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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

Tesamorelin — pharmacology

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

Document identifier
CEI-MN-021/2
Series
Compound monograph
Version
4.2
Published
01 Dec 2023
Last reviewed
01 Sep 2024
Next review
01 Sep 2026
Identifier
10.71829/cei.mono.21
Certainty
Moderate
Cycle
2023 Q4

§2Pharmacology

§2.1Molecular targets

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

TargetInteractionNote
GHRH receptor (GHRHR)AgonistPituitary somatotroph receptor; stimulates pulsatile endogenous growth hormone release

§2.2Mechanism of action

Tesamorelin stimulates the pituitary to release endogenous growth hormone in a pulsatile pattern, preserving the physiological feedback architecture that exogenous growth hormone bypasses. Downstream IGF-1 elevation drives lipolysis with a preferential effect on visceral adipose tissue. Because feedback is intact, the risk of the supraphysiological IGF-1 exposure associated with exogenous growth hormone is reduced, though not abolished.[1,2]

§2.3Pharmacokinetics

Terminal half-life
≈26–38 min
Time to maximum concentration
≈0.15 h
Volume of distribution
≈9.4 L/kg
Plasma protein binding
not extensively bound
Clearance
≈30–40 L/h
Bioavailability
≈4 % (subcutaneous, in healthy subjects)

Rapid proteolytic degradation. The short half-life is not a limitation because the pharmacodynamic effect is mediated by a downstream hormone cascade with its own kinetics.

Reconstructed plasma concentration–time profilePlasma concentration plotted against time after dosing, reconstructed from published pharmacokinetic parameters.0.00.20.40.60.8011223Time 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

  • Cortisol conversion — growth hormone inhibits 11β-hydroxysteroid dehydrogenase type 1 and may unmask central hypoadrenalism
  • Cytochrome P450 substrate metabolism may be modestly altered by growth hormone

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. 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
  2. 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

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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