Randomized phase I trial outcomes show safe and sustainable inhibition of classical and lectin complement pathways by empasiprubart

Abstract Activation of classical and lectin complement pathways contributes to several human diseases. Empasiprubart is a humanized recycling monoclonal antibody that inhibits both pathways by binding to the CCP2 domain of complement factor 2 (C2), an interaction that is dependent on both Ca2+ and p...

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Main Authors: Inge Van de Walle, Laura Bracke, Heidi Gytz Olesen, Tonke van Bragt, Stéphanie Cadour, Phillip De Decker, Giorgia Ciurlia, Erwin Pannecoucke, Emma K. Persson, Olivier Van de Steen, Xinghong Leng, Gregers Rom Andersen, Domenica Gandini, C. Erik Hack
Format: Article
Language:English
Published: Nature Portfolio 2025-08-01
Series:Nature Communications
Online Access:https://doi.org/10.1038/s41467-025-62925-1
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author Inge Van de Walle
Laura Bracke
Heidi Gytz Olesen
Tonke van Bragt
Stéphanie Cadour
Phillip De Decker
Giorgia Ciurlia
Erwin Pannecoucke
Emma K. Persson
Olivier Van de Steen
Xinghong Leng
Gregers Rom Andersen
Domenica Gandini
C. Erik Hack
author_facet Inge Van de Walle
Laura Bracke
Heidi Gytz Olesen
Tonke van Bragt
Stéphanie Cadour
Phillip De Decker
Giorgia Ciurlia
Erwin Pannecoucke
Emma K. Persson
Olivier Van de Steen
Xinghong Leng
Gregers Rom Andersen
Domenica Gandini
C. Erik Hack
author_sort Inge Van de Walle
collection DOAJ
description Abstract Activation of classical and lectin complement pathways contributes to several human diseases. Empasiprubart is a humanized recycling monoclonal antibody that inhibits both pathways by binding to the CCP2 domain of complement factor 2 (C2), an interaction that is dependent on both Ca2+ and pH. Here, we resolve the crystal structure of empasiprubart complexed with C2, providing the molecular basis of its Ca2+ dependency, and report a randomized, double-blind, placebo-controlled trial to assess the safety and tolerability (primary objectives) in addition to pharmacokinetics, pharmacodynamics, and immunogenicity (secondary objectives) of empasiprubart in 78 healthy participants (NCT04532125). A single intravenous (IV) dose of empasiprubart reduces circulating C2 levels by up to 99% and dose-dependently inhibits the classical and lectin pathways. Multiple IV empasiprubart doses reinforce reductions in free C2 levels, which persist until the endpoint of the study at 41 weeks. This prolonged reduction is in line with the empasiprubart elimination half-life (70–88 days). Single and multiple ascending doses of empasiprubart are generally safe and well tolerated. Overall, our results reveal in atomic detail the mechanism of empasiprubart and demonstrate that it is a first-in-class anti-C2 therapeutic antibody for use in complement-mediated diseases.
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spelling doaj-art-ec939bfa9eb44ec4b3703c20fa33a6312025-08-20T03:47:12ZengNature PortfolioNature Communications2041-17232025-08-0116111510.1038/s41467-025-62925-1Randomized phase I trial outcomes show safe and sustainable inhibition of classical and lectin complement pathways by empasiprubartInge Van de Walle0Laura Bracke1Heidi Gytz Olesen2Tonke van Bragt3Stéphanie Cadour4Phillip De Decker5Giorgia Ciurlia6Erwin Pannecoucke7Emma K. Persson8Olivier Van de Steen9Xinghong Leng10Gregers Rom Andersen11Domenica Gandini12C. Erik Hack13argenxargenxDepartment of Molecular Biology and Genetics - Protein ScienceCurare Consulting BVargenxargenxargenxargenxargenxargenxargenxDepartment of Molecular Biology and Genetics - Protein ScienceargenxargenxAbstract Activation of classical and lectin complement pathways contributes to several human diseases. Empasiprubart is a humanized recycling monoclonal antibody that inhibits both pathways by binding to the CCP2 domain of complement factor 2 (C2), an interaction that is dependent on both Ca2+ and pH. Here, we resolve the crystal structure of empasiprubart complexed with C2, providing the molecular basis of its Ca2+ dependency, and report a randomized, double-blind, placebo-controlled trial to assess the safety and tolerability (primary objectives) in addition to pharmacokinetics, pharmacodynamics, and immunogenicity (secondary objectives) of empasiprubart in 78 healthy participants (NCT04532125). A single intravenous (IV) dose of empasiprubart reduces circulating C2 levels by up to 99% and dose-dependently inhibits the classical and lectin pathways. Multiple IV empasiprubart doses reinforce reductions in free C2 levels, which persist until the endpoint of the study at 41 weeks. This prolonged reduction is in line with the empasiprubart elimination half-life (70–88 days). Single and multiple ascending doses of empasiprubart are generally safe and well tolerated. Overall, our results reveal in atomic detail the mechanism of empasiprubart and demonstrate that it is a first-in-class anti-C2 therapeutic antibody for use in complement-mediated diseases.https://doi.org/10.1038/s41467-025-62925-1
spellingShingle Inge Van de Walle
Laura Bracke
Heidi Gytz Olesen
Tonke van Bragt
Stéphanie Cadour
Phillip De Decker
Giorgia Ciurlia
Erwin Pannecoucke
Emma K. Persson
Olivier Van de Steen
Xinghong Leng
Gregers Rom Andersen
Domenica Gandini
C. Erik Hack
Randomized phase I trial outcomes show safe and sustainable inhibition of classical and lectin complement pathways by empasiprubart
Nature Communications
title Randomized phase I trial outcomes show safe and sustainable inhibition of classical and lectin complement pathways by empasiprubart
title_full Randomized phase I trial outcomes show safe and sustainable inhibition of classical and lectin complement pathways by empasiprubart
title_fullStr Randomized phase I trial outcomes show safe and sustainable inhibition of classical and lectin complement pathways by empasiprubart
title_full_unstemmed Randomized phase I trial outcomes show safe and sustainable inhibition of classical and lectin complement pathways by empasiprubart
title_short Randomized phase I trial outcomes show safe and sustainable inhibition of classical and lectin complement pathways by empasiprubart
title_sort randomized phase i trial outcomes show safe and sustainable inhibition of classical and lectin complement pathways by empasiprubart
url https://doi.org/10.1038/s41467-025-62925-1
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