RECORD // DOSAGE
Sermorelin Dosage in the Research Literature
The doses, routes, and timing documented in the published studies — logged as study protocol, never as a recommendation to administer.
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This page reports what doses researchers used in published sermorelin dosage studies — nothing more. It is a record of study protocols, not instructions. The numbers below are tied to specific populations (GH-deficient children, older men, healthy volunteers) and specific research questions. They are written as 'studied at X in [population]' precisely because a dose that answered a research question is not a usage recommendation. No part of this page tells anyone to administer sermorelin.
Sermorelin dosing in the research literature
Sermorelin dosing in the published record spans a few well-defined research contexts. In the pediatric GH-deficiency efficacy study, GHRH(1-29) was given at 30 mcg/kg/day subcutaneously at bedtime [4]. In the aging-research study in older men, doses were 0.5 mg and 1 mg subcutaneously twice daily for 14 days [5]. In pharmacokinetic work in healthy men, intravenous doses of 0.25-2 mcg/kg elicited GH release, with maximal release at 1-2 mcg/kg [3]. Historically, a single intravenous bolus (commonly ~1 mcg/kg) was used diagnostically to test pituitary GH reserve.
These are study doses in defined populations, reported here as documented protocol. This record does not convert them into a personal regimen, and the absence of robust long-term adult outcome data is itself part of the dosing picture.
Routes studied
Three routes appear in the literature. Subcutaneous injection — delivery into the fatty layer just under the skin — is the primary research route [4][5]. Intravenous administration was used in diagnostic and pharmacokinetic studies, where doses of 0.25-2 mcg/kg elicited GH release in healthy men [3]. Intranasal delivery (a nasal spray) was tested historically but showed only ~3-5% bioavailability [3] — meaning only a small fraction of the dose reached the bloodstream. That low figure is consistent with the broader observation that oral, sublingual, and troche 'sermorelin' formats absorb poorly, because peptides are degraded in the gut and cross mucous membranes inefficiently.
The route differences are not cosmetic: a separate dose-response study of a related GHRH(1-29) analog reported that roughly a tenfold-higher subcutaneous dose and a thirtyfold-higher intranasal dose were needed to match the intravenous route, which frames why subcutaneous injection dominates the research record [13].
Dose-response: how little raised GH
The pharmacokinetic record is precise about thresholds. In 30 healthy men, intravenous GHRH(1-29)NH2 elicited significant GH release at doses as low as 0.25 mcg/kg, with maximal release at 1-2 mcg/kg [3]. That is a steep, low-dose response: the pituitary answers a small upstream signal. The relevant figures — 0.25 mcg/kg threshold, 1-2 mcg/kg maximal, ~3 hours of GH elevation despite ~10-12 minute clearance — are reported here as the measured pharmacology of the molecule, logged to source [3], and not as a dose any person should administer.
Why is sermorelin studied with bedtime dosing?
Endogenous GH is secreted in pulses, largest during slow-wave sleep; bedtime GHRH(1-29) dosing was used in the pediatric and elderly trials to reinforce the natural nocturnal GH pulse [4]. GHRH's sleep-endocrine effects are also time-of-administration dependent.
When was sermorelin dosed in the studies?
Trials commonly dosed GHRH(1-29) subcutaneously at bedtime to align with the nocturnal GH pulse [4]; GHRH's sleep-endocrine effects are time-of-administration dependent. This is study protocol, not a usage recommendation.
Half-life and the supplied form
Sermorelin's plasma half-life is short — ~10-12 minutes after intravenous administration — yet a single dose elevates serum GH for roughly 3 hours [3]. Because aqueous peptide solutions degrade, sermorelin acetate is supplied as a lyophilized powder, reconstituted with sterile diluent and typically refrigerated once in solution; compounded preparations are made under USP <797> sterile-compounding standards [3]. The native peptide's brevity is what drove development of longer-acting analogs such as those using D-Ala2 substitution and DAC albumin binding.