Independent · non-commercial · publishes on a quarterly cycle|Current cycle 2026 Q3
Compound Evidence InstituteEvidence synthesis · established 2023Graded assessments of compounds, trials, methods and supply
Document set current to 30 July 2026
Compound monograph · §2

Teduglutide — pharmacology

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

Document identifier
CEI-MN-020/2
Series
Compound monograph
Version
4.1
Published
30 May 2023
Last reviewed
30 Jan 2024
Next review
30 Jan 2026
Identifier
10.71829/cei.mono.20
Certainty
Moderate
Cycle
2023 Q2

§2Pharmacology

§2.1Molecular targets

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

TargetInteractionNote
GLP-2 receptor (GLP2R)AgonistExpressed on intestinal subepithelial myofibroblasts and enteric neurons rather than on enterocytes directly

§2.2Mechanism of action

GLP-2 receptor agonism promotes intestinal mucosal growth, increases villus height and crypt depth, slows gastric emptying and reduces intestinal secretion. The therapeutic consequence in short-bowel syndrome is improved fluid and nutrient absorption and reduced dependence on parenteral support. The trophic mechanism is also the source of the principal safety concern: any agent that promotes intestinal mucosal proliferation carries a theoretical neoplasia risk that requires colonoscopic surveillance.[1,2]

§2.3Pharmacokinetics

Terminal half-life
≈2 h in adults
Time to maximum concentration
3–5 h
Volume of distribution
≈26 L
Plasma protein binding
not extensively bound
Clearance
≈123 mL/h/kg
Bioavailability
≈88 %

Renal clearance with proteolytic degradation. Dose reduction is required in moderate and severe renal impairment.

Reconstructed plasma concentration–time profilePlasma concentration plotted against time after dosing, reconstructed from published pharmacokinetic parameters.0.00.20.40.602468Time after first dose (hours)Relative concentrationt max ≈ 1 ht½ ≈ 2 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

  • Increased absorption of oral medicines including benzodiazepines, psychotropics and narrow-therapeutic-index agents — dose reduction may be needed

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. Drucker DJ. Mechanisms of action and therapeutic application of glucagon-like peptide-1. Cell Metabolism 2018;27(4):740–756. doi:10.1016/j.cmet.2018.03.001 · PMID 29617641
  2. Müller TD, Finan B, Bloom SR, D’Alessio D, Drucker DJ, Flatt PR, Fritsche A, Gribble F, Grill HJ, Habener JF, Holst JJ, Langhans W, Meier JJ, Nauck MA, Perez-Tilve D, Pocai A, Reimann F, Sandoval DA, Schwartz TW, Seeley RJ. Glucagon-like peptide 1 (GLP-1). Molecular Metabolism 2019;30:72–130. doi:10.1016/j.molmet.2019.09.010 · PMID 31767182

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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