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Gp62.5

GHRP-6 Research

Mostly mechanism / observationalLimited safety

9 peer-reviewed studies

What the evidence says

Mostly mechanism / observational

Most GHRP-6 studies are mechanism or observational rather than RCTs that measure a clinical effect — keep findings provisional.

Most evidence is from mixed-quality randomised trials published 2002–2024 with a typical study size of 69 participants.

Based on 9 studies · 1 RCT · 725 total participants

Confidence

Low

By outcome

GH / IGF-1 axis
Mostly mechanism / observational6 studies
Cardio / tissue protection (preclinical)
Mostly mechanism / observational3 studies
Appetite & food intake
Too few graded studies2 studies
Safety profile
Too few graded studies2 studies
Lean body mass & muscle growth
Too few graded studies1 study

Steady research

1 study in the last 5 years

200220132024

1Pilotn=9 · very small study2013

GHRP-6 is a growth hormone secretagogue that also enhances tissue viability in different organs.

Cabrales A, Gil J, Fernández E, Valenzuela C, et al. · Eur J Pharm Sci (2013)

Phase-1 pharmacokinetic study in nine healthy men given a single IV bolus of 100, 200 or 400 mcg/kg GHRP-6, quantified by a validated LC-MS method
Disposition best fitted a bi-exponential model; distribution half-life 7.6 ± 1.9 min and elimination half-life 2.5 ± 1.1 h
Exposure (AUC) tended to increase proportionally with dose — i.e. a short-acting hexapeptide

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2Pilotn=69 · small study2009

During administration of GHRP6 no side effects were observed. GHRP6 alone as a provocative test is highly specific, but with limited sensitivity for the diagnosis of GH deficiency in adults.

Alaioubi B, Mann K, Petersenn S. · Horm Metab Res (2009)

49 patients with suspected hypothalamic/pituitary disease plus 20 healthy controls underwent GHRP-6 (1 mcg/kg) testing; patients also had the insulin tolerance test
Mean GH peak was 3.0 mcg/L in the GH-deficient group vs 14.8 mcg/L in the GH-sufficient group; optimal cut-point 3.5 mcg/L (80% sensitivity, 95% specificity)
Demonstrates GHRP-6's transient, GH-raising effect used as a diagnostic provocative stimulus in humans

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3Observationaln=542 · large study2006

This study confirms that the combined provocative test is adequate to separate normal and GH-deficient subjects.

Kelestimur F, Popovic V, Leal A, Van Dam PS, et al. · Clin Endocrinol (Oxf) (2006)

GHRH + GHRP-6-induced GH peaks evaluated in 542 subjects (healthy normal-weight, overweight, obese, morbidly obese, and GH-deficient patients)
Adiposity had a strong negative effect on the elicited GH peak (r = -0.503, P < 0.0001) — GH response falls with rising body fat
Established BMI-adjusted cut-offs for the combined GHRH + GHRP-6 provocative test

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4Pilotn=69 · small study2010

GHRP6 led to significant activation of the hypothalamic-pituitary-adrenal axis.

Alaioubi B, Mann K, Petersenn S. · Horm Metab Res (2010)

49 patients with suspected HPA-axis dysfunction and 20 healthy controls received GHRP-6 (1 mcg/kg); serum cortisol over 90 min was the main outcome
Mean cortisol peak was 227 nmol/L in adrenal-insufficient vs 395 nmol/L in adrenal-sufficient patients; ROC threshold ~299 nmol/L
Confirms that GHRP-6 activates the HPA axis and raises cortisol — relevant as an off-target effect for performance use

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5Animal2005

GHRP treatment significantly improved left ventricular function and remodeling in CHF rats... GHRP suppressed cardiomyocyte apoptosis.

Xu XB, Pang JJ, Cao JM, Ni C. · Am J Physiol Heart Circ Physiol (2005)

Pressure-overload chronic-heart-failure rats were treated with one of four GH-releasing peptides (GHRP-1, -2, -6 or hexarelin, 100 mcg/kg) or saline, twice daily for 3 weeks
GHRP treatment improved LV ejection fraction and remodeling, alleviated cardiac cachexia, and suppressed cardiomyocyte apoptosis
Lowered elevated stress hormones (catecholamines, renin, angiotensin II, aldosterone, endothelin-1, ANP) and raised cardiac GHS-receptor mRNA

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6Animal2002

GH and GHRP-6 modulate IGF-I expression in the central nervous system... coincident with activation of intracellular signaling pathways used by IGF-I and increased expression of proteins involved in cell survival or neuroprotection.

Frago LM, Pañeda C, Dickson SL, Hewson AK, et al. · Endocrinology (2002)

Adult male rats treated with GHRP-6 (or GH) for 1 week showed increased IGF-I mRNA in hypothalamus, cerebellum and hippocampus
GHRP-6 activated pro-survival signaling (phosphorylation of Akt and Bad) and raised the antiapoptotic protein Bcl-2 in the same regions
Supports a cytoprotective / neuroprotective mechanism downstream of the GH/IGF-1 axis

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7Animal2011

Intra-VTA delivery of the ghrelin receptor antagonist [Lys-3]-GHRP-6 selectively reduced caloric intake of high-fat chow and reduced body weight gain.

King SJ, Isaacs AM, O'Farrell E, Abizaid A. · Horm Behav (2011)

In rats, ghrelin (the natural GHS-R1a agonist) increased chow intake and body-weight gain and the motivation to work for palatable food
The ghrelin-receptor antagonist [D-Lys3]-GHRP-6 conversely reduced high-fat caloric intake and body-weight gain
Illustrates the GHS-R1a appetite/reward axis that GHRP-6 (as an agonist) stimulates — i.e. why GHRP-6 increases hunger

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8Review2006

These ligands have several cardiovascular activities, including a cardioprotective effect against myocardial ischemia, and vasoactive and cardiotropic effects in both experimental models and humans.

Cao JM, Ong H, Chen C. · Trends Endocrinol Metab (2006)

Review of ghrelin and synthetic GH secretagogues (including GHRP-6) and their cardiovascular actions via GHS-R1a and peripheral binding sites
Summarizes cardioprotection against myocardial ischemia plus vasoactive and cardiotropic effects in experimental models
Notes that cardiovascular GHS-receptor signalling pathways are not fully documented

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9RCTn=36 · small study2024

EGF + GHRP6 therapy was safe. The functional benefits of treatment in this study supported a Phase III study.

Hernández-Bernal F, Estenoz-García D, Gutiérrez-Ronquillo JH, et al. · Front Neurol (2024)

Multicentric, randomized, open-label, controlled phase I/II trial: 36 acute ischemic stroke patients given EGF + GHRP-6 (3.5 or 5 mg i.v., BID for 7 days) vs standard care
Primary endpoint was safety over 6 months; serious adverse events were not increased vs control (30% and 20% in treated groups vs 56% control)
Treated patients showed a favourable neurological (NIHSS) and functional (Barthel, modified Rankin) recovery signal at 90 and 180 days with a moderate-to-strong effect size

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View in Research Library

GHRP-6 Research

Mostly mechanism / observational

Pharmacokinetic study of Growth Hormone-Releasing Peptide 6 (GHRP-6) in nine male healthy volunteers.

Diagnosis of growth hormone deficiency in adults: provocative testing with GHRP6 in comparison to the insulin tolerance test.

Effect of obesity and morbid obesity on the growth hormone (GH) secretion elicited by the combined GHRH + GHRP-6 test.

Diagnosis of adrenal insufficiency using the GHRP-6 Test: comparison with the insulin tolerance test in patients with hypothalamic-pituitary-adrenal disease.

GH-releasing peptides improve cardiac dysfunction and cachexia and suppress stress-related hormones and cardiomyocyte apoptosis in rats with heart failure.

Growth hormone (GH) and GH-releasing peptide-6 increase brain insulin-like growth factor-I expression and activate intracellular signaling pathways involved in neuroprotection.

Motivation to obtain preferred foods is enhanced by ghrelin in the ventral tegmental area.

Effects of ghrelin and synthetic GH secretagogues on the cardiovascular system.

Combination therapy of Epidermal Growth Factor and Growth Hormone-Releasing Hexapeptide in acute ischemic stroke: a phase I/II non-blinded, randomized clinical trial.