Physiology‐based pharmacokinetic model with relative transcriptomics to evaluate tissue distribution and receptor occupancy of anifrolumab

Abstract Type I interferons contribute to the pathogenesis of several autoimmune disorders, including systemic lupus erythematosus (SLE), systemic sclerosis, cutaneous lupus erythematosus, and myositis. Anifrolumab is a monoclonal antibody that binds to subunit 1 of the type I interferon receptor (I...

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Main Authors: Pradeep Sharma, David W. Boulton, Lynn N. Bertagnolli, Weifeng Tang
Format: Article
Language:English
Published: Wiley 2025-01-01
Series:CPT: Pharmacometrics & Systems Pharmacology
Online Access:https://doi.org/10.1002/psp4.13245
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author Pradeep Sharma
David W. Boulton
Lynn N. Bertagnolli
Weifeng Tang
author_facet Pradeep Sharma
David W. Boulton
Lynn N. Bertagnolli
Weifeng Tang
author_sort Pradeep Sharma
collection DOAJ
description Abstract Type I interferons contribute to the pathogenesis of several autoimmune disorders, including systemic lupus erythematosus (SLE), systemic sclerosis, cutaneous lupus erythematosus, and myositis. Anifrolumab is a monoclonal antibody that binds to subunit 1 of the type I interferon receptor (IFNAR1). Results of phase IIb and phase III trials led to the approval of intravenous anifrolumab 300 mg every 4 weeks (Q4W) alongside standard therapy in patients with moderate‐to‐severe SLE. Here, we built a population physiology‐based pharmacokinetic (PBPK) model of anifrolumab by utilizing the physiochemical properties of anifrolumab, binding kinetics to the Fc gamma neonatal receptor, and target‐mediated drug disposition properties. A novel relative transcriptomics approach was employed to determine IFNAR1 expression in tissues (blood, skin, gastrointestinal tract, lungs, and muscle) using mRNA abundances from bioinformatic databases. The IFNAR1 expression and PBPK model were validated by testing their ability to predict clinical pharmacokinetics over a large dose range from different clinical scenarios after subcutaneous and intravenous anifrolumab dosing. The validated PBPK model predicted high unbound local concentrations of anifrolumab in blood, skin, gastrointestinal tract, lungs, and muscle, which exceeded its IFNAR1 dissociation equilibrium constant values. The model also predicted high IFNAR1 occupancy with subcutaneous and intravenous anifrolumab dosing. The model predicted more sustained IFNAR1 occupancy ≥90% with subcutaneous anifrolumab 120 mg once‐weekly dosing vs. intravenous 300 mg Q4W dosing. The results informed the dosing of phase III studies of anifrolumab in new indications and present a novel approach to PBPK modeling coupled with relative transcriptomics in simulating pharmacokinetics of therapeutic monoclonal antibodies.
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spelling doaj-art-6eae4ea9280b4de9a344f4d1d6c2c2d72025-01-07T20:48:59ZengWileyCPT: Pharmacometrics & Systems Pharmacology2163-83062025-01-0114110511710.1002/psp4.13245Physiology‐based pharmacokinetic model with relative transcriptomics to evaluate tissue distribution and receptor occupancy of anifrolumabPradeep Sharma0David W. Boulton1Lynn N. Bertagnolli2Weifeng Tang3Clinical Pharmacology and Quantitative Pharmacology, Clinical Pharmacology and Safety Sciences R&D, AstraZeneca Cambridge UKClinical Pharmacology and Quantitative Pharmacology, Clinical Pharmacology and Safety Sciences R&D, AstraZeneca Gaithersburg Maryland USAClinical Pharmacology and Quantitative Pharmacology, Clinical Pharmacology and Safety Sciences R&D, AstraZeneca Gaithersburg Maryland USAClinical Pharmacology and Quantitative Pharmacology, Clinical Pharmacology and Safety Sciences R&D, AstraZeneca Gaithersburg Maryland USAAbstract Type I interferons contribute to the pathogenesis of several autoimmune disorders, including systemic lupus erythematosus (SLE), systemic sclerosis, cutaneous lupus erythematosus, and myositis. Anifrolumab is a monoclonal antibody that binds to subunit 1 of the type I interferon receptor (IFNAR1). Results of phase IIb and phase III trials led to the approval of intravenous anifrolumab 300 mg every 4 weeks (Q4W) alongside standard therapy in patients with moderate‐to‐severe SLE. Here, we built a population physiology‐based pharmacokinetic (PBPK) model of anifrolumab by utilizing the physiochemical properties of anifrolumab, binding kinetics to the Fc gamma neonatal receptor, and target‐mediated drug disposition properties. A novel relative transcriptomics approach was employed to determine IFNAR1 expression in tissues (blood, skin, gastrointestinal tract, lungs, and muscle) using mRNA abundances from bioinformatic databases. The IFNAR1 expression and PBPK model were validated by testing their ability to predict clinical pharmacokinetics over a large dose range from different clinical scenarios after subcutaneous and intravenous anifrolumab dosing. The validated PBPK model predicted high unbound local concentrations of anifrolumab in blood, skin, gastrointestinal tract, lungs, and muscle, which exceeded its IFNAR1 dissociation equilibrium constant values. The model also predicted high IFNAR1 occupancy with subcutaneous and intravenous anifrolumab dosing. The model predicted more sustained IFNAR1 occupancy ≥90% with subcutaneous anifrolumab 120 mg once‐weekly dosing vs. intravenous 300 mg Q4W dosing. The results informed the dosing of phase III studies of anifrolumab in new indications and present a novel approach to PBPK modeling coupled with relative transcriptomics in simulating pharmacokinetics of therapeutic monoclonal antibodies.https://doi.org/10.1002/psp4.13245
spellingShingle Pradeep Sharma
David W. Boulton
Lynn N. Bertagnolli
Weifeng Tang
Physiology‐based pharmacokinetic model with relative transcriptomics to evaluate tissue distribution and receptor occupancy of anifrolumab
CPT: Pharmacometrics & Systems Pharmacology
title Physiology‐based pharmacokinetic model with relative transcriptomics to evaluate tissue distribution and receptor occupancy of anifrolumab
title_full Physiology‐based pharmacokinetic model with relative transcriptomics to evaluate tissue distribution and receptor occupancy of anifrolumab
title_fullStr Physiology‐based pharmacokinetic model with relative transcriptomics to evaluate tissue distribution and receptor occupancy of anifrolumab
title_full_unstemmed Physiology‐based pharmacokinetic model with relative transcriptomics to evaluate tissue distribution and receptor occupancy of anifrolumab
title_short Physiology‐based pharmacokinetic model with relative transcriptomics to evaluate tissue distribution and receptor occupancy of anifrolumab
title_sort physiology based pharmacokinetic model with relative transcriptomics to evaluate tissue distribution and receptor occupancy of anifrolumab
url https://doi.org/10.1002/psp4.13245
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