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Gp22.5

GHRP-2 Research

Mostly mechanism / observational

47 peer-reviewed studies

What the evidence says

Mostly mechanism / observational

Most GHRP-2 studies are mechanism or observational rather than RCTs that measure a clinical effect — keep findings provisional.

Most evidence is from high-quality randomised trials published 1995–2023 with a typical study size of 56 participants.

Based on 47 studies · 41 RCTs · 136 total participants

Confidence

Moderate confidence

By outcome

GH / IGF-1 & lean massRaises GH/IGF-1 short-term as a biomarker, with no outcome data for marketed physique uses; also raises cortisol and prolactin. · Not established (no outcome data)
Mostly mechanism / observational34 studies
Appetite & body weight
Mostly mechanism / observational5 studies
Safety profile
Mostly mechanism / observational5 studies
Glucose & insulin sensitivity
Too few graded studies2 studies

Slowing down

Only 1 study in the last 5 years

199520092023

1RCT2004

Iranmanesh A, Bowers CY, Veldhuis JD · J Clin Endocrinol Metab (2004)

GHRP-2 Research

Mostly mechanism / observational

Activation of somatostatin-receptor subtype-2/-5 suppresses the mass, frequency, and irregularity of growth hormone (GH)-releasing peptide-2-stimulated GH secretion in men.

The somatotropic axis in critical illness: effect of continuous growth hormone (GH)-releasing hormone and GH-releasing peptide-2 infusion.

Reactivation of pituitary hormone release and metabolic improvement by infusion of growth hormone-releasing peptide and thyrotropin-releasing hormone in patients with protracted critical illness.

Novel relationships of age, visceral adiposity, insulin-like growth factor (IGF)-I and IGF binding protein concentrations to growth hormone (GH) releasing-hormone and GH releasing-peptide efficacies in men during experimental hypogonadal clamp.

GH responses to intravenous bolus infusions of GH releasing hormone and GH releasing peptide 2 separately and in combination in adult volunteers.

Gender, sex-steroid, and secretagogue-selective recovery from growth hormone-induced feedback in older women and men.

The combined administration of GH-releasing peptide-2 (GHRP-2), TRH and GnRH to men with prolonged critical illness evokes superior endocrine and metabolic effects compared to treatment with GHRP-2 alone.

Reduction of free fatty acids by acipimox enhances the growth hormone (GH) responses to GH-releasing peptide 2 in elderly men.

Neuroendocrinology of prolonged critical illness: effects of exogenous thyrotropin-releasing hormone and its combination with growth hormone secretagogues.

Tripartite neuroendocrine activation of the human growth hormone (GH) axis in women by continuous 24-hour GH-releasing peptide infusion: pulsatile, entropic, and nyctohemeral mechanisms.

Oral estradiol administration modulates continuous intravenous growth hormone (GH)-releasing peptide-2-driven GH secretion in postmenopausal women.

Thyrotrophin and prolactin release in prolonged critical illness: dynamics of spontaneous secretion and effects of growth hormone-secretagogues.

Contributions of gender and systemic estradiol and testosterone concentrations to maximal secretagogue drive of burst-like growth hormone secretion in healthy middle-aged and older adults.

Differential pulsatile secretagogue control of GH secretion in healthy men.

Aromatase and 5alpha-reductase inhibition during an exogenous testosterone clamp unveils selective sex steroid modulation of somatostatin and growth hormone secretagogue actions in healthy older men.

Secretagogue type, sex-steroid milieu, and abdominal visceral adiposity individually determine secretagogue-stimulated cortisol secretion.

Short-term testosterone supplementation relieves growth hormone autonegative feedback in men.

Growth hormone-releasing peptide-2 infusion synchronizes growth hormone, thyrotrophin and prolactin release in prolonged critical illness.

Growth hormone (GH)-releasing effects of synthetic peptide GH-releasing peptide-2 and GH-releasing hormone (1-29NH2) in children with GH insufficiency and idiopathic short stature.

Determinants of GH-releasing hormone and GH-releasing peptide synergy in men.