<p>Tividenofusp alfa (tividenofusp alfa-eknm; AVLAYAH<sup>™</sup>) is an intravenous brain-penetrant enzyme replacement therapy being developed by Denali Therapeutics for the treatment of mucopolysaccharidosis type&#xa0;II (MPS&#xa0;II). Also known as Hunter syndrome, MPS&#xa0;II is a rare X-linked recessive lysosomal storage disease caused by a deficiency of the lysosomal enzyme iduronate-2-sulfatase resulting in accumulation of glycosaminoglycans, heparan sulphate and dermatan sulphate. Consisting of the iduronate-2-sulfatase enzyme fused to a transferrin receptor-binding Fc domain, tividenofusp alfa has been designed to enable distribution of exogenous iduronate-2-sulfatase into both the central nervous system and peripheral tissues. Based on a reduction in cerebrospinal fluid heparan sulphate levels in patients with MPS&#xa0;II treated with tividenofusp alfa in a phase&#xa0;I/II trial, in March 2026 tividenofusp alfa was approved in the USA, under accelerated approval, for the treatment of neurologic manifestations of MPS&#xa0;II when initiated in presymptomatic or symptomatic paediatric patients weighing ≥ 5&#xa0;kg prior to advanced neurologic impairment. Continued approval for tividenofusp alfa may be contingent upon verification of clinical benefit in a confirmatory trial. Tividenofusp alfa has also been granted Priority Medicine designation by the European Medicines Agency. This article summarises the milestones in the development of tividenofusp alfa leading to this first approval for MPS&#xa0;II.</p>

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Tividenofusp Alfa: First Approval

  • Matt Shirley

摘要

Tividenofusp alfa (tividenofusp alfa-eknm; AVLAYAH) is an intravenous brain-penetrant enzyme replacement therapy being developed by Denali Therapeutics for the treatment of mucopolysaccharidosis type II (MPS II). Also known as Hunter syndrome, MPS II is a rare X-linked recessive lysosomal storage disease caused by a deficiency of the lysosomal enzyme iduronate-2-sulfatase resulting in accumulation of glycosaminoglycans, heparan sulphate and dermatan sulphate. Consisting of the iduronate-2-sulfatase enzyme fused to a transferrin receptor-binding Fc domain, tividenofusp alfa has been designed to enable distribution of exogenous iduronate-2-sulfatase into both the central nervous system and peripheral tissues. Based on a reduction in cerebrospinal fluid heparan sulphate levels in patients with MPS II treated with tividenofusp alfa in a phase I/II trial, in March 2026 tividenofusp alfa was approved in the USA, under accelerated approval, for the treatment of neurologic manifestations of MPS II when initiated in presymptomatic or symptomatic paediatric patients weighing ≥ 5 kg prior to advanced neurologic impairment. Continued approval for tividenofusp alfa may be contingent upon verification of clinical benefit in a confirmatory trial. Tividenofusp alfa has also been granted Priority Medicine designation by the European Medicines Agency. This article summarises the milestones in the development of tividenofusp alfa leading to this first approval for MPS II.