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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

Maridebart cafraglutide — pharmacology

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

Document identifier
CEI-MN-018/2
Series
Compound monograph
Version
3.3
Published
19 Jan 2025
Last reviewed
19 May 2025
Next review
19 May 2027
Identifier
10.71829/cei.mono.18
Certainty
Low
Cycle
2025 Q1

§2Pharmacology

§2.1Molecular targets

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

TargetInteractionNote
GIP receptor (GIPR)AntagonistAntibody arm
GLP-1 receptor (GLP1R)AgonistConjugated peptide arms

§2.2Mechanism of action

GLP-1 receptor agonism supplies appetite suppression; GIP receptor antagonism is proposed to act on adipose tissue and central pathways in a manner that also reduces adiposity. The antibody scaffold gives a very long half-life permitting monthly or less frequent administration, which is the principal practical differentiator.[1,2]

§2.3Pharmacokinetics

Terminal half-life
≈21 days
Time to maximum concentration
several days
Volume of distribution
consistent with an IgG (small, largely vascular)
Plasma protein binding
not applicable in the small-molecule sense
Clearance
antibody-typical, FcRn-dependent
Bioavailability
antibody-typical subcutaneous bioavailability

Reticuloendothelial catabolism with FcRn recycling. The very long half-life means an adverse effect, once initiated, cannot be terminated by stopping treatment for several weeks — a consideration the Institute regards as material to benefit–risk.

Reconstructed plasma concentration–time profilePlasma concentration plotted against time after dosing, reconstructed from published pharmacokinetic parameters.0.01.02.00200400600800Time after first dose (hours)Relative concentrationt max ≈ 625 ht½ ≈ 504 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

  • Antibody-typical; no cytochrome interaction expected

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. Samms RJ, Coghlan MP, Sloop KW. How may GIP enhance the therapeutic efficacy of GLP-1?. Trends in Endocrinology & Metabolism 2020;31(6):410–421. doi:10.1016/j.tem.2020.02.006 · PMID 32396843
  2. Coskun T, Sloop KW, Loghin C, Alsina-Fernandez J, Urva S, Bokvist KB, Cui X, Briere DA, Cabrera O, Roell WC, Kuchibhotla U, Moyers JS, Benson CT, Gimeno RE, D’Alessio DA, Haupt A. LY3298176, a novel dual GIP and GLP-1 receptor agonist for the treatment of type 2 diabetes mellitus: from discovery to clinical proof of concept. Molecular Metabolism 2018;18:3–14. doi:10.1016/j.molmet.2018.09.009 · PMID 30473097

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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