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Compound Evidence InstituteEvidence synthesis · established 2023Graded assessments of compounds, trials, methods and supply
Document set current to 30 July 2026
Compound monograph · §2

Sermorelin — pharmacology

Molecular targets, mechanism of action, pharmacokinetics and interactions as characterised in humans.

Document identifier
CEI-MN-022/2
Series
Compound monograph
Version
3.3
Published
15 Feb 2026
Last reviewed
15 Jun 2026
Next review
15 Jun 2028
Identifier
10.71829/cei.mono.22
Certainty
Low
Cycle
2026 Q1

§2Pharmacology

§2.1Molecular targets

Table 2. Molecular targets recorded for Sermorelin, with the character of the interaction and the potency where the Institute holds it.

TargetInteractionNote
GHRH receptor (GHRHR)AgonistFull agonist activity equivalent to native GHRH(1-44)

§2.2Mechanism of action

Sermorelin stimulates pituitary growth-hormone release through the GHRH receptor. Its very short half-life confines the pharmacodynamic effect to a single secretory pulse, which is why its established clinical use was diagnostic — as a provocative test of pituitary somatotroph reserve — rather than therapeutic.[1,2]

§2.3Pharmacokinetics

Terminal half-life
≈11–12 min
Time to maximum concentration
≈5–20 min (intravenous), 15–30 min (subcutaneous)
Volume of distribution
≈24–32 L
Plasma protein binding
not extensively bound
Clearance
high
Bioavailability
not formally established

Rapid cleavage at the Tyr1-Ala2 bond by dipeptidyl peptidase-4, producing the inactive GRF(3-29) fragment, followed by further proteolysis.

Reconstructed plasma concentration–time profilePlasma concentration plotted against time after dosing, reconstructed from published pharmacokinetic parameters.0.00.20.40.60.801122Time after first dose (hours)Relative concentrationt max ≈ 0 ht½ ≈ 1 h
Modelled profileSimulated observationsDose administration
Figure 2. Illustrative. Plasma concentration–time profile reconstructed by the Institute from the published half-life and time-to-maximum-concentration parameters using a one-compartment model with first-order absorption. The curve is not digitised from a published figure and its vertical scale is relative. It is published to convey the shape of the profile and the approach to steady state, not to supply a concentration at any time point.

§2.4Interactions

  • Glucocorticoids, thyroid hormone, somatostatin analogues, muscarinic antagonists and cyclo-oxygenase inhibitors all modify the growth-hormone response and confound diagnostic use

References cited on this page

References are numbered in order of first citation in this document. Each superscript in the text links to its entry below.

  1. Prakash A, Goa KL. Sermorelin: a review of its use in the diagnosis and treatment of children with idiopathic growth hormone deficiency. BioDrugs 1999;12(2):139–157. doi:10.2165/00063030-199912020-00007 · PMID 18031173
  2. Falutz J, Allas S, Blot K, Potvin D, Kotler D, Somero M, Berger D, Brown S, Richmond G, Fessel J, Turner R, Grinspoon S. Metabolic effects of a growth hormone-releasing factor in patients with HIV. New England Journal of Medicine 2007;357(23):2359–2370. doi:10.1056/NEJMoa072375 · PMID 18052660

Identifiers are reproduced only where the Institute holds them. Where a digital object identifier or PubMed identifier is not shown, the Institute has recorded the journal and year and has not constructed an identifier.

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