Research monograph / dose context

Sermorelin dosage: the doses, routes, and timing the studies actually used.

A research-context record of how GHRH(1-29) was administered across the published studies — what was given, to which population, by which route. Not a usage recommendation.

Before the details

This page reports how sermorelin was studied, not how anyone should use it. It gives no human dosing instructions. Every figure below is a dose that appeared in a published study, with the population and route it was used in — because a dose only means something attached to who received it and how. Sermorelin's short stay in the blood (a half-life of about 10-12 minutes) shaped most of these designs, which is why timing and route get as much attention here as the numbers themselves.

Sermorelin dosage: doses studied in the GHRH(1-29) literature

Sermorelin dosage in the research record clusters by purpose. The pediatric efficacy study used 30 mcg/kg/day subcutaneously at bedtime in GH-deficient children, accelerating first-year height velocity from about 4.1 to roughly 7-8 cm/year [1]. Aging research in older men used 0.5 mg and 1 mg subcutaneously twice daily for 14 days, producing dose-related rises in 24-hour GH and IGF-1 [2]. Diagnostic GHRH stimulation historically used a single intravenous bolus — commonly around 1 mcg/kg — to test pituitary GH reserve. Pharmacokinetic work used intravenous doses of 0.25-2 mcg/kg, with measurable GH release from as little as 0.25 mcg/kg and maximal release at 1-2 mcg/kg [3].

A dose-response study of the GHRH analog [Nle27]GHRH(1-29)-NH2 in normal men found dose-responsive GH stimulation across intravenous, subcutaneous, and intranasal routes, but required a tenfold higher subcutaneous dose and a thirtyfold higher intranasal dose to match the intravenous effect — a direct illustration of how route changes the dose required [12]. These are studied doses in defined populations, reported as research context only.

Sermorelin half-life and pharmacokinetics

Sermorelin's half-life is short: on the order of 10-12 minutes in plasma after intravenous administration [3]. GHRH(1-29) is rapidly eliminated — yet, despite that clearance, a single dose elevates serum GH for roughly 3 hours, because the GH pulse it triggers outlasts the peptide itself [3].

That brevity is the engineering problem the whole analog family was built to solve. The native peptide's short life motivated longer-acting designs — the D-Ala2 substitution that resists one cleavage enzyme, and the Drug Affinity Complex (DAC, an albumin-binding group) behind CJC-1295 with DAC — which sustain GH and IGF-1 over much longer windows [3]. The sermorelin vs CJC-1295 page works through that native-versus-stabilized contrast in detail. Pharmacokinetics also constrain route: intranasal bioavailability of GHRH(1-29) was only about 3-5% [3], which is the research basis for why oral and sublingual sermorelin products are widely criticized as ineffective.

Routes studied

Three routes appear in the record. Subcutaneous injection was the primary route in the efficacy and aging studies [1][2]. Intravenous administration was used for diagnostic GH-stimulation testing and for pharmacokinetic work [3]. Intranasal delivery was studied historically but showed only ~3-5% bioavailability [3], and the cross-route comparison of [Nle27]GHRH(1-29)-NH2 confirmed that subcutaneous and especially intranasal routes need substantially higher doses than intravenous to achieve the same GH response [12]. Route choice in the studies tracked the goal: subcutaneous for sustained dosing, intravenous for diagnostics and PK.

Why bedtime administration was studied

Research protocols used bedtime subcutaneous dosing to coincide with the post-sleep-onset GH pulse. The body's largest endogenous GH pulse occurs shortly after sleep onset, so GHRH research used nocturnal dosing to augment that natural pulse rather than introduce an out-of-phase stimulus [10]. Single nightly injections of GHRH(1-29) in healthy elderly men were specifically studied for their effect on the GH/IGF-1 axis [10], and GHRH's sleep-endocrine effects are known to depend on the time of administration [12]. This describes how studies were designed; it is not a usage recommendation.

Timing of administration in the studies

The timing logic in the studies is consistent: align the stimulus with the body's own rhythm. The largest natural GH pulse follows sleep onset, GHRH's effects are time-of-administration dependent [12], and the pediatric efficacy protocol dosed at bedtime [1]. Where studies departed from nocturnal dosing — the twice-daily older-men protocol, the intravenous diagnostic and PK work — the goal was different (steady-state GH/IGF-1 elevation, or acute stimulation testing) [2][3]. Timing in the record is an endpoint-driven design choice, reported here as such.

Treatment durations used in the research

Study durations varied widely, so there is no single "enough" window. The older-men GH/IGF-1 study ran 14 days [2]; the GHRH-analog cognition trial ran 20 weeks [6]; pediatric growth therapy operated on a year-scale, with the height-velocity result measured over the first year [1]. Outcomes were endpoint- and population-specific: a two-week course was sufficient to move GH/IGF-1 in older men, but a cognition or growth endpoint required months to years. Duration in this literature is defined by the question being asked, not by a fixed protocol.

Formulation and stability notes

Sermorelin acetate is supplied as a lyophilized (freeze-dried) powder because aqueous peptide solutions are susceptible to degradation. It is reconstituted with sterile diluent and, once reconstituted, typically refrigerated. Compounded preparations are prepared under USP <797> sterile-compounding standards. The very low intranasal bioavailability (~3-5%) reported for GHRH(1-29) [3] is the same pharmacology that underlies criticism of oral, sublingual, and troche "sermorelin" formulations — peptides are degraded in the gut and poorly absorbed across mucosa, so non-injectable formats face a steep bioavailability problem.