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

Orforglipron — pharmacology

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

Document identifier
CEI-MN-011/2
Series
Compound monograph
Version
1.0
Published
30 Apr 2026
Last reviewed
30 Apr 2026
Next review
30 Apr 2028
Identifier
10.71829/cei.mono.11
Certainty
Moderate
Cycle
2026 Q2

§2Pharmacology

§2.1Molecular targets

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

TargetInteractionNote
GLP-1 receptor (GLP1R)Biased partial agonistPartial cyclic-AMP efficacy with minimal beta-arrestin recruitment; the bias is proposed to limit receptor internalisation and desensitisation

§2.2Mechanism of action

Orforglipron activates the GLP-1 receptor from a non-peptide scaffold, producing the insulinotropic, glucagonostatic and central appetite effects of the class from an orally bioavailable molecule that does not require an absorption enhancer. Its partial agonism and signalling bias mean the maximum achievable receptor activation is below that of the injectable peptides, yet clinical weight effects approach those of subcutaneous semaglutide, which the Institute records as an important and not fully explained observation.[1,2]

§2.3Pharmacokinetics

Terminal half-life
≈29–49 h
Time to maximum concentration
4–6 h
Volume of distribution
not published
Plasma protein binding
high
Clearance
not published
Bioavailability
sufficient for once-daily oral dosing without a permeation enhancer

Hepatic metabolism with CYP3A4 involvement reported in early characterisation. No food or water restriction is required, which distinguishes it operationally from oral semaglutide.

Reconstructed plasma concentration–time profilePlasma concentration plotted against time after dosing, reconstructed from published pharmacokinetic parameters.0.00.20.40.60.80200400600800Time after first dose (hours)Relative concentrationt max ≈ 523 ht½ ≈ 49 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

  • Potential for interaction with CYP3A4 inhibitors and inducers, unlike the peptide GLP-1 receptor agonists which have no meaningful cytochrome interaction

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. Wharton S, Blevins T, Connery L, Rosenstock J, Raha S, Liu R, Ma X, Mather KJ, Haupt A, Robins D, Pratt E, Kazda C, Konig M. Daily oral GLP-1 receptor agonist orforglipron for adults with obesity. New England Journal of Medicine 2023;389(10):877–888. doi:10.1056/NEJMoa2302392 · PMID 37342922
  2. Frías JP, Hsia S, Eyde S, Liu R, Ma X, Konig M, Kazda C, Mather KJ, Haupt A, Pratt E, Robins D. Efficacy and safety of oral orforglipron in patients with type 2 diabetes: a multicentre, randomised, dose-response, phase 2 study. The Lancet 2023;402(10400):472–483. doi:10.1016/S0140-6736(23)01302-8 · PMID 37369232

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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