BackgroundSanfilippo type B is a mucopolysaccharidosis (MPS) with a major neuronopathic component characterized by heparan sulfate (HS) accumulation due to mutations in the NAGLU gene encoding alfa-N-acetyl-glucosaminidase. Enzyme replacement therapy for neuronopathic MPS requires efficient enzyme delivery throughout the brain in order to normalize HS levels, prevent brain atrophy, and potentially delay cognitive decline.MethodsIn this phase I/II open-label study, patients with MPS type IIIB (n = 22) were treated with tralesinidase alfa administered i.c.v. The patients were monitored for drug exposure; total HS and HS nonreducing end (HS-NRE) levels in both cerebrospinal fluid (CSF) and plasma; anti-drug antibody response; brain, spleen, and liver volumes as measured by MRI; and cognitive development as measured by age-equivalent (AEq) scores.ResultsIn the Part 1 dose escalation (30, 100, and 300 mg) phase, a 300 mg dose of tralesinidase alfa was necessary to achieve normalization of HS and HS-NRE levels in the CSF and plasma. In Part 2, 300 mg tralesinidase alfa sustained HS and HS-NRE normalization in the CSF and stabilized cortical gray matter volume (CGMV) over 48 weeks of treatment. Resolution of hepatomegaly and a reduction in spleen volume were observed in most patients. Significant correlations were also established between the change in cognitive AEq score and plasma drug exposure, plasma HS-NRE levels, and CGMV.ConclusionAdministration of tralesinidase alfa i.c.v. effectively normalized HS and HS-NRE levels as a prerequisite for clinical efficacy. Peripheral drug exposure data suggest a role for the glymphatic system in altering tralesinidase alfa efficacy.Trial registrationClinicaltrials.gov NCT02754076.FUNDINGBioMarin Pharmaceutical Inc. and Allievex Corporation.
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http://dx.doi.org/10.1172/JCI165076 | DOI Listing |
Toxicol Rep
March 2023
Allievex Corporation, Marblehead, MA, USA.
Mucopolysaccharidosis Type IIIB (MPS IIIB) is an ultrarare, fatal pediatric disease with no approved therapy. It is caused by mutations in the gene encoding for lysosomal enzyme alpha-N-acetylglucosaminidase (NAGLU). Tralesinidase alfa (TA) is a fusion protein comprised of recombinant NAGLU and a modified human insulin-like growth factor 2 that is being developed as an enzyme replacement therapy for MPS IIIB.
View Article and Find Full Text PDFJ Clin Invest
January 2023
Allievex Corporation, Marblehead, Massachusetts, USA.
J Pharmacol Exp Ther
September 2022
Departments of Animal Science (N.M.E., B.N.V., A.S.H., J.K.J., E.M.S., M.J.), Veterinary Clinical Science (N.M.E., N.D.J.), Veterinary Pathology (S.J.H., J.D.S.), Veterinary Diagnostics and Production Animal Medicine (S.T.M., R.L.P.), and Biomedical Science (S.T.M.), Iowa State University, Ames, Iowa; StageBio, Frederick, Maryland (M.T.B.); BioMarin Pharmaceutical Inc., Novato, California (S.C., H.P., X.Y.L., H.Z., R.L., B.E.C., A.G., G.C., A.C.M., A.C., B.R.V., J.C.M.W., C.A.O., J.P., E.M.); The Lundquist Institute (formerly Los Angeles Biomedical Research Institute) at Harbor-UCLA Medical Center, Torrance, California (M.T.E., A.B.A., H.R.N., J.D.C.); Department of Pediatrics, Washington University in St Louis, St Louis, Missouri (H.R.N., J.D.C.); Department of Pediatrics, University of Minnesota, Minneapolis, Minnesota (I.N., B.A.M., R.L., A.P.); and Allievex Corporation, Marblehead, Massachusetts (J.K., E.Z.)
Mucopolysaccharidosis type IIIB (MPS IIIB; Sanfilippo syndrome B; OMIM #252920) is a lethal, pediatric, neuropathic, autosomal recessive, and lysosomal storage disease with no approved therapy. Patients are deficient in the activity of N-acetyl-alpha-glucosaminidase (NAGLU; EC 3.2.
View Article and Find Full Text PDFPLoS One
September 2019
Research, BioMarin Pharmaceutical, Inc., Novato, CA, United States of America.
Sanfilippo syndrome type B (Sanfilippo B; Mucopolysaccharidosis type IIIB) occurs due to genetic deficiency of lysosomal alpha-N-acetylglucosaminidase (NAGLU) and subsequent lysosomal accumulation of heparan sulfate (HS), which coincides with devastating neurodegenerative disease. Because NAGLU expressed in Chinese hamster ovary cells is not mannose-6-phosphorylated, we developed an insulin-like growth factor 2 (IGF2)-tagged NAGLU molecule (BMN 250; tralesinidase alfa) that binds avidly to the IGF2 / cation-independent mannose 6-phosphate receptor (CI-MPR) for glycosylation independent lysosomal targeting. BMN 250 is currently being developed as an investigational enzyme replacement therapy for Sanfilippo B.
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