GHRP-6 Research, Specifications & Scientific Information

Q: What is GHRP-6?

GHRP-6 is a synthetic hexapeptide, His-D-Trp-Ala-Trp-D-Phe-Lys-NH2, first described in 1984 as [His1,Lys6] GHRP. It acts directly on pituitary somatotrophs to release growth hormone and was the founding member of the growth hormone-releasing peptide family . It is a laboratory reagent and is not approved by the U.S. Food and Drug Administration for any indication.

Q: How does GHRP-6 work?

Through the growth hormone secretagogue receptor, a class A G protein-coupled receptor cloned from pituitary and hypothalamus in 1996 and shown three years later to be the receptor for ghrelin, an acylated peptide from the stomach . Somatostatin opposes the response: both somatostatin-14 and somatostatin-28 inhibited it in the original characterisation, with somatostatin-28 the more active of the two .

Q: Why is GHRP-6 historically important?

Because the receptor was found by looking for it. GHRP-6 and its relatives were synthetic compounds with no known endogenous counterpart; the search for what they bound produced the growth hormone secretagogue receptor , and the search for that receptor’s natural ligand produced ghrelin . The sequence of events is set out in the review literature on the class .

Q: Is GHRP-6 FDA approved?

No. GHRP-6 has not been approved by the U.S. Food and Drug Administration for any indication, and it holds no approval in any other jurisdiction. Its clinical literature consists of investigator-initiated pharmacological studies rather than a registrational programme.

Q: How does GHRP-6 differ from GHRP-2?

They are hexapeptides at the same receptor differing at positions 1 and 2: GHRP-6 has histidine and D-tryptophan where GHRP-2 has D-alanine and D-2-naphthylalanine. In conscious swine, GHRP-2 was more potent but less efficacious than GHRP-6 . Only GHRP-2 has reached an approved diagnostic use anywhere.

Q: How does GHRP-6 differ from ipamorelin?

Ipamorelin is a pentapeptide identified from a series lacking the central Ala-Trp dipeptide that GHRP-6 carries. In primary rat pituitary cells the two released growth hormone with similar potency and efficacy, but in conscious swine GHRP-6 raised ACTH and cortisol while ipamorelin did not .

Q: Does GHRP-6 raise cortisol?

In the one published direct comparison, yes. Administration of GHRP-6 and of GHRP-2 to conscious swine increased plasma ACTH and cortisol, while ipamorelin did not; none of the compounds tested altered FSH, LH, prolactin or TSH . That finding is from swine.

Q: Has GHRP-6 been studied in humans?

Yes, as a pharmacological probe rather than as a candidate medicine. Published studies measured growth hormone responses to intravenous administration — alone and combined with growth hormone-releasing hormone — in people with type 2 diabetes at normal weight and overweight , in hyperthyroidism , and in prolactinoma before and after dopamine agonist therapy .

GHRP-6 is a synthetic hexapeptide first described in 1984 and the founding member of the growth hormone-releasing peptide family. It is an agonist at the growth hormone secretagogue receptor, the receptor for ghrelin, and it is not approved by the FDA for any indication.

By Elegance Peptides Editorial TeamPublished September 22, 2026Updated September 22, 2026

Category: GHRH analogues and GH secretagogues

Introduction

GHRP-6 is the compound that started the field, and its scientific importance is out of proportion to anything it ever became. Described in 1984 as [His1,Lys6] GHRP, it was a synthetic hexapeptide that released growth hormone from the pituitary without releasing luteinising hormone, follicle-stimulating hormone, thyroid-stimulating hormone or prolactin, across rats, monkeys, lambs, calves and chicks ^[1]. It behaved, in the authors' words, like a hypophysiotropic hormone — except that no such hormone was known.

That anomaly drove two decades of work. Searching for what this synthetic peptide bound produced the growth hormone secretagogue receptor in 1996 ^[3]; searching for that receptor's natural ligand produced ghrelin in 1999 ^[8]. GHRP-6 itself never became a medicine anywhere. It remains a reference compound and a pharmacological probe, and this page describes it as one.

What Is GHRP-6?

GHRP-6 is a synthetic hexapeptide: His-D-Trp-Ala-Trp-D-Phe-Lys-NH2. Two of its six residues are D-enantiomers and the C-terminus is an amide, which is what allows a peptide this short to survive in plasma at all.

It is an agonist at the growth hormone secretagogue receptor — the ghrelin receptor — and acts directly on pituitary somatotrophs rather than through the hypothalamus ^{[1, 3]}. That places it in the same family as GHRP-2 and ipamorelin, and on the opposite side of a pharmacological divide from the growth hormone-releasing hormone analogues sermorelin, tesamorelin and the CJC-1295 forms.

It holds no regulatory approval in any country. Its human literature consists of investigator-initiated studies in which it was used to interrogate somatotroph function in one clinical condition or another, not to treat anything.

One naming oddity is worth recording. The FDA/NCATS Global Substance Registration System lists this substance under the preferred name Hexapeptide-2, its cosmetic-ingredient name, with GHRP-6 as a synonym.

GHRP-6 Specifications

Compound name: GHRP-6
Full chemical name: L-Histidyl-D-tryptophyl-L-alanyl-L-tryptophyl-D-phenylalanyl-L-lysinamide
Aliases: Growth hormone-releasing peptide 6, [His1,Lys6] GHRP, growth hormone releasing hexapeptide, Hexapeptide-2, His-D-Trp-Ala-Trp-D-Phe-Lys-NH2
Development code: Not publicly characterised
CAS number: 87616-84-0
PubChem CID: 9919153
UNII: 4H7N4I6X6A
Compound type: Synthetic hexapeptide
Peptide family: Growth hormone secretagogues (ghrelin receptor agonists)
Amino acid sequence: His-D-Trp-Ala-Trp-D-Phe-Lys-NH₂
Sequence length: 6 residues
Molecular formula: C46H56N12O6
Molecular weight: 873.01 g/mol
Primary target: Growth hormone secretagogue receptor 1a (GHS-R1a, the ghrelin receptor)
Secondary targets: Not publicly characterised
Receptor family: Class A (rhodopsin-like) G protein-coupled receptors
Agonist / antagonist status: Agonist at the growth hormone secretagogue receptor

GHRP-6 is written in three-letter notation because two of its six residues are D-enantiomers, which single-letter code cannot express. Position 1 is L-histidine, position 2 D-tryptophan, position 3 L-alanine, position 4 L-tryptophan, position 5 D-phenylalanine and position 6 L-lysine, with a C-terminal amide. It is the compound described in the 1984 discovery paper as [His1,Lys6] GHRP. The FDA/NCATS Global Substance Registration System records it as a chemical substance under UNII 4H7N4I6X6A with CAS registry number 87616-84-0, molecular formula C46H56N12O6 and a calculated mass of 873.02; note that the register's preferred name for it is Hexapeptide-2, the cosmetic-ingredient name, with GHRP-6 listed as a synonym. PubChem carries more than one record with this molecular formula; the identifier published here, 9919153, is the one the register cross-links. The molecular formula and mass agree with the supplier catalog values. Any figure on this page is a reference value: the certificate of analysis supplied with a laboratory order is the record for a given lot.

Values that a public register does not carry are shown as not publicly characterised rather than estimated. Identifiers are reference values; the certificate of analysis supplied with a laboratory order is the record for a given lot.

How Does GHRP-6 Work?

The receptor is the growth hormone secretagogue receptor 1a, a class A rhodopsin-like G protein-coupled receptor found in pituitary and hypothalamus and coupling principally through Gq and phospholipase C ^[3]. Its endogenous ligand is ghrelin ^[8].

Because that route is independent of the growth hormone-releasing hormone receptor and its Gs/cyclic AMP signalling, engaging both together produces a larger response than either alone — an observation made repeatedly in the human studies that administered GHRP-6 and GHRH in the same participants ^{[7, 5]}.

The response is also opposed by the other arm of the axis. In the original characterisation, both somatostatin-14 and somatostatin-28 inhibited the growth hormone response to the hexapeptide, with somatostatin-28 about four times more active in vitro and 7.5 times more active in vivo ^[1]. The compound does not override the normal regulation of the axis; it works within it.

GHRP-6 Mechanism of Action

In vitro research

In the pituitary incubate assay used in the discovery work, the minimum and maximum active concentrations ranged from 1 to 10 ng/ml ^[1]. In primary rat pituitary cells measured decades later against the rest of the family, GHRP-6 released growth hormone with an EC50 of 2.2 ± 0.3 nmol/l at an Emax defined as 100 per cent, the reference point against which ipamorelin was reported at 1.3 ± 0.4 nmol/l and 85 ± 5 per cent ^[6].

The receptor assignment for the family was established pharmacologically, by the differing blockade produced by GHRP antagonists and growth hormone-releasing hormone antagonists ^[6], and then molecularly, by cloning the receptor from pituitary and hypothalamic tissue and showing it mediates the action of these synthetic compounds ^[3]. The endogenous ligand found at that receptor, ghrelin, is an acylated 28-residue peptide from the stomach and bears no sequence resemblance to the hexapeptide that led to it ^[8].

What Is GHRP-6 Being Researched For?

Published research on GHRP-6 falls into three groups, and the first is historical rather than active:

Receptor and ligand discovery — the work that produced the growth hormone secretagogue receptor and ghrelin ^{[3, 8, 10]}.
Somatotroph function as a clinical probe — growth hormone responses in type 2 diabetes, hyperthyroidism and prolactinoma ^{[7, 2, 5]}.
Rodent models of feeding and body composition — central administration and repeated peripheral administration ^{[9, 11]}.

There has never been a registrational programme for this compound, and there is no approved use anywhere. None of the research described here is research into, or evidence about, research-grade material supplied for laboratory use.

Human Research on GHRP-6

Human clinical research

Results from pharmaceutical clinical trials describe the investigational material and populations used in those studies and should not be interpreted as establishing the effects of research-grade materials offered for laboratory use.

Growth hormone response in type 2 diabetes

Population. 21 patients with non-insulin-dependent diabetes mellitus, divided into a normal-weight group (BMI 23.31 ± 0.62 kg/m², group A) and an overweight group (BMI 27.62 ± 0.72 kg/m², group B), with 8 normal-weight control participants ^[7].

Endpoint and duration. Each participant received GHRP-6 90 µg intravenously, GHRH 100 µg intravenously, and both together, on three separate occasions. Growth hormone peak and area under the curve over 120 minutes were the measures ^[7].

Result. Growth hormone responses to GHRP-6 did not differ across the three groups — peaks of 50.95 ± 11.55, 51.96 ± 7.71 and 70.07 ± 15.59 mU/L (p > 0.05) with correspondingly non-significant differences in area under the curve. The response to GHRH, by contrast, was reduced in the overweight diabetic group relative to the normal-weight diabetic group (peak 8.25 ± 1.90 versus 22.19 ± 8.81, p < 0.05) ^[7].

Limitations. 29 participants in total, a single-centre pharmacological study with a hormone concentration as its endpoint. Its value is comparative — it distinguishes the behaviour of two receptor systems in the same people — not therapeutic.

Growth hormone response in hyperthyroidism and in prolactinoma

Population. Patients with hyperthyroidism in one study ^[2]; patients with microprolactinoma and macroprolactinoma, studied before and after bromocriptine therapy, in another ^[5].

Endpoint and duration. Growth hormone responses to GHRP-6, to GHRH, and in the prolactinoma study to both combined ^{[2, 5]}.

Result. Both studies used the compound to ask whether somatotroph responsiveness is altered by the endocrine condition under study, and whether the two receptor routes are affected differently. The prolactinoma study additionally examined whether dopamine agonist therapy changed the response ^[5].

Limitations. Small, single-centre, condition-specific pharmacological studies. They characterise a hormonal response in a disease population; none of them measured a clinical outcome, and none assessed repeated administration.

Preclinical Research on GHRP-6

Animal research

The 1984 characterisation is unusually broad by modern standards. The hexapeptide was active in rats, monkeys, lambs, calves and, under particular experimental conditions, chicks — which the authors took as evidence that its action was not species-dependent. It was active by intravenous, subcutaneous and intraperitoneal routes in rats. After intravenous administration, growth hormone rose within two minutes, peaked at 10 to 20 minutes, and had usually returned to baseline by two hours — a longer response than either of the larger growth hormone-releasing factors tested alongside it. Administered once or twice daily to immature rats for 9 or 25 days, it increased body-weight gain above control, and at the end of those studies the pituitary remained fully responsive ^[1].

Later rodent work moved to the hypothalamus. Central administration of ghrelin and of growth hormone secretagogues induced feeding and activated brain regions associated with appetite, placing this receptor in the circuitry that regulates food intake rather than only in the pituitary ^[9]. A further study found that the effects of GHRP-6 on body-weight gain and fat mass accrual in rodents depended on insulin and glucose status — that is, the same compound produced different body-composition results in different metabolic contexts ^[11].

The comparative swine pharmacology is where the compound's hormonal profile is clearest: GHRP-6 raised plasma ACTH and cortisol, as did GHRP-2, while ipamorelin did not; none of the three altered FSH, LH, prolactin or TSH. In swine, GHRP-6's ED50 was 3.9 ± 1.4 nmol/kg with an Emax of 74 ± 7 ng growth hormone per ml plasma ^[6].

Findings described in this section were observed in animals, and nothing in them establishes anything about humans.

Other Areas of GHRP-6 Research

In vitro research

The most consequential thing GHRP-6 did was to be inexplicable. A synthetic peptide that acts like a hormone implies a receptor, and a receptor implies a ligand. The receptor arrived first, cloned from pituitary and hypothalamus and shown to be the route through which this class of compound acts ^[3]; the ligand followed, isolated from stomach and found to be an acylated peptide with an octanoyl group on its third residue — a post-translational modification essential for its activity and, at the time, without precedent among mammalian peptide hormones ^[8].

The review literature of the 1990s captures the field in the interval between those two events, when the clinical and basic properties of the growth hormone-releasing peptides were well described and their endogenous counterpart was still unknown ^[4]. The fuller account of how the chemistry programme led to the receptor and the hormone is set out in a later review of the class ^[10].

This is history of science rather than pharmacology of a product, and it is the main reason GHRP-6 still appears in reference collections.

Current Research Status

Regulatory status (United States): Not approved. GHRP-6 has not been approved by the U.S. Food and Drug Administration for any indication, diagnostic or therapeutic.
Investigational status: No approval in any jurisdiction and no active clinical development programme has been identified. Its clinical literature consists of investigator-initiated pharmacological and diagnostic studies, chiefly from the 1990s, in which it served as a probe of pituitary somatotroph function in various metabolic and endocrine conditions.
Highest research phase reached: Investigator-initiated clinical pharmacology studies; no registrational programme and no approval
Approved uses: None
Approval is compound-specific: No

Status as of September 22, 2026. This block is rendered from maintained fields, not from prose, so it cannot go stale in one place and stay current in another.

Chemical & Molecular Characteristics

GHRP-6 is a hexapeptide with two D-residues and a C-terminal amide, and its register record carries a small trap for anyone matching identifiers.

The residues. Position 1 L-histidine, position 2 D-tryptophan, position 3 L-alanine, position 4 L-tryptophan, position 5 D-phenylalanine, position 6 L-lysine, C-terminal amide. The D-residues at 2 and 5 and the amide are what make a six-residue peptide survive in plasma.

The register's preferred name is not GHRP-6. The Global Substance Registration System records this substance as Hexapeptide-2 under UNII 4H7N4I6X6A, with GHRP-6, growth hormone releasing hexapeptide and the full chemical name among its synonyms. Anyone searching a register by the name GHRP-6 alone may not find it, and — a sharper hazard — a search for that name in PubChem returns records for a different compound among its hits.

More than one PubChem record shares the formula. Two PubChem compound identifiers carry the molecular formula C46H56N12O6 at a mass of 873.0. The identifier published here, 9919153, is the one the substance register cross-links. CAS registry number 87616-84-0 resolves to this substance and agrees with the supplier catalog.

Analytical Specifications

Physical form: Lyophilized powder
Appearance: White to off-white lyophilized solid
Lot number: RP-2609-076
Tested purity: ≥99% by HPLC
Storage: −20 °C, protect from light, desiccate

Analytical figures are lot-specific. Fields the catalog does not carry for the current lot are omitted rather than filled with a typical value. The certificate of analysis and the safety data sheet for the exact lot supplied are provided with a laboratory order; no purity figure on this page is a substitute for that document.

Frequently Asked Questions

What is GHRP-6?

GHRP-6 is a synthetic hexapeptide, His-D-Trp-Ala-Trp-D-Phe-Lys-NH2, first described in 1984 as [His1,Lys6] GHRP. It acts directly on pituitary somatotrophs to release growth hormone and was the founding member of the growth hormone-releasing peptide family ^[1]. It is a laboratory reagent and is not approved by the U.S. Food and Drug Administration for any indication.

How does GHRP-6 work?

Through the growth hormone secretagogue receptor, a class A G protein-coupled receptor cloned from pituitary and hypothalamus in 1996 ^[3] and shown three years later to be the receptor for ghrelin, an acylated peptide from the stomach ^[8]. Somatostatin opposes the response: both somatostatin-14 and somatostatin-28 inhibited it in the original characterisation, with somatostatin-28 the more active of the two ^[1].

Why is GHRP-6 historically important?

Because the receptor was found by looking for it. GHRP-6 and its relatives were synthetic compounds with no known endogenous counterpart; the search for what they bound produced the growth hormone secretagogue receptor ^[3], and the search for that receptor’s natural ligand produced ghrelin ^[8]. The sequence of events is set out in the review literature on the class ^[10].

Is GHRP-6 FDA approved?

No. GHRP-6 has not been approved by the U.S. Food and Drug Administration for any indication, and it holds no approval in any other jurisdiction. Its clinical literature consists of investigator-initiated pharmacological studies rather than a registrational programme.

How does GHRP-6 differ from GHRP-2?

They are hexapeptides at the same receptor differing at positions 1 and 2: GHRP-6 has histidine and D-tryptophan where GHRP-2 has D-alanine and D-2-naphthylalanine. In conscious swine, GHRP-2 was more potent but less efficacious than GHRP-6 ^[6]. Only GHRP-2 has reached an approved diagnostic use anywhere.

How does GHRP-6 differ from ipamorelin?

Ipamorelin is a pentapeptide identified from a series lacking the central Ala-Trp dipeptide that GHRP-6 carries. In primary rat pituitary cells the two released growth hormone with similar potency and efficacy, but in conscious swine GHRP-6 raised ACTH and cortisol while ipamorelin did not ^[6].

Does GHRP-6 raise cortisol?

In the one published direct comparison, yes. Administration of GHRP-6 and of GHRP-2 to conscious swine increased plasma ACTH and cortisol, while ipamorelin did not; none of the compounds tested altered FSH, LH, prolactin or TSH ^[6]. That finding is from swine.

Has GHRP-6 been studied in humans?

Yes, as a pharmacological probe rather than as a candidate medicine. Published studies measured growth hormone responses to intravenous administration — alone and combined with growth hormone-releasing hormone — in people with type 2 diabetes at normal weight and overweight ^[7], in hyperthyroidism ^[2], and in prolactinoma before and after dopamine agonist therapy ^[5].

Scientific References

Bowers CY, Momany FA, Reynolds GA, et al.. On the in vitro and in vivo activity of a new synthetic hexapeptide that acts on the pituitary to specifically release growth hormone Endocrinology; 1984. PMID 6714155 doi:10.1210/endo-114-5-1537
Ramos-Dias JC, Pimentel-Filho F, Reis AF, et al.. Different growth hormone (GH) response to GH-releasing peptide and GH-releasing hormone in hyperthyroidism The Journal of clinical endocrinology and metabolism; 1996. PMID 8636330 doi:10.1210/jcem.81.4.8636330
Howard AD, Feighner SD, Cully DF, et al.. A receptor in pituitary and hypothalamus that functions in growth hormone release Science (New York, N.Y.); 1996. PMID 8688086 doi:10.1126/science.273.5277.974
Argente J, García-Segura LM, Pozo J, et al.. Growth hormone-releasing peptides: clinical and basic aspects Hormone research; 1996. PMID 8950613 doi:10.1159/000185015
Popovic V, Simic M, Ilic L, et al.. Growth hormone secretion elicited by GHRH, GHRP-6 or GHRH plus GHRP-6 in patients with microprolactinoma and macroprolactinoma before and after bromocriptine therapy Clinical endocrinology; 1998. PMID 9509075 doi:10.1046/j.1365-2265.1998.00360.x
Raun K, Hansen BS, Johansen NL, et al.. Ipamorelin, the first selective growth hormone secretagogue European journal of endocrinology; 1998. PMID 9849822 doi:10.1530/eje.0.1390552
Micić D, Macut D, Popović V, et al.. Growth hormone (GH) response to GH-releasing peptide-6 and GH-releasing hormone in normal-weight and overweight patients with non-insulin-dependent diabetes mellitus Metabolism: clinical and experimental; 1999. PMID 10206449 doi:10.1016/s0026-0495(99)90115-4
Kojima M, Hosoda H, Date Y, et al.. Ghrelin is a growth-hormone-releasing acylated peptide from stomach Nature; 1999. PMID 10604470 doi:10.1038/45230
Lawrence CB, Snape AC, Baudoin FM, et al.. Acute central ghrelin and GH secretagogues induce feeding and activate brain appetite centers Endocrinology; 2002. PMID 11751604 doi:10.1210/endo.143.1.8561
Smith RG. Development of growth hormone secretagogues Endocrine reviews; 2005. PMID 15814848 doi:10.1210/er.2004-0019
Granado M, García-Cáceres C, Frago LM, et al.. The positive effects of growth hormone-releasing peptide-6 on weight gain and fat mass accrual depend on the insulin/glucose status Endocrinology; 2010. PMID 20219977 doi:10.1210/en.2009-1394

Every identifier above is resolved against PubMed, Crossref or ClinicalTrials.gov at build time, and the title returned by the register is compared with the title stored here. A page does not publish if a reference fails to resolve.

Research-Use Information

For in vitro research use only. This material is a laboratory reagent. It is not a drug, food, dietary supplement, or cosmetic and is not for human or veterinary use, including ingestion, injection, or any other administration. No information on this page describes or implies any effect in humans or animals. Sold only to researchers under our Terms of Sale.