GHRP-2 Reconstitution Calculator

No. GHRP-2 (pralmorelin; D-Ala-D-β-naphthyl-Ala-Ala-Trp-D-Phe-Lys-NH₂) is approved only in Japan, solely as an intravenous diagnostic agent for GH deficiency, the single GHRP-family member with clinical approval. No jurisdiction has approved it for performance, body-composition, or anti-aging use; online "research" vials are unregulated with unverified composition, and novel analogues engineered to evade doping detection circulate on the black market. GHRP-2 is on the WADA Prohibited List.

Subcutaneous injection is the standard self-administration route (community protocol). Clinical diagnostics use 100 μg IV boluses, which raise both recombinant and pituitary GH without altering the isoform Rec/Pit ratio (observational). Intranasal delivery is systemically effective: a 12-month intranasal course improved body weight and hypoglycemia in an anorexia nervosa patient (case report), and urinary metabolites confirm absorption up to 47 h after nasal dosing. Oral GHRP-2 releases GH in swine and cattle, but human oral pharmacokinetics are unpublished; oral dosing uses larger amounts than injection (animal). Community consensus: 100–300 μg SC 2–3× daily on an empty stomach, typically pre-bed (pre-sleep dosing, most common timing) (community protocol).

Yes. GHRP-2 directly stimulates pituitary ACTH secretion via the ghrelin receptor (GHS-R1a), independent of CRH (mechanistic). In 47 patients tested, a peak cortisol ≥11.6 μg/dL ruled out secondary hypoadrenalism with 89.7% sensitivity and 88.9% specificity, i.e., the peptide provokes meaningful adrenal activation in most individuals. Prolactin and cortisol elevations are among the most commonly reported adverse effects of unregulated GHRP-2 use. Expect a transient post-dose cortisol rise; persistent elevated morning cortisol with fluid retention or insomnia warrants discontinuation (practitioner consensus).

No human pregnancy or lactation data exist, do not use while pregnant or breastfeeding (community protocol). GHRP-2 alters GH, ACTH, cortisol, and appetite signaling, with dysglycaemia among reported endocrine disturbances. In patients 65+, the GHRP-2 stimulation test is considered relatively safe among endocrine provocative tests and is used routinely in Japanese clinics, so age alone is not a contraindication. Baseline cortisol and fasting glucose checks before first use are reasonable given the ACTH/cortisol and glycaemic effects (practitioner consensus).

GH-response attenuation develops within days of continuous daily dosing. Healthy young men given daily SC GHRP-2 for 5 days showed significantly blunted GH responses and no IGF-I elevation. Chronic clinical exposure is limited to case data: 12 months of intranasal use in one patient with sustained weight benefit and no serious adverse events reported. Community practice: cycle 8–12 weeks on, 2–4 weeks off; during the on-phase take 2–3 short-acting doses/day and check IGF-1 at week 4–6, a flat IGF-1 suggests desensitization or dosing mistimed against endogenous GH pulses (community protocol).

GHRP-2 is 2–3× more potent than GHRP-6 at releasing GH and is the only clinically approved GHRP. Ipamorelin is viewed as more GH-selective with less ACTH/prolactin spillover, whereas GHRP-2's stronger ACTH and hunger (orexigenic) profile makes appetite increase a notable effect. CJC-1295 (with or without DAC) belongs to the GHRH-analogue class, a different receptor target, and GHRPs plus GHRH analogues are frequently stacked in self-administration regimens. GHRP-2 is short-acting (hours); CJC-1295 with DAC supplies a long-acting GHRH background (community protocol).

Animal data only, plausible but unproven in humans. In a rat rotator-cuff tear model, GHRP-2 reduced M1 macrophage polarization and improved histological scores, bone mineral density, and maximal failure load/stiffness at 4–8 weeks postsurgery (animal). In tumor-bearing mice it reversed 5-fluorouracil chemotherapy-induced anorexia (animal). No human injury or healing trials exist; musculoskeletal benefit in people remains extrapolation.

Anti-doping urine detection: parent GHRP-2, GHRP-2 free acid, and GHRP-2(1–3) free acid were detectable up to 47 h after nasal dosing. After IV dosing, parent peptide plus the AA-3 metabolite (D-Ala-D-β-naphthyl-Ala-Ala-OH) are detectable, and GHRP-2 temporarily masks recombinant hGH in the isoform immunoassay, which is why WADA laboratories pair urine mass spectrometry with the isoform test. Standard workplace drug panels do not screen for peptides. Storage: keep lyophilized powder frozen; after reconstituting with bacteriostatic water, refrigerate at 2–8°C and use within ~3 weeks (community protocol).