GHR-2 (GHRP-2)
A synthetic growth hormone secretagogue that stimulates natural GH release, studied for body composition, recovery, and anti-aging.
GHRP-2 (pralmorelin) is the most clinically legitimate of the growth hormone-releasing peptides, because it is the only one with a real regulatory approval — Japan licensed it in 2004 as a single-dose intravenous diagnostic agent for growth hormone deficiency, and it is genuinely good at that job. What it does not have is evidence for the reasons most people take it: no controlled trial has ever measured body composition with GHRP-2 as the intervention. It raises GH reliably, raises IGF-1 over weeks of dosing, and also raises ACTH, cortisol and prolactin — less than GHRP-6, more than ipamorelin. In the US it is not approved for anything, sits in FDA's 503A Category 3 and 503B Category 2, and is named by name on the WADA Prohibited List under S2.2.4 with routine urinary detection.
What is GHR-2 (GHRP-2)?
GHRP-2 (Growth Hormone Releasing Peptide-2) is a synthetic hexapeptide that acts as a potent growth hormone secretagogue. It stimulates the pituitary gland to release growth hormone through the ghrelin receptor (GHS-R1a). It is one of the most studied GHRPs and has been used as a diagnostic tool for growth hormone deficiency.
What GHR-2 (GHRP-2) Is Investigated For
GHRP-2 is investigated for growth hormone optimization, body composition improvement, recovery from training, and sleep quality, with a well-characterized ghrelin-receptor (GHS-R1a) mechanism that stimulates pulsatile GH release. The strongest evidence is for its diagnostic use — it is formally approved in Japan as pralmorelin for intravenous GH-stimulation testing, one of the few GHRPs worldwide to achieve any regulatory indication. Human clinical data on chronic wellness dosing is moderate: well-characterized GH release kinetics and IGF-1 elevation in the 3–6 week range, with stacking against GHRH analogs like CJC-1295 producing synergistic pulses. The honest caveats are meaningful: no FDA approval exists for any indication in the US, long-term human safety data beyond the diagnostic-use population is essentially absent, and GHRP-2 elevates cortisol and prolactin more than ipamorelin though less than GHRP-6. It is named on WADA's Prohibited List (S2.2.4, as GHRP-2/pralmorelin) at all times, and LC-MS/MS urinary detection is routine. In the US, FDA lists GHRP-2 in 503B Category 2 (significant safety risks) and in 503A Category 3 (nominated without adequate support), so there is no settled compounding pathway. Dominikowski and colleagues (Front Endocrinol 2026) reviewed the emerging landscape of GH-IGF1-axis peptides under self-administration — GHRP-2 among them — stratifying candidates by evidence quality (from regulatory-grade RCTs to complete absence of human data) and cataloguing the class-level adverse-event pattern clinicians encounter in patients presenting after unregulated use: endocrine and metabolic disturbances (prolactin and cortisol elevations, appetite changes, dysglycaemia), fluid-retention syndromes, musculoskeletal symptoms (myalgia and arthralgia), and injection-site reactions.
History & Discovery
GHRP-2, also known as pralmorelin, was developed in the 1990s building on the original GHRP series pioneered by Cyril Bowers and colleagues at Tulane University, whose work in the 1980s established that short synthetic enkephalin-derived peptides could release growth hormone through a distinct receptor from GHRH. GHRP-2 (sometimes designated KP-102 in early Japanese literature) emerged from a series developed by Polygen in Germany together with Bowers's group at Tulane. Kaken Pharmaceutical acquired worldwide manufacturing and marketing rights and sublicensed the US and Canada to Wyeth, formerly American Home Products — which is why the compound also carries the development codes GPA 748 and WAY-GPA-748 — while retaining Japan for itself. Kaken took it through to a Japanese approval for intravenous use in GH-stimulation testing, one of the few GHRPs worldwide to achieve a formal regulatory indication. The Japanese preparation is marketed as 注射用GHRP科研100, GHRP Kaken 100 for Injection: a lyophilized vial containing 100 mcg of pralmorelin hydrochloride with 25 mg of D-mannitol, reconstituted in 10 mL of saline immediately before use. Outside Japan, GHRP-2 was never approved as a therapeutic drug. It migrated into the wellness, bodybuilding, and research-chemical markets during the 2000s, where it became a common component of GH-optimization stacks, typically paired with a GHRH analog such as CJC-1295 or sermorelin to exploit the dual-pathway rationale described in the GHRP literature. The order of those discoveries is worth getting right, because it is frequently reversed. The receptor came first: Howard, Feighner and colleagues at Merck cloned the orphan growth hormone secretagogue receptor in 1996, identifying it precisely by its responsiveness to the synthetic GHRPs. Its endogenous ligand was found three years later, when Kojima, Kangawa and colleagues identified ghrelin in 1999. Only then could GHS-R1a be called the ghrelin receptor at all — and only then did GHRP-2 become legible as an early synthetic ghrelin mimetic rather than the orphan peptide it had been for its first decade.
How It Works
GHRP-2 tells your pituitary gland to release more growth hormone by mimicking a natural hunger hormone called ghrelin. This results in a pulse of growth hormone similar to what your body produces naturally during deep sleep.
GHRP-2 binds to the growth hormone secretagogue receptor (GHS-R1a), the same receptor targeted by endogenous ghrelin. This triggers calcium influx in somatotroph cells, leading to GH release. Unlike direct GH administration, GHRP-2 maintains the pulsatile nature of GH secretion and preserves negative feedback mechanisms. It also has mild effects on ACTH and cortisol release.
Evidence Snapshot
Human Clinical Evidence
Moderate for endocrine pharmacology and diagnostics; absent for body composition. GHRP-2 is a formally approved diagnostic agent in Japan, and the diagnostic literature is genuinely strong — a cortisol cut-off of 11.6 mcg/dl predicts secondary hypoadrenalism with 89.7% sensitivity and 88.9% specificity (PMID 27020037), the ACTH response screens pituitary adrenal insufficiency at 83% sensitivity and 88% specificity (PMID 35795807), and a 2026 study extends this to distinguishing hypothalamic from pituitary adrenal insufficiency (PMID 42732957). Pharmacokinetics and GH-release kinetics are well characterized (PMID 9543135), as is synergy with GHRH (PMID 7559885). Chronic dosing data exist but are thin: one 30-day continuous subcutaneous infusion study in older adults showed sustained GH pulsatility and elevated IGF-1 without tachyphylaxis (PMID 11322505). Food intake rose dose-dependently up to 33.5% in a placebo-controlled infusion study (PMID 16861611). What does not exist is any controlled trial measuring body composition, lean mass or fat mass as an endpoint — that use case rests on mechanism and anecdote, not on evidence.
Animal / Preclinical
Extensive. Well-characterized mechanism and pharmacokinetics in animal models.
Mechanistic Rationale
Strong. GHS-R1a binding and downstream signaling are well-understood.
Research Gaps & Open Questions
What the current literature has not yet settled about GHR-2 (GHRP-2):
- 01Long-term (>12 month) human safety data outside the diagnostic-use population is essentially absent — Japanese diagnostic-use experience informs single-dose IV safety, not chronic subcutaneous wellness dosing.
- 02Whether GHRP-2's mild cortisol and prolactin elevation carries clinically meaningful consequences at chronic wellness doses has not been quantified in a dedicated long-duration trial.
- 03Optimal dosing cadence (two vs. three times daily) and the dose-response curve for IGF-1 at chronic wellness-range doses have not been compared head-to-head in published human work.
- 04Whether stacking with a GHRH analog meaningfully improves clinical endpoints over monotherapy — as opposed to just amplifying the acute GH pulse — has not been tested with body-composition or functional endpoints in a controlled human study.
- 05Pituitary desensitization with chronic use — GHRP-2 is often described as less desensitizing than hexarelin but this comparison rests on short-duration studies rather than long-duration human data.
- 06Independent replication of cardiovascular and tissue-repair findings outside the Japanese and European GHRP research programs has begun but remains thin — a 2025 Chinese rat rotator-cuff study reported improved tendon-bone healing with reduced M1 macrophage production (PMID 39672241), which is exactly the kind of outside-program replication that was previously absent.
- 07No controlled human trial has ever measured body composition, lean mass or fat mass as an endpoint for GHRP-2, despite body composition being among the most common reasons people seek it out. The chronic human data amount to a single 30-day infusion study measuring hormones, not physique.
- 08Whether the desensitization seen in animals applies to human protocols is unresolved, and the animal data cut both ways: repeated same-day injections at two-hour intervals blunt the GH response in calves and swine, while once-daily subcutaneous dosing for 30 days in swine continued to stimulate GH release, and a 30-day continuous human infusion showed no loss of effect. Dosing frequency, not duration, may be what drives tolerance.
Forms & Administration
GHRP-2 is administered via subcutaneous injection, typically 2-3 times daily. It is often combined with a GHRH analog for enhanced effect. Timing around meals and sleep is important for optimal results. All injectable peptides should only be administered under the guidance of a qualified healthcare provider. Never self-administer without clinician oversight.
Dosing & Protocols
The ranges below reflect protocols commonly discussed in the literature and by clinicians — not a prescription. Actual dosing for any individual should be determined by a qualified healthcare provider who knows the patient.
Typical Range
Protocols commonly discussed for GHRP-2 run 100–300 mcg per dose, most frequently 100 mcg per injection two to three times daily. The Japanese diagnostic protocol for GH deficiency testing uses a single intravenous 100 mcg dose, which is not equivalent to a chronic wellness protocol but informs the lower bound of pharmacologically active doses. Total daily doses above ~1 mg tend to saturate the GH response; larger single doses amplify cortisol and prolactin effects more than they amplify GH release.
Frequency
GHRP-2 is short-acting (plasma half-life roughly 15–60 minutes), so dosing is typically split across two to three discrete pulses per day — commonly morning, post-workout or midday, and bedtime. The standard stacking rationale with a GHRH analog (CJC-1295 no-DAC, sermorelin, or tesamorelin) rests on two distinct receptor pathways: GHRP-2 acts at the ghrelin/GHS-R1a receptor on somatotrophs, while GHRH analogs act at the GHRH receptor. Combined, the two produce a GH pulse substantially greater than either alone — a synergistic rather than additive effect that is the basis for nearly every 'GHRP-2 + GHRH' protocol.
Timing Considerations
Time of day
Bedtime is the most common window, aligned with the natural nocturnal GH pulse; multi-dose protocols typically add a mid-morning fasted dose and a pre-workout dose.
Relative to meals
Fasted — at least 30 minutes before food and 2+ hours after a meal. Elevated insulin and amino acids substantially blunt the GH response.
Relative to exercise
Independent of training, though a pre-workout dose on training days is common in multi-dose protocols.
Cycle Length
Commonly discussed protocols run 8–12 weeks on followed by a 4-week break, partly to limit sustained cortisol and prolactin exposure and partly as a generic conservative default across GH secretagogues. Pituitary desensitization is a theoretical concern with continuous ghrelin-receptor stimulation, though the human evidence for meaningful tachyphylaxis with GHRP-2 specifically is thinner than for hexarelin. No long-duration human trial has compared continuous versus cycled use in a wellness population.
Protocol Notes
GHRP-2 is supplied as a lyophilized powder (typically 2 mg or 5 mg per vial) and reconstituted in bacteriostatic water. A 5 mg vial in 2 mL of BAC water yields 2,500 mcg/mL, making 100 mcg roughly 0.04 mL or 4 units on an insulin syringe. Subcutaneous injection into the abdominal fat pad is the standard route outside the diagnostic IV setting. Because GHRP-2 acts through the ghrelin receptor, timing on a relatively empty stomach matters: circulating amino acids and elevated insulin blunt GH release, so most protocols call for injection at least 30 minutes before eating or at least 2 hours after a meal. Bedtime dosing is often used to align with the natural nocturnal GH pulse; morning fasted dosing is the other common window. When stacked with CJC-1295 no-DAC or sermorelin, the two peptides are typically drawn into the same syringe and injected together.
GHRP-2 is not FDA-approved for any indication in the United States; its only current regulatory approval is as an intravenous diagnostic agent for GH deficiency in Japan. The numbers above describe commonly-referenced wellness protocols, not a prescription. Use should be supervised by a qualified clinician with appropriate IGF-1, glucose, cortisol, and prolactin monitoring.
Timeline of Effects
Onset
Sleep-depth changes and subjective recovery improvement are typically the first reported signals, often within 1–2 weeks of consistent daily dosing. Appetite stimulation — milder than with GHRP-6 but present — can appear within days. GH pulses are immediate (peak within 15–30 minutes of injection), but downstream IGF-1 elevation requires several days of repeat dosing to accumulate meaningfully in serum.
Peak Effect
Serum IGF-1 typically rises progressively over the first 3–6 weeks and plateaus. Subjective body-composition and recovery benefits most commonly plateau around the 2–3 month mark. Whether continued dosing beyond that point adds benefit or simply maintains the plateau has not been established from controlled human data.
After Discontinuation
Because GHRP-2 does not suppress endogenous GHRH or ghrelin production, endogenous pulsatile GH secretion returns to baseline within days of stopping dosing. IGF-1 drifts back toward pre-treatment levels over 2–4 weeks. Cortisol and prolactin elevations, to the extent they were present, normalize quickly. No post-cycle therapy is required — GHRP-2 does not suppress the HPG axis.
Monitoring & Measurement
Bloodwork & Labs
- •IGF-1 (serum) — the practical response marker, since GH itself is pulsatile and a single random GH level is uninterpretable. The one chronic human study showed IGF-1 rising within 24 hours and holding for 30 days
- •Fasting glucose and HbA1c — GH opposes insulin action and GHRP-2's cortisol rise compounds it
- •Prolactin and cortisol — GHRP-2 is not selective; modest rises are expected pharmacology rather than a complication, but a doubling of either warrants reassessment
- •Morning cortisol or ACTH if symptoms of HPA disturbance appear — GHRP-2 raised ACTH roughly 38-fold in Cushing's disease, so it is a genuine corticotroph stimulus
- •Thyroid panel — GH-IGF1 axis manipulation interacts with thyroid status, and uncorrected hypothyroidism blunts the GH response
Functional & Performance Tests
- •DEXA for lean and fat mass — worth doing precisely because no trial has ever measured this endpoint for GHRP-2, so your own before-and-after is the only data you will have
- •Grip strength or another simple functional measure, to distinguish fluid retention from genuine change
When to Test
Baseline, 6 weeks, and 12 weeks.
Interpretation & Notes
The single most important point is that IGF-1, not GH, is the marker to follow — GHRP-2 produces pulses, so a spot GH level reflects when the blood was drawn more than whether the protocol is working. Expect IGF-1 to climb over 3 to 6 weeks and plateau. Because GHRP-2 is non-selective, modest prolactin and cortisol elevations are part of normal pharmacology; the question is whether they stay modest. Watch glucose carefully in anyone with insulin resistance, since GH and cortisol both push the same direction. Note that none of the chronic-use monitoring here is validated by trial data — the Japanese approval covers a single diagnostic dose, and no regulator has ever reviewed GHRP-2 for repeated administration. Panels are available through LabCorp, Quest, Marek Health and Ulta Lab Tests.
Common Questions
How does GHRP-2 differ from GHRP-6?
GHRP-2 is more potent for GH release at comparable doses and produces noticeably less hunger. Both raise cortisol and prolactin, but GHRP-6 does so more — GHRP-2 sits between GHRP-6 and ipamorelin on selectivity rather than being clean. One honest caveat: this ranking is near-universal in the field and consistent with how the two behave clinically, but it rests on cross-study comparison rather than a head-to-head trial of GHRP-2 against GHRP-6 on cortisol and prolactin endpoints. The sharper practical difference is that GHRP-2 has a real regulatory approval as a diagnostic agent and GHRP-6 has none.
Can GHRP-2 be combined with CJC-1295?
Yes, and the rationale is better evidenced than most peptide stacking claims. The two act at different receptors — GHRP-2 at the ghrelin receptor GHS-R1a, CJC-1295 at the GHRH receptor — and the combination produces a GH pulse larger than either alone. That synergy has been demonstrated directly: in children of short stature, the GH response to GHRH combined with GHRP-2 was synergistic rather than additive, mirroring earlier adult observations (PMID 7559885). What has never been tested is whether that larger acute pulse translates into better body-composition or functional outcomes than either agent alone.
What is GHRP-2 actually approved for?
One thing, in one country. Japan approved it in October 2004 as pralmorelin hydrochloride, marketed by Kaken as GHRP Kaken 100 for Injection — a lyophilized 100 mcg vial used as a single intravenous dose to diagnose growth hormone deficiency. The protocol is specific: reconstitute in 10 mL of saline immediately before use, inject slowly while fasting, and sample GH before dosing and at 15, 30, 45 and 60 minutes. Adults receive 100 mcg; children aged 4 to under 18 receive 2 mcg/kg, capped at 100 mcg above 50 kg. A peak GH at or below 15 ng/mL indicates severe GH deficiency, or 9 ng/mL when a recombinant GH standard is used. That is a single-dose diagnostic test, not a therapy — it says nothing about the safety of injecting GHRP-2 repeatedly for months, which is what wellness protocols describe.
Will GHRP-2 improve my body composition?
Nobody knows, and the honest answer is that the evidence most people assume exists does not. No controlled human trial has used GHRP-2 and measured lean mass, fat mass or any body-composition endpoint. What is established is upstream of that: GHRP-2 raises GH pulses acutely, and a 30-day continuous subcutaneous infusion in older adults with reduced GH secretion raised IGF-1 within 24 hours and kept it elevated for the full month (PMID 11322505). Whether sustained IGF-1 elevation at these doses produces meaningful changes in physique or function has not been tested. Treat body composition as a mechanistic expectation, not a demonstrated outcome.
Is GHRP-2 contraindicated in pregnancy?
Yes — and unusually for a research peptide, this is a formal regulatory contraindication rather than a precaution inferred from missing data. The Japanese package insert for GHRP Kaken 100 lists under section 2, contraindications, pregnant women or women who may be pregnant. That is a regulator's judgment on a product that only ever gets given as a single diagnostic dose, which makes repeated self-administration during pregnancy harder to defend, not easier.
Who GHR-2 (GHRP-2) Is NOT For
- •Active or recent-history cancer — GH and IGF-1 elevation may accelerate proliferation of existing malignancies; clinicians universally exclude patients with active cancer from GH-secretagogue protocols.
- •Pregnancy — no human pregnancy safety data; reproductive-toxicology characterization is absent, and sustained GH/IGF-1 elevation has not been studied in pregnancy.
- •Breastfeeding — no data on transfer into breast milk or effects on nursing infants.
- •Diabetes or uncontrolled insulin resistance — GH opposes insulin action and can worsen glycemic control; GHRP-2's mild cortisol elevation compounds this concern. Glucose monitoring is the minimum standard if use is pursued.
- •Active acromegaly, pituitary adenoma, or Cushing's disease — further stimulation of GH-producing cells or HPA-axis activity is contraindicated; GHRP-2 is notably used as a provocation test in Cushing's workup precisely because it amplifies ACTH/cortisol release in affected patients.
- •Pediatric use outside a diagnosed GH deficiency under specialist supervision — development-related signaling effects from unmonitored secretagogue use are a concern. Japanese pediatric data exist for the diagnostic use case but not for chronic wellness dosing.
Drug & Supplement Interactions
Documented clinical drug interactions for GHRP-2 outside the diagnostic setting are sparse; most of what follows is theoretical and derived from GH-pathway overlap with known drug classes. Glucose-regulating medications — insulin, sulfonylureas, and GLP-1 receptor agonists — interact with GH's counter-regulatory effect on glucose and may require dose adjustment as IGF-1 rises over weeks of use. Corticosteroids (prednisone, dexamethasone) complicate the picture in both directions: acute glucocorticoid administration can actually enhance GH response to GHRP-2, while chronic glucocorticoid exposure suppresses spontaneous GH secretion and may blunt cumulative IGF-1 gains. This pharmacological quirk is part of why GHRP-2 is used in Cushing's-disease workup. Somatostatin analogs (octreotide, lanreotide) directly oppose GH release and will pharmacologically antagonize GHRP-2. Thyroid hormone status matters — uncorrected hypothyroidism blunts the GH response. Estrogens modulate GH/IGF-1 coupling, with oral estrogens in particular reducing hepatic IGF-1 generation, which affects interpretation of IGF-1 monitoring labs. Dopamine agonists used for hyperprolactinemia may attenuate GHRP-2's small prolactin-elevating effect. Patients on any regular medication should disclose GHRP-2 use to their prescribing clinician; absence of documented interaction is not evidence of absence.
Safety Profile
Common Side Effects
Cautions
- • Not FDA-approved for anti-aging
- • Can affect blood sugar levels
- • Should be monitored by clinician
- • May affect cortisol and prolactin
What We Don't Know
Long-term effects of sustained GH elevation through GHRP-2 use are not fully characterized in anti-aging contexts.
Legal Status
United States
GHRP-2 is not FDA-approved for any medical indication in the United States, and it is not on the 503A Bulks List. FDA's May 2026 list places GHRP-2 in 503A Category 3 (nominated without adequate support), and since September 29, 2023 GHRP-2 for injectable and nasal routes has been in 503B Category 2 (bulk drug substances that may present significant safety risks). FDA cites immunogenicity risk from aggregation and peptide-related impurities, an unnatural amino acid that complicates characterization, and reports of serious adverse events — increased insulin requirements, deaths in critically ill study subjects, infection and pancreatitis — though causality has not been established. GHRP-2 was not part of FDA's April 2026 Category 2 changes. It is widely sold in the research-chemical market labeled 'not for human consumption,' which is not an authorized channel for human use. Regulatory posture is actively evolving.
International
GHRP-2 is approved in Japan under the name pralmorelin (marketed by Kaken Pharmaceutical as GHRP Kaken) specifically as an intravenous diagnostic agent for growth hormone deficiency testing — not as a chronic therapeutic. The European Medicines Agency and UK MHRA have not authorized GHRP-2 as a medicine. Australia's TGA classifies GH secretagogues as Schedule 4 prescription-only substances. Canada treats it as an unapproved investigational agent.
Sports & Competition
GHRP-2 is explicitly prohibited under WADA's S2.2.4 (growth hormone releasing factors), which names GHRP-2 (pralmorelin) among the GH-releasing peptides — prohibited at all times, both in and out of competition. LC-MS/MS urinary detection methods for GHRP-2 and its metabolites are well-established and used routinely in anti-doping laboratories. Athletes subject to WADA, USADA, UKAD, or equivalent bodies must avoid it.
Regulatory status changes over time. Verify current local rules with a qualified professional.
Myths & Misconceptions
Myth
GHRP-2 is FDA-approved because it has regulatory approval somewhere.
Reality
GHRP-2's only current approval is Japanese, as an intravenous diagnostic agent for GH deficiency — not as a chronic therapeutic and not in the United States. The FDA has not approved GHRP-2 for any indication. Conflating 'approved somewhere' with 'approved here' is a common marketing sleight of hand in the peptide space.
Myth
GHRP-2 is a clean, selective GH secretagogue on par with ipamorelin.
Reality
GHRP-2 is more selective than GHRP-6 or hexarelin but meaningfully less selective than ipamorelin. It raises ACTH, cortisol, and prolactin at clinically relevant doses — modestly at typical wellness protocols, more noticeably at higher doses. Ipamorelin was specifically designed to eliminate those off-target effects and is the reference 'clean' GHRP; GHRP-2 sits between ipamorelin and the older compounds on the selectivity spectrum.
Myth
GHRP-2 + CJC-1295 produces natural, physiological GH pulses identical to endogenous secretion.
Reality
The combination does produce large, pulsatile GH releases through two distinct receptor pathways, and the pulses do preserve negative feedback. But the amplitude and frequency are pharmacologically imposed, not physiological; stacking exogenous agents at multiple dosing windows per day is not the same thing as the body's native circadian GH rhythm. 'Physiological pathway' is accurate; 'physiological pattern' overstates it.
Myth
GHRP-2 is not detectable in drug testing because it is a short peptide that breaks down quickly.
Reality
LC-MS/MS urinary detection methods for GHRP-2 and its metabolites are well-validated and used routinely in WADA-accredited labs. Short plasma half-life does not equal undetectability — metabolites are excreted in urine and remain measurable for a window after dosing. Athletes have tested positive for GHRP-2 under WADA code.
Myth
GHRP-2 is safe to use during pregnancy because it just 'tells your body to release its own GH.'
Reality
No human pregnancy safety data exists for GHRP-2. Endogenous GH physiology changes substantially during pregnancy, and pharmacologically imposed GH pulsing has not been studied in reproductive-toxicology frameworks. 'Stimulates your own hormones' is not a safety argument in pregnancy — it is a gap in the evidence base.
Published Research
36 studiesDifferentiating hypothalamic from pituitary adrenal insufficiency: underlying causes and diagnostic utility of the corticotropin-releasing hormone and growth hormone-releasing peptide-2 stimulation tests
The emerging landscape of performance-enhancing peptides modulating GH-IGF1 axis: bridging the gap between clinical evidence and patient self-administration
Dominikowski et al., Front Endocrinol 2026 — a current review of GH-IGF1 axis peptides used outside medical supervision, naming GHRP-2 explicitly among the growth hormone secretagogues. It stratifies agents by evidence quality, from regulatory-grade randomized data to a complete absence of human studies, and catalogues the adverse-effect pattern clinicians actually encounter: endocrine and metabolic disturbances including prolactin and cortisol elevations, appetite changes and dysglycaemia, fluid-retention syndromes, musculoskeletal myalgia and arthralgia, and injection-site reactions.
Growth Hormone-Releasing Peptide 2 May Be Associated With Decreased M1 Macrophage Production and Increased Histologic and Biomechanical Tendon-Bone Healing Properties in a Rat Rotator Cuff Tear Model
Assessment of anterior pituitary reserve capacity based on growth hormone response to growth hormone-releasing peptide-2 test in the elderly
Clinical Usefulness of the Growth Hormone-Releasing Peptide-2 Test for Hypothalamic-Pituitary Disorder
Suzuki et al., J Endocr Soc 2022 — the best modern diagnostic-accuracy data for the GHRP-2 test in hypothalamic-pituitary disorder. ROC analysis showed the ACTH response was useful for screening pituitary adrenal insufficiency at a cut-off of 1.55-fold, with 83% sensitivity and 88% specificity.
Evaluation of growth hormone-releasing peptide-2 for diagnosis of thyrotropin-producing pituitary adenomas
Growth Hormone Releasing Peptide-2 Attenuation of Protein Kinase C-Induced Inflammation in Human Ovarian Granulosa Cells
Investigation of the clinical significance of the growth hormone-releasing peptide-2 test for the diagnosis of secondary adrenal failure
Arimura et al., Endocr J 2016 — the diagnostic-validation study for GHRP-2 beyond growth hormone. Using a peak serum cortisol cut-off of 11.6 mcg/dl, the GHRP-2 test predicted secondary hypoadrenalism with 88.9% specificity and 89.7% sensitivity, supporting its use as an alternative to the insulin tolerance test for adrenal axis assessment.
One-year intranasal application of growth hormone releasing peptide-2 improves body weight and hypoglycemia in a severely emaciated anorexia nervosa patient
Synthesis of Mono-PEGylated Growth Hormone Releasing Peptide-2 and Investigation of its Biological Activity
Growth hormone response to growth hormone-releasing peptide-2 in growth hormone-deficient little mice
Influence of intravenous administration of growth hormone releasing peptide-2 (GHRP-2) on detection of growth hormone doping: growth hormone isoform profiles in Japanese male subjects
Okano et al., Drug Test Anal 2010 — a human administration study with a finding that matters beyond detection. After GHRP-2 dosing, GH isoform recombinant-to-pituitary ratios fell to 39.9 to 43.9% of the elevated ratio produced by recombinant GH, meaning GHRP-2 is not only detectable by the isoform differential immunoassay but can also MASK recombinant GH doping on that assay.
Identification of the growth-hormone-releasing peptide-2 (GHRP-2) in a nutritional supplement
Growth hormone releasing peptide-2, a ghrelin agonist, attenuates lipopolysaccharide-induced acute lung injury in rats
Determination of growth hormone secretagogue pralmorelin (GHRP-2) and its metabolite in human urine by liquid chromatography/electrospray ionization tandem mass spectrometry
Concordant and discordant adrenocorticotropin (ACTH) responses induced by growth hormone-releasing peptide-2 (GHRP-2), corticotropin-releasing hormone (CRH) and insulin-induced hypoglycemia in patients with hypothalamopituitary disorders: evidence for direct ACTH releasing activity of GHRP-2
Comparison of pituitary-adrenal responsiveness between insulin tolerance test and growth hormone-releasing peptide-2 test: a pilot study
Exaggerated response of adrenocorticotropic hormone to growth hormone-releasing peptide-2 test in Cushing's disease. Case report
Sakihara et al., Neurol Med Chir 2009 — the most vivid illustration of GHRP-2's off-target corticotroph activity. In Cushing's disease, 100 mcg of GHRP-2 raised plasma ACTH from 66 pg/ml to 2490 pg/ml, roughly a 38-fold increase. This is why GHRP-2 is used as a provocation agent in Cushing's workup and why it cannot be described as a clean, GH-selective secretagogue.
Growth hormone-releasing peptide-2 stimulates secretion and synthesis of adrenocorticotropic hormone in mouse pituitary
The effect of growth hormone releasing peptide-2 on upper gastrointestinal contractile activity and food intake in conscious dogs
Diagnostic usefulness of the growth hormone-releasing peptide-2 test as a substitute for the insulin tolerance test in hypopituitarism
Obese subjects respond to the stimulatory effect of the ghrelin agonist growth hormone-releasing peptide-2 on food intake
Laferrere et al., Obesity 2006 — the controlled demonstration that GHRP-2 drives eating, not just growth hormone. In a double-blind placebo-controlled study, GHRP-2 infusion increased ad libitum food intake dose-dependently, by 10.2 +/- 3.9% at the low dose (p=0.011) and 33.5 +/- 5.8% at the high dose (p=0.000) versus placebo. This is the best quantification of the orexigenic effect anywhere in the GHRP literature.
Pralmorelin: GHRP 2, GPA 748, growth hormone-releasing peptide 2, KP-102 D, KP-102 LN, KP-102D, KP-102LN
Drugs in R&D 2004 — the regulatory and licensing record for pralmorelin, and the source that corrects the commonly repeated development history. The series was developed by Polygen in Germany and Tulane University under Cyril Bowers; Kaken acquired worldwide manufacturing and marketing rights and sublicensed the US and Canada to Wyeth, formerly American Home Products, retaining Japan. It also sets the diagnostic threshold: ROC analysis gave a GH peak cut-off of 15.0 mcg/l for separating GH-deficient patients from healthy controls.
Chicken ghrelin and growth hormone-releasing peptide-2 inhibit food intake of neonatal chicks
Growth hormone/insulin-like growth factor-1 response to acute and chronic growth hormone-releasing peptide-2, growth hormone-releasing hormone 1-44NH2 and in combination in older men and women with decreased growth hormone secretion
Bowers et al., Endocrine 2001 — the only chronic human dosing data on this page, and the evidence behind the claim that IGF-1 climbs over weeks. GHRP-2 was infused subcutaneously at 1 mcg/kg/h continuously for 30 days in older men and women with reduced GH secretion. Normal pulsatile GH secretion and serum IGF-1 both increased after 24 hours and remained elevated across the full 30 days, with no evidence of the tachyphylaxis that repeated same-day bolus dosing produces in animals.
Interactive regulation of postmenopausal growth hormone insulin-like growth factor axis by estrogen and growth hormone-releasing peptide-2
Effects of the administration of growth hormone-releasing peptide-2 (GHRP-2) orally by gavage and in feed on growth hormone release in swine
The effects of growth hormone-releasing peptide-2 (GHRP-2) on the release of growth hormone and growth performance in swine
Preservation of growth hormone secretion in response to growth hormone-releasing peptide-2 during prednisone therapy
Growth hormone-releasing peptide-2 infusion synchronizes growth hormone, thyrotrophin and prolactin release in prolonged critical illness
Van den Berghe et al., Eur J Endocrinol 1999 — GHRP-2 in prolonged critical illness, and an unusual finding about pituitary rhythm. Infusion of GHRP-2, but not GHRH or TRH, markedly synchronized the serum profiles of GH, TSH and prolactin (all p<=0.007), suggesting the ghrelin-receptor pathway restores pulsatile coordination that is lost in chronic critical illness rather than simply raising hormone levels.
Effect of growth hormone-releasing peptide-2 (GHRP-2) and GH-releasing hormone (GHRH) on the the cAMP levels and GH release from cultured acromegalic tumours
Pharmacokinetics and pharmacodynamics of growth hormone-releasing peptide-2: a phase I study in children
Pihoker et al., JCEM 1998 — the human pharmacokinetic source underlying the half-life and onset figures used throughout this page. In children, GHRP-2 showed a terminal half-life of 0.55 +/- 0.14 hours, with the GH response peaking at 50.7 +/- 17.2 ng/ml at 0.42 +/- 0.16 hours — roughly 25 minutes, which is why protocols describe a pulse rather than sustained exposure.
Treatment effects of intranasal growth hormone releasing peptide-2 in children with short stature
Characteristics of growth hormone secretion responsiveness to growth hormone-releasing peptide-2 (GHRP-2 or KP102) in calves
Effects of growth hormone-releasing peptide-2 (GHRP-2) on membrane Ca2+ permeability in cultured ovine somatotrophs
Diagnostic studies with intravenous and intranasal growth hormone-releasing peptide-2 in children of short stature
Pihoker et al., JCEM 1995 — the clinical evidence behind the GHRH-plus-GHRP stacking rationale. In 12 children of short stature, the GH response to GHRH combined with GHRP-2 was synergistic rather than additive, mirroring earlier observations in adults of normal stature. The mean peak GH response to 15 mcg/kg intranasally was 31.3 mcg/l.
Quick Facts
- Class
- Growth Hormone Secretagogue
- Tier
- C
- Evidence
- Moderate
- Safety
- Moderate Data
- Updated
- Nov 2026
- Citations
- 36PubMed
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Clinical Trials
View Clinical TrialsLinks to ClinicalTrials.gov for reference. Listing does not imply endorsement.