GHRP-2

GHRP-2 (pralmorelin, KP-102) is a synthetic hexapeptide growth hormone secretagogue and ghrelin mimetic that binds the growth hormone secretagogue receptor (GHS-R1a) in the pituitary and hypothalamus. Occupancy at somatotrophs produces short, high-amplitude pulses of endogenous GH rather than a flat exogenous level, leaving the negative feedback loop intact.

It was among the first secretagogues developed and is approved in Japan as a diagnostic agent for growth hormone deficiency; it holds no therapeutic approval in the US or Europe. Published work spans intravenous, subcutaneous, intranasal and oral administration, with clinical use in paediatric GH deficiency, appetite stimulation and provocative diagnostic testing, plus animal work on tendon healing.

On the selectivity spectrum, GHRP-2 is intermediate. Raun et al. (1998) established ipamorelin as the first selective secretagogue, with no meaningful ACTH or cortisol release even at doses more than 200 times the GH-effective dose, while both GHRP-2 and GHRP-6 raised plasma ACTH and cortisol. Arvat et al. (1997) found GHRP-2 and hexarelin both produced GH responses exceeding GHRH, alongside ACTH and cortisol release comparable to the corticotropin-releasing hormone test and prolactin release below that of TRH. GHRP-6 and hexarelin sit at the less selective end, with stronger orexigenic effect and larger cortisol, prolactin and ACTH spikes.

Desensitisation is the distinguishing liability against ipamorelin, which is why cycling is treated as mandatory rather than optional. Subcutaneous bolus is the practical route; injection-site handling and reconstitution with bacteriostatic water apply as for other GHRPs.

GHRP-2 is a ghrelin mimetic acting at GHS-R1a. GH secretion depends on two arms: hypothalamic GHRH, which drives synthesis and release from somatotrophs, and ghrelin, which triggers release of stored GH while suppressing somatostatin, the inhibitory brake. GHRP-2 reproduces the ghrelin arm.

Receptor activation signals through calcium channel modulation, cyclic AMP activation and protein kinase C. Action is dual-site: directly on pituitary somatotrophs to trigger release, and on the hypothalamic arcuate nucleus to modulate regulation from above. Combined stimulation plus disinhibition is why GHRPs generate pulses larger than either mechanism alone.

Kinetics are brief. GH peaks at approximately 15 minutes and returns to baseline within 90 to 120 minutes; GHRP-2's own half-life is approximately 15 to 30 minutes. Hence 2 to 3 daily administrations to sustain elevated GH exposure. Doi et al. (2004) characterised GHRP-2 as showing superior GH-releasing activity to exogenous GHRH in conscious rats, with less sensitivity to suppression by endogenous somatostatin, and activity in conscious dogs where GHRH was ineffective.

Downstream, hepatic GH signalling raises IGF-1, the effector for muscle protein synthesis, lipid metabolism, tissue repair and collagen production.

GHRH dependency is a key mechanistic constraint: Alba et al. (2005) showed GHRP-2 could not restore adequate GH secretion in GHRH knockout mice without functional GHRH signalling. This is the rationale for pairing with a GHRH analogue such as CJC-1295 without DAC — GHRP-2 triggers the pulse while the GHRH analogue amplifies and extends it, with reported synergy of 77 to 225% greater GH release than either compound alone.

Selectivity: moderate cortisol and prolactin elevation at standard doses, with ACTH and cortisol responses similar to the corticotropin-releasing hormone test and prolactin release lower than TRH (Arvat et al., 1997). Insulin opposes GH release, which underpins fasted administration.

Somatotropic axis: GHS-R1a agonism produces dose-dependent, high-amplitude GH pulses, with a single injection elevating GH above baseline for approximately 90 minutes. Pharmacological testing showed GH-releasing activity superior to exogenous GHRH and reduced sensitivity to somatostatin suppression.

Anabolic: elevated GH and IGF-1 support muscle protein synthesis, nutrient partitioning and inhibition of catabolism. Phung et al. (2000) reported average daily gain up 22.35% and feed efficiency up 20.64% over 30 days of chronic administration in swine.

Metabolic: GH-driven lipolysis via hormone-sensitive lipase activation, hydrolysing stored triglycerides to free fatty acids; reduced adiposity, particularly abdominal, is the common report. Enhanced insulin regulation is part of the ghrelin-mimetic profile, though GH itself can impair insulin sensitivity.

Orexigenic: moderate, receptor-mediated appetite stimulation — Laferrere et al. (2005) recorded a 35.9% increase in food intake, with every subject increasing intake, milder than GHRP-6.

Musculoskeletal repair: accelerated cellular repair and tissue regeneration; Li et al. (2025) showed reduced M1 macrophage polarisation with improved histologic score, bone mineral density, maximal failure load and stiffness in a rat rotator cuff model — preliminary, single-study evidence.

Skeletal: increased bone strength with support for calcium regulation.

Sleep architecture: improved subjective sleep quality and REM cycles, relevant given the dominant nocturnal GH pulse between 10 PM and 2 AM.

Cardiovascular and immune: supports cardiomyocyte survival and repair; enhanced thymic function and immune response.

Hepatic: may reduce hepatic inflammation and stimulate healing via localised stem cell activity.

CNS: anti-ageing and neuroprotective effects, improved mood with reduced impulsivity.

Diagnostic: approved in Japan as a provocative test for GH deficiency, validated in both paediatric and elderly populations.

No published human data establishes body composition or performance timelines for GHRP-2 as used in practice — daily subcutaneous bolus for optimisation. What follows is aggregated user reporting plus extrapolation from the GH literature.

Weeks 1 to 2. The endocrine response is immediate: GH peaks at approximately 15 minutes post-injection and returns to baseline within 90 to 120 minutes. Earliest reported effects are improved sleep quality with evening dosing, moderate orexigenic effect, and mild fluid retention.

Weeks 2 to 4. Inter-session recovery improves; early body composition shifts may become apparent; sleep effects stabilise.

Weeks 4 to 8. Cumulative GH and IGF-1 elevation becomes visible — reduced body fat, improved muscle fullness, better skin quality, improved training recovery and enhanced well-being.

Weeks 8 to 16. Continued body composition and performance gains, with possible partial attenuation of the peak GH response under chronic dosing. Phung et al. (2000) observed attenuation between day 1 and day 10 in swine while growth-promoting effects persisted across 30 days. Hexarelin data show attenuation by 16 weeks of twice-daily use that reverses fully after 4 weeks off, which is the basis for cycling.

Users consistently describe the effect as more subtle than exogenous HGH but meaningful alongside solid training and nutrition. Response magnitude varies with age — lower baseline GH in older individuals tends to produce more pronounced effects — plus body composition, training status, sleep and nutrition. A few users report cortisol-like effects at higher doses (irritability, disrupted sleep) that resolve on dose reduction, consistent with GHRP-2's non-selective ACTH and prolactin activity. Monitoring IGF-1 at 4 to 6 weeks confirms the peptide is working and that levels are not excessive.

Published dosing is unrelated to practical use: intranasal 5 to 15 mcg/kg in children, subcutaneous infusion at 1 mcg/kg/hour in the food intake study, stepwise subcutaneous 0.3, 1.0 and 3.0 mcg/kg/day in the graded dose study, and intravenous 0.1 to 10 mcg/kg in animals. No published dose-finding studies exist for the subcutaneous bolus protocols used in practice; the protocols below reflect clinical practice patterns as reported by users.

Reconstitution: 5 mg vial with 2 mL bacteriostatic water, yielding 250 mcg per 10 insulin units (2.5 mg/mL, 25 mcg per unit). Diluent down the vial wall, swirl, do not shake. Use 0.3 mL (30 unit) syringes — the therapeutic window falls at 4 to 12 units, where a 1 mL barrel has poor resolution.

Solo: 100 to 300 mcg per injection, 2 to 3 times daily, fasted, timed morning, pre-workout and/or pre-bed. Body-weight tiering in practice: under 150 lbs, 100 to 150 mcg per injection; 150 to 200 lbs, 150 to 200 mcg; over 200 lbs, 200 to 300 mcg. With CJC-1295 without DAC, 100 to 200 mcg of each per injection, 2 to 3 times daily, mixable in the same syringe; reported synergy is 77 to 225% greater GH release than either alone. An anti-ageing pattern of 150 mcg once nightly pre-sleep aligns the dose with the slow-wave-sleep GH pulse.

Fasted administration is mechanistically required: insulin and GH are inversely related, so dose at least 1 hour before food or 2 to 3 hours after, and delay eating 30 minutes post-injection. Exploiting the orexigenic effect means dosing 30 minutes pre-meal.

Cycling: hexarelin data show partial, fully reversible attenuation after 16 weeks of twice-daily use, resolving after 4 weeks off. Practical cycles are 12 to 16 weeks on with 4 weeks off, 8 to 16 weeks solo, 8 to 12 weeks combined with CJC-1295, or 8 to 12 weeks with a 4-week washout. Avoid stacking two GHRPs — they compete at the same receptor.

GHRP-2 (KP-102, Pralmorelin) has human and animal data dating to the 1990s and is approved in Japan as a diagnostic agent for GH deficiency.

Appetite: Laferrere et al. (2005) infused GHRP-2 subcutaneously at 1 mcg/kg/hour versus saline for 270 minutes in 7 lean healthy males before a buffet meal. Intake rose 35.9% (101.3 to 136.0 kJ/kg); every subject increased intake, with significant rises in serum GH. First demonstration that GHRP-2, like ghrelin, increases food intake in humans.

Paediatric growth: Pihoker et al. (1997) treated 15 children of short stature with intranasal GHRP-2 at 5 to 15 mcg/kg twice daily for 3 months, then three times daily; height velocity rose from 3.7 to 6.1 cm/year at 6 months and 6.0 cm/year at 18 to 24 months, with increased GH binding protein and no side effects. Mericq et al. (1998) gave 6 prepubertal GH-deficient children graded subcutaneous doses of 0.3, 1.0 and 3.0 mcg/kg/day over successive 2-month periods: dosewise increases in overnight GH secretion, short-lived with little late-night effect, improved growth velocity, no toxicities; longer-acting formulations were judged necessary.

Selectivity: Arvat et al. (1997) compared GHRP-2 and hexarelin — both produced GH responses exceeding GHRH, but both also stimulated ACTH and cortisol at levels similar to hCRH and prolactin below TRH. Raun et al. (1998) established ipamorelin as the first selective secretagogue, with no meaningful ACTH or cortisol release even above 200 times the GH-effective dose, while GHRP-2 and GHRP-6 raised both.

Pharmacology and animal data: Doi et al. (2004) found superior GH-releasing activity versus exogenous GHRH in conscious rats, lower sensitivity to endogenous somatostatin, activity in dogs where GHRH failed, and growth acceleration over 3 weeks. Phung et al. (2000) in swine showed dose-dependent GH release peaking at 15 minutes and returning to baseline by 120 minutes, average daily gain +22.35% and feed efficiency +20.64% over 30 days, with some attenuation between day 1 and day 10. Alba et al. (2005) showed GHRP-2 requires intact GHRH signalling. Li et al. (2025), a single rat rotator cuff study, showed reduced M1 macrophage polarisation with better histology, bone mineral density, failure load and stiffness — preliminary.