ARWR
Published on 06/06/2025 at 09:57
ARO-C3, an investigational RNAi Therapeutic Targeting Complement C3, Reduces Proteinuria, Hematuria, and Complement Activity in IgAN Patients
Seungyeup Han1, Sug Kyun Shin2, Muh Geot Wong3, Seung Hyeok Han4, Adrian Liew5, Ashley Frazer-Abel6, James Hamilton7, Grigoriy Shekhtman7, Eric Garcia-Medel7, Hamid Moradi7, Ran Fu7, Jonathan Barratt8
1Keimyung University Dongsan Hospital, Daegu, Korea, 2National Health Insurance Service Ilsan Hospital, Goyang, Korea 3Concord Repatriation General Hospital, University of Sydney, Sydney, Australia, 4Yonsei University College of Medicine, Sinchon Severance Hospital, Seoul, Korea, 5Mount Elizabeth Novena Hospital, Singapore 6Exsera Biolabs, University of Colorado, Aurora, USA, 7Arrowhead Pharmaceuticals, Pasadena, USA, 8University of Leicester, Leicester, United Kingdom
Disclosures
Background
Dysregulated activation of the complement cascade mediates tissue injury in complement-mediated kidney diseases such as IgA Nephropathy
The central role of complement component 3 (C3) in the cascade makes it a unique therapeutic target for complement inhibition
ARO-C3 is an siRNA designed to achieve potent and durable complement inhibition by targeting hepatic synthesis of C3
ARO-C3 is Designed to Target and Silence C3 mRNA Expression in the Liver, Reducing Serum C3 Protein Levels
ARO-C3 is a synthetic, double-stranded oligonucleotide
Chemical modifications enhance pharmacokinetics (PK) and pharmacodynamics (PD)
The GalNAc (N-Acetylgalactosamine) ligand facilitates uptake into hepatocytes via asialoglycoprotein receptor
Complement Mediates Glomerular Injury in IgAN
Gd-IgA-containing Immune Complexes
Complement Cascade
Inflammation and Tissue Injury
Disclaimer
Arrowhead Pharmaceuticals Inc. published this content on June 04, 2025, and is solely responsible for the information contained herein. Distributed via Public Technologies (PUBT), unedited and unaltered, on June 06, 2025 at 13:56 UTC.