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GHRP-2

Pralmorelin

GHRP-2 (pralmorelin) is a synthetic hexapeptide growth-hormone secretagogue that activates the ghrelin/GH-secretagogue receptor (GHS-R1a) to trigger a pulse of growth hormone (GH) release from the pituitary. Its only established, validated human use is as a single-dose intravenous diagnostic agent for GH deficiency (approved in Japan as a provocative pituitary-function test); it is not an approved therapy. It is sold through unregulated research-chemical channels for physique/anti-aging goals, but there are essentially no rigorous long-term human safety trials for that use pattern. It is not selective for GH — it reliably co-stimulates ACTH/cortisol and prolactin, can raise blood glucose and reduce insulin sensitivity, and stimulates appetite (a ghrelin-receptor effect). Product sold outside a pharmacy is unregulated, may be mislabeled or contaminated, and chronic self-injection carries unknown risks including the theoretical concerns that attach to any sustained elevation of GH/IGF-1 (glucose dysregulation, fluid retention, and the unresolved question of cancer/mortality risk). This monograph is risk-forward and is not dosing guidance.

Clinical readoutPeptide · gh-secretagogue
Hepatic strainLow
CardiovascularNone
HPTA suppressionNone
Half-life
1 h
Route
Intravenous for the val…
Evidence
C
Active
Acute/short-lived GH pu…
1 h2 h3 h4 h5 h
Illustrative single-compartment washout · each mark = one half-life · t½ ≈ Short. Human plasma half-life is not well characterized in the retrieved primary literature; pharmacodynamically the GH response peaks within ~60 minutes of an intravenous dose and the provocative test is complete within ~2 hours.
Pharmacology

Mechanism of action

GHRP-2 is a synthetic agonist of the growth-hormone-secretagogue receptor (GHS-R1a), the same G-protein-coupled receptor activated by endogenous ghrelin. It acts at both the pituitary somatotroph and the hypothalamus, promoting pulsatile GH release; its action is synergistic with GHRH and appears to work partly by opposing somatostatin (somatotropin-release-inhibiting) tone rather than by simple GHRH mimicry. Because GHS-R1a is also expressed on other pituitary cell populations and drives central pathways, GHRP-2 is not GH-selective: in humans it also increases ACTH and cortisol secretion and can stimulate prolactin release, and as a ghrelin-receptor agonist it stimulates appetite/food intake. Downstream, the GH pulse raises hepatic IGF-1.
Kinetics

Pharmacokinetics

Half-life

Short. Human plasma half-life is not well characterized in the retrieved primary literature; pharmacodynamically the GH response peaks within ~60 minutes of an intravenous dose and the provocative test is complete within ~2 hours.

Active duration

Acute/short-lived GH pulse (order of 1-2 hours after a single IV dose); repeated/continuous exposure produces partial desensitization of the GH response over time.

Route

Intravenous for the validated diagnostic test (100 µg adults; 2 µg/kg children). It is also biologically active by subcutaneous, intranasal and oral routes, though non-IV/oral bioavailability is lower; non-medical users typically self-inject subcutaneously (not an endorsed practice).

Metabolism & clearance

Peptide is metabolized; a characteristic metabolite (D-Ala-D-beta-(2-naphthyl)-Ala-Ala-OH, 'AA-3') and unchanged parent are recoverable in human urine, indicating renal elimination of parent and metabolite.

For monitoring and washout planning, not drug-test evasion.

Reported effects

Physiological & performance effects

  • Induces a transient, dose-related surge in serum growth hormone from the pituitary (basis for its use as a GH-provocative diagnostic test)
  • Raises hepatic IGF-1 with repeated exposure
  • Co-stimulates ACTH and cortisol release (an intended readout in some pituitary-adrenal reserve testing, but an off-target effect for physique users)
  • Can increase prolactin secretion via pituitary GHS-R
  • Stimulates appetite / food intake (ghrelin-receptor effect)
  • GH response is blunted by older age, adiposity/obesity, and is markedly reduced in true GH deficiency (the diagnostic basis)
Safety

Adverse effects by system

Cardiovascular

No robust human cardiovascular outcome data for GHRP-2 itself. Acute diagnostic dosing is generally well tolerated. Any sustained GH/IGF-1 elevation carries theoretical cardiovascular concerns (fluid retention, blood-pressure and cardiac remodeling seen with chronic GH excess); GHS-R is expressed in cardiovascular tissue, but GHRP-2-specific long-term human cardiac data are absent.

Hepatic

No evidence of direct hepatotoxicity in the retrieved literature; GHRP-2 is a peptide, not 17-alpha-alkylated. The liver is the site of GH-driven IGF-1 production but no signal of liver injury from GHRP-2 is documented. Long-term human liver-safety data are lacking.

Endocrine / HPTA

Primary endocrine concern. Not GH-selective: reliably co-stimulates ACTH and cortisol and can raise prolactin. Sustained GH/IGF-1 elevation can reduce insulin sensitivity and raise blood glucose. Repeated/continuous exposure causes partial desensitization of the GH axis. Effects on the reproductive HPG axis are not established (see hptaSuppression).

Reproductive

No adequate human data on fertility or reproductive outcomes. Prolactin elevation could theoretically affect the gonadal axis, but this is not characterized for GHRP-2. Avoid in pregnancy/breastfeeding (no safety data).

Neuropsychiatric

No well-documented psychiatric adverse effects in the retrieved human diagnostic-use literature. As a ghrelin-system agonist it acts on central appetite/reward circuits, but GHRP-2-specific neuropsychiatric human data are absent.

Renal

No specific human renal toxicity reported; parent drug and metabolite are renally excreted, so impaired kidney function could alter clearance. No adequate long-term human renal-safety data.

Hematologic

No known specific hematologic effects; no adequate human data.

Dermatologic

No characteristic dermatologic toxicity reported for the compound. Injection-site reactions are a generic risk of any self-administered subcutaneous peptide (non-endorsed use); unregulated product raises infection/contamination risk.

Recovery

HPTA suppression & recovery

Suppression: Not characterized for the reproductive (HPG) axis; the relevant axis effect is on the GH and HPA (cortisol) axes

GHRP-2 is a GH secretagogue, not an androgen, so classic testosterone-axis (HPTA) suppression is not its primary concern and single-SERM recovery frameworks are not applicable/indicated here. Its documented endocrine actions are co-stimulation of ACTH/cortisol and prolactin and partial desensitization of the GH response with repeated dosing; the durability of any GH-axis desensitization after stopping is not well studied in the retrieved literature. Anyone using this, or with abnormal cortisol, prolactin, glucose or IGF-1 findings, should stop and consult a board-certified endocrinologist rather than self-manage. This is conservative, non-optimizing guidance.

Bloodwork & vitals

Monitoring

Recommended labs & checks
Fasting glucose and HbA1c (glucose dysregulation risk)IGF-1ProlactinMorning cortisol / ACTH (axis is perturbed by the drug)Thyroid function (TSH, free T4) as part of pituitary-axis evaluation

Cadence: Baseline before any use, then clinician-directed periodic review. Any non-diagnostic ongoing use should be under an endocrinologist; there is no validated safe long-term self-monitoring schedule because long-term human data are absent.

Warning signs — seek care
  • New or worsening high blood sugar (excessive thirst, frequent urination, fatigue)
  • Persistent headache, visual changes, or galactorrhea (possible prolactin/pituitary effects)
  • Swelling/edema, joint pain, or carpal-tunnel-type symptoms (GH-excess features)
  • Injection-site infection, fever, or systemic illness
  • Symptoms of adrenal dysfunction (profound fatigue, dizziness, low blood pressure)
Do not use if

Contraindications

  • Active or history of malignancy, or elevated cancer risk (GH/IGF-1 elevation is theoretically undesirable; long-term cancer/mortality safety of GH secretagogues is explicitly unresolved)
  • Diabetes mellitus or impaired glucose tolerance / insulin resistance (GH secretagogues can raise blood glucose and reduce insulin sensitivity)
  • Pregnancy and breastfeeding (no safety data)
  • Prolactin-sensitive conditions or prolactinoma (GHS-R-expressing prolactinomas can respond to GHRP with prolactin release)
  • Untreated adrenal insufficiency or unstable HPA-axis disease (drug perturbs ACTH/cortisol)
  • Use of non-pharmaceutical, unregulated 'research chemical' product of unknown identity/purity
  • Any use without physician supervision and baseline evaluation
Combinations

Interaction profile

  • MajorWith insulin: Metabolic / glucose
  • ModerateWith another GH secretagogue: Metabolic / glucose
  • ModerateWith growth hormone: Metabolic / glucose
  • ModerateWith IGF-1: Metabolic / glucose
  • ModerateWith a GLP-1 / incretin agonist: Metabolic / glucose
  • ContraindicatedWith DNP: Additive cardiovascular strain

Check a specific combination in the interaction checker.

Harm reduction

Reducing harm & when to stop

  • This compound has no validated human use beyond a single-dose diagnostic test; there is no adequate long-term human safety evidence for repeated physique/anti-aging use. Treat any such use as experimental and unquantified in risk.
  • Do not use without a clinician. Get baseline bloodwork (glucose/HbA1c, IGF-1, prolactin, morning cortisol/ACTH, thyroid) and involve a board-certified endocrinologist, especially if any result is abnormal.
  • Stop and seek medical care for signs of high blood sugar, persistent headache or visual change, galactorrhea, significant swelling/joint pain, or injection-site infection/fever.
  • Because it co-stimulates cortisol and prolactin and can raise blood glucose, it is a poor choice for anyone with diabetes/prediabetes, adrenal or pituitary disease, or prolactin-sensitive conditions.
  • Product sold through non-pharmacy 'research chemical' channels is unregulated and may be mislabeled, underdosed, or contaminated; purity and identity cannot be assumed.
  • Avoid entirely in pregnancy, breastfeeding, active or prior cancer, and elevated cancer risk given unresolved GH/IGF-1 long-term safety.
  • This document is harm-reduction information, not medical advice or an endorsement of use, and contains no dosing-optimization guidance.
Evidence

Citations (12)

Every clinical claim above is tied to a primary source. Overall evidence grade C — graded to the best available evidence for its core claims.

  1. 01

    GHRP-2 (pralmorelin) is a synthetic hexapeptide growth-hormone secretagogue used as an intravenous diagnostic agent for GH deficiency, with a validated adult cut-off (peak GH ~15 µg/L, ~9 µg/L on the WHO 98/574 standard) after a 100 µg IV dose; GH peaks within 60 min.

    CohortPMID 17609397 ↗

  2. 02

    The GHRP-2 test is used and recommended in Japan as a convenient, safe GH-stimulation test for diagnosing severe adult GH deficiency (peak GH cut-off ~9 µg/L).

    ReviewPMID 25070016 ↗

  3. 03

    GHRP-2 is a diagnostic GH-releasing peptide; the pediatric IV dose used is 2 µg/kg and the test reliably separates GH-deficient from non-deficient children, correlating with the insulin tolerance test.

    CohortPMID 20662346 ↗

  4. 04

    GHRP-2 acts via GHS-R (ghrelin/GH-secretagogue receptor) expressed on human pituitary somatotrophs; the same receptor is expressed on prolactinomas, which can respond to GHRP with prolactin secretion.

    PreclinicalPMID 9467586 ↗

  5. 05

    GHRPs act at pituitary and hypothalamic GHRP receptors, are synergistic with GHRH, appear to counteract somatostatin, retain activity by IV/SC/intranasal/oral routes, undergo partial desensitization (more with continuous than intermittent dosing), and chronic administration raises IGF-1; the GH response declines with older age.

    ReviewGrowth hormone-releasing peptides.PMID 9186261 ↗

  6. 06

    The GHRP-2 provocative test co-stimulates ACTH and cortisol in humans; measuring ACTH/cortisol during the test aids detection of secondary adrenal insufficiency, indicating GHRP-2 is not GH-selective.

    CohortPMID 35795807 ↗

  7. 07

    GH response to the GHRP-2 test correlates with adrenocortical (ACTH/cortisol) function in elderly patients, again reflecting co-activation of the HPA axis.

    CohortPMID 37295337 ↗

  8. 08

    GHRP-2 and GHRP-6 increase plasma ACTH and cortisol (shown preclinically in swine), whereas the more selective ipamorelin does not — establishing that GHRP-2 is a non-selective secretagogue affecting the corticotropic axis.

    PreclinicalIpamorelin, the first selective growth hormone secretagogue.PMID 9849822 ↗

  9. 09

    After IV administration in human volunteers, unchanged GHRP-2 and its metabolite AA-3 (D-Ala-D-beta-(2-naphthyl)-Ala-Ala-OH) are excreted and detectable in urine, indicating renal elimination of parent and metabolite.

    CohortDetermination of growth hormone secretagogue pralmorelin (GHRP-2) and its metabolite in human urine by LC/ESI-MS/MS.PMID 20552695 ↗

  10. 10

    Growth-hormone secretagogues are generally well tolerated in short-term human studies but few long-term rigorously controlled studies exist; a notable concern is increased blood glucose from decreased insulin sensitivity, and long-term safety including cancer incidence and mortality remains unestablished.

    ReviewThe Safety and Efficacy of Growth Hormone Secretagogues.PMID 28400207 ↗

  11. 11

    Pralmorelin mimics ghrelin, may influence food intake, was developed as a GH-deficiency diagnostic (cut-off peak GH 15 µg/L), and its therapeutic development for GH deficiency/short stature was not brought to broad approval outside the diagnostic indication.

    ReviewPralmorelin: GHRP 2, GPA 748, growth hormone-releasing peptide 2, KP-102 D, KP-102 LN, KP-102D, KP-102LN.PMID 15230633 ↗

  12. 12

    GHRP-2 stimulates GH secretion in children with and without GH deficiency and was developed as a pituitary GH-secretory diagnostic test.

    Case seriesPMID 9401554 ↗

Last reviewed 2026-07-06 · Verified against PubMed · Educational, not medical advice