Ghrp-2
GHRP-2 is a synthetic peptide belonging to the “growth hormone secretagogues” (GHS), studied for its ability to acutely stimulate the secretion of growth hormone (GH) and, to a variable extent, prolactin and ACTH/cortisol. It is not a nutrient and is not found in foods; use outside regulated research/clinical settings involves risks and uncertainties regarding quality, purity, and safety.
Growth hormone (GH) secretagogue peptide active at the ghrelin receptor (GHS-R1a)
GHRP-2 is a synthetic peptide belonging to the “growth hormone secretagogues” (GHS), studied for its ability to acutely stimulate the secretion of growth hormone (GH) and, to a variable extent, prolactin and ACTH/cortisol. It is not a nutrient and is not found in foods; use outside regulated research/clinical settings entails risks and uncertainties regarding quality, purity, and safety.
Mechanism of action
Agonism of the GHS-R1a receptor (ghrelin receptor) at the hypothalamic and pituitary levels: (1) it stimulates the release of GHRH and/or enhances the pituitary response to GHRH; (2) it functionally reduces the inhibitory tone of somatostatin; (3) it promotes pulsatile GH secretion. It may also increase prolactin and ACTH/cortisol (off-target effect/hypothalamic-pituitary-adrenal axis). The increase in IGF-1 is a downstream effect of GH and depends on the liver and nutritional status. Activation of GHS-R1a is also associated with orexigenic signals (increased appetite) and modulation of carbohydrate/lipid metabolism, with a potential impact on insulin sensitivity and blood glucose in some contexts.
Supported benefits
- Acute increase in GH secretion (pulsatile response) in human subjects under experimental conditions (strong)
- Increase in IGF-1 with repeated administrations (secondary effect mediated by GH), variable by population and protocol (moderate)
- Possible increase in appetite and energy intake (orexigenic effect via GHS-R1a), with individual variability (moderate)
- Potential support for body composition markers in specific contexts (e.g., catabolic states/older adults) via the GH/IGF-1 axis; evidence is heterogeneous and inconclusive for healthy populations (limited)
Safety & side effects
- Increased appetite (orexigenic effect), with possible increases in caloric intake and weight in some subjects
- Water retention/edema and a sensation of “fullness” or bloating (effects associated with increased GH/IGF-1 in some contexts)
- Headache, flushing, paresthesia, or dizziness (reported with GH secretagogues in some studies)
- Injection site reactions (pain, redness, induration) with parenteral routes
- Increase in prolactin and/or ACTH/cortisol: potential effects on mood, sleep, blood pressure, and metabolism (variable)
- Possible alterations in blood glucose and insulin sensitivity (direction and magnitude depend on context, dose, and metabolic status)
FAQ
Is GHRP-2 a dietary supplement?
No. It is a synthetic peptide studied as a GH secretagogue. It is not a nutrient and does not come from food sources.
Does it always increase IGF-1?
IGF-1 may increase as a downstream effect of increased GH, but the extent depends on dose, frequency, duration, age, nutritional status, and liver function. It is neither a guaranteed nor a uniform effect.
Which hormones besides GH can it affect?
In several studies it may also increase prolactin and ACTH/cortisol, with potential implications for metabolism, stress, and related symptoms.
Is it relevant for athletic performance?
Evidence of a direct improvement in performance in healthy subjects is weak/heterogeneous. In addition, it is generally prohibited under anti-doping regulations.
Why is the oral route not used in studies?
Peptides are degraded in the gastrointestinal tract and have low oral bioavailability; for this reason, research uses parenteral routes.
The information provided is for informational and educational purposes only. It does not constitute medical advice. Use must be evaluated and authorized by a qualified healthcare professional.
Mechanism of action
Agonism of the GHS-R1a receptor (ghrelin receptor) at the hypothalamic and pituitary level: (1) stimulates the release of GHRH and/or enhances the pituitary response to GHRH; (2) functionally reduces the inhibitory tone of somatostatin; (3) promotes pulsatile GH secretion. It may also increase prolactin and ACTH/cortisol (off-target effect/hypothalamic-pituitary-adrenal axis). The increase in IGF-1 is a downstream effect of GH and depends on the liver and nutritional status. Activation of GHS-R1a is also associated with orexigenic signaling (increased appetite) and modulation of carbohydrate/lipid metabolism, with potential impact on insulin sensitivity and blood glucose in some contexts.
Scientific benefits
Contraindications
- Pregnancy and breastfeeding (lack of adequate safety data)
- Pediatric age outside regulated clinical protocols
- Active or suspected neoplasms: the GH/IGF-1 axis is mitogenic/anti-apoptotic in various tissues; high caution in the absence of a medical indication
- Uncontrolled diabetes or conditions of glycemic instability (potential impact on carbohydrate metabolism)
- Unevaluated pituitary disorders (risk of unpredictable endocrine axis responses)
- Untreated obstructive sleep apnea syndrome or significant edema (possible worsening of fluid retention in some contexts)
Side effects
- Increased appetite (orexigenic), possible increase in caloric intake and weight in some subjects
- Fluid retention/edema and a sensation of “fullness” or bloating (effects associated with increased GH/IGF-1 in some contexts)
- Headache, flushing, paresthesias, or dizziness (reported with GH secretagogues in some studies)
- Injection site reactions (pain, redness, induration) for parenteral routes
- Increase in prolactin and/or ACTH/cortisol: potential effects on mood, sleep, blood pressure, and metabolism (variable)
- Possible alterations in blood glucose and insulin sensitivity (direction and magnitude depend on context, dose, and metabolic status)
Interactions
- Drugs that affect blood glucose/insulin (e.g. insulin, sulfonylureas, corticosteroids): possible modification of glycemic control
- Glucocorticoids: may interfere with the GH/IGF-1 axis and increase metabolic risks; furthermore, GHRP-2 may increase ACTH/cortisol
- Dopaminergic/antidopaminergic agents: potential indirect interaction via prolactin (since GHRP-2 may increase prolactin)
- Other GH secretagogues or exogenous GH: possible additive effects and increased risk of adverse events related to GH/IGF-1
Regulatory status
Not generally approved as a drug for common use; mainly used in research. In many jurisdictions, sale for human use may be restricted or unauthorized. In the anti-doping field, GH secretagogues (including GHRPs) are typically prohibited.
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