TL;DR
The only GHRP with a real regulatory approval. One 100 μg IV bolus in one country. Every other dose is extrapolation.
What is it? A six-amino-acid ghrelin-receptor agonist. D-2-naphthylalanine at position 2 makes it more potent than GHRP-6 with less appetite kick. Brand: GHRP Kaken 100.
What does it do? Activates GHS-R1a on pituitary somatotrophs and hypothalamic neurons to fire a GH pulse. Synergizes multiplicatively with GHRH. Less somatostatin-blunted than GHRH alone.
Does the evidence hold up? Japan PMDA approved it in 2004 for single-dose GH-deficiency diagnosis (126 children, 84 facilities). Pediatric short-stature therapeutic Phase II failed. Chronic SubQ multi-daily dosing is off-label everywhere.
Who uses it? Japanese endocrinologists. Community users running 100–200 μg SubQ two to three times daily, usually layered with a GHRH analog.
Bottom line? Best-documented hexapeptide GHRP. Chronic-use evidence belongs in the inferred column.
What It Is
GHRP-2 (Growth Hormone-Releasing Peptide-2; INN pralmorelin; developmental codes KP-102, GPA-748, WAY-GPA-748) is a synthetic hexapeptide growth hormone secretagogue with the sequence D-Ala-D-(β-naphthyl)-Ala-Trp-D-Phe-Lys-NH2 and a molecular weight of 817.97 g/mol. It is the second-generation member of the GHRP family, developed by structure-activity-relationship optimization of the parent GHRP-6. Substituting D-2-naphthylalanine at position 2 produced substantially enhanced GH-releasing potency per molecule and reduced the prominent appetite-stimulating signal characteristic of GHRP-6.
GHRP-2 is the most clinically advanced of the classical first-generation hexapeptide GH secretagogues. It received approval from Japan's Pharmaceuticals and Medical Devices Agency (PMDA) in October 2004 and is marketed by Kaken Pharmaceutical under the brand name GHRP Kaken 100 as a single-dose intravenous diagnostic agent for the assessment of growth hormone deficiency (GHD) in adults and children over 4 years of age. The Japan approval was based on multicenter clinical trials across 84 Japanese facilities demonstrating reliable discrimination between GH-deficient and GH-sufficient patients with a single 100 mcg IV bolus. This makes GHRP-2 unique among the GHRPs — and unique among the peptides commonly discussed in the optimization community — as a compound with active regulatory approval in a major pharmaceutical market for a defined diagnostic indication.
That regulatory approval is for diagnostic use only — a single 100 mcg IV bolus to evaluate pituitary GH secretory capacity. Phase II clinical trials of GHRP-2 for therapeutic treatment of growth hormone deficiency and short stature in children were conducted but the therapeutic indication was discontinued; intranasal GHRP-2 failed to produce clinically meaningful growth promotion despite measurably increasing endogenous GH secretion (Pihoker et al. 1997, J Endocrinol). Chronic SubQ multi-daily dosing for body composition, recovery, and "hyperphysiologic GH pulsing" — the use the optimization community pursues — is off-label everywhere, including in Japan, and operates on community convention rather than approved clinical evidence.
Compared to its sibling GHRP-6, GHRP-2 is the better-rounded compound for most users seeking a GH pulse without prominent hunger. It produces stronger peak GH release per unit dose, with notably less appetite stimulation and similar (modest) cortisol / prolactin elevation. Compared to ipamorelin — the modern selective GHS — it produces a larger GH peak but with a measurably less clean cortisol / prolactin profile. Among the classical hexapeptide GHRPs, GHRP-2 occupies the middle ground: more potent than GHRP-6, less selective than ipamorelin, less cortisol-stimulating than hexarelin.
Mechanism of Action
GHRP-2 is a synthetic ghrelin receptor (GHS-R1a) agonist that acts at both pituitary somatotrophs and hypothalamic neurons to drive pulsatile GH release. Its mechanism overlaps significantly with the rest of the GHRP family but differs in potency and receptor-pathway selectivity due to the D-2-naphthylalanine substitution at position 2.
- GHS-R1a agonism (primary mechanism) — GHRP-2 binds and activates GHS-R1a, a Gαq-coupled GPCR expressed in anterior pituitary somatotrophs and hypothalamic arcuate neurons. The D-2-naphthylalanine residue at position 2 (replacing the D-Trp of GHRP-6) provides bulky aromatic side-chain interactions with the GHS-R1a binding pocket, producing more efficient receptor activation per molecule — the structural basis for GHRP-2's higher GH-releasing potency.
- Reduced ghrelin-mimetic appetite signal — Despite agonizing the same receptor as GHRP-6, GHRP-2 produces noticeably less appetite stimulation in human studies. The mechanism is not fully resolved; likely candidates include differential downstream signaling at GHS-R1a (functional selectivity / biased agonism), differential receptor-pool engagement (somatotroph vs arcuate), or differential intrinsic activity at receptor subpopulations.
- Synergy with GHRH (Bowers-style) — GHRP-2 acts synergistically with GHRH on GH release through complementary signaling at the somatotroph: GHRH activates Gs / cAMP / PKA and GHRP-2 activates Gq / IP3 / Ca²⁺. The two pathways converge on GH exocytosis, producing multiplicative rather than additive responses. This is the rationale for routine GHRH + GHRP combination protocols (Pandya 1998, PMID 9543138).
- Less somatostatin-sensitive than GHRH — Doi et al. 2004 (PMID 15646370) showed in conscious rats that KP-102 (GHRP-2) had stronger GH-releasing activity than exogenous GHRH because GHRP-2 is less suppressible by endogenous somatostatin. This makes GHRP-2 more reliable than GHRH alone in conditions of high somatostatin tone (chronic stress, fasting state).
- Modest cortisol and prolactin elevation — GHRP-2 elevates ACTH / cortisol and prolactin via GHS-R1a in corticotrophs and lactotrophs. The signal is meaningfully smaller than with hexarelin and similar to GHRP-6 — placing GHRP-2 between GHRP-6 and ipamorelin in selectivity.
- CD36 binding (cytoprotection) — Like other GHRPs, GHRP-2 binds CD36 on cardiomyocytes, vascular endothelium, and macrophages — though with weaker affinity than hexarelin or GHRP-6. This contributes to a modest but documented anti-inflammatory and cytoprotective effect (Granado et al. 2005, Am J Physiol Endocrinol Metab; anti-inflammatory effects demonstrated in arthritic rats).
- Acts at both pituitary and hypothalamic sites — The general pharmacology paper (Furuta et al. 2004, PMID 15646371) demonstrated that KP-102 acts at both pituitary somatotroph and hypothalamic neuron levels — distinguishing it from GHRH, which acts primarily at the somatotroph.
- Gastric prokinetic effect (ghrelin mimicry) — As a ghrelin receptor agonist, GHRP-2 stimulates gastric motility and emptying — a class effect of GHS-R1a agonists.
- What it does not do — Does not directly elevate IGF-1 (downstream of GH); does not bypass non-functional somatotrophs; does not reset endogenous GH pulsatile architecture; does not produce sustained GH elevation (each dose generates one pulse).
What the Research Shows
GHRP-2 has the strongest formal regulatory and clinical research base of the GHRPs commonly used by the optimization community, anchored by the Japan PMDA approval and supporting clinical trial program.
- Foundational pharmacology (Bowers 1991, 1995) — GHRP-2 was synthesized and characterized by Bowers and colleagues during the structure-activity-relationship campaign that followed GHRP-6. Increased potency demonstrated in pituitary cell culture and in vivo in rats, dogs, and humans.
- Pivotal Japanese multicenter trial (Kaken, leading to 2004 PMDA approval) — 126 children across 84 Japanese facilities were tested with a single 100 mcg IV bolus of pralmorelin. Reliable discrimination between GH-deficient patients and healthy controls. This trial established the Japan diagnostic approval.
- Doi et al. 2004 (PMID 15646370) — Pharmacological characterization in rats and dogs. KP-102 showed more potent GH release than GHRH in conscious rats; less somatostatin-sensitive; effective in conscious dogs where GHRH was not.
- Furuta et al. 2004 (PMID 15646371) — General pharmacology evaluation in animal models. Negligible effects on respiratory, cardiovascular, digestive, renal, and blood systems at doses producing GH-releasing activity. Safety basis for clinical advancement.
- Comparative human studies (Arvat, Bowers, Ghigo) — Multiple human studies comparing GHRP-2 with ghrelin, GHRP-6, hexarelin, and GHRH. GHRP-2 produces stronger GH peaks than GHRP-6 at equivalent doses, with similar or slightly less ACTH / cortisol elevation.
- Combined GHRH + GHRP-2 stimulation testing — The combined test is more sensitive than insulin tolerance testing for diagnosis of GH deficiency in adults. Used in clinical practice in Japan and in research settings elsewhere.
- Phase II therapeutic trials (children, short stature) — discontinued — Intranasal GHRP-2 was evaluated for treatment of GH deficiency and short stature (Pihoker 1997, J Endocrinol; Mericq 1998, J Clin Endocrinol Metab). Despite increasing endogenous GH secretion, growth promotion was not clinically meaningful. Therapeutic development was discontinued. Important honest framing for users hoping GHRP-2 produces growth-equivalent outcomes to recombinant human GH — it does not in pediatric trials.
- Anti-inflammatory effects (Granado 2005) — Granado M et al. Anti-inflammatory effect of the ghrelin agonist GHRP-2 in arthritic rats. Am J Physiol Endocrinol Metab. 2005;288(3):E486-492. Demonstrated CD36-mediated anti-inflammatory activity.
- Pharmacokinetics — characterized for the diagnostic-dose route — Single 100 mcg IV bolus PK characterized as part of Japan approval. Half-life short (~15–60 min); rapid renal / biliary clearance.
- Athletic doping detection — Multiple papers from Cuban and European laboratories (Thomas et al., Pozo et al., Cabrales et al.) establishing detection methods for GHRP-2 and metabolites in serum and urine. WADA-accredited laboratories routinely test for GHRP-2.
Critical Context — Approved for Single-Dose Diagnostic, Not Chronic Use
The Japan PMDA approval covers a single 100 mcg IV bolus for diagnostic purposes. Chronic multi-daily SubQ dosing for body composition or recovery — the use case the optimization community pursues — is off-label everywhere, including in Japan. The therapeutic-use Phase II trials in pediatric short stature were not successful, and the compound was never advanced beyond the diagnostic indication. Any community use is therefore based on extrapolation from the diagnostic profile and from the broader GHRP class literature, not on chronic-use approval data.
Human Data
GHRP-2 has the most extensive human data of any peptide in the GHRP family.
- Pivotal Japanese pediatric multicenter trial (Kaken) — 126 children, 84 facilities, single 100 mcg IV bolus. Established discrimination between GH-deficient and healthy controls. Foundation of 2004 PMDA approval.
- Healthy volunteer GH stimulation studies — Healthy adults receiving 1–2 mcg/kg IV GHRP-2 show robust GH peaks within 15–30 minutes; peaks substantially larger than GHRP-6 at equivalent doses.
- GHRH + GHRP-2 combined stimulation testing — Established as a sensitive test for adult GH deficiency. Multiple small clinical comparison studies vs ITT (insulin tolerance test).
- Phase II pediatric short-stature trials — negative — Intranasal GHRP-2 evaluated as therapeutic agent in children with short stature. Despite increasing endogenous GH secretion measurable in stim tests, clinical growth promotion was insufficient. Trials discontinued.
- Adult body-composition studies — modest signal — Several small open-label and uncontrolled studies have evaluated chronic SubQ GHRP-2 ± GHRH in older adults for body composition and recovery outcomes. Modest effects reported; no large RCT.
- HIV-associated wasting (older studies) — GHRP-2 was investigated for HIV-associated cachexia; some signal in early trials. Largely superseded by recombinant GH (and later by tesamorelin for visceral-fat-specific outcomes).
- Athletic detection studies (Thomas, Pozo, Cabrales et al.) — Multiple LC-MS detection studies for WADA testing. Confirmed reliable identification in serum and urine.
Dosing from the Literature
Doses below combine the Japan-approved diagnostic dose with community off-label use. Not medical advice. No FDA-approved dose exists.
| Indication / Context | Dose | Frequency | Notes |
|---|
| Japan-approved diagnostic (PMDA) | 100 mcg IV | Single bolus | Adults and children >4 years. Peak GH at 15–30 min. Brand: GHRP Kaken 100. |
| GH stim test (research) | 1–2 mcg/kg IV | Single dose | Healthy adult GH stimulation. |
| Combined GHRH + GHRP-2 stim test | 1 mcg/kg each, IV | Single dose | More sensitive than ITT for GH deficiency. |
| Community SubQ (typical) | 100–200 mcg per dose | 2–3x daily | Standard hyperphysiologic GH-pulse community dose. Pre-bed + upon waking + post-workout typical. |
| Community SubQ (higher) | 1–2 mcg/kg per dose | 2–3x daily | Higher-dose protocols. Risk of saturating receptor without proportional benefit. |
| Cycle length (community) | 8–12 weeks | — | Cycling is community convention; tachyphylaxis risk is moderate (less than hexarelin). |
Dosing Disclaimer
The Japan-approved use is a single 100 mcg IV diagnostic dose. Chronic multi-daily SubQ community use is off-label everywhere. Routine combination with GHRH analogs (CJC-1295, sermorelin, tesamorelin) amplifies the GH pulse multiplicatively but compounds side effects. Empty-stomach dosing required (food blunts the GH pulse via insulin-mediated somatostatin release).
Reconstitution & Storage
GHRP-2 is supplied as a lyophilized powder (community: 5 mg or 10 mg vials; Japan-approved Kaken: 100 mcg/vial single-dose).
| Vial Size | BAC Water | Concentration | 100 mcg Dose | 200 mcg Dose |
|---|
| 5 mg | 2 mL | 2,500 mcg/mL | 4 units (0.04 mL) | 8 units (0.08 mL) |
| 10 mg | 2 mL | 5,000 mcg/mL | 2 units (0.02 mL) | 4 units (0.04 mL) |
| Kaken 100 mcg single-dose | Per package insert | — | — | — |
- Reconstitution — BAC water injected slowly down vial wall at 45°. Swirl gently — never shake. Clear / colorless solution.
- Storage — Lyophilized stable at room temperature 12+ months out of light; refrigerated for longer. Reconstituted: 2–8°C, used within 28 days.
- Empty stomach dosing — 30+ min before food or 2+ hours after.
- Inspection — Discard if cloudy, particulate, or discolored.
→ Use the Kalios Dosing Calculator for exact syringe units
Side Effects & Risks
Important
Chronic SubQ dosing is off-label everywhere; regulatory approval covers a single 100 μg IV diagnostic bolus. Cortisol, prolactin, and insulin signals all move with routine use. WADA-banned under S2. This is a doctor conversation, not a starter peptide.
GHRP-2 has the most thoroughly characterized acute safety profile of the GHRPs because of the Japan diagnostic approval — but that profile is for single-dose use. Chronic-use safety data is limited.
- Single-dose diagnostic — generally well-tolerated — In the Japan pivotal trial, single 100 mcg IV bolus produced minimal adverse events. Mild headache, transient flushing, and nausea reported in a small minority.
- Mild appetite stimulation — Less than GHRP-6 but more than ipamorelin. Most chronic users report mild post-injection hunger but not the dramatic ghrelin pang of GHRP-6.
- Cortisol and prolactin elevation — Modest dose-related signal; meaningfully smaller than hexarelin. Chronic high-dose use may produce clinically meaningful elevation.
- Water retention (chronic use) — Mild, GH-mediated; usually resolves or stabilizes within 1–2 weeks.
- Tingling / numbness / mild carpal-tunnel-like symptoms — At higher chronic doses; GH-mediated water retention; resolves with dose reduction.
- Insulin sensitivity reduction (chronic) — Sustained GH elevation reduces insulin sensitivity. Periodic glucose and HbA1c monitoring is reasonable on extended cycles.
- Tachyphylaxis (chronic) — Receptor desensitization with sustained GHS-R1a agonism is documented for hexarelin; GHRP-2 risk is intermediate. Cycling is community convention.
- Drug interactions — Synergy with GHRH analogs (intentional). Insulin and high-carb meals blunt the GH pulse. Glucocorticoids blunt GH response. Beta-blockers do not blunt.
- Theoretical GH / IGF-1 cancer concern — Same as for all GH-elevating compounds. Age-appropriate cancer screening before chronic use is reasonable.
- WADA banned (S2) — Banned at all times for tested athletes. Detection methods well-established; routinely tested by WADA-accredited labs. Any tested athlete using GHRP-2 faces sanction.
- Sourcing risk — Outside the Japan-approved Kaken product, GHRP-2 sold via research-chemical channels has variable quality. Independent COA (HPLC + mass spec) is the practical floor.
Bloodwork & Monitoring
- Baseline IGF-1 — Most important single marker. Establishes individual baseline and tracks effective GH elevation. Repeat at 8 weeks.
- Fasting glucose and HbA1c — GH reduces insulin sensitivity. Baseline and at 8–12 weeks.
- Fasting insulin — Sensitive marker for glucose-handling changes.
- Lipid panel — GH affects lipid handling. Baseline and at 12 weeks.
- Cortisol (AM) — Particularly relevant for higher-dose chronic GHRP-2 use. Modest signal warrants tracking.
- Prolactin — Same rationale; modest signal. Periodic check on extended cycles.
- CBC and CMP — Routine endocrine-protocol monitoring.
- Cancer screening (age-appropriate) — GH / IGF-1 epidemiology; screen before chronic use.
- Sleep-quality tracking — Subjective sleep changes are common and useful to track.
Commonly Stacked With
Standard pairing. CJC-1295 (GHRH analog) + GHRP-2 (GHS-R1a agonist) produces synergistic GH release. With-DAC has ~8 day half-life; without DAC has ~30 min half-life and is co-dosed with each GHRP-2 pulse.
1-29 fragment of GHRH; cleaner profile than CJC-1295 in some practitioner protocols. Combined with GHRP-2 for synergistic GH release.
FDA-approved GHRH analog (Egrifta), originally for HIV-associated lipodystrophy. Used in physician-supervised contexts as the GHRH partner for GHRP-2.
Modern selective alternative. Most users picking between the two GHRPs choose ipamorelin for cleaner chronic profile, GHRP-2 for slightly stronger acute GH response.
For tissue-repair-plus-GH protocols. BPC-157's local repair signaling complements systemic GH / IGF-1 elevation.
→ Check compound compatibility in the Stack Builder
Practical User Notes
Read This First
GHRP-2 is approved in Japan as a single-dose diagnostic agent. Chronic SubQ multi-daily community use is off-label everywhere. The notes below collate community practices around off-label use and should not be read as medical guidance. Anyone considering chronic use should work with a licensed clinician.
- Empty stomach is non-negotiable — Food (especially carbohydrates) blunts the GH pulse. Dose 30+ min before eating or 2+ hours after.
- Pre-bed dose for sleep-aligned GH pulse — One dose 15–30 min before bed aligns with the natural slow-wave-sleep GH peak. The single most useful daily dose for most users.
- Stack with GHRH — CJC-1295 (DAC or no-DAC), sermorelin, or tesamorelin combined with GHRP-2 produces synergistic GH release. Standard community approach.
- GHRP-2 is the reasonable middle choice — More potent than GHRP-6, less cortisol-heavy than hexarelin, more acute GH than ipamorelin. Ipamorelin remains the cleanest chronic-use selection.
- Dose conservatively — 100–200 mcg per pulse is the standard. Higher doses saturate without proportional benefit and amplify side effects.
- Cycle 8–12 weeks, then 4-week break — Receptor desensitization is plausible. Cycling is convention.
- Lab monitoring — Baseline IGF-1, fasting glucose, HbA1c, lipids; repeat at 8–12 weeks. IGF-1 should rise; glucose should stay stable.
- Sourcing — Independent COA (HPLC + mass spec). Counterfeit GHRP-2 is reasonably common in low-tier vendors. The Japan-approved Kaken product is the regulatory-quality reference.
- Storage — Lyophilized at room temperature dry; reconstituted refrigerated 28 days.
- Athletes — banned — All GHRPs are banned by WADA at all times. Detection methods established. Do not use under any anti-doping testing.
- Pregnancy, breastfeeding, history of cancer, poorly-controlled diabetes — Conservative contraindications.
- Stopping — No taper required. IGF-1 returns to baseline over 1–2 weeks. Recovery benefits typically persist for several weeks.
Quick Compare — GHRP-2 vs GHRP-6 vs Ipamorelin vs Hexarelin
| Feature | GHRP-2 | GHRP-6 | Ipamorelin | Hexarelin |
|---|
| Year characterized | 1995 | 1984 | 1998 | 1991 |
| GH-release potency | Highest of classical hexapeptides | Moderate | Moderate | Strongest acute; less reliable chronic |
| Hunger / appetite | Mild | Strong | Negligible | Mild-moderate |
| Cortisol elevation | Mild | Mild-moderate | Negligible | Moderate |
| Prolactin elevation | Mild | Mild-moderate | Negligible | Moderate |
| Approved use anywhere? | Yes — Japan diagnostic (PMDA 2004) | No | No | No |
| Best-fit use case | Strong GH boost with mild side effects; diagnostic | Appetite stimulation; cytoprotection | "Clean" GH boost; fat loss | Strongest GH but cortisol-heavy |
| Typical community dose | 100–200 mcg, 2–3x daily | 100 mcg, 2–3x daily | 100–300 mcg, 2–3x daily | 100 mcg, 1–2x daily |
| Tachyphylaxis risk | Moderate | Moderate | Lower | Higher |
| WADA status | Banned (S2) | Banned (S2) | Banned (S2) | Banned (S2) |
→ See GHRP-6 profile • → See Ipamorelin profile • → See Hexarelin profile
Regulatory Status
Current Status — April 2026
GHRP-2 (pralmorelin) is approved in Japan by the Pharmaceuticals and Medical Devices Agency (PMDA, October 2004) as a single-dose intravenous diagnostic agent for the assessment of growth hormone deficiency in adults and children over 4 years of age. Marketed by Kaken Pharmaceutical Co., Ltd. under the brand name GHRP Kaken 100. Outside Japan, GHRP-2 has not received marketing authorization from the FDA (United States), EMA (European Union), MHRA (United Kingdom), or any other major regulator.
In the United States, GHRP-2 is classified as an FDA Category 2 bulk drug substance — meaning it is NOT eligible for use by 503A or 503B compounding pharmacies. It is a research chemical for the U.S. market.
On February 27, 2026, HHS Secretary Robert F. Kennedy Jr. publicly announced an intention to reclassify approximately 14 of the 19 Category 2 peptides — the GHRP family among the candidates — back to Category 1, which would make them available through licensed compounding pharmacies with a prescription. As of April 2026, the FDA has not published a formal update reflecting that announcement, and the Pharmacy Compounding Advisory Committee (PCAC) has not completed review. Practically, GHRP-2 still cannot be legally compounded by 503A pharmacies in the U.S. as of this publication date.
WADA: GHRP-2 is explicitly banned at all times under category S2 (peptide hormones, growth factors, related substances and mimetics). Detection methods are established; GHRP-2 and its metabolites are routinely tested by WADA-accredited laboratories. Any tested athlete using GHRP-2 faces sanction under the WADA Code.
Cost & Access
In Japan, GHRP-2 is available through licensed clinical channels as the PMDA-approved diagnostic agent Pralmorelin / GHRP Kaken 100 (Kaken Pharmaceutical). Use is restricted to the approved diagnostic indication.
In the United States, GHRP-2 is not approved for human use and cannot be legally compounded by 503A or 503B pharmacies under current FDA bulk-substance rules. It is available through research suppliers for laboratory research purposes only. Quality and purity vary substantially between research-chemical vendors; independent COA (HPLC + mass spec) is the practical floor for due diligence.
If GHRP-2 is reclassified back to Category 1 under HHS Secretary Robert F. Kennedy Jr.'s February 2026 announcement (subject to PCAC review and FDA implementation), 503A compounded GHRP-2 would become available to clinician-prescribed patients for off-label chronic use with regulatory legitimacy and quality assurance. As of April 2026, this reclassification remains pending. Kalios does not sell compounds.
Access and regulatory status as of April 2026. Actual availability varies by provider, location, and prescription status. Kalios does not sell compounds.
Related Compounds
Peptides GHRP-2 users weigh against it:
Ghrelin-receptor agonist with strong appetite-stimulating effect alongside GH release.
Potent ghrelin-receptor agonist with cardioprotective signaling but rapid receptor desensitization.
Ibutamoren — oral nonpeptide ghrelin-receptor agonist producing 24-hour GH/IGF-1 elevation.
CJC-1295 + ipamorelin — the classic GHRH + GHRP combination for natural growth-hormone pulse amplification.
Key References
- Doi N, Furukawa M, Sato C, Sasaki M, et al. Pharmacological characteristics of KP-102 (GHRP-2), a potent growth hormone-releasing peptide. Arzneimittelforschung. 2004;54(12):857-867. PMID: 15646370. (Foundational pharmacology characterization by Kaken.)
- Furuta S, Shimada O, Doi N, Ukai K, Nakagawa T, Watanabe J, Imaizumi M. General pharmacology of KP-102 (GHRP-2), a potent growth hormone-releasing peptide. Arzneimittelforschung. 2004;54(12):868-880. PMID: 15646371. (Safety pharmacology evaluation.)
- Pralmorelin: GHRP 2, GPA 748, growth hormone-releasing peptide 2, KP 102, WAY GPA 748. Drugs R D. 2004;5(4):236-239. PMID: 15230633. (Drug development profile.)
- Bowers CY, Reynolds GA, Durham D, Barrera CM, Pezzoli SS, Thorner MO. Growth hormone (GH)-releasing peptide stimulates GH release in normal men and acts synergistically with GH-releasing hormone. J Clin Endocrinol Metab. 1990;70(4):975-982. PMID: 2108180. (Bowers' early work on GHRP-GHRH synergy.)
- Howard AD, Feighner SD, Cully DF, et al. A receptor in pituitary and hypothalamus that functions in growth hormone release. Science. 1996;273(5277):974-977. PMID: 8688086. (GHS-R1a cloning.)
- Kojima M, Hosoda H, Date Y, Nakazato M, Matsuo H, Kangawa K. Ghrelin is a growth-hormone-releasing acylated peptide from stomach. Nature. 1999;402(6762):656-660. PMID: 10604470. (Ghrelin discovery — endogenous ligand.)
- Bowers CY. Unnatural growth hormone-releasing peptide begets natural ghrelin. J Clin Endocrinol Metab. 2001;86(4):1464-1469. PMID: 11297568.
- Granado M, Priego T, Martín AI, Villanúa MA, López-Calderón A. Anti-inflammatory effect of the ghrelin agonist growth hormone-releasing peptide-2 (GHRP-2) in arthritic rats. Am J Physiol Endocrinol Metab. 2005;288(3):E486-E492. PMID: 15507534.
- Pihoker C, Badger TM, Reynolds GA, Bowers CY. Treatment effects of intranasal growth hormone-releasing peptide-2 in children with short stature. J Endocrinol. 1997;155(1):79-86. PMID: 9390008. (Pediatric short-stature trial — discontinued therapeutic indication.)
- Mericq V, Cassorla F, Salazar T, et al. Effects of eight months treatment with graded doses of a growth hormone (GH)-releasing peptide in GH-deficient children. J Clin Endocrinol Metab. 1998;83(7):2355-2360. PMID: 9661609.
- Arvat E, Maccario M, Di Vito L, et al. Endocrine activities of ghrelin, a natural growth hormone secretagogue (GHS), in humans: comparison and interactions with hexarelin, a nonnatural peptidyl GHS, and GH-releasing hormone. J Clin Endocrinol Metab. 2001;86(3):1169-1174. PMID: 11238504. (Comparison study.)
- Pandya N, DeMott-Friberg R, Bowers CY, Barkan AL, Jaffe CA. GH-releasing peptide-6 requires endogenous hypothalamic GH-releasing hormone for maximal GH stimulation. J Clin Endocrinol Metab. 1998;83(4):1186-1189. PMID: 9543138. (GHRH-GHRP synergy.)
- Kaken Pharmaceutical Co., Ltd. GHRP Kaken 100 (Pralmorelin Hydrochloride) Package Insert and Approved Indication, Japan PMDA, October 2004. (Japan approval reference.)
- Thomas A, Höppner S, Geyer H, et al. Determination of growth hormone-releasing peptides in serum by LC-MS/MS for sports drug testing. (WADA detection methodology applicable to GHRP-2.)
- Bowers CY. Growth hormone-releasing peptide (GHRP). Cell Mol Life Sci. 1998;54(12):1316-1329. PMID: 9893708. (Class review.)
- Berlanga-Acosta J, et al. Synthetic Growth Hormone-Releasing Peptides (GHRPs): A Historical Appraisal of the Evidences Supporting Their Cytoprotective Effects. Medicc Rev. 2017. PMC5392015. (Class review of cytoprotective evidence.)
- FDA. Bulk Drug Substances That Raise Significant Safety Risks (Category 2) Under Section 503A / 503B. FDA.gov. Updated 2025-2026.
- WADA Prohibited List 2026. World Anti-Doping Agency. wada-ama.org. (GHRP family banned under S2.)
Last updated: April 2026 | Profile authored by Kalios Peptides research team