Miglustat: a first-in-class enzyme stabilizer for cipaglucosidase alfa for the treatment of late-onset Pompe disease

Late-onset Pompe disease (LOPD) is a rare inherited disorder caused by deficiency of the lysosomal enzyme acid α-glucosidase (GAA), leading to an accumulation of lysosomal glycogen in tissues, profoundly affecting muscles. Patients with LOPD typically have some residual GAA activity but experience progressive skeletal muscle dysfunction resulting in muscle weakness and respiratory failure. Enzyme replacement therapy (ERT) with alglucosidase alfa, a recombinant human GAA (rhGAA), was the first disease-specific therapy for Pompe disease. Despite efficacy in the first years of use, many patients receiving alglucosidase alfa experience a decline in function over time. This may reflect the inherent challenges associated with rhGAA ERT, such as enzyme inactivation at the near-neutral pH of blood, inefficient target cell uptake, and a necessity for complete lysosomal processing once inside target cells. Cipaglucosidase alfa, a second-generation rhGAA, aims to address these challenges through natural enrichment with bis-mannose-6-phosphate-containing <i>N</i>-glycans to enhance cellular uptake while retaining capacity for complete postdelivery processing. Co-administration of cipaglucosidase alfa with the small molecule stabilizer miglustat (N-butyldeoxynojirimycin) enhances cipaglucosidase alfa stability in the bloodstream after infusion. We discuss published and new preclinical and clinical data on the efficacy and safety of miglustat in combination with cipaglucosidase alfa for treating LOPD. Studies in Pompe mouse models and patients with Pompe disease showed that stabilization by miglustat improved cipaglucosidase alfa exposure and availability for uptake into target tissues and was associated with improved functional outcomes and biomarker levels compared with cipaglucosidase alfa alone. In patients with Pompe disease, the once every 2 weeks dosing regimen of miglustat was well tolerated, with a low frequency of miglustat-related gastrointestinal events compared with daily miglustat regimens at higher doses used in the treatment of other diseases. <b><i>Trial registration</i>:</b> New data are reported for NCT02675465 (ATB200-02), NCT03729362 (PROPEL), and NCT04138277 (PROPEL open-label extension, ATB200-07); all registered at ClinicalTrials.gov (https://clinicaltrials.gov).

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Journal
Therapeutic Advances in Rare Disease
Published
2026-02-26
DOI
https://doi.org/10.1177/26330040261425686
Primary Topic
Lysosomal Storage Disorders Research
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article
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article

Miglustat: a first-in-class enzyme stabilizer for cipaglucosidase alfa for the treatment of late-onset Pompe disease

Stephan Wenninger, Nadine A. M. E. van der Beek, Giancarlo Parenti, Jon J. Brudvig et al.
Therapeutic Advances in Rare Disease
Lysosomal Storage Disorders Research
article

Miglustat: a first-in-class enzyme stabilizer for cipaglucosidase alfa for the treatment of late-onset Pompe disease

Stephan Wenninger, Nadine A. M. E. van der Beek, Giancarlo Parenti, Jon J. Brudvig, Barry J. Byrne, Jufen Zhang, Fred Holdbrook, Franklin K. Johnson, V Jain, Ans T. van der Ploeg, Priya S. Kishnani, Benedikt Schoser, Brian Fox, Mark Roberts
article en

Abstract

Late-onset Pompe disease (LOPD) is a rare inherited disorder caused by deficiency of the lysosomal enzyme acid α-glucosidase (GAA), leading to an accumulation of lysosomal glycogen in tissues, profoundly affecting muscles. Patients with LOPD typically have some residual GAA activity but experience progressive skeletal muscle dysfunction resulting in muscle weakness and respiratory failure. Enzyme replacement therapy (ERT) with alglucosidase alfa, a recombinant human GAA (rhGAA), was the first disease-specific therapy for Pompe disease. Despite efficacy in the first years of use, many patients receiving alglucosidase alfa experience a decline in function over time. This may reflect the inherent challenges associated with rhGAA ERT, such as enzyme inactivation at the near-neutral pH of blood, inefficient target cell uptake, and a necessity for complete lysosomal processing once inside target cells. Cipaglucosidase alfa, a second-generation rhGAA, aims to address these challenges through natural enrichment with bis-mannose-6-phosphate-containing <i>N</i>-glycans to enhance cellular uptake while retaining capacity for complete postdelivery processing. Co-administration of cipaglucosidase alfa with the small molecule stabilizer miglustat (N-butyldeoxynojirimycin) enhances cipaglucosidase alfa stability in the bloodstream after infusion. We discuss published and new preclinical and clinical data on the efficacy and safety of miglustat in combination with cipaglucosidase alfa for treating LOPD. Studies in Pompe mouse models and patients with Pompe disease showed that stabilization by miglustat improved cipaglucosidase alfa exposure and availability for uptake into target tissues and was associated with improved functional outcomes and biomarker levels compared with cipaglucosidase alfa alone. In patients with Pompe disease, the once every 2 weeks dosing regimen of miglustat was well tolerated, with a low frequency of miglustat-related gastrointestinal events compared with daily miglustat regimens at higher doses used in the treatment of other diseases. <b><i>Trial registration</i>:</b> New data are reported for NCT02675465 (ATB200-02), NCT03729362 (PROPEL), and NCT04138277 (PROPEL open-label extension, ATB200-07); all registered at ClinicalTrials.gov (https://clinicaltrials.gov).

Therapeutic Advances in Rare DiseaseVol. 7
Cincinnati Children's Hospital Medical Center (US), University of California, Irvine (US), Salford Royal NHS Foundation Trust (GB), Erasmus MC (NL), University of Florida (US), Duke Medical Center (US), University of Kansas Medical Center (US), Friedrich Baur Stiftung (DE), Amicus Therapeutics (United States) (US), University of Naples Federico II (IT), Ludwig-Maximilians-Universität München (DE)
Good health and well-being
Openalex Percentile: Top 40%
Lysosomal Storage Disorders Research
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