TY - JOUR
T1 - Interim analysis of post-marketing surveillance study of intracerebroventricular idursulfase therapy for neuronopathic mucopolysaccharidosis type II
T2 - Safety and effectiveness in clinical practice in Japan
AU - Kosuga, Motomichi
AU - So, Tetsumin
AU - Chinen, Yasutsugu
AU - Okamoto, Shungo
AU - Fukuda, Tokiko
AU - Yamamoto, Eiichi
AU - Ikari, Azuma
AU - Kumagai, Tadayuki
AU - Musha, Ikuma
AU - Wada, Yasunori
AU - Kakiuchi, Toshihiko
AU - Ueda, Yuki
AU - Egawa, Kiyoshi
AU - Yamada, Yuki
AU - Furujo, Mahoko
AU - Dateki, Sumito
AU - Nakajima, Yoko
AU - Ozawa, Naoko
AU - Okuyama, Torayuki
N1 - Publisher Copyright:
© 2026 The Authors. Published by Elsevier Inc. This is an open access article under the CC BY license. http://creativecommons.org/licenses/by/4.0/
PY - 2026/9/1
Y1 - 2026/9/1
N2 - Mucopolysaccharidosis type II (MPS II) results from iduronate-2-sulfatase (IDS) enzyme deficiency due to IDS gene mutations. Most patients with neuronopathic MPS II experience progressive neurological decline; however, effectiveness of standard treatment, intravenous idursulfase, is limited by blood-brain barrier transfer. Intracerebroventricular (ICV) idursulfase beta, approved in Japan in 2021, directly delivers idursulfase beta into cerebral ventricles. This post-marketing surveillance reports long-term effectiveness and safety of ICV idursulfase beta (30 mg every 4 weeks) in all treated patients from April 2021 through August 2024. Outcomes included cerebrospinal fluid (CSF) heparan sulfate (HS) levels (quarterly), developmental age (DA; Kyoto Scale of Psychological Development, annually), and safety. Thirty-seven Japanese male patients across 21 sites were enrolled (safety population n = 36; effectiveness population n = 35). Mean CSF HS concentrations decreased from 7.36 to 3.19 μg/mL from baseline to week 24, with reduction sustained through week 100. Patients who initiated treatment within 3 years of age had DA progression aligned with healthy cohorts, regardless of mutation type; however, those starting later had no comparable benefit. Adverse events (AEs) occurred in 20 patients (55.6%). Procedure-related serious AEs (SAEs) occurred in 2 patients (bacterial meningitis, device-related infection, pyrexia). Treatment-related AEs affected 14 patients (38.9%), mainly pyrexia (27.8%, including one SAE). One SAE (membranous glomerulonephritis) was not intervention related. No deaths, anaphylaxis, or anti-IDS antibodies in CSF were detected. ICV idursulfase beta demonstrated sustained CSF HS reduction with no new safety signals. Earlier treatment initiation (≤3 years) was associated with improved neurodevelopmental outcomes, regardless of mutation type.
AB - Mucopolysaccharidosis type II (MPS II) results from iduronate-2-sulfatase (IDS) enzyme deficiency due to IDS gene mutations. Most patients with neuronopathic MPS II experience progressive neurological decline; however, effectiveness of standard treatment, intravenous idursulfase, is limited by blood-brain barrier transfer. Intracerebroventricular (ICV) idursulfase beta, approved in Japan in 2021, directly delivers idursulfase beta into cerebral ventricles. This post-marketing surveillance reports long-term effectiveness and safety of ICV idursulfase beta (30 mg every 4 weeks) in all treated patients from April 2021 through August 2024. Outcomes included cerebrospinal fluid (CSF) heparan sulfate (HS) levels (quarterly), developmental age (DA; Kyoto Scale of Psychological Development, annually), and safety. Thirty-seven Japanese male patients across 21 sites were enrolled (safety population n = 36; effectiveness population n = 35). Mean CSF HS concentrations decreased from 7.36 to 3.19 μg/mL from baseline to week 24, with reduction sustained through week 100. Patients who initiated treatment within 3 years of age had DA progression aligned with healthy cohorts, regardless of mutation type; however, those starting later had no comparable benefit. Adverse events (AEs) occurred in 20 patients (55.6%). Procedure-related serious AEs (SAEs) occurred in 2 patients (bacterial meningitis, device-related infection, pyrexia). Treatment-related AEs affected 14 patients (38.9%), mainly pyrexia (27.8%, including one SAE). One SAE (membranous glomerulonephritis) was not intervention related. No deaths, anaphylaxis, or anti-IDS antibodies in CSF were detected. ICV idursulfase beta demonstrated sustained CSF HS reduction with no new safety signals. Earlier treatment initiation (≤3 years) was associated with improved neurodevelopmental outcomes, regardless of mutation type.
KW - Developmental age
KW - Enzyme replacement therapy
KW - Idursulfase beta
KW - Intracerebroventricular
KW - Mucopolysaccharidosis II
UR - https://www.scopus.com/pages/publications/105048812688
UR - https://www.scopus.com/pages/publications/105048812688#tab=citedBy
U2 - 10.1016/j.ymgme.2026.110243
DO - 10.1016/j.ymgme.2026.110243
M3 - Article
C2 - 42679455
AN - SCOPUS:105048812688
SN - 1096-7192
VL - 149
JO - Molecular Genetics and Metabolism
JF - Molecular Genetics and Metabolism
IS - 1-2
M1 - 110243
ER -