GHRP-1
An early-generation GH-releasing heptapeptide from the same Bowers series as GHRP-6, almost entirely displaced by ipamorelin and GHRP-2 and rarely worth sourcing today.
Also known as Growth Hormone Releasing Peptide-1
Human trials — Studied in people, typically early phase or small — promising rather than proven.
Small early human studies from the Bowers GHRP series demonstrated GH release, but GHRP-1 was never developed further and there is no modern human pharmacokinetic, dose-response or safety data. Sourcing quality is also poorer than for the mainstream GHRPs because demand is so low.
How it works
GHRP-1 belongs to the original series of synthetic met-enkephalin-derived GH-releasing peptides developed by Cyril Bowers, and shares the core pharmacology of GHRP-2 and GHRP-6: GHS-R1a agonism at the somatotroph plus suppression of hypothalamic somatostatin tone. Its GH-releasing potency sits below GHRP-2 and hexarelin, and its selectivity profile was never characterised in humans to the depth of the other members of the family. It has no distinguishing advantage, which is precisely why it disappeared from both the clinical pipeline and the grey market. Anyone using it is effectively running a weaker GHRP-2 with less published data.
Targets: GHS-R1a (ghrelin receptor), Pituitary somatotrophs, Hypothalamic somatostatin neurons
Dosing
| Protocol | Dose | Frequency | Route |
|---|---|---|---|
| Extrapolated GHRP protocolFasted, one dose at bedtime. | 100 mcg – 200 mcg | one to three times daily | subcutaneous |
- · There is no established human dosing schedule for GHRP-1. This range is borrowed wholesale from GHRP-2 and GHRP-6 practice and should be treated as a guess, not a protocol.
Titration
Start at the low end - 100 mcg once daily - given how thin the human data is.
Cycling
By analogy with the class, eight to twelve weeks then a four-week break. There is no data specific to this compound.
Pharmacology
- Half-life
- Not established in humans; assumed to be in the 15-to-60-minute range typical of the hexapeptide GHRPs.
- Onset
- GH pulse within 15 to 30 minutes of injection, by analogy with the rest of the class.
- Routes
- subcutaneous, intramuscular
- Molecule
- Synthetic heptapeptide GHRP (GHS-R1a agonist)
- Sequence length
- 7 amino acids
Handling
- Diluent
- Bacteriostatic water
- Typical mix
- 2 or 3 mL
- Vial sizes
- 5 mg
- Lyophilised
- Refrigerate; freeze for long-term.
- Reconstituted
- Refrigerated, use within about 30 days.
- Light sensitive
- Yes — keep it out of the light
Mixing
A 5 mg vial in 2.5 mL gives 2000 mcg/mL; 5 units on a U-100 syringe is 100 mcg.
Side effects
- commonIncreased appetite— Expected from the class; magnitude not characterised for this specific peptide.
- commonWater retention
- commonInjection-site reaction
- commonFlushing or head rush
- uncommonElevated cortisol and prolactin— Class effect; not specifically quantified for GHRP-1.
Do not use if
- Active malignancy.
- Poorly controlled diabetes.
- Pregnancy and breastfeeding.
Combining it
- synergycjc-1295-no-dac — GHRH plus GHRP synergy is a class effect and should apply here.
- redundantipamorelin — Same receptor, and ipamorelin has vastly more supporting data.
- redundantghrp-2 — Same receptor and same series.
What to monitor
- · IGF-1 at baseline and 8 to 12 weeks - the only way to know whether it is doing anything.
- · Prolactin and cortisol if used chronically.
Legal status
Never approved anywhere; sold as a research chemical. Prohibited in sport under WADA S2.
References
- Bowers et al., early GH-releasing peptide series characterisation (preclinical)
Mechanism in depth
There is very little to say about GHRP-1 that is specific to GHRP-1, and pretending otherwise would be inventing content. It is a heptapeptide from the same Bowers met-enkephalin-derived series that produced GHRP-2 and GHRP-6, sharing the same GHS-R1a pharmacology: Gq/PLC signalling at the somatotroph, hypothalamic somatostatin suppression, and the same GHRH synergy the family shows. Its GH-releasing potency sits below GHRP-2 and hexarelin, and unlike them it was never characterised in humans to any depth - there is no dose-response study, no selectivity profiling against ACTH and prolactin, no pharmacokinetics. It never distinguished itself on any axis, which is exactly why it disappeared from both the clinical pipeline and, mostly, from the grey market. Anyone running it is running a less-studied, probably weaker GHRP-2. The honest framing is that this compound's Extended tier is thin because the underlying evidence is thin, not because nobody looked.
What usually goes wrong
Sourcing is the practical problem. Demand for GHRP-1 is low enough that the vendors carrying it are usually the ones carrying everything, and low-volume products get less quality attention, not more. Because there is no established dose-response, the 100 to 200 mcg range everyone quotes is borrowed wholesale from GHRP-2 and GHRP-6 practice and may be wrong in either direction. And because the selectivity profile is unknown, you cannot predict whether you will get GHRP-2-like prolactin drift, hexarelin-like cortisol, or neither. The failure mode specific to this compound is spending money and months on something that is strictly dominated by better-characterised alternatives.
Bloodwork worth running
| Marker | When | Why it matters |
|---|---|---|
| IGF-1 | Baseline and at 8 weeks. If it has not moved, stop; there is no argument for persisting with an uncharacterised compound that is not producing a measurable effect. | With a compound this poorly characterised, IGF-1 is not a monitoring marker - it is the only evidence you will have that anything is happening at all.Act if: Flat IGF-1 at 8 weeks means stop. |
| Prolactin and morning cortisol | Baseline and at 8 weeks. | The selectivity of GHRP-1 against ACTH and prolactin has never been profiled in humans. That means you are the profiling study, and you should collect the data.Act if: Any rise above the reference range means switch to a compound where this question has been answered. |
| Fasting glucose | Baseline and 12 weeks. | Class effect, presumed rather than demonstrated.Act if: Crossing 100 mg/dL is a reason to stop. |
Pharmacokinetics
- Metabolism
- Presumed peptidase hydrolysis by analogy with the rest of the family. Not studied.
- Elimination
- Not characterised.
Receptor targets
- GHS-R1a, pituitary somatotroph — Lower potency than GHRP-2 and hexarelin; no quantitative human data
GH release by the standard GHS-R1a route. Magnitude and dose-response uncharacterised in humans.
- GHS-R1a, hypothalamic somatostatin neurons — Not characterised
Presumed somatostatin suppression by class analogy. Not demonstrated for this compound specifically.
What to expect, and when
Presumed to follow the class: GH rising within 15 minutes, peaking by 30, gone within two hours. This is extrapolation, not observation - no human onset data for GHRP-1 was located. Any IGF-1 change would follow the usual 8-to-12-week timeline.
Stacking and comparisons
The GHRH-plus-GHRP synergy is a class effect and should apply here, but nobody has demonstrated it for this specific peptide. Every other GHRP in this class - ipamorelin, GHRP-2, GHRP-6, hexarelin - has more human data and at least as much potency, so there is no stacking scenario where GHRP-1 is the correct choice. If someone has a vial, the sensible use is with 100 mcg of a GHRH analogue and an IGF-1 draw at eight weeks to find out whether it does anything.
Against every other GHRP: worse. Less potent than GHRP-2 and hexarelin, less selective than ipamorelin as far as anyone knows, and less studied than any of them. There is no goal for which GHRP-1 is the best available answer. The only honest reason to use it is curiosity or because you already own a vial.
Rough cost
$30–$80/month. Approximate and unreliable. GHRP-1 is stocked by few vendors and priced inconsistently, often higher than GHRP-2 or GHRP-6 despite being less useful, simply because volume is low. Figures are rough observations.
Genuinely uncertain
- No human pharmacokinetic data of any kind: no half-life, tmax, bioavailability, clearance or volume of distribution.
- No human dose-response study, so the 100 to 200 mcg dosing range is entirely borrowed from other GHRPs.
- The selectivity profile against ACTH, cortisol and prolactin has never been characterised in humans.
- The sequence Ala-His-D-2-Nal-Ala-Trp-D-Phe-Lys-NH2 is reported in secondary sources but was not resolved from a primary structural reference, and no molecular weight is given in the Core record because none was confidently established.
- The Core record's claim that early human studies from the Bowers series demonstrated GH release is plausible and consistent with the history, but no specific GHRP-1 human study was located in this session.
- Product identity and purity risk is higher than for mainstream GHRPs because of low demand and low vendor attention.
Papers
- GH releasing peptides - structure and kinetics Bowers CY, Journal of Pediatric Endocrinology, 1993 · PMID 8374685
Further reading rather than evidence for GHRP-1 specifically. Bowers' own account of the peptide series this compound belongs to.
- Growth hormone-releasing peptides: clinical and basic aspects Argente J, García-Segura LM, Pozo J, Chowen JA, Hormone Research, 1996 · PMID 8950613
Further reading. A contemporary review covering the GHRP series as a whole.