide-2 stimulates GH secretion in GH-deficient patients with mutated GH-releasing hormone receptor. Journal of Clinical Endocrinology and Metabolism 86(7):3279-3283. PMID 11443201. DOI 10.1210/jcem.86.7.7694. Eleven people with a homozygous receptor mutation and eight controls.
  19. Nakagawa T, Ukai K, Ohyama T, Koida M, Okamura H (1996). Effects of the synthesized growth hormone releasing peptide, KP-102, on growth hormone release in sodium glutamate monohydrate-treated low growth rats. Life Sciences 59(9):705-712. PMID 8761023. DOI 10.1016/0024-3205(96)00356-6. Rats with both arcuate nuclei destroyed, and direct injection into that nucleus.
  20. Xu R, Zhao Y, Chen C (2002). Growth hormone-releasing peptide-2 reduces inward rectifying K+ currents via a PKA-cAMP-mediated signalling pathway in ovine somatotropes. Journal of Physiology 545(2):421-433. PMID 12456822. DOI 10.1113/jphysiol.2002.030916. Patch-clamp work in sheep pituitary cells.
  21. Raun K, Hansen BS, Johansen NL, Thøgersen H, Madsen K, Ankersen M, Andersen PH (1998). Ipamorelin, the first selective growth hormone secretagogue. European Journal of Endocrinology 139(5):552-561. PMID 9849822. DOI 10.1530/eje.0.1390552. Conscious pigs; the study that measured the difference in selectivity between GHRP-2, GHRP-6 and ipamorelin.
  22. Chihara K, Shimatsu A, Hizuka N, Tanaka T, Seino Y, Kato Y (2007). A simple diagnostic test using GH-releasing peptide-2 in adult GH deficiency. European Journal of Endocrinology 157(1):19-27. PMID 17609397. DOI 10.1530/EJE-07-0066. Seventy-seven healthy people and 58 patients, with the cut-off derived against the insulin tolerance test. The accompanying commentary is PMID 17609398.
  23. Mericq V, Cassorla F, Bowers CY, Avila A, Gonen B, Merriam GR (2003). Changes in appetite and body weight in response to long-term oral administration of the ghrelin agonist GHRP-2 in growth hormone deficient children. Journal of Pediatric Endocrinology and Metabolism 16(7):981-985. PMID 14513874. DOI 10.1515/jpem.2003.16.7.981. Ten children over twelve months; the body mass index endpoint was missed.
  24. Bowers CY, Granda R, Mohan S, Kuipers J, Baylink D, Veldhuis JD (2004). Sustained elevation of pulsatile growth hormone secretion and IGF-I, IGFBP-3 and IGFBP-5 concentrations during 30-day continuous subcutaneous infusion of GH-releasing peptide-2 in older men and women. Journal of Clinical Endocrinology and Metabolism 89(5):2290-2300. PMID 15126555. DOI 10.1210/jc.2003-031799. With the earlier report by Bowers CY, Granda-Ayala R (2001), Endocrine 14(1):79-86, PMID 11322505.
  25. Van den Berghe G, de Zegher F, Bowers CY, Wouters P, Muller P, Soetens F, Vlasselaers D, Schetz M, Verwaest C, Lauwers P, Bouillon R (1996). Pituitary responsiveness to GH-releasing hormone, GH-releasing peptide-2 and thyrotrophin-releasing hormone in critical illness. Clinical Endocrinology (Oxford) 45(3):341-351. PMID 8949573. DOI 10.1046/j.1365-2265.1996.00805.x.
  26. Van den Berghe G, Wouters P, Weekers F, Mohan S, Baxter RC, Veldhuis JD, Bowers CY, Bouillon R (1999). Reactivation of pituitary hormone release and metabolic improvement by infusion of growth hormone-releasing peptide and thyrotropin-releasing hormone in patients with protracted critical illness. Journal of Clinical Endocrinology and Metabolism 84(4):1311-1323. PMID 10199772. DOI 10.1210/jcem.84.4.5636. This is the paper the FDA links from its category 2 entry.
  27. Van den Berghe G, Baxter RC, Weekers F, Wouters P, Bowers CY, Iranmanesh A, Veldhuis JD, Bouillon R (2002). The combined administration of GH-releasing peptide-2 (GHRP-2), TRH and GnRH to men with prolonged critical illness evokes superior endocrine and metabolic effects compared to treatment with GHRP-2 alone. Clinical Endocrinology (Oxford) 56(5):655-669. PMID 12030918. DOI 10.1046/j.1365-2265.2002.01255.x. The largest of the intensive care studies; the peptide on its own left the metabolic markers unchanged.
  28. Maas HCM, de Vries WR, Maitimu I, Bol E, Bowers CY, Koppeschaar HP (2000). Growth hormone responses during strenuous exercise: the role of GH-releasing hormone and GH-releasing peptide-2. Medicine and Science in Sports and Exercise 32(7):1226-1232. PMID 10912886. DOI 10.1097/00005768-200007000-00007. Eight healthy men; the only exercise study, and it measured only the hormone response.
  29. Okano M, Nishitani Y, Sato M, Ikekita A, Kageyama S (2010). Influence of intravenous administration of growth hormone releasing peptide-2 (GHRP-2) on detection of growth hormone doping: growth hormone isoform profiles in Japanese male subjects. Drug Testing and Analysis 2(11-12):548-556. PMID 21249726. DOI 10.1002/dta.166. A reference population of 100 men and three treatment arms of five to ten men each.
  30. Okano M, Sato M, Ikekita A, Kageyama S (2010). Determination of growth hormone secretagogue pralmorelin (GHRP-2) and its metabolite in human urine by liquid chromatography/electrospray ionization tandem mass spectrometry. Rapid Communications in Mass Spectrometry 24(14):2046-2056. PMID 20552695. DOI 10.1002/rcm.4619. The work that identified the marker fragment AA-3; both substances were found in all ten volunteers.
  31. Thomas A, Kohler M, Mester J, Geyer H, Schänzer W, Petrou M, Thevis M (2010). Identification of the growth-hormone-releasing peptide-2 (GHRP-2) in a nutritional supplement. Drug Testing and Analysis 2(3):144-148. PMID 20878896. DOI 10.1002/dta.120. Identified and quantified in tablets sold openly as a supplement, where it was not declared. The Cologne laboratory's annual report on confiscated black-market products for 2009 is PMID 21204286.
  32. Pihoker C, Middleton R, Reynolds GA, Bowers CY, Badger TM (1995). Diagnostic studies with intravenous and intranasal growth hormone-releasing peptide-2 in children of short stature. Journal of Clinical Endocrinology and Metabolism 80(10):2987-2992. PMID 7559885. DOI 10.1210/jcem.80.10.7559885. Twenty-four short children; the first published comparison against the conventional stimulation tests.
  33. openFDA drug label API, queried 10 September 2026. A substance-name search for pralmorelin and a full-text search for GHRP-2 both returned no record, while the control search for somatropin in the same run returned 25 records.
  34. Health Canada Drug Product Database, active ingredient API, queried 10 September 2026. A search for pralmorelin returned an empty response; the control search for somatropin in the same run returned several entries, among them drug codes 8187 and 43174.
  35. Annex to section 2 subsection 3 of the German Anti-Doping Act (AntiDopG), published at BGBl. 2023 I No. 67, 1-5, section II.2.4, full text read on 10 September 2026. It names "GHRP-2, also known as pralmorelin" as the first example, followed by GHRP-2-Gly, GHRP-6, GHRP-6-Gly and hexarelin. Germany has no marketing authorisation for the substance.
  36. Registers that returned no readable result on 10 September 2026, so that the status entries resting on them are inferences rather than direct findings: the European Medicines Agency full-text search (HTTP 401); products.mhra.gov.uk and swissmedicinfo.ch (search shell rendered in the browser only, no server-side result list); swissmedic.ch overview page (HTTP 404); the Russian state medicines register grls.rosminzdrav.ru, where the control search for somatropin failed as well; the Australian ARTG, which did not respond; and the FDA warning letter search, which returned no result list, so no statement is made about warning letters.
  37. Semenistaya E, Zvereva I, Thomas A, Thevis M, Krotov G, Rodchenkov G (2015). Determination of growth hormone releasing peptides metabolites in human urine after nasal administration of GHRP-1, GHRP-2, GHRP-6, hexarelin and ipamorelin. Drug Testing and Analysis 7(10):919-925. PMID 25869809. DOI 10.1002/dta.1787. GHRP-2 had the longest detection window of the five, at 47 hours.
  38. Thomas A, Walpurgis K, Krug O, Schänzer W, Thevis M (2012). Determination of prohibited, small peptides in urine for sports drug testing by means of nano-liquid chromatography/benchtop quadrupole orbitrap tandem-mass spectrometry. Journal of Chromatography A 1259:251-257. PMID 22901302. DOI 10.1016/j.chroma.2012.07.022. Eleven prohibited peptides in one screen, with detection limits of 2 to 10 pg/ml. The related excretion study after a single dose by mouth is PMID 21298258.

Cite this page

The facts on this page were checked on 10 September 2026, and the registers behind the status table were queried on that same day. Two things could move: the Japanese licence, and any FDA action on the compounding list.

myPeptides Research & Editing. (2026). GHRP-2: what the studies show, status and safety. Version 1.0, 10 September 2026. myPeptides Peptide Register. Retrieved from https://mypep.app/peptides/ghrp-2

How pages in this register are compiled and graded is described under methodology; the full register is at peptides.

VersionDateChange
1.02026-09-10Initial publication

Last verified: 10 September 2026. Next review: on any change to the Japanese licence, on any FDA action concerning the substance, or on the publication of a registered trial.

Identifiers

IdentifierValue
CAS number158861-67-7
PubChem CID6918245
UNIIE6S6E1F19M
InChIKeyHRNLPPBUBKMZMT-RDRUQFPZSA-N
ChEMBLCHEMBL106593
WikidataQ21098924
Molecular formulaC45H55N9O6
Molecular weight818
SequenceD-Ala-D-2-Nal-Ala-Trp-D-Phe-Lys-NH2

Cite this page

Use this reference when you quote the page, and the JSON export when you process it automatically.

myPeptides Research & Editing (2026). GHRP-2: what the studies show, status and safety (Version 1.0). myPeptides. https://mypep.app/peptides/ghrp-2

Machine-readable version (JSON)

Last reviewed: September 2026

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