Research Evidence
GH Stimulation and Diagnostic Use
The Japanese approval of pralmorelin was based on clinical data showing that a single intravenous dose reliably distinguishes GH-sufficient from GH-deficient subjects. Healthy individuals produce plasma GH responses above 15 mcg/L, while patients with severe adult GH deficiency consistently fall below this threshold. This led to pralmorelin's approval as a diagnostic provocative test in 2004.
Pediatric Growth Study
Mericq, Bowers, and colleagues (1998) conducted an eight-month study treating six prepubertal GH-deficient children with stepwise increasing subcutaneous doses of GHRP-2 (0.3, 1.0, and 3.0 mcg/kg/day). The study demonstrated dose-dependent increases in overnight episodic GH secretion, higher growth velocity during treatment compared to pre- and post-treatment periods, and no observed side effects or toxicities. A final two-month period combining GHRP-2 with GHRH produced further augmentation of GH output.
Comparative Hormonal Profiling
Arvat et al. (1997) conducted the definitive head-to-head comparison of GHRP-2, hexarelin, GHRH, TRH, and hCRH in healthy young adults. The study established that GHRP-2 and hexarelin produced GH responses exceeding maximal-dose GHRH, with similar slight stimulatory effects on prolactin (lower than TRH) and ACTH/cortisol (comparable to hCRH). This work remains a cornerstone reference for understanding GHRP-2's hormonal selectivity profile.
Appetite and Food Intake
Laferrere et al. (2005) demonstrated in a controlled crossover study that GHRP-2 significantly increases caloric intake in healthy men through ghrelin receptor-mediated appetite stimulation. This confirmed that GHRP-2, like endogenous ghrelin, has orexigenic properties, though clinical observation consistently shows the effect is less intense than that of GHRP-6.
Cytoprotective Properties
A comprehensive 2017 review by Berlanga-Acosta et al. catalogued evidence for GHRP-mediated cytoprotection, documenting cardioprotective, neuroprotective, and anti-inflammatory effects in preclinical models. These effects appear to be mediated in part through CD36 receptor binding and are independent of GH release, suggesting additional therapeutic dimensions beyond growth hormone secretion.