moss-agal

Moss-agal is a recombinant form of human **alpha-galactosidase A** produced in the moss (*Physcomitrella patens*) expression system, developed for **enzyme replacement therapy** in patients with **Fabry disease**. It features a highly homogeneous N-glycosylation profile with >90% mannose-terminated glycans and is notable for lacking plant-type glyco-forms, reducing immunogenic risk. Its tissue uptake is mediated by mannose receptor targeting—distinct from mammalian cell-produced alpha-galactosidase which utilizes mannose-6-phosphate receptor mediated endocytosis—allowing efficient targeting of renal, endothelial, and macrophage cells. Moss-agal demonstrates comparable efficacy to approved enzyme replacement therapies in reducing **globotriaosylceramide (Gb3)** and **lyso-Gb3** levels, with a short plasma half-life and rapid tissue uptake. Clinical studies have shown it is well tolerated in patients, with promising reduction in Gb3 excretion and no serious safety concerns in Phase 1 trials. This is the first moss-made clinical drug and represents a novel bioproduction modality[1][3][7].

Brand names

moss-aGal

Other names

moss aGalactosidasemoss alpha-galactosidasemoss-made alpha-galactosidaserecombinant human alpha-galactosidase A produced in moss