GHRP-1: what the studies show, status and safety
Summary
GHRP-1 is a lab-made peptide of seven building blocks that prompts the pituitary gland to release growth hormone, by docking onto the receptor for the hunger hormone ghrelin. Cyril Bowers and his colleagues described it in the early 1990s, and four small studies gave it to people between 1993 and 2000. All four gave a single dose and measured a hormone level, and no study has ever tested repeated dosing. No country has approved it, the world anti-doping list names it, and two better-known peptides, ipamorelin and NN703, were built from its skeleton.
Key findings at a glance
- The largest study of GHRP-1 alone covered 22 children. In children with a growth hormone deficiency it produced a response in 60 percent of them, against 68 percent for the natural releasing hormone. Peaks were 7.5 ± 8.0 µg/l and 11.2 ± 12.1 µg/l [1].
- The largest study of any kind covered 68 women, and it was not about treatment. Twenty minutes after an injection into a vein, growth hormone reached a middle value of 78 µg/l in the control group, five to seven times what breastfeeding mothers reached [2].
- It reaches beyond growth hormone. In 23 children and adolescents, cortisol rose (p < 0.05), the thyroid signal TSH fell and free thyroxine rose (both p < 0.01). Prolactin, LH and FSH did not move [3].
- The only industrial attempt collapsed. A phase 2 trial in dialysis patients was registered in 2006, enrolled three people and was stopped in 2007 for lack of enrolment. No results were ever posted [4].
- It is named on the anti-doping list. Section S2.2.4 of the 2026 Prohibited List prints "GHRP-1" in full, banned at all times [5].
- In Australia, possessing it without authority is illegal. The Poisons Standard lists growth hormone releasing peptides as a class, both as prescription-only and in the appendix that carries that rule [6].
- Nobody has measured how the body handles it. There is no published human pharmacokinetic study of GHRP-1. For GHRP-2 a full one exists, in ten children, giving a terminal half-life of 0.55 ± 0.14 hours [7].
What it is
GHRP-1 is a synthetic peptide of seven building blocks. It is not a hormone, and it is not a fragment of anything the body makes. Cyril Bowers, at Tulane University Medical Center in New Orleans, stands behind all of the early human work, and his name appears on every one of those papers. The 1993 paper that worked out how it acts calls it a second generation peptide in its title [8].
That title matters, because the number in the name misleads. GHRP-6 came first. A historical review calls it the first synthetic peptide that released growth hormone in a dose-related way, in the test tube and in animals. GHRP-1 and the others were made afterwards [9].
Bowers himself counted GHRP-1 in 1993 among three such peptides that had by then been given to people [10].
Two better-known peptides descend from it. Ipamorelin was found in a series of compounds that lack the central pair of building blocks of GHRP-1, alanine and tryptophan [11]. NN703, an orally active follow-up from Novo Nordisk, was derived from GHRP-1 by way of ipamorelin [12].
The build of the molecule explains why it survives in the body at all. Two of its seven building blocks are mirror images of the natural form, and one of them, a naphthalene-bearing alanine, does not occur in proteins. The tail end is capped as well [13]. Enzymes that cut ordinary proteins handle such a chain far less readily.
Quick facts
| Field | Value | Ref |
|---|---|---|
| Generic name | None. It never received an official international name | [13] |
| Development code | KP 101; the depot form in the one registered trial was called GHRP-1/AG | [4], [13] |
| Class | Growth hormone releasing peptide, switching on the ghrelin receptor | [9], [14] |
| Sequence | Ala-His-D-2-Nal-Ala-Trp-D-Phe-Lys-NH2 | [13] |
| Structure | Seven building blocks, capped at one end, two of them mirror images, one not found in proteins | [13] |
| Formula and mass | C51H62N12O7, 955.1 g/mol | [13] |
| How long it lasts in people | Never measured. No human pharmacokinetic study exists | [7] |
| Status | Human studies stopped after 2000, approved nowhere | [4] |
| Discoverer | Cyril Y. Bowers, Tulane University Medical Center | [8], [10] |
| CAS registry number | 141925-59-9 | [13] |
| PubChem CID | 10350910 | [13] |
| UNII | 39EVI31P0W | [13] |
| Entry in an official reference book | None | [13] |
How it works
GHRP-1 docks onto the receptor for the hunger hormone ghrelin, and the pituitary gland responds by releasing growth hormone [14].
- Calcium, not the usual messenger. In cultured rat pituitary cells GHRP-1 raised growth hormone release by up to threefold without changing levels of cAMP, the messenger that the natural releasing hormone GHRH uses. Instead it raised calcium inside the cell by up to 45.5 ± 5.6 nM. Blocking the calcium channels stopped both [8].
- A separate route from GHRH. In children with a growth hormone deficiency, giving both peptides together produced a peak far above the sum of the two given alone [1]. Two substances sharing one receptor cannot do that.
- The receptor was identified years later. GHRP-1 was given to people before anyone knew what it acted on. The receptor was found in 1996, and later work confirmed that GHRP-1 competes with ghrelin for it [14], [15].
- Binding sites outside the pituitary. In human heart tissue, GHRP-1 displaced a labelled tracer from heart membranes, as did GHRP-2, GHRP-6 and hexarelin. Binding is not an effect, and no heart measurement in people has ever been taken with this peptide [16].
- A direct hand on the thyroid. In cultured human thyroid tissue, GHRP-1 damped the response to TSH in step with the dose, while GHRH did not [17].
The distinction from GHRH matters throughout this page. GHRH and its copies, such as sermorelin, work through a different receptor and a different messenger. The two families can be told apart by the fact that their effects add up to more than the sum of their parts.
One caution belongs here. Most of what is written about how this family works comes from studies of other members of it. For GHRP-1 itself the record is patchy, and the selectivity of one member cannot be assumed for another [11].
What the studies found
Growth hormone in healthy children
Human, single dose Fifteen short but otherwise healthy children and adolescents received 1 µg/kg into a vein. Growth hormone climbed in all of them and peaked after 15 to 30 minutes. The rise was larger in the nine who had entered puberty than in the six who had not (p < 0.05). The response to GHRH in the same children was similar or slightly higher [3].
Eleven of the 23 people in that study also received 1 µg/kg of GHRH for comparison. No absolute peak values are published for the healthy children, so the size of the effect in them cannot be stated.
Eight young patients with pituitary failure were tested alongside them. Six responded to neither peptide. The one with a partial deficiency peaked at 6.5 µg/l five minutes after GHRP-1 and at 9.2 µg/l fifteen minutes after GHRH, and one further patient reached 10 µg/l after GHRH alone [3].
Children with a growth hormone deficiency
Human, single dose This is the largest study of GHRP-1 on its own. Twenty-two children with a documented deficiency were tested on three separate days, at least a week apart, receiving GHRP-1, GHRH or both. GHRP-1 produced a significant response in 60 percent of them, GHRH in 68 percent [1].
Peaks were 7.5 ± 8.0 µg/l after GHRP-1 and 11.2 ± 12.1 µg/l after GHRH. For GHRP-1 the spread is wider than the average itself, which means the children responded very differently from one another. The rise also lasted a shorter time than after GHRH, and both were smaller than what had been seen in healthy children [1].
Together the two peptides reached 34.2 ± 44.8 µg/l, well above the sum of the separate responses, and 86 percent of the children responded [1].
Three test days at least one week apart, each peptide at 1 microgram per kilogram into a vein. The combined response is larger than the two separate ones added up. Note the spread: after GHRP-1 alone it is wider than the average. Source [1].
Women after childbirth
Human, single dose The largest study of all used GHRP-1 as a tool rather than as a treatment. Ten women who had not been pregnant and 58 mothers received a single 100 µg injection into a vein, in a randomised, placebo-controlled design [2].
The mothers were tested at one of two points: either a median of 48 hours after delivery, range 42 to 54 hours, or a median of ten weeks after, range 3 to 25 weeks [2].
Twenty minutes later, growth hormone reached a middle value of 78 µg/l in the control group. That was seven times what breastfeeding mothers reached two days after giving birth, and five times what they reached at ten weeks [2].
The higher a woman's starting prolactin, the smaller and slower her growth hormone response. Middle prolactin values were 5 µg/l in controls, 102 µg/l two days after birth and 27 µg/l at ten weeks [2].
Forms of growth hormone released
Human, single dose A follow-up measured which forms of growth hormone appear after stimulation, in 10 newborns, 10 women shortly after birth, 18 women ten weeks after and 9 who had not been pregnant. In newborns the less common forms made up a middle value of 10 percent, range 7.2 to 19.4 percent, the same as in adults who had not been pregnant [18].
Shortly after birth, total levels after GHRP-1 were lower and the share of those less common forms higher. By ten weeks the response had partly recovered [18]. This is physiology, not a test of any use for the peptide.
Taken by mouth
Human, mixed routes Bowers compared growth hormone responses after injection into a vein, injection under the skin and swallowing. He reported that GHRP-6, GHRP-1 and GHRP-2 release growth hormone in that increasing order, and that all three work when swallowed, writing that near maximal amounts can be released after oral GHRP-1 [10].
This is the only source on oral use in people, and it is the discoverer summarising his own unpublished data. The accessible text gives no doses, no participant numbers and no peak values, so nothing can be checked. No independent group has confirmed it for GHRP-1.
The thyroid, in the test tube
Human tissue Cultured human thyroid follicles were exposed to GHRP-1 at 6 to 600 µg/l and to GHRH at 6 to 1200 µg/l. Neither changed the resting release of thyroid hormone. GHRP-1, but not GHRH, damped the release triggered by TSH and by forskolin, in step with the dose [17].
The authors placed the point of action below the messenger cAMP. The finding sits alongside the falling TSH seen in children, and it suggests the thyroid effect is not simply a consequence of growth hormone.
Animal studies, and where they disagree
Animal data In eight young lambs, only the highest of three doses raised growth hormone. Peaks were 2.2 ± 0.9 ng/ml after saline, then 9.3 ± 2.5, 8.8 ± 2.4 and 35.1 ± 5.8 ng/ml as the dose rose, against 51.6 ± 10.5 ng/ml for GHRH at 0.3 nmol/kg.
The authors noted that spontaneous peaks of 20 ng/ml occur, which leaves the two lower doses without a usable effect [19].
That is the opposite of the human picture, where these peptides release more growth hormone than GHRH does. In sheep pituitary cells GHRP-1 was ten times weaker than the releasing factor, with a half-maximal dose of 10⁻⁷ M, the same as GHRP-6 [20]. In the same system GHRP-2 was ten times more potent than either [21].
Animal data In rats with heart failure, four peptides of this family, including GHRP-1, were given at 100 µg/kg twice daily for three weeks. Heart function and wasting both improved, stress hormones fell and heart muscle cell death was suppressed [22].
Those results are reported for the four peptides as one group. Nothing can be said from them about GHRP-1 on its own.
The only registered trial
Phase 2, terminated In September 2006, QLT Inc. registered a randomised, double-blind, vehicle-controlled crossover trial of a depot form called GHRP-1/AG. It was to run at Tulane and the Mayo Clinic, in adults on haemodialysis with signs of malnutrition, over 12 weeks [4].
Safety was the primary measure, alongside a malnutrition score, calorie intake and body weight. Growth hormone, IGF-1, prolactin and cortisol were secondary. The trial enrolled three people and stopped in May 2007, with lack of enrolment given as the reason. No results were ever posted [4].
What is still unknown
- What repeated dosing does. No study has ever given GHRP-1 to a person on more than one day and published the result [1], [2], [3], [4].
- How the body handles it. Half-life, clearance and how much reaches the blood are all unmeasured [7].
- How tightly it binds. No binding strength at the human ghrelin receptor has been published, only the fact that it binds [15].
- Muscle, body fat, strength, recovery and sleep. Nothing has been measured, in anyone, for any of these.
- Whether it releases ACTH. Only cortisol was measured, and it rose. Whether the trigger hormone above it moves, as with GHRP-2 and GHRP-6, is untested [3].
- What it does in healthy adults. The human record covers children, adolescents and women around childbirth [1], [2], [3].
Side effects and safety
No authority has ever weighed benefits against risks, because no application was ever filed. Everything below comes from hormone measurements taken alongside single test doses. The one trial that set out to collect safety data stopped after three participants and published nothing [4].
What was measured, in people:
- Cortisol rose after a single injection of 1 µg/kg in children and adolescents (p < 0.05). The paper gives no absolute values [3].
- The thyroid signal shifted. In the same 23 people, TSH fell and free thyroxine rose, both at p < 0.01, with all values staying inside the normal range [3]. Human thyroid tissue in culture shows a direct effect that would fit [17].
- Prolactin did not move, nor did LH or FSH [3]. Reviews credit this family in general with releasing prolactin and cortisol [16], so the absence here is worth noting, in the only study that looked.
- No side effects were reported in any human study of GHRP-1. None of them asked in a structured way, so this is an absence of data rather than a finding.
Two risks come from the wider family rather than from GHRP-1 itself.
The first is that the response fades with continued use. A 24-hour infusion of GHRP-6 cut the growth hormone released by a later dose from 19 ± 3.0 to 4.1 ± 1.6 µg/l·h. The peak fell from 25 ± 2.9 to 7.9 ± 2.9 µg/l, both at p < 0.05 [23]. Nobody has tested this with GHRP-1.
The second is what is actually in grey-market material. The doping control literature describes peptides of this class as openly available over the internet [24]. Nobody has published an analysis of what such products actually contain.
Cautions here come from the studies, since no label exists. The one trial that defined them excluded a long list of conditions [4]. Among them were insulin-treated diabetes, active heart disease, active infection, anaemia, liver disease, overactive parathyroid glands and nervous system disorders. Those are trial exclusions, not formal contraindications.
Who the human data come from is a limit in itself. Twenty-three of the people studied were children and adolescents, and 115 more were women around childbirth or newborns [1], [2], [3], [18]. Nobody has given this peptide to a healthy adult and published what happened.
The absence of GHRP-1 from the American compounding lists says nothing about its safety. GHRP-2, GHRP-6 and ipamorelin sit there in the risk category, because somebody put them forward and the agency then assessed them [25]. GHRP-1 was apparently never put forward, so no view was ever taken.
The gaps are worth stating plainly. There is no pharmacokinetic data and no measured binding strength. Nothing has been published on repeated dosing, immune reactions, interactions, pregnancy or storage and stability.
Doses used in studies
The doses below are simply what the cited studies gave, listed so that the results can be understood. They are not advice on how to use anything. Most human entries are single test doses given in hospital, and animal doses cannot be scaled to people.
| Study | Model or population | Dose | Route | Frequency | Duration | Ref |
|---|---|---|---|---|---|---|
| Laron 1993, children and adolescents | 15 short healthy young people, 8 with pituitary failure | 1 µg/kg | Into a vein | Once | Once | [3] |
| Mericq 1995, growth hormone deficiency | 22 children before puberty | 1 µg/kg, alone or with 1 µg/kg GHRH | Into a vein | Once per test day | Three test days | [1] |
| de Zegher 1998, after childbirth | 68 women | 100 µg in total | Into a vein | Once | Once | [2] |
| Bowers 1993, comparison of routes | Healthy younger adults | 1 µg/kg with GHRH; no doses given for the other routes | Vein, skin, mouth | Once | Once | [10] |
| Semenistaya 2015, excretion study | One volunteer | Not stated in the paper | Into the nose | Once | Samples over 2 days | [26] |
| NCT00381602, the terminated trial | 3 adults on haemodialysis | 70 mg depot | Under the skin | Once per period | 12 weeks, stopped early | [4] |
| Charrier 1998, lambs | 8 young lambs | 1.2, 2.4 and 6 nmol/kg | Into a vein | Once per level | Once | [19] |
| Wu 1994, sheep pituitary cells | Cells in culture | Half-maximal at 10⁻⁷ M | In the medium | Twice, an hour apart | In the test tube | [20] |
| Kraiem 1995, human thyroid tissue | Follicles in culture | 6 to 600 µg/l | In the medium | Once | In the test tube | [17] |
| Xu 2005, rats with heart failure | Rats, four peptides compared | 100 µg/kg | Under the skin | Twice daily | 3 weeks | [22] |
| Akman 1993, rat pituitary cells | Cells in culture | A dose series; values not stated | In the medium | Once | In the test tube | [8] |
One gap in that table is worth naming. The academic human studies worked with 1 µg/kg or 100 µg in total, while the single industrial attempt used a 70 mg depot, roughly a thousand times more. The depot released its contents slowly over weeks, in a different population, so the two figures are not comparable.
Development and approval status
From the Bowers laboratory to a named prohibition
- Early 1990sDescribed by Cyril Bowers in New OrleansCalled a second generation peptide, after GHRP-6, refs [8], [9]
- 1993First human tests, in short children and adolescentsCortisol rises, TSH falls, prolactin does not move, ref [3]
- 1995The largest study of GHRP-1 alone, in 22 childrenA response in 60 percent, and a synergy with GHRH, ref [1]
- 1998Ipamorelin published, built from the GHRP-1 skeletonTwo central building blocks removed, and selective, ref [11]
- 1998 to 2000Last academic human studies, in women after childbirth68 and 47 participants, the peptide used as a tool, refs [2], [18]
- 2001NN703 derived from GHRP-1 by way of ipamorelinAn orally active follow-up from Novo Nordisk, ref [12]
- 2006 to 2007The one registered trial starts and is stoppedThree people enrolled, lack of enrolment given as the reason, ref [4]
- 2015 to 2016Doping laboratories publish detection methodsSix fragments identified; the peptide itself is not found in urine, ref [26]
- 2026Named on the anti-doping list, and covered by class in AustraliaBanned at all times, and possession without authority is illegal, refs [5], [6]
- Early 1990s — the peptide comes out of the Bowers laboratory and is characterised in rat pituitary cells [8].
- 1993 to 1995 — the human programme is small and quick: 23 young people, then 22 children with a deficiency [1], [3].
- 1998 to 2000 — two studies use it to probe pituitary function in women after childbirth. Academic work then stops [2], [18].
- 2006 to 2007 — the only registered trial enrols three people and is terminated [4]. A search of the trials register returns no other study of this peptide [27].
- 2026 — the substance stands named on the anti-doping list and covered by a class entry in Australian law [5], [6].
Why development stopped is not documented anywhere. Three things happened around it. GHRP-2 proved ten times more potent in a head-to-head system [21]. The skeleton was deliberately refined into ipamorelin and NN703 [11], [12]. And the natural ligand ghrelin was isolated in 1999, which moved the whole field [15].
None of that is a documented cause, and this page does not claim it was.
Every one of these studies gave a single dose. The registered phase 2 trial, the only one designed to run for weeks, enrolled three people before it was stopped. Sources [1], [2], [3], [4], [18].
| Market | Status | Note | Ref |
|---|---|---|---|
| United States | Not approved | No label; not on either compounding list | [25], [28] |
| European Union | Not approved | Register search blocked; no authorisation known | [29] |
| Germany | Not approved | Covered by an open-ended clause in the anti-doping annex | [30] |
| United Kingdom | Not approved | Register search returned no usable page | [31] |
| Australia | Prescription-only | Covered as a class; possession without authority is illegal | [6] |
| Canada | Not approved | No entry in the database | [32] |
| Russia | Unknown | Register returned no usable result list | [33] |
Every query behind this table was run on 10 September 2026. Three rows deserve a caveat. The European, British and Russian registers could not be searched properly that day [29], [31], [33]. Those rows rest on something weaker: no brand name for GHRP-1 appears anywhere in the literature.
The German row needs a second distinction. The annex to the anti-doping law lists growth hormone releasing peptides as a group and names GHRP-2, GHRP-6 and hexarelin as examples. GHRP-1 is not among them, but the list is expressly open-ended [30].
The Australian row works the same way. The Poisons Standard carries a class entry for these peptides rather than naming this one, both in the prescription-only schedule and in the appendix that forbids possession without authority [6].
Anti-doping
GHRP-1 is banned in sport at all times, in and out of competition. Unlike most other rulebooks, the anti-doping list names it rather than catching it by a general clause.
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" [5]. The 2025 list carried it too, spelled GHRP1.
Testing looks for fragments rather than for the peptide. After a dose through the nose, GHRP-1 itself could not be found in urine at all. Six fragments were identified, and one of them stayed detectable for 27 hours [26].
Routine screens cover it alongside other small peptides. One method that injects urine directly reaches detection limits of 50 to 500 pg/ml [34]. Another, covering GHRP-1 alongside ten further prohibited peptides, reaches 2 to 10 pg/ml [35]. The wider picture for this family is at peptides banned in sport.
Compared with related peptides
| Peptide | Class | Approval | Anti-doping | Distinguishing finding |
|---|---|---|---|---|
| GHRP-1 | Growth hormone releasing peptide, seven building blocks | None, anywhere | Named, S2.2.4 [5] | No human pharmacokinetic study exists [7] |
| GHRP-2 | Growth hormone releasing peptide, six building blocks | None, anywhere | Named, S2.2.4 [5] | Ten times more potent in the same sheep system [21]; a full human study gives a half-life of 0.55 ± 0.14 hours [7] |
| GHRP-6 | Growth hormone releasing peptide, six building blocks | None, anywhere | Named, S2.2.4 [5] | The first of the family, and the one the others were built from [9] |
| Hexarelin | Growth hormone releasing peptide, six building blocks | None, anywhere | Named, S2.2.4 [5] | Built from GHRP-6, not from GHRP-1, by changing one building block [36] |
| Ipamorelin | Growth hormone secretagogue, five building blocks | None, anywhere | Named, S2.2.4 [5] | Built from the GHRP-1 skeleton, and selective: in pigs it raised neither ACTH nor cortisol above what GHRH did, at more than 200 times the dose giving half its maximum growth hormone response [11] |
| Sermorelin | Copy of the natural releasing hormone GHRH | Approved in the past, withdrawn | Named, S2.2.4 [5] | A different receptor entirely, which is why the two add up to more than their sum [1] |
Two lines run through this table. The first separates the copies of the natural releasing hormone GHRH, such as sermorelin, from the peptides that act on the ghrelin receptor. Everything else in the table sits on the ghrelin side.
The second runs through the ghrelin group and is about how much is known. GHRP-2 has an official generic name, a full human pharmacokinetic study and a place by name in German and Australian law [7], [21]. GHRP-1 has none of these. It is the least documented member of a family that is thinly documented to begin with.
One row in that table needs care. Hexarelin sits close to GHRP-1 in every list and in every doping screen, but the two were built along different lines, and neither is a variant of the other [36].
Its lasting contribution was as a starting point. Ipamorelin removed two of its central building blocks and gained selectivity [11], and NN703 went a step further towards a molecule that works when swallowed [12].
Common misconceptions
- "GHRP-1 is the oldest one, because of the number." The numbering does not track discovery. GHRP-6 came first, and the paper that worked out how GHRP-1 acts calls it a second generation peptide in its own title [8], [9].
- "GHRP-1 and hexarelin are much the same." Same family, different lines. GHRP-1 has seven building blocks; hexarelin has six and comes directly from GHRP-6, by making one of them harder for enzymes to cut [36]. They differ in registry number and in legal status.
- "GHRP-1 and GHRP-2 are interchangeable." In the same sheep system GHRP-2 was ten times more potent [21]. GHRP-2 also has an official generic name and a full human pharmacokinetic study; GHRP-1 has neither [7].
- "Ipamorelin is selective, so GHRP-1 is too." Ipamorelin was built from the GHRP-1 skeleton precisely to avoid the stress hormones. In pigs it raised neither ACTH nor cortisol above the levels GHRH produced, even at more than 200 times the dose that gave half its maximum growth hormone response [11]. Cortisol rose measurably after GHRP-1 in people [3].
- "It protects the heart." The rat study gave four peptides and reported them as one group [22]. The human finding is that GHRP-1 displaces a tracer from heart membranes, which is binding, not effect [16]. No heart measurement has ever been taken in a person given this peptide.
- "Older papers about GHRP tell us about GHRP-1." Often they do not. Several much-cited papers of the early 1990s say GHRP and mean GHRP-6 [37], [38]. Any number taken from that literature has to be traced back to the peptide actually given.
- "It was well tolerated in the studies." Nobody collected side effects in a structured way. The only trial designed to do so stopped after three people [4]. What exists are hormone measurements in 23 children and adolescents, and those did move [3].
- "It is not on the FDA risk list, so it is safer." It is absent because nobody ever nominated it, so the agency never looked. The reasoning applied to GHRP-2 and GHRP-6 fits it just as well [25].
Frequently asked questions
Is GHRP-1 approved anywhere?
No. No country has licensed it as a medicine, for any condition. It never received an official generic name and never had a brand name, because no product containing it was ever authorised. The register searches behind this page were run on 10 September 2026.
What is GHRP-1?
It is a lab-made peptide of seven building blocks, written as Ala-His-D-2-Nal-Ala-Trp-D-Phe-Lys-NH2. It switches on the receptor for the hunger hormone ghrelin and thereby sets off a burst of growth hormone. Two of its building blocks are mirror images and one is not found in proteins at all.
Was GHRP-1 the first growth hormone releasing peptide?
No, despite the number in its name. GHRP-6 came first, and a historical review calls it the first synthetic peptide that released growth hormone in a dose-related way. The paper that worked out how GHRP-1 acts calls it a second generation peptide in its own title.
What did the studies of GHRP-1 find?
That it releases growth hormone, and little else. In 22 children with a growth hormone deficiency it produced a response in 60 percent of them, with peaks of 7.5 ± 8.0 µg/l against 11.2 ± 12.1 µg/l for the natural releasing hormone. The spread there is wider than the signal itself.
What are the known side effects of GHRP-1?
The measured ones are hormonal, and they come from a single study of 23 children and adolescents. Cortisol rose (p < 0.05), the thyroid signal TSH fell and free thyroxine rose (both p < 0.01), while prolactin, LH and FSH did not move. Nobody has ever collected side effects from GHRP-1 in a structured way.
How long does GHRP-1 stay in the body?
Nobody has published an answer. There is no human pharmacokinetic study of GHRP-1, so its half-life, its clearance and how much of it reaches the blood are all unmeasured. For the closely related GHRP-2 a full study in children exists, with a terminal half-life of 0.55 ± 0.14 hours. That number belongs to GHRP-2, not to this peptide.
Is GHRP-1 banned in sport?
Yes, at all times, in and out of competition. Section S2.2.4 of the 2026 Prohibited List names it in full, alongside GHRP-2, GHRP-6 and hexarelin. Testing laboratories look for its fragments rather than the peptide itself, because the peptide is gone from urine by the time a sample is taken.
Is GHRP-1 legal to possess in Australia?
No, not without authority. The Poisons Standard of June 2026 carries a class entry for growth hormone releasing peptides in its prescription-only schedule, and repeats that class in an appendix headed with the rule that possession without authority is illegal. GHRP-1 is covered by the class rather than named.
How does GHRP-1 differ from ipamorelin?
Ipamorelin was built from the GHRP-1 skeleton by removing two central building blocks, and it was built to be selective. In pigs it raised neither ACTH nor cortisol above what GHRH did, at more than 200 times the dose giving half its maximum growth hormone response. GHRP-1 raised cortisol measurably in people, so ipamorelin's selectivity cannot be transferred to it.
What is still unknown about GHRP-1?
Almost everything a person would want to know. There is no study of repeated dosing, no pharmacokinetic data, no measured binding strength at the receptor, and no data at all on muscle, body fat, recovery or sleep. The one trial designed to collect safety data stopped after three participants.
Sources
- Mericq V, Cassorla F, Garcia H, Avila A, Bowers CY, Merriam GR (1995). Growth hormone (GH) responses to GH-releasing peptide and to GH-releasing hormone in GH-deficient children. Journal of Clinical Endocrinology and Metabolism 80(5):1681-1684. PMID 7745018. DOI 10.1210/jcem.80.5.7745018
- de Zegher F, Spitz B, Van den Berghe G, Lemmens D, Vanweser K, Keppens K, Bowers CY (1998). Postpartum hyperprolactinemia and hyporesponsiveness of growth hormone (GH) to GH-releasing peptide. Journal of Clinical Endocrinology and Metabolism 83(1):103-106. PMID 9435424. DOI 10.1210/jcem.83.1.4483
- Laron Z, Bowers CY, Hirsch D, Almonte AS, Pelz M, Keret R, Gil-Ad I (1993). Growth hormone-releasing activity of growth hormone-releasing peptide-1 (a synthetic heptapeptide) in children and adolescents. Acta Endocrinologica (Copenhagen) 129(5):424-426. PMID 8279223. DOI 10.1530/acta.0.1290424
- ClinicalTrials.gov, NCT00381602. A phase 2, randomised, crossover, vehicle-controlled, double-blind, multicentre study of GHRP-1/AG in subjects with end-stage renal disease on haemodialysis. Sponsor QLT Inc.; status terminated, reason "Lack of enrolment"; 3 participants enrolled; September 2006 to May 2007; no results posted. Full study record retrieved through API v2 on 10 September 2026. https://clinicaltrials.gov/study/NCT00381602
- World Anti-Doping Agency. The 2026 Prohibited List, section S2.2.4, third bullet, naming GHRP-1 among the growth hormone releasing peptides. Full text read 10 September 2026. The 2025 list carries the same entry, spelled GHRP1.
- Therapeutic Goods (Poisons Standard—June 2026) Instrument 2026, F2026L00633, registered 28 May 2026. Schedule 4 entry "# GROWTH HORMONE RELEASING PEPTIDES (GHRPs)."; Appendix D, clause 5, item 19. Text extract read 10 September 2026. https://www.legislation.gov.au/F2026L00633/asmade
- 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 — cited as the contrast: a complete human study exists for GHRP-2 and none for GHRP-1, in any source read for this page.
- Akman MS, Girard M, O'Brien LF, Ho AK, Chik CL (1993). Mechanisms of action of a second generation growth hormone-releasing peptide (Ala-His-D-beta Nal-Ala-Trp-D-Phe-Lys-NH2) in rat anterior pituitary cells. Endocrinology 132(3):1286-1291. PMID 8095015. DOI 10.1210/endo.132.3.8095015
- Cabrales A, Berlanga J, et al. (2017). Synthetic growth hormone-releasing peptides (GHRPs): a historical appraisal of the evidences supporting their cytoprotective effects. PMCID PMC5392015. Full text read 10 September 2026.
- Bowers CY (1993). GH releasing peptides — structure and kinetics. Journal of Pediatric Endocrinology 6(1):21-31. PMID 8374685. DOI 10.1515/jpem.1993.6.1.21 — the only source on oral use in people; the accessible abstract gives no doses and no participant numbers.
- 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
- Ahnfelt-Rønne I, Nowak J, Olsen UB (2001). Do growth hormone-releasing peptides act as ghrelin secretagogues? Endocrine 14(1):133-135. PMID 11322495. DOI 10.1385/ENDO:14:1:133
- PubChem. Compound CID 10350910, growth hormone-releasing peptide 1; formula C51H62N12O7, 955.1 g/mol, CAS 141925-59-9, UNII 39EVI31P0W, ChEMBL427926, InChIKey NWQWNCILOXTTHF-HLCSKTDOSA-N, synonym "KP 101". Retrieved 10 September 2026. https://pubchem.ncbi.nlm.nih.gov/compound/10350910
- Ferro P, Krotov G, Zvereva I, Rodchenkov G, Segura J (2017). Structure-activity relationship for peptidic growth hormone secretagogues. Drug Testing and Analysis 9(1):87-95. PMID 26811125. DOI 10.1002/dta.1947
- Bowers CY (2012). History to the discovery of ghrelin. Methods in Enzymology 514:3-32. PMID 22975043. DOI 10.1016/B978-0-12-381272-8.00001-5
- Muccioli G, Broglio F, Valetto MR, Ghè C, Catapano F, Graziani A, Papotti M, Bisi G, Deghenghi R, Ghigo E (2000). Growth hormone-releasing peptides and the cardiovascular system. Annales d'Endocrinologie (Paris) 61(1):27-31. PMID 10790589
- Kraiem Z, Bowers CY, Sobel E, Laron Z (1995). Growth hormone (GH)-releasing heptapeptide, but not GH-releasing hormone, inhibits thyrotropin-stimulated thyroid hormone secretion and cAMP formation in cultured human thyroid follicles. European Journal of Endocrinology 133(1):117-120. PMID 7627332. DOI 10.1530/eje.0.1330117
- Boguszewski CL, Boguszewski MC, de Zegher F, Carlsson B, Carlsson LM (2000). Growth hormone isoforms in newborns and postpartum women. European Journal of Endocrinology 142(4):353-358. PMID 10754476. DOI 10.1530/eje.0.1420353
- Charrier J, Fraysse A, Guilhermet R, Serra-Pujol R, Formal M, Bowers CY (1998). In vivo effects of the GH-releasing heptapeptide GHRP-1 in lambs. Reproduction Nutrition Development 38(3):245-254. PMID 9698275. DOI 10.1051/rnd:19980304
- Wu D, Chen C, Zhang J, Katoh K, Clarke I (1994). Effects in vitro of new growth hormone releasing peptide (GHRP-1) on growth hormone secretion from ovine pituitary cells in primary culture. Journal of Neuroendocrinology 6(2):185-190. PMID 8049717. DOI 10.1111/j.1365-2826.1994.tb00571.x
- Wu D, Chen C, Katoh K, Zhang J, Clarke IJ (1994). The effect of GH-releasing peptide-2 (GHRP-2 or KP 102) on GH secretion from primary cultured ovine pituitary cells can be abolished by a specific GH-releasing factor (GRF) receptor antagonist. Journal of Endocrinology 140(2):R9-R13. PMID 8169551. DOI 10.1677/joe.0.140r009
- Xu XB, Pang JJ, Cao JM, Ni C, Xu RK, Peng XZ, Yu XX, Guo S, Chen MC, Chen C (2005). GH-releasing peptides improve cardiac dysfunction and cachexia and suppress stress-related hormones and cardiomyocyte apoptosis in rats with heart failure. American Journal of Physiology. Heart and Circulatory Physiology 289(4):H1643-H1651. PMID 15951341. DOI 10.1152/ajpheart.01042.2004
- Huhn WC, Hartman ML, Pezzoli SS, Thorner MO (1993). Twenty-four-hour growth hormone (GH)-releasing peptide (GHRP) infusion enhances pulsatile GH secretion and specifically attenuates the response to a subsequent GHRP bolus. Journal of Clinical Endocrinology and Metabolism 76(5):1202-1208. PMID 8496311 — the substance given was GHRP-6, and the figures are cited here as a finding for the family, not for GHRP-1.
- Thomas A, Delahaut P, Krug O, Schänzer W, Thevis M (2012). Metabolism of growth hormone releasing peptides. Analytical Chemistry 84(23):10252-10259. PMID 23101768. DOI 10.1021/ac302034w
- U.S. Food and Drug Administration. Certain bulk drug substances for use in compounding that may present significant safety risks. Full page text read 10 September 2026; GHRP-2, GHRP-6 and ipamorelin acetate appear in category 2, added 29 September 2023, and GHRP-1 does not appear. https://www.fda.gov/drugs/human-drug-compounding/certain-bulk-drug-substances-use-compounding-may-present-significant-safety-risks
- 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
- ClinicalTrials.gov API v2. Query for "GHRP-1" on 10 September 2026 returned exactly one study, NCT00381602; a query for the spelled-out term returned eight studies, none of them testing this peptide.
- openFDA and Drugs@FDA. Label endpoint query for "GHRP-1" on 10 September 2026 returned HTTP 404 with no matches; the alphabetical Drugs@FDA listing for the letter G holds no product containing it. https://api.fda.gov/drug/label.json
- European Medicines Agency. Full-text search and medicines listing attempted on 10 September 2026; the site returned HTTP 401 and no server-rendered result list. No European register finding of our own exists.
- Annex to section 2(3) of the German Anti-Doping Act (AntiDopG), published at BGBl. 2023 I, No. 67, 1-5, section II.2.4. The entry covers peptides acting like growth hormone releasing factors and gives GHRP-2, GHRP-2-Gly, GHRP-6, GHRP-6-Gly and hexarelin as examples, introduced by "for example" and therefore not exhaustive. Full text read 10 September 2026. https://www.gesetze-im-internet.de/antidopg/anlage.html
- MHRA. products.mhra.gov.uk returned only a search shell without a rendered result list on 10 September 2026. No British register finding of our own exists.
- Health Canada. Drug Product Database, active ingredient and brand name APIs, queries for "GHRP" and "growth hormone releasing" on 10 September 2026, 0 results each; the control query for somatropin returned several in the same run. https://health-products.canada.ca/api/drug/
- State Register of Medicines of the Russian Federation (GRLS). Query on 10 September 2026 returned HTTP 200 but no usable result list, so no finding can be drawn either way.
- Thomas A, Görgens C, Guddat S, Thieme D, Dellanna F, Schänzer W, Thevis M (2016). Simplifying and expanding the screening for peptides <2 kDa by direct urine injection, liquid chromatography, and ion mobility mass spectrometry. Journal of Separation Science 39(2):333-341. PMID 26578461. DOI 10.1002/jssc.201501060
- 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
- Deghenghi R, Cananzi MM, Torsello A, Battisti C, Muller EE, Locatelli V (1994). GH-releasing activity of Hexarelin, a new growth hormone releasing peptide, in infant and adult rats. Life Sciences 54(18):1321-1328. PMID 7910650. DOI 10.1016/0024-3205(94)00510-9
- Robinson BM, Friberg RD, Bowers CY, Barkan AL (1992). Acute growth hormone (GH) response to GH-releasing hexapeptide in humans is independent of endogenous GH-releasing hormone. Journal of Clinical Endocrinology and Metabolism 75(4):1121-1124. PMID 1400881 — the peptide given was GHRP-6.
- Hartman ML, Farello G, Pezzoli SS, Thorner MO (1992). Oral administration of growth hormone (GH)-releasing peptide stimulates GH secretion in normal men. Journal of Clinical Endocrinology and Metabolism 74(6):1378-1384. PMID 1592884 — the peptide given was GHRP-6.
Cite this page
The facts on this page were checked on 10 September 2026, and every register query behind the status table was run on that date. Nobody has developed GHRP-1 since 2007, so the anti-doping and legal entries are the parts most likely to change.
myPeptides Research & Editing. (2026). GHRP-1: what the studies show, status and safety. Version 1.0, 10 September 2026. myPeptides Peptide Register. Retrieved from https://mypep.app/peptides/ghrp-1
How pages in this register are compiled and graded is described under methodology; the full register is at peptides.
| Version | Date | Change |
|---|---|---|
| 1.0 | 2026-09-10 | Initial publication |
Last verified: 10 September 2026. Next review: on any change to the anti-doping list, to the Australian Poisons Standard or to the FDA compounding lists, or on any new human study.