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PerformancePralmorelinGrowth Hormone-Releasing Peptide-2

GHRP-2

Growth-hormone-releasing peptide · ghrelin-receptor (GHS-R1a) agonist · Japanese diagnostic agent

GHRP-2 (pralmorelin) is a synthetic hexapeptide growth-hormone secretagogue and an agonist at the ghrelin receptor GHS-R1a. Of all the growth-hormone-releasing peptides it has the most real regulatory standing: it is an approved diagnostic agent in Japan, marketed by Kaken Pharmaceutical as 'GHRP Kaken 100' to assess the pituitary's growth-hormone secretory capacity. It is a potent releaser of growth hormone in humans — releasing more than a maximal dose of GHRH — and, like GHRP-6, it synergizes with GHRH because the two act through different receptors. Three honesty caveats define it: it is approved only as a diagnostic in one country and for no therapeutic, wellness, or anti-aging use anywhere; it is not growth-hormone-selective, raising ACTH, cortisol, and prolactin as a class effect; and it measurably increases appetite in humans. It is prohibited in sport at all times.

The short version

GHRP-2 is a small lab-made peptide (six amino acids) that signals the pituitary gland to release growth hormone — through the ghrelin receptor, a different doorway than the body's own growth-hormone-releasing hormone uses.

It is the most 'real' of the growth-hormone-releasing peptides in regulatory terms: in Japan it is an approved medical test (sold as 'GHRP Kaken 100') used to check whether someone's pituitary can make enough growth hormone. That is a diagnostic use, though — not a treatment, and not an anti-aging product, anywhere.

Two honest points temper the marketing. GHRP-2 is not 'clean': along with growth hormone it also raises stress-related hormones (ACTH, cortisol) and prolactin. And it makes people hungrier — in a human study it increased food intake by about a third. It is also banned in competitive sport at all times.

01

Molecular identity

Specs

Molecular weight
818.0 g/mol (free base)
PubChem CID 6918245
Molecular formula
C45H55N9O6
PubChem CID 6918245
Monoisotopic mass
817.43 Da (free base)
PubChem CID 6918245
CAS / UNII
158861-67-7 · E6S6E1F19M
PubChem CID 6918245
Half-life
~33 min (elimination, human IV)
Sequence (6 AA)
D-Ala-D-2-Nal-Ala-Trp-D-Phe-Lys-NH₂PubChem CID 6918245
Structure / class
Synthetic GHRP-class hexapeptide (GHS-R1a agonist)Research literature
Molecular target
GHS-R1a (ghrelin receptor) on pituitary somatotrophsResearch literature
Regulatory status
Diagnostic-approved in Japan (GHRP Kaken 100); not therapeutic anywhere · WADA S2.2.4PMID 15230633 / WADA
02

Plain English

Mechanism

GHRP-2 is an agonist (a molecule that switches a receptor on) at the growth-hormone-secretagogue receptor GHS-R1a — the same receptor activated by the body's own ghrelin (the hunger hormone). Because it acts on this receptor rather than the GHRH receptor (the docking site for the body's own growth-hormone-releasing hormone), its growth-hormone-releasing mechanism is distinct from that of GHRH analogs (lab-made copies) such as sermorelin or CJC-1295, and the two classes synergize (combine for a bigger effect than either alone): in humans, a ghrelin-receptor agonist combined with GHRH produces growth-hormone release greater than either alone, whereas combining two secretagogues (GH-release triggers) that share the ghrelin receptor does not add in the same way.

GHRP-2 is a powerful growth-hormone releaser. In direct human study it released more growth hormone than the maximal (largest possible) effect of GHRH. It is not, however, growth-hormone-selective (it does not act on GH alone): alongside GH it produces a class co-release of ACTH (the hormone that drives the adrenal glands), cortisol (the body's main stress hormone), and prolactin (the milk-signaling hormone) — the prolactin rise being smaller than that produced by TRH (a thyroid-signaling hormone), and the ACTH/cortisol rise comparable to that produced by CRH (the brain's stress-axis trigger). This off-target (beyond the intended target) hormonal signature is intrinsic to the GHRP class, not an impurity effect.

As a ghrelin-receptor agonist, GHRP-2 also stimulates appetite. Unlike GHRP-6 — where the quantified human food-intake data belongs to ghrelin itself — GHRP-2 has its own direct human evidence: a subcutaneous infusion (a slow delivery into the fat under the skin) in healthy men increased food intake by about 36% and raised pre-meal hunger ratings. GHRP-2 is therefore an active orexigenic (appetite-stimulating agent) in humans, not an appetite-neutral secretagogue.

Sources:PMID 11238504PMID 9285939PMID 15699539

03

Why people reach for it

Potential benefits

GHRP-2 is the GH-releasing peptide with the most real regulatory standing — here's what draws people to it.

  • A powerful growth-hormone triggerIts headline appeal: in direct human study GHRP-2 released more GH than a maximal dose of GHRH, making it one of the strongest GH-releasing peptides per microgram.
  • Raise your own GH, not inject itIt fires the body's own GH pulse through the ghrelin receptor, so the natural feedback and rhythm stay in the loop rather than being overridden by outside hormone.
  • The GHRP with genuine regulatory tractionIt is an approved diagnostic agent in Japan (Kaken's 'GHRP Kaken 100') for assessing pituitary GH capacity — more real-world standing than any other peptide in this family.
  • Pairs synergistically with a GHRH analogBecause it works the ghrelin receptor, it stacks with a GHRH peptide for a combined pulse bigger than either alone — most commonly CJC-1295.
  • Appetite drive that can fuel a bulkIt measurably raises hunger (about +36% food intake in a human study) — a drawback when cutting, but something people deliberately use to eat enough during a weight-gain phase.

Sources:PMID 9285939PMID 11238504PMID 15699539

What people reach for GHRP-2 for, drawn from what the research reports (acute and diagnostic human data) and how it's used — not proven chronic outcomes or medical claims. Note it also raises cortisol, ACTH, and prolactin as a class effect.

04

Implied timing

Best time to dose

Implied best time

Bedtime (empty stomach)

Most people inject GHRP-2 at bedtime on an empty stomach, with extra fasted doses (morning or pre-workout) optional through the day.

  • GHRP-2 amplifies the body's own GH release, and the single largest natural GH pulse fires in early slow-wave (deep) sleep — a bedtime dose stacks the peptide's pulse on top of that nocturnal surge.
  • Food is the reason for the empty stomach: a meal raises insulin and somatostatin (GH's off-switch), both of which blunt the pulse, so the dose goes ~2 hours clear of eating (hold food 30–60 min after, too).
  • It can be pulsed 2–3× daily, all fasted, with injections spaced ≥3 hours apart — but the bedtime dose is the anchor.
  • Expect a real hunger surge in the 30–60 minutes after a dose; timing an injection where that appetite is manageable (or aligned with a planned meal) is part of the practical scheduling.

No study establishes an ideal time of day for GHRP-2 — this is reasoned from its GH-secretagogue mechanism and how it's used. As a rule of thumb peptide dosing lands in the midday-to-evening window; for GHRP-2 the lean is bedtime, fasted.

Sources:PMID 15699539

05

How to run it

Dosing & protocol

GHRP-2 is injected subcutaneously — the practical route the on-page calculator is built for. Two timing rules drive every card below: (1) inject on an empty stomach, because dietary fat and carbohydrate raise insulin and somatostatin (GH's off-switch), blunting the pulse; and (2) bedtime is the highest-leverage injection window, riding the body's own largest GH surge in deep sleep. Its human-evidence base is single-dose acute and diagnostic — the ranges and cycle below are practitioner and community convention built from that evidence, not a proven chronic regimen.

Practitioner convention extrapolated from acute human PK + diagnostic data — no published chronic-efficacy human trial exists. GHRP-2 is approved only as a diagnostic in Japan, not for wellness or anti-aging anywhere. WADA S2.2.4: prohibited in sport at all times.

Tiered dose ranges

Subcutaneous doses of 100–300 mcg per injection, run 1–3× daily on an empty stomach.

Entry / sensitivity check:
100 mcg once daily (bedtime) — establishes tolerance before adding frequency; the on-page calculator default.
Standard:
100–200 mcg 1–2× daily — the most common community range for ongoing GH-axis goals (bedtime ± fasted morning or pre-workout).
High-frequency:
100–300 mcg up to 3× daily — reserved for active recovery or loading phases; appetite and cortisol/prolactin burden increase with frequency, so this tier is time-limited.
Food window:
Hold food for at least 30–60 minutes after injection. Fat and carbohydrate blunt the GH pulse via somatostatin; a 2-hour pre-dose fast is the stricter practitioner convention.

Subcutaneous administration

Inject into subcutaneous fat; rotate sites to prevent lipohypertrophy.

Injection site:
Abdomen (2–3 cm from the navel), lateral love-handle area, or outer thigh. Rotate between sites across the day's doses.
Measuring the dose:
Drawn on a U-100 insulin syringe from the reconstituted vial. At the standard mix (5 mg vial + 2 mL BAC water = 2,500 mcg/mL): 100 mcg = 4 IU · 200 mcg = 8 IU · 300 mcg = 12 IU. The on-page calculator updates these live for any vial size.
Time of day:
Bedtime is the primary window — the body's largest GH pulse occurs in early slow-wave sleep and GHRP-2 amplifies it. A fasted morning or pre-workout dose is the common second injection. Space multiple daily doses ≥ 3 hours apart.
Appetite alert:
GHRP-2 increased food intake by ~35.9% in a controlled human study (Laferrère 2005). Expect real hunger in the 30–60 minutes post-injection — plan the post-dose meal accordingly (protein-forward; see Cofactors).

Cycle & washout

GHS-R1a desensitization occurs with continuous daily stimulation — pulsed cycling is the convention.

Standard cycle:
8–12 weeks of daily use, then a break. Some protocols use a 5-on / 2-off weekly pattern within a longer cycle to limit tachyphylaxis (diminishing response).
Washout:
4–8-week break between cycles. Because GHRP-2 also raises cortisol and prolactin, monitoring those markers during the washout is prudent on longer runs.
Honesty note:
There is no published chronic-use human trial behind any cycle length. These durations are practitioner patterns, not evidence-grounded endpoints.

Reconstitution at a glance

The on-page calculator does this live; quick reference for the default 5 mg vial:

Mixing:
5 mg vial + 2 mL bacteriostatic water = 2,500 mcg per mL. On a 100-unit (1 mL) U-100 insulin syringe: 100 mcg = 4 IU · 150 mcg = 6 IU · 200 mcg = 8 IU · 300 mcg = 12 IU.

Sources:PMID 15699539PMID 15230633PMID 11238504

06

Substrate the signal needs

Nutritional cofactor precision

GHRP-2 fires the ghrelin receptor (GHS-R1a) to spike a GH pulse — and that receptor is also the hunger switch, so appetite rises ~36% as a documented side effect. The cofactors below address three questions: what nutrient relieves the brake on GH release (somatostatin), what offsets GHRP-2's specific off-target costs (glucose drift, cortisol, prolactin, and the appetite surge), and what raw material does the resulting GH/IGF-1 signal need to do its job.

Reasoned from GHS-R1a / GH/IGF-1 physiology plus GHRP-2's documented human off-target profile (appetite +35.9%; cortisol/ACTH/prolactin co-release) — not a GHRP-2 nutrition study. Supplement doses are community convention ranges.

AMPLIFY — relieve the somatostatin brake

Somatostatin is GH's off-switch. Two nutrients blunt it, widening the pulse GHRP-2 triggers.

L-Arginine:
3–6 g on an empty stomach 30–60 min before the GHRP-2 injection. L-arginine suppresses somatostatin release, so the pituitary pulse is less dampened. Take the lower end (3 g) first — higher doses cause GI discomfort in some users.
Alpha-GPC:
300–600 mg taken ~30 min before injection (pre-bed or pre-workout). Alpha-GPC raises acetylcholine tone, which independently blunts somatostatin and potentiates the GH response. It also provides mild cognitive sharpness useful for the pre-workout window.

MITIGATE — offset GHRP-2's specific costs

GHRP-2 is not a clean secretagogue: it raises glucose, cortisol, prolactin, and appetite. Mitigate each.

Berberine 500 mg:
Taken with the post-dose meal (the protein meal ~30–60 min after injection). GH transiently raises blood glucose via insulin resistance; berberine is an AMPK activator that counteracts that glucose drift without blunting the GH pulse itself — unlike insulin secretagogues or metformin.
Alpha-lipoic acid (ALA) 600 mg:
With the same post-dose meal. ALA improves insulin sensitivity and acts as an antioxidant — a complementary second angle on the glucose-handling cost.
Cortisol / prolactin awareness:
GHRP-2 co-releases ACTH, cortisol, and prolactin alongside GH. This is an intrinsic class effect, not resolvable by a single supplement. The practical mitigation: run short cycles (8–12 weeks), avoid stacking GHRP-2 onto an already high-cortisol / under-recovery state (poor sleep, overtraining, chronic stress), and consider monitoring cortisol + prolactin markers on longer runs. If cortisol/prolactin off-target is unacceptable, Ipamorelin is the cleaner ghrelin-receptor option.
Appetite management:
GHRP-2 increased food intake by ~35.9% in healthy men (Laferrère 2005 — this file's cited figure). This is not a cofactor to suppress — it is an opening. Schedule the post-dose meal as a protein-forward intake (1.6–2.0 g protein/kg/day total; leucine-rich sources: chicken, cottage cheese, Greek yogurt). Steering the hunger toward protein turns the orexigenic effect into a GH/IGF-1 substrate advantage.

SUPPLY — feed the GH/IGF-1 signal

GH's downstream messenger (IGF-1) drives protein synthesis and tissue remodeling. Supply the substrate.

Dietary protein 1.6–2.0 g/kg/day:
The raw material for the muscle and connective-tissue synthesis IGF-1 drives. Time at least one serving (25–40 g, leucine-rich) in the window 30–90 minutes after injection — the post-dose meal when hunger peaks.
ZMA (zinc + magnesium + B6) before bed:
Zinc 25–30 mg + magnesium glycinate 300–400 mg + B6, taken 30 min before the bedtime GHRP-2 injection. Low zinc tracks with lower IGF-1; magnesium supports deep-sleep architecture (the GH pulse is sleep-dependent); B6 is a cofactor for neurotransmitter synthesis. ZMA is the single stack that supplies substrate and improves the sleep window simultaneously.
Vitamin D 2,000–5,000 IU/day:
Vitamin D receptors are expressed throughout the GH/IGF-1 axis; deficiency is associated with blunted GH responses. Dose to target serum 25-OH-D in the sufficient range (≥40 ng/mL).

Sources:PMID 15699539PMID 9285939

07

Combinations + timing

Stacking notes + timing windows

GHRP-2 occupies the ghrelin-receptor arm of GH release. The productive pairings come from the other arm (the GHRH receptor) or from a different goal entirely (tissue repair). Pairing two ghrelin-receptor agonists — GHRP-2 + Ipamorelin, GHRP-2 + GHRP-6, GHRP-2 + Hexarelin — is receptor-level redundancy: they compete for the same docking site and do not add; that pairing is convention folklore, not pharmacology.

Cross-class GHRH + GHRP synergy is grounded in human pharmacology (Arvat 2001). The specific branded combinations and recovery pairings are practitioner convention, not head-to-head trials. GHRP-2 itself has no chronic human trial, so any stack is doubly unproven. Doses are community ranges.

GHRP-2 + CJC-1295

The canonical GHRP-2 pairing — ghrelin arm + GHRH arm = synergistic GH pulse proven in human pharmacology.

Why it works:
CJC-1295 (a GHRH analog with drug-affinity complex for extended half-life) acts on the GHRH receptor (growth-hormone-releasing-hormone receptor), a completely separate docking site from GHS-R1a. In humans, co-administering a ghrelin-receptor agonist with GHRH produces greater-than-additive GH release — each molecule amplifies the other's signal because they converge on the pituitary through independent pathways.
The protocol:
GHRP-2 100–200 mcg SC + CJC-1295 100–200 mcg SC, co-injected once daily (bedtime preferred) or 1–2× daily. Because CJC-1295 with DAC has a multi-day half-life, some users inject it 1–2× per week and run GHRP-2 daily in between — the CJC-1295 maintains a GHRH background; GHRP-2 delivers the acute pulse.
Outcome:
The combination users reach for when maximizing GH output is the explicit goal — body composition, recovery, anti-aging conventions. The appetite and cortisol/prolactin costs of GHRP-2 still apply; the Cofactors above address them.

GHRP-2 + Sermorelin or Tesamorelin

Alternative GHRH partners — same synergy mechanism, different pharmacokinetic profiles.

Why it works:
Sermorelin (the first 29 AA of GHRH, short-acting) and Tesamorelin (stabilized GHRH analog, the only GHRH analog with FDA approval — for HIV-associated lipodystrophy) both act on the GHRH receptor. The same GHRH + GHRP synergy applies. Sermorelin's shorter half-life means the timing sensitivity is higher (must inject together); tesamorelin's stability makes it somewhat more forgiving.
The protocol:
GHRP-2 100–200 mcg SC + sermorelin 200–500 mcg SC, co-injected on the same schedule (bedtime ± fasted morning). With tesamorelin: 1–2 mg SC daily (its studied dose), combined with GHRP-2 at the standard range on the same or proximate injection.
Outcome:
Users reach for sermorelin when seeking a shorter-acting, lower-cost GHRH partner. Tesamorelin is chosen when the documented human evidence trail is the priority — it has the richest GHRH-analog clinical data set. Either way, GHRP-2's off-target cortisol/prolactin/appetite profile is unchanged by the GHRH partner.

GHRP-2 + BPC-157 + TB-500

Recovery backdrop — the GH/IGF-1 surge from GHRP-2 amplifies the local tissue repair driven by the other two.

Why it works:
BPC-157 rebuilds gut lining and connective tissue and brings angiogenesis (new blood vessels) to the repair site; TB-500 (Thymosin β4) migrates repair cells into damaged tissue. GHRP-2 adds an anabolic backdrop — the GH/IGF-1 axis is the systemic signal that upregulates collagen synthesis and protein accretion, amplifying the local repair work the other two do. Three different levers: local repair + cell migration + systemic anabolic signal.
The protocol:
GHRP-2 100–200 mcg SC 1–2× daily (bedtime ± morning); BPC-157 250–500 mcg SC once daily near the injury site; TB-500 on its own loading-then-maintenance schedule (higher weekly dose for the first 2–4 weeks, then a lower maintenance dose). All three can be drawn into separate syringes or injected at nearby sites.
Outcome:
The combination users reach for on active recovery from soft-tissue injury, surgery, or heavy training blocks where gut health, connective tissue, and anabolic drive overlap. GHRP-2's appetite effect in this context becomes an asset — the extra hunger feeds the repair.

Sources:PMID 11238504PMID 15699539

08

Reconstitution math

Reconstitution calculator

Reconstitution calculator

Calculated for a 1 mL U-100 insulin syringe (100 units/mL).

mg
mL

Units per dose

4

Draw to this mark on a U-100 syringe

Volume per dose
0.04 mL
Doses per vial
50
Concentration
2.5 mg/mL

One vial lasts

Daily
50 days
Every other day
100 days
5×/week
70 days

Research use only. Not for human consumption. Outputs are reference values based on research literature — verify all measurements independently.

09

From the studies

Side effects from research

The two characteristic off-target (beyond the intended target) signals are hormonal and orexigenic (appetite-raising). GHRP-2 is not growth-hormone-selective (it does not act on GH alone): in human study it raised ACTH (the adrenal-driving hormone), cortisol (the main stress hormone), and prolactin (the milk-signaling hormone) alongside growth hormone — the prolactin rise smaller than that from TRH (a thyroid-signaling hormone), the ACTH/cortisol rise comparable to that from CRH (the brain's stress-axis trigger). This co-release is a property of the GHRP class.

GHRP-2 also stimulates appetite. In a controlled human infusion study (a slow steady delivery) it increased food intake by about 36% and raised pre-meal hunger ratings — direct evidence that GHRP-2 is an active orexigenic (appetite-stimulating agent), not appetite-neutral.

GHRP-2 is approved only as a diagnostic agent (a medical test) in Japan and is not an approved therapeutic (treatment) anywhere; there is no modern chronic-use (long-term) clinical safety dataset for wellness or anti-aging purposes, and claims of long-term benefit are not supported by a published chronic human trial.

Sources:PMID 9285939PMID 15699539PMID 15230633

10

As reported in literature

Research dosing ranges

These are the doses actually used in the published studies — the evidence the practical figures above lean on, shown separately so research data is never mistaken for an endorsed chronic dose. GHRP-2's human data is acute (single-use) and diagnostic rather than chronic (long-term). The three best-characterized contexts are: the single-dose growth-hormone-provocation test (a one-time injection used to measure the pituitary's GH output) that underlies its Japanese diagnostic approval, a Phase I (first-in-human) pharmacokinetic study (how the body absorbs and clears the drug) in children, and a short appetite-infusion study (a slow few-hour delivery) in healthy men. There is no published chronic-efficacy human trial — US therapeutic development was discontinued at Phase II (the mid-stage human-trial step). These are not endorsed protocols.

DoseRouteModelOutcomeSources:
100 µgIV bolusHuman (GH-deficiency diagnosis)Approved diagnostic GH-provocation test in Japan ('GHRP Kaken 100')PMID 15230633
1 µg/kgIV bolusHuman (10 prepubertal short-stature children)Peak GH ~50.7 ng/mL; elimination half-life ~33 min (Phase I PK)PMID 9543135
1 µg/kg/h × 270 minSC infusionHuman (7 lean healthy men)Food intake +35.9%; higher pre-meal hunger ratingsPMID 15699539
11

Quick answers

Frequently asked

Is GHRP-2 an approved drug?

Only in one country and only for diagnosis. In Japan, GHRP-2 (pralmorelin) is approved as a diagnostic agent — marketed by Kaken Pharmaceutical as 'GHRP Kaken 100' — to assess the pituitary's growth-hormone secretory capacity. It is not approved for any therapeutic, wellness, or anti-aging use anywhere, it is not FDA-approved, and US therapeutic development was discontinued at Phase II.

How is GHRP-2 different from GHRP-6?

Both are hexapeptide agonists at the same ghrelin receptor (GHS-R1a) and both raise cortisol and prolactin. GHRP-2 is commonly described as the stronger growth-hormone releaser per microgram and is the one with real regulatory traction (the Japanese diagnostic). Importantly, GHRP-2 is not appetite-neutral: it measurably increased food intake (about 36%) in a human study — the 'cleaner than GHRP-6' framing is relative, not absolute.

Does GHRP-2 raise cortisol?

Yes. In direct human study GHRP-2 raised ACTH, cortisol, and prolactin alongside growth hormone. The ACTH/cortisol response was comparable to that produced by CRH and the prolactin response was smaller than that from TRH. This co-release is an intrinsic class effect of the growth-hormone-releasing peptides, so 'cortisol-free' marketing is not supported by the primary data.

How does GHRP-2 differ from sermorelin or CJC-1295?

Sermorelin and CJC-1295 are GHRH-receptor agonists; GHRP-2 acts on a different receptor — the ghrelin receptor (GHS-R1a). Because they work through independent pathways, combining a GHRP with a GHRH analog produces synergistic growth-hormone release.

Is GHRP-2 banned in sport?

Yes. Growth-hormone secretagogues including GHRP-2 (pralmorelin) are named on the WADA Prohibited List under Section S2.2.4 (GH-releasing peptides) and are prohibited at all times, in and out of competition.

What is GHRP-2's half-life?

In a Phase I intravenous study in children, GHRP-2 had an elimination half-life of about 33 minutes after a single 1 µg/kg dose.

12

Primary sources

References

  • PubChem CID 6918245PubChem — Pralmorelin / GHRP-2 free base (CID 6918245)
  • PMID 15230633Pralmorelin (KP-102, GPA-748) Adis R&D profile 2004 — Japanese diagnostic approval, discontinued US development (Drugs R D)
  • PMID 9285939Arvat et al. 1997 — GHRP-2 & hexarelin GH potency and ACTH/cortisol/prolactin co-release in humans (Peptides)
  • PMID 11238504Arvat et al. 2001 — ghrelin/GHS-R agonism, GHRH synergy, distinct receptors (JCEM)
  • PMID 9543135Pihoker et al. 1998 — Phase I pharmacokinetics of GHRP-2 in children, ~33 min elimination half-life (JCEM)
  • PMID 15699539Laferrère et al. 2005 — GHRP-2 increases food intake (+35.9%) in healthy men (JCEM)
  • WADA Prohibited List S2.2.4WADA Prohibited List — S2.2.4 GH-Releasing Peptides (GHRP-2/pralmorelin named)

Research use only · Not medical advice · Updated 2026-06-01