GHRP-2

GHRP-2 (Growth Hormone Releasing Peptide-2, also called pralmorelin or KP-102) is a synthetic hexapeptide with the sequence D-Ala-D-2-Nal-Ala-Trp-D-Phe-Lys-NH₂. It activates the growth hormone secretagogue receptor 1a (GHSR1a, the ghrelin receptor) on pituitary somatotrophs and triggers pulsatile GH release. It was developed by Cyril Bowers and colleagues at Tulane University as part of the second-generation GHRP class following GHRP-6 (the original peptide in the family). GHRP-2 has higher GH-releasing potency than GHRP-6 but produces a less pronounced increase in appetite.

The molecule was developed in the late 1980s as a refinement of GHRP-6. The structural modifications (D-amino acid substitutions, naphthylalanine at position 2) produced a peptide with greater binding affinity for GHSR1a and stronger downstream GH release. GHRP-2 is approximately 5 to 10 times more potent than GHRP-6 at raw GH stimulation per dose.

The compound received approval in Japan as KP-102/Pralmorelin for diagnostic use in evaluating GH deficiency. Patients receive an intravenous bolus and the GH response is measured. This is the only formal regulatory approval for any GHRP family member. Therapeutic use approvals have not been pursued in any major jurisdiction.

Adult anabolic use of GHRP-2 has continued since the early 2000s, often in combination with GHRH analogs (sermorelin, CJC-1295) to produce synergistic GH release. The combination practice exploits the different receptor systems (GHRH receptor and ghrelin receptor) on the same pituitary cell to produce a stronger pulse than either compound alone.

The Clinical Evidence Base

The published clinical evidence for GHRP-2 is concentrated in pharmacology and endocrine-physiology studies rather than disease-focused efficacy trials.

GH stimulation studies. Multiple Phase 1 and pharmacology studies from the 1990s and 2000s have established the GH-releasing profile of GHRP-2 in healthy subjects and patients with various endocrine conditions. The Arvat et al. 1997 paper is the most cited reference, comparing GHRP-2 with hexarelin across multiple dose levels and measuring GH, prolactin, ACTH, and cortisol responses.

Diagnostic use in GH deficiency. The Japanese KP-102/Pralmorelin approval supported clinical use of GHRP-2 as a diagnostic agent for evaluating pituitary GH responsiveness. The compound is administered intravenously and the GH response is interpreted to distinguish between hypothalamic and pituitary causes of growth hormone deficiency.

Synergy with GHRH analogs. Studies in the 1990s and 2000s established that combining GHRP-2 with GHRH (or GHRH analogs like sermorelin) produces GH responses 3 to 5 times larger than either compound alone. The synergy is mediated by the different receptor systems engaged simultaneously.

Long-term therapeutic use. Trials of chronic GHRP-2 administration for GH deficiency, age-related GH decline, or sarcopenia have not produced approved therapeutic indications. The cumulative trial dataset for chronic use is small compared with established GH replacement therapy (somatropin) or the GHRH analog tesamorelin.

The structural problem with the GHRP-2 clinical evidence is that the published trials are largely pharmacology studies rather than disease-focused efficacy programs. No Phase 3 trial in any specific indication has been completed, which limits the regulatory and clinical positioning of the compound.

GHRP-2 binds the ghrelin receptor (GHSR1a) on pituitary somatotrophs and hypothalamic neurons. The receptor activation produces a multi-component response.

GH release. Primary effect. GHSR1a activation on pituitary somatotrophs triggers a GH pulse through cAMP increase and intracellular calcium mobilization. The GH-releasing potency of GHRP-2 is substantially greater than GHRP-6 and slightly greater than hexarelin in head-to-head studies.

Cortisol and ACTH increase. Secondary effect. GHRP-2 stimulates the hypothalamic-pituitary-adrenal (HPA) axis through central mechanisms probably involving CRH or arginine vasopressin (AVP). The Arvat et al. 1997 study in Peptides reported that all tested doses of GHRP-2 stimulated ACTH and cortisol to a similar extent, with the response comparable in magnitude to that produced by human CRH. This is the main difference from ipamorelin, which produces GH release without meaningful cortisol increase.

Prolactin increase. Modest. GHRP-2 raises prolactin to a smaller extent than GH, but the increase is measurable and contributes to the overall endocrine effects.

Appetite stimulation. Mild to moderate. GHRP-2 stimulates appetite through ghrelin receptor effects on hypothalamic feeding centers, but the effect is smaller than for GHRP-6 (which is the GHRP most associated with strong appetite stimulation). Some users report measurable hunger increases, particularly at higher doses.

The pharmacokinetic profile is short. GHRP-2 has a plasma half-life of approximately 30 to 60 minutes. The GH-releasing effect is pulsatile, with the GH pulse peaking around 15 to 30 minutes after subcutaneous injection and resolving within 2 to 3 hours.

Regulatory status

Japan. GHRP-2 (as KP-102/Pralmorelin) has approved use as a diagnostic agent for evaluating GH deficiency. This is the only formal regulatory approval for any GHRP family member.

United States. GHRP-2 has no FDA approval. The compound was added to the FDA Category 2 bulks list under Section 503A in September 2023, prohibiting compounding pharmacy preparation. The compound is one of those scheduled for reconsideration at the PCAC meeting on July 23 and 24, 2026. Whether the diagnostic-only Japanese approval is sufficient to support Category 1 reclassification is uncertain.

EU and UK. No EMA or MHRA approval. The compound has not been formally evaluated for therapeutic use by major Western regulators.

WADA status. GHRP-2 is on the WADA Prohibited List under section S2 (Peptide Hormones, Growth Factors, Related Substances, and Mimetics). Use in competitive sport is a doping violation in-competition and out-of-competition. Detection methods for GHRP-2 metabolites are established.

The compound continues to be sold by online research-chemical vendors as "for laboratory use only," with the same quality control concerns that apply to the broader research-chemical peptide market.

Dosing protocols and literature-reported ranges are documented in the approved label or trial publications referenced above.

The safety profile of GHRP-2 is well characterized through pharmacology studies. The most consistent findings are:

Cortisol and ACTH increase. The most clinically meaningful adverse effect. GHRP-2 produces measurable HPA axis activation that can be problematic with chronic dosing. Sustained cortisol increase has metabolic and immune consequences that are undesirable in most adult anabolic contexts.

Prolactin increase. Modest. May cause minor effects on libido or breast tissue at higher doses. Generally not clinically significant at therapeutic doses.

Mild appetite stimulation. Less pronounced than with GHRP-6 but still present. Some users report measurable hunger increases.

Injection-site reactions. Common with subcutaneous administration. Generally mild and self-limited.

Headache, flushing, mild fatigue. Reported at low rates.

Mild glucose increase. GH-induced insulin resistance is a class effect at higher cumulative doses.

The cortisol increase is the key safety distinction from ipamorelin, which retains the GH-releasing potency without meaningfully raising cortisol. This is why ipamorelin has largely displaced GHRP-2 in adult anabolic compounding settings since the early 2000s. For diagnostic use (single-dose pituitary testing), the cortisol increase is irrelevant. For chronic anabolic use, it is a substantial drawback.

The GHRP family includes several compounds with different selectivity profiles.

GHRP-2 vs GHRP-6. GHRP-2 is more potent at GH stimulation (approximately 5 to 10 times) but produces less appetite stimulation. GHRP-6 is the older, less selective compound with stronger appetite effects.

GHRP-2 vs Hexarelin. Hexarelin has the strongest cardiac protective effects in the GHRP class. The GH-releasing potency is comparable to GHRP-2. Cortisol and prolactin effects are also comparable.

GHRP-2 vs Ipamorelin. Ipamorelin retains GH-releasing potency while substantially reducing cortisol, ACTH, prolactin, and appetite effects. This selectivity advantage is why ipamorelin has displaced GHRP-2 in most adult anabolic settings.

GHRP-2 vs MK-677. MK-677 is a non-peptide ghrelin receptor agonist with oral bioavailability. The mechanism is the same but the route of administration differs. MK-677 has a larger Phase 2 evidence base (1,200+ subjects).

GHRP-2 vs GHRH analogs (sermorelin, CJC-1295, tesamorelin). These act on the GHRH receptor rather than the ghrelin receptor. Combining a GHRP (like GHRP-2) with a GHRH analog produces synergistic GH release through engagement of both receptor systems simultaneously.

For practical adult anabolic use, ipamorelin has largely displaced GHRP-2 due to the cortisol selectivity advantage. GHRP-2 retains a niche position as the most potent of the older GHRPs and as the only approved GH secretagogue (in Japan, for diagnostic use).