Hexarelin half-life & pharmacokinetics

Reported half-life

Approximately 70-100 minutes plasma half-life — longer than ipamorelin (~2 hours equivalent biological action), GHRP-6, and GHRP-2. The relative half-life extension reflects the protease-resistant D-amino-acid substitutions and N-methylated tryptophan that confer enhanced metabolic stability.

The half-life and pharmacokinetic profile of Hexarelin reported above is drawn from the published pre-clinical literature. Plasma half-life describes the time taken for the circulating concentration to fall by half after a single dose; tissue half-life — which may be longer for peptides retained in specific organs or matrices — is a distinct and often more relevant parameter for healing research, where the duration of exposure at the injury site matters more than the systemic exposure profile.

Routes of administration studied

• Subcutaneous injection (research; standard route)
• Intravenous bolus (research; pharmacology characterisation)
• Intranasal (limited research; bioavailability low)

Different routes produce materially different pharmacokinetic profiles for the same peptide. Subcutaneous administration generally produces flatter, more sustained plasma profiles than intravenous bolus dosing; intraperitoneal administration (common in rodent models) is not directly translatable to human routes; oral administration faces the additional challenge of luminal and brush-border peptidase degradation, which is why most research peptides have very low oral bioavailability without protective formulation.

Drug class

Synthetic hexapeptide GHRP-class secretagogue; ghrelin-receptor (GHSR-1a) full agonist with additional direct CD36 receptor binding on cardiomyocytes.

Mechanism context

Half-life interpretation depends on the underlying mechanism. Hexarelin acts as follows:

Hexarelin is a 6-amino-acid synthetic peptide (His-D-2-Me-Trp-Ala-Trp-D-Phe-Lys-NH2) developed by Mediolanum Farmaceutici as an analogue of GHRP-6 with structural modifications designed to enhance GH-releasing potency. The two key modifications are 2-methylation of D-tryptophan at position 2 (improving GHSR-1a binding affinity) and C-terminal amidation (extending metabolic stability against carboxypeptidase degradation). The molecular weight of 887 Da and pentapeptide-equivalent size place hexarelin alongside ipamorelin and GHRP-2 as the small, GHSR-targeted GHRPs.

See the full Hexarelin research profile for the complete mechanism summary, history, study citations, and references.

Practical considerations

Short plasma half-life does not necessarily mean short duration of biological effect. Many peptides — including BPC-157, GHK-Cu, and the thymosin-derived compounds — exhibit tissue retention or mechanistic effects (gene expression, signalling cascades) that outlast plasma exposure by hours to days. The pharmacological half-life and the biological-effect half-life are distinct parameters that must both be specified in any rigorous research design. Repeated-dose protocols should account for accumulation only where tissue half-life is genuinely long; for most peptides with short plasma half-life and rapid degradation, accumulation is not a practical concern.

For dose ranges in published research, see the dosing reference page. For reconstitution guidance, see the reconstitution reference page.