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GHRP-1

Also known as growth hormone-releasing peptide-1, GHRP1

The least-studied member of the GHRP family; a few small human studies, no development beyond them.

early-clinical Growth hormone research chemical

At a glance

Category
Growth hormone
Status
research chemical
Route
intravenous and intranasal in the published human studies; subcutaneous in non-medical use
Half-life
Not established in any published human pharmacokinetic study. GH release after a bolus peaks at 15-30 minutes and has largely resolved within a few hours, but that is a pharmacodynamic observation and not a measured half-life
Onset
GH rises within minutes of an intravenous bolus, peaking at 15-30 minutes
Molecular weight
approximately 955 g/mol
Sequence
Ala-His-D-2-Nal-Ala-Trp-D-Phe-Lys-NH2 (a C-terminally amidated synthetic heptapeptide)

Not approved for human use anywhere and never developed as a medicine. It was studied in a small number of academic human experiments in the early 1990s and then abandoned in favour of GHRP-2 and GHRP-6, which received far more attention. Material sold today is labelled for laboratory research use only and is not manufactured to injectable-medicine standards. Unlike GHRP-2, GHRP-6, ipamorelin and MK-677, GHRP-1 does not appear on the FDA's category 2 list of compounding bulk substances that may present significant safety risks 5 — because it was never nominated, not because the FDA assessed it and cleared it.

Doping status: Prohibited at all times (WADA S2, growth hormone secretagogues)

Checked against the WADA 2026 Prohibited List. For a specific product and country, Global DRO is the lookup athletes are expected to use — the List names substances, not brand names.

This is a short entry. There is little or no published research on this compound, so there is correspondingly little to report. Empty dosing or reconstitution sections mean no credible figures exist — not that they were left out.

Mechanism of action

GHRP-1 is a synthetic heptapeptide agonist of the growth hormone secretagogue receptor 1a (GHS-R1a), the ghrelin receptor. It belongs to the same family as GHRP-2, GHRP-6, hexarelin and ipamorelin, all of which descend from Bowers' work on met-enkephalin-derived GH-releasing peptides in the 1970s and 1980s — a line of research that predated the discovery of ghrelin itself in 1999 and was in effect the discovery of the receptor before its natural ligand was known.

Like the other GHRPs it acts at two levels: directly on pituitary somatotrophs, where GHS-R1a couples through Gq and phospholipase C to trigger GH exocytosis, and on the hypothalamus, where it amplifies GHRH release and suppresses somatostatin tone. Bowers described this as a dual and complementary action, and it is why GHRPs produce a larger GH pulse than a GHRH analogue alone and act synergistically with one. GHRP-1 is not fully selective, but its profile is not identical to its siblings' either. In the one published human study — a 1 mcg/kg intravenous bolus in 15 healthy children and 8 patients with pituitary insufficiency — it produced a transitory rise in plasma cortisol and a significant rise in free thyroxine with a fall in TSH, both thyroid changes remaining within normal limits, while prolactin did not change 1. That last point matters, because prolactin does rise with GHRP-2 and hexarelin, and it is routinely assumed to rise with GHRP-1 by analogy. Whether GHRP-1's selectivity profile genuinely differs from GHRP-2's has never been established, because the direct comparison was not done.

What the research shows

Almost nothing is known about GHRP-1 specifically. There is a small early-1990s literature demonstrating that it releases growth hormone in humans, and a modern doping-control literature that detects its urinary metabolites — and essentially nothing else. There is no dose-finding study, no repeat-dose safety study, no efficacy study for any outcome, and no pharmacokinetic study. Everything else claimed about it is extrapolated from GHRP-2 and GHRP-6, which are different molecules studied to a different depth.

Research in humans

The principal published human study administered GHRP-1 as a bolus to healthy children and adolescents and to patients with pituitary insufficiency: all healthy children responded with a progressive rise in plasma GH peaking at 15-30 minutes, with larger responses in pubertal than prepubertal subjects, together with a transient rise in cortisol and free thyroxine and a fall in TSH 1. A 2015 anti-doping study characterised urinary metabolites in humans after intranasal administration of GHRP-1 alongside GHRP-2, GHRP-6, hexarelin and ipamorelin 2, which confirms human exposure but was not an efficacy or safety study. Beyond these, there is no clinical trial literature. There is no study of repeated dosing, and no study of any downstream outcome such as body composition, recovery or IGF-1 over time.

Animal and lab research

GHRP-1 appears in the early comparative pharmacology of the GHRP series as one of several analogues tested for GH-releasing potency in rats and other species. It was not the lead compound in any programme, and there is no substantial independent animal dataset — no toxicology programme, no carcinogenicity work, nothing of the kind required for a medicine.

Caveats. The published human work is small, uncontrolled, single-dose and thirty years old, and was designed to test a pharmacological principle rather than a therapeutic use. There is no comparison with GHRP-2 or ipamorelin that would establish any advantage. There is no toxicology. Material sold as GHRP-1 is not manufactured to injectable standards, and identity and purity are not independently verified. Because GHRPs raise cortisol and prolactin to varying degrees and GHRP-1's profile is uncharacterised, even the standard claim that it is 'like GHRP-2' is unverified.

What it is used for

  • Research: as a GHS-R1a agonist in pharmacology experiments, and as a reference compound in anti-doping metabolite detection
  • Non-medical: used for the same purposes as other GHRPs — raising GH and IGF-1 for body composition or recovery — with no human evidence for any of those outcomes

Dosing

Route
intravenous and intranasal in published research; subcutaneous in non-medical use
  • There is no established dose. No dose-finding study has been published for GHRP-1 in humans, and the studies that exist administered single doses to demonstrate a GH response, not a regimen.
  • Figures circulating for GHRP-1 are copied from GHRP-2 or GHRP-6 protocols. They are not data about this compound, and the equipotency assumption behind them has never been tested.
  • Leaving the studied-dose fields empty is deliberate, because no dose-finding study exists. The section below records the borrowed numbers that circulate anyway, as a description of user practice rather than of anything established about GHRP-1.
  • The unit trap is acute for this class: the dose that circulates is around 100 micrograms, while the vials are sold labelled in milligrams (commonly 5 mg or 10 mg). A 5 mg vial holds roughly fifty such doses, and confusing mcg with mg here is a fifty- to hundredfold overdose.

These figures describe what the literature and published protocols report. They are not advice and not a dosing instruction.

Protocols

Secretagogue 'saturation dose' pattern, borrowed from GHRP-2/6 (user-reported)

user protocol — not validated

Source: Peptide forums and vendor pages, which reuse the GHRP-2/GHRP-6 schedule

This is not a validated schedule. It is a pattern that circulates among users and sellers, reproduced because it is what people actually follow — not because it has been tested. No trial established these doses, this interval or this duration, and nobody is checking what is in the vial. Treat every number below as an assertion, not a finding.

Reported per-dose amountaround 100 mcg subcutaneously (sometimes framed as roughly 1 mcg/kg), described as a 'saturation dose'
Reported frequencyone to three times daily, typically before bed and/or before meals, often paired with a GHRH analogue such as CJC-1295 or mod-GRF(1-29)
Reported cycle lengthrun continuously for weeks to months in most accounts, with no consistent off-period

This is not a GHRP-1 protocol; it is the GHRP-2/GHRP-6 protocol with the name changed. Every number here is copied from its better-known siblings, and the assumption that GHRP-1 is equipotent has never been tested — the one published human study used a single 1 mcg/kg intravenous bolus, not a repeated subcutaneous regimen 1. The '100 mcg saturation dose' idea is community lore about the point beyond which more peptide gives little extra GH; it is not established for this molecule. Expected class effects that users report include hunger, water retention, tingling and a transient blood-pressure drop; note that prolactin, commonly assumed to rise, did not change in the one human study of GHRP-1 1, while cortisol and free thyroxine did 1. No safety data of any kind exist for repeated dosing in humans.

Schedules are reproduced as their source states them. Units, IU and milligrams explains why the figures are not interchangeable between products.

Reconstitution

Solvent
bacteriostatic water (0.9% benzyl alcohol) is what suppliers specify for research peptides of this class
Storage
Lyophilised powder is generally stored frozen and protected from light; reconstituted solution refrigerated. Any specific stability figures for GHRP-1 come from supplier claims rather than published stability studies.

No reconstitution example is given because no credible dose exists to calculate one from. Reconstitution instructions circulating for GHRP-1 are supplier text, not the product of stability testing.

Safety

Side effects

  • Transitory rise in plasma cortisol, observed after a 1 mcg/kg intravenous bolus in the one published human study 1
  • Rise in free thyroxine with a fall in TSH, observed in the same study, both remaining within normal limits 1
  • Increased hunger, an expected class effect of ghrelin receptor agonism, though it was not among the endpoints of the published study
  • Prolactin did not change in the published human study 1, despite the common assumption that GHRP-1 raises prolactin the way GHRP-2 and hexarelin do
  • Effects reported for other GHRPs but not specifically documented for GHRP-1: flushing, water retention, tingling, transient drop in blood pressure, injection site reactions, and reduced insulin sensitivity with sustained elevation of GH and IGF-1
  • No systematic safety data of any kind exists for repeated administration in humans

Do not use if

  • Active or suspected malignancy — GH secretagogues raise IGF-1, which is mitogenic and anti-apoptotic; this is an absolute contraindication for every approved drug that raises GH
  • Diabetes mellitus and impaired glucose tolerance, since sustained GH elevation reduces insulin sensitivity
  • Pregnancy and breastfeeding: no data whatsoever
  • Children and adolescents outside a supervised research setting, given effects on the growth axis
  • Competitive athletes under the WADA code: prohibited at all times
  • In general: there is no human safety dataset for repeated use, so no informed risk assessment is possible

Interactions

Not systematically studied. By class, somatostatin analogues (octreotide, lanreotide) and supraphysiological glucocorticoids blunt or abolish the GH response, GHRH analogues act synergistically with GHRPs, and raised GH and IGF-1 reduce insulin sensitivity and may increase insulin and antidiabetic requirements. None of these has been demonstrated for GHRP-1 specifically.

Sources