GHRP-2

GHRP-2 (also called pralmorelin) is a growth hormone releaser known for strongly prompting the pituitary gland to release the body's own growth hormone, by acting on the ghrelin (hunger hormone) receptor. It also raises cortisol and prolactin, and its growth-hormone effect can fade with sustained use. It's not FDA-approved in the US, where its childhood short-stature program was discontinued, though it's approved in Japan as a diagnostic test for adult growth hormone deficiency; outside Japan it's sold only as a research peptide, and it's banned in drug-tested sport.

GHRP-2 has been studied as a potent trigger of growth-hormone release, and a childhood-treatment trial reported increased height velocity over 6 to 24 months. It also produces dose-dependent rises in the stress hormone cortisol and in prolactin, and the response can fade with sustained use (tachyphylaxis). No large adult trials have been published for the body-composition uses people pursue.

Not FDA-approved for any indication. Wyeth-Ayerst advanced GHRP-2 through Phase II/III clinical evaluation in pediatric short stature in the late 1990s and early 2000s; clinical development was discontinued before US market approval. Kaken Pharmaceutical received Japanese regulatory approval for pralmorelin (GHRP-2) as a diagnostic agent for adult GH deficiency — Japan is the only major jurisdiction with an approved indication. The compound is available outside Japan exclusively as a research peptide through unregulated research-peptide supply chains. Not DEA-scheduled. WADA-banned in regulated sport — explicitly named under Section S2.2.4 (Growth Hormone Releasing Factors → GH-releasing peptides subsection) of the 2026 Prohibited List as "GHRP-2 (pralmorelin)" alongside alexamorelin, examorelin (hexarelin), GHRP-1, GHRP-3, GHRP-4, GHRP-5, and GHRP-6.[⁷]

GHRP-2 is not FDA-approved in the US and is banned in regulated sport (WADA). VialWise is a research and educational reference, not medical advice — consult a licensed professional.

⚠️ For research and educational purposes only. GHRP-2 (pralmorelin) is not approved by the FDA for any indication. Wyeth-Ayerst discontinued US clinical development before market approval. Pralmorelin is approved in Japan as a diagnostic agent for adult GH deficiency (Kaken Pharmaceutical); outside Japan it is available exclusively as a research peptide through unregulated supply chains. Information in this entry is informational, not medical advice. Always confirm dose calculations with the in-app calculator and consult appropriate professional guidance before any protocol decisions.

⚠️ Precision matters at low doses. GHRP-2 is dosed in micrograms (mcg), not milligrams. Typical research-community doses ( per dose) at typical reconstitution concentrations ( vial / 2.5 mL BAC water = =) produce small draws in the range on a U-100 syringe. Lower-concentration setups ( / 5 mL =) produce draws — generally easier precision. Always verify draws against the in-app calculator. Same precision concern as Ipamorelin, Hexarelin, and the other GHS-class peptides.

⚠️ GHRP-2 has the strongest GH-releasing potency of any older-generation GHRP but produces dose-dependent cortisol and prolactin elevation distinct from the cleaner ghrelin-receptor agonists. The Adams 1996 *Molecular Endocrinology* study established that GHRP-2 was considerably more potent than GHRP-6 in human pituitary somatotropinoma cell cultures.[⁵] In healthy subjects, IV GHRP-2 produces a near-maximal GH peak (~50 µg/L), placing it among the most potent acute GH secretagogues characterized.[³] The clinical-utility tradeoff is the same as hexarelin: meaningful cortisol/prolactin elevation at higher per-dose amounts and tachyphylaxis with sustained dosing. Ipamorelin is the modern default for sustained GH-axis stimulation specifically because it retains GHRP-class potency while substantially improving cortisol/prolactin selectivity. GHRP-2 is best understood as the historically-most-clinically-developed GHRP — Wyeth-Ayerst Phase II/III for pediatric short stature plus Kaken Pharmaceutical's approved Japanese diagnostic indication — but with the same tolerability-vs-potency tradeoff that limited the older GHRP class generally.

⚠️ GHRP-2 vs the rest of the GHS-axis cluster — explicit cluster context for navigating the library. The library now has multiple ghrelin-receptor-agonist entries with substantially different pharmacology and clinical-development histories: - Ipamorelin — pentapeptide; the cleanest GHRP for sustained use; minimal cortisol/prolactin elevation at any dose; minimal tachyphylaxis. The default research-community choice for sustained GH-axis stimulation. - Hexarelin — hexapeptide; high acute GH-stimulating potency; dose-dependent cortisol/prolactin elevation; meaningful tachyphylaxis; Mediolanum Phase II discontinued. - GHRP-2 / Pralmorelin (this entry) — hexapeptide; near-maximal acute GH response at low IV doses; the only GHRP with an approved national-regulator indication (Japan, diagnostic GH-deficiency testing); Wyeth-Ayerst US Phase II/III for pediatric short stature discontinued; the historical clinical-development leader of the GHRP class. - GHRP-6 — hexapeptide; the original Bowers/Momany GHRP from which both GHRP-2 and hexarelin were derived; substantially less potent than GHRP-2 in head-to-head pharmacology;[⁵] notable for the central appetite-stimulation effect (the "hunger peptide" framing) demonstrated by Locke 1995 in rats. - MK-677 / Ibutamoren — non-peptide oral small-molecule ghrelin agonist; very long half-life (~24 hours); CHF-safety-signal concern in elderly populations (Adunsky 2011 phase 2b DSMB termination); active phase 3 program at Lumos Pharma. Among the older GHRPs (GHRP-1, GHRP-2/pralmorelin, GHRP-3, GHRP-4, GHRP-5, GHRP-6, hexarelin/examorelin) the modern research-community use is dominated by GHRP-2 and hexarelin, with GHRP-6 a distant third and GHRP-1/-3/-4/-5 essentially absent. Ipamorelin emerged as the modern preferred GHRP because it kept the GH-stimulating potency while substantially improving the side-effect-profile selectivity.

⚠️ WADA-banned — explicitly named under Section S2.2.4 (Growth Hormone Releasing Factors → GHRP subsection) using the INN-plus-research-name format "GHRP-2 (pralmorelin)". The 2026 WADA Prohibited List Section S2.2.4 names *"GH-releasing peptides (GHRPs) [e.g. alexamorelin, examorelin (hexarelin), GHRP-1, GHRP-2 (pralmorelin), GHRP-3, GHRP-4, GHRP-5 and GHRP-6]"*.[⁷] Same WADA subsection (S2.2.4) as Ipamorelin, Hexarelin, CJC-1295, Sermorelin, Tesamorelin, and MK-677. Prohibited at all times. The "(pralmorelin)" parenthetical in WADA's listing reflects pralmorelin's INN status — it is the only GHRP-class peptide with an approved national-regulator indication (Japan), so the INN is the canonical regulatory name.

According to PubMed-indexed research, GHRP-2 is a synthetic hexapeptide growth hormone-releasing peptide (GHRP) with the sequence d-Ala-D-β-naphthyl-alanine-Ala-Trp-D-Phe-Lys-NH2. The compound was developed at Tulane University in the laboratory of Cyril Y. Bowers (the same Bowers research program that produced the original GHRP-6 in the 1980s) as a second-generation GHRP, with the D-β-naphthyl-alanine residue conferring substantially greater potency than GHRP-6.[¹] The INN spelling is "pralmorelin"; "GHRP-2" is the developmental designation used in the great majority of clinical trials and the dominant name in research-community use. Wyeth-Ayerst licensed the compound for US clinical development under codes KP-102 / GPA-748 and advanced it through Phase II/III clinical evaluation for pediatric short stature in the late 1990s and early 2000s — but US clinical development was discontinued before market approval. Kaken Pharmaceutical (Japan) received Japanese regulatory approval for pralmorelin as a diagnostic agent for adult GH deficiency — Japan is the only major jurisdiction with an approved indication, making pralmorelin the only GHRP-class peptide with an approved finished pharmaceutical product anywhere in the world.

Mechanism. Based on articles retrieved from PubMed, GHRP-2 acts as an agonist at the ghrelin receptor (GHS-R1a) at both pituitary and hypothalamic levels to stimulate GH release.[⁵] The mechanism is shared with all GHRP-class peptides plus the non-peptide ghrelin-mimetic MK-677. The Adams 1996 *Molecular Endocrinology* study established that GHRP-2 acts via protein kinase C-dependent phosphatidylinositol hydrolysis at the human pituitary somatotroph, with the cAMP-second-messenger pathway providing additional crosstalk in tumors expressing constitutively-active Gs-protein (gsp oncogenes).[⁵] Critically, the Adams 1996 study established that GHRP-2 was considerably more potent than GHRP-6 in stimulating GH secretion from human pituitary somatotropinoma cell cultures — a finding that anchored the subsequent clinical development of GHRP-2 (rather than GHRP-6) as the lead GHRP class candidate for both pediatric short-stature treatment and adult GH-deficiency diagnostic testing.

Bitar 1991 receptor-pharmacology context. The Bitar 1991 *Biochemical and Biophysical Research Communications* study established that GHRP and GHRH act through distinct receptors — substance P/bombesin antagonists dose-dependently inhibited GHRP-induced GH release (IC50 0.2–6 µM range across multiple antagonists) but had only 10–15% inhibitory effect on GHRH-stimulated GH release.[⁶] Conversely, the GHRH antagonist DC21-366 inhibited GHRH-stimulated GH release (IC50 0.16 µM) but did not inhibit GHRP-stimulated GH release. This established the dual-receptor model of GH stimulation — GHRP and GHRH activate different receptors, with subsequent identification of the ghrelin receptor (GHS-R1a) for the GHRP class and the GHRH receptor for GHRH. The dual-receptor framework is the basis for the synergistic GHRP-plus-GHRH combination protocol used across the GHS-axis library (GHRP-2 plus CJC-1295 no-DAC, sermorelin, or tesamorelin).

Pediatric short-stature clinical-development thread (Pihoker 1997 / Pihoker 1998).[³][⁴] The Wyeth-Ayerst Phase II/III pediatric short-stature program was anchored on two Pihoker-Bowers studies. Pihoker 1998 *Journal of Clinical Endocrinology & Metabolism* established the pediatric Phase I PK/PD profile in 10 prepubertal children receiving IV: elimination half-life 0.55 ± 0.14 h, Cmax 7.4 ± 3.8 ng/mL, EC50 1.09 ± 0.59 ng/mL, peak GH response 50.7 ± 17.2 ng/mL.[³] Pihoker 1997 *Journal of Endocrinology* established the chronic-intranasal-treatment efficacy profile: 15 children with short stature received intranasal GHRP-2 ( twice daily, escalated to three times daily) for 6 months (n=15) to 18–24 months (n=6); height velocity increased from 3.7 ± 0.2 cm/year to 6.1 ± 0.3 cm/year at 6 months and was sustained at 6.0 ± 0.4 cm/year at 18–24 months.[⁴] GHRP-2-stimulated GH response did not decline over the treatment period, suggesting that GH-response tachyphylaxis to chronic intranasal GHRP-2 dosing in this pediatric population was less severe than the chronic-SC-hexarelin tachyphylaxis demonstrated in adults by Rahim 1999 (see hexarelin entry). The Pihoker dataset is the most clinically-relevant published evidence for GHRP-2 efficacy — though limited to pediatric short stature, not the adult body-composition/recovery use case that dominates research-community use.

Postmenopausal GH/IGF axis thread (Veldhuis 2001). The Veldhuis 2001 *Endocrine* review/clinical-investigation article characterized the estrogen-GHRP-2 interaction in postmenopausal women.[²] The framework synthesized: (a) estrogen is the proximate sex steroid sustaining GH secretion across the human lifespan in both sexes; (b) GHRP-2 stimulates GH at the somatotroph level and likely also at the hypothalamic level via somatostatin-tone modulation; (c) in hyposomatotropic postmenopausal women, GHRP-2 produces meaningful GH/IGF-1 elevation that interacts with estrogen status. This is the foundational "GHRP-2 in adult use" reference for the entry — though Veldhuis 2001 frames GHRP-2 as an investigational tool rather than as a clinical therapy, it remains the most comprehensive published characterization of GHRP-2's effects in adult endocrine physiology.

Japan diagnostic approval (Kaken Pharmaceutical). Pralmorelin is approved in Japan as a diagnostic agent for adult growth hormone deficiency, marketed by Kaken Pharmaceutical. The diagnostic protocol is a single IV bolus dose ( per the Japanese labeling) with subsequent GH measurements at 15 / 30 / 60 / 90 / 120 minutes. The diagnostic cutoff for adult GH deficiency is peak-stimulated GH below 9 ng/mL (varies by clinical context). The Japanese diagnostic indication is the only currently-approved use of any GHRP-class peptide anywhere in the world. US, EU, and other major-jurisdiction regulators have not approved pralmorelin for any indication.

Regulatory status (US — current). GHRP-2 (pralmorelin) is not FDA-approved for any indication. Wyeth-Ayerst's pediatric short-stature clinical development program was discontinued before market approval. The compound is available outside Japan exclusively as a research peptide through unregulated research-peptide supply chains; not legally compoundable through US 503A pharmacies (the compound is not on the 503A bulks list, and per the broader peptide-bulks-list regulatory situation as of 2024, is not approved for compounding). Not DEA-scheduled.

Regulatory status (sport — WADA). GHRP-2 is WADA-banned under Section S2.2.4 (Growth Hormone Releasing Factors → GHRP subsection) of the 2026 Prohibited List, named explicitly as "GHRP-2 (pralmorelin)" alongside alexamorelin, examorelin (hexarelin), GHRP-1, GHRP-3, GHRP-4, GHRP-5, and GHRP-6.[⁷] Same WADA subsection as Ipamorelin, Hexarelin, CJC-1295, Sermorelin, Tesamorelin, and MK-677. Prohibited at all times.

Common research interests. GHRP-2 is used in research-community contexts for: - Acute GH stimulation for body composition and recovery — the dominant research-community use case. Typically used in 4–6 week cycles to manage tachyphylaxis. The relative-potency advantage of GHRP-2 over GHRP-6 per Adams 1996[⁵] is the typical rationale for choosing GHRP-2 over GHRP-6 in this context. - Combined with low-dose GHRH analog (CJC-1295 no-DAC, sermorelin, tesamorelin) — the same synergistic-GHRP-plus-GHRH-analog framework described for hexarelin, with the dual-receptor pharmacology established by Bitar 1991.[⁶] Reduces required per-dose GHRP-2 amount and produces stronger GH response than GHRP-2 alone. - Diagnostic GH-stimulation testing (clinical context, Japan) — the only currently-approved clinical use, exclusively in Japan, exclusively for adult GH-deficiency diagnostic workup. - Investigational / experimental endocrine pharmacology — Veldhuis-style clinical research on GH-axis regulation in aging, hypopituitarism, and related contexts.

Commonly reported

• Cortisol elevation — dose-dependent; the same hormonal-selectivity concern documented for hexarelin's GHRP class. Pihoker 1998 reported the PK/PD profile but did not characterize cortisol elevation specifically in the pediatric cohort; adult clinical trials have documented cortisol elevation comparable to hexarelin at equivalent µg/kg doses.
• Prolactin elevation — dose-dependent; same hormonal-selectivity concern as hexarelin
• Tachyphylaxis (GH-response decline with sustained use) — characterized in adult chronic-administration contexts; less prominent in the Pihoker 1997 pediatric intranasal treatment dataset where GH response was sustained over 18–24 months
• Injection site reactions — typical of subcutaneous peptide injection
• Water retention / fluid retention — common; same as other GHS-class compounds
• Increased appetite — common; ghrelin-receptor agonism is the mechanism. The appetite effect is generally less pronounced than for GHRP-6 (the "hunger peptide") but more pronounced than for the cleaner Ipamorelin
• Tingling or numbness in extremities — uncommon; suggests carpal-tunnel-syndrome-like effect; warrants dose reduction
• Joint stiffness — uncommon
• Sleep changes (typically improved sleep quality at modest doses; sleep disturbance at high doses) — mixed reports
• Long-term safety in adults using GHRP-2 off-label is not well characterized in published literature. The Pihoker 1997 pediatric intranasal treatment dataset extends to 18–24 months in 6 children — among the longest published exposures.[⁴] Multi-year off-label use in the research community is not characterized.
• CHF-related concerns — the Adunsky 2011 *Annals of Internal Medicine* phase 2b trial of MK-677 (a non-peptide ghrelin agonist with similar receptor target) was terminated by the DSMB for CHF safety signal in elderly population; whether the same concern applies to GHRP-2 in a different population is theoretical but mechanistically plausible. See [mk-677.md](./mk-677.md).

Serious

• Severe headache with visual changes — could suggest acute intracranial pressure elevation or pituitary pathology; rare but warrants immediate medical evaluation
• New-onset glucose dysregulation with symptoms (polyuria, polydipsia, blurred vision) — GH-axis activation can worsen insulin resistance; new-onset diabetic symptoms warrant immediate medical evaluation
• Severe or persistent injection-site reaction (induration, abscess, signs of infection) — warrants medical evaluation
• Signs of pituitary apoplexy (severe sudden headache, visual loss, ophthalmoplegia) — extremely rare but theoretically possible with strong GH-axis stimulation in individuals with undiagnosed pituitary pathology
• Allergic reaction (hives, swelling, difficulty breathing) — extremely rare but warrants immediate medical evaluation

Active malignancy or known IGF-1R-positive tumors — GH/IGF-1 axis activation is contraindicated

Active hyperprolactinemia or prolactinoma — additive concerns

Active hypercortisolism or Cushing's syndrome — additive concerns

Pregnancy and lactation — no human data outside the Japanese diagnostic-approval context; default to contraindicated

Pediatric use — no FDA-approved indication; the Pihoker 1997/1998 pediatric data exist but were generated in a Wyeth-Ayerst clinical-trial context that did not lead to US market approval

Concurrent corticosteroid therapy — additive cortisol effects

Active diabetes / impaired glucose tolerance — caution; GH-axis stimulation may worsen insulin resistance

Regulatory note (US): GHRP-2 is not FDA-approved for any indication and is not legally compoundable through US 503A pharmacies.

Regulatory note (sport): WADA-banned in regulated sport — explicitly named under Section S2.2.4 of the 2026 Prohibited List as "GHRP-2 (pralmorelin)".[⁷]

Not DEA-scheduled.

Peptide

A short chain of amino acids, the building blocks of proteins. Many compounds in this library are peptides.

Growth hormone secretagogue

A compound that signals the body to release its own growth hormone, rather than supplying growth hormone directly.

Ghrelin receptor

a receptor that, when activated, triggers growth hormone release and hunger.

Tachyphylaxis

a fading of a compound's effect with repeated use.

WADA Prohibited List

The list of substances banned in regulated sport by the World Anti-Doping Agency.

1. Bowers CY, Momany FA, Reynolds GA, Hong A. (1984). On the in vitro and in vivo activity of a new synthetic hexapeptide that acts on the pituitary to specifically release growth hormone. Endocrinology, 114(5):1537–1545.(PMID 6714155)
2. Veldhuis JD, Evans WS, Bowers CY, Anderson S. (2001). Interactive regulation of postmenopausal growth hormone insulin-like growth factor axis by estrogen and growth hormone-releasing peptide-2. Endocrine, 14(1):45–62 (February 2001).(PMID 11322501)
3. Pihoker C, Kearns GL, French D, Bowers CY. (1998). Pharmacokinetics and pharmacodynamics of growth hormone-releasing peptide-2: a phase I study in children. Journal of Clinical Endocrinology & Metabolism, 83(4):1168–1172 (April 1998).(PMID 9543135)
4. Pihoker C, Badger TM, Reynolds GA, Bowers CY. (1997). Treatment effects of intranasal growth hormone releasing peptide-2 in children with short stature. Journal of Endocrinology, 155(1):79–86 (October 1997).(PMID 9390009)
5. Adams EF, Lei T, Buchfelder M, Bowers CY, Fahlbusch R. (1996). Protein kinase C-dependent growth hormone releasing peptides stimulate cyclic adenosine 3',5'-monophosphate production by human pituitary somatotropinomas expressing gsp oncogenes: evidence for crosstalk between transduction pathways. Molecular Endocrinology, 10(4):432–438 (April 1996).(PMID 8721987)
6. Bitar KG, Bowers CY, Coy DH. (1991). Effect of substance P/bombesin antagonists on the release of growth hormone by GHRP and GHRH. Biochemical and Biophysical Research Communications, 180(1):156–161 (October 15, 1991).(PMID 1718273)
7. World Anti-Doping Agency. The 2026 Prohibited List, International Standard (effective 1 January 2026). Canonical PDF: wada-ama.org/sites/default/files/2025-09/2026list_en_final_clean_september_2025.pdf (linked from the WADA landing page; local archival copy in `docs/legal/wada-2026-prohibited-list.pdf`). GHRP-2 is named explicitly under Section S2.2.4 (Growth Hormone Releasing Factors → GHRP subsection) — page 8 of the canonical PDF — as "GHRP-2 (pralmorelin)". Verbatim from the canonical PDF: under S2.2.4 ("Growth hormone releasing factors, including, but not limited to:"), the GHRP bullet reads "GH-releasing peptides (GHRPs) [e.g. alexamorelin, examorelin (hexarelin), GHRP-1, GHRP-2 (pralmorelin), GHRP-3, GHRP-4, GHRP-5 and GHRP-6]". Same S2.2.4 subsection as Ipamorelin, Hexarelin, CJC-1295, Sermorelin, Tesamorelin, and MK-677. Prohibited at all times.

• Hexarelin — discussed together in this entry's stacks section
• MK-677 (Ibutamoren) — discussed together in this entry's stacks section
• Testosterone — discussed together in this entry's stacks section
• IGF-1 LR3 — discussed together in this entry's stacks section
• CJC-1295 / Ipamorelin Blend — same mechanism class
• CJC-1295 — same mechanism class